1 - ILO

m
51042
©
Vth International
Pneumoconiosis Conference
V Conferencia
Internacional de Neumoconiosis
Caracas - Venezuela
29 October to 3 November 1978
Organized by
Comité Nacional
de Neumoconiosis
International
Labour Office
Publisher: Wirtschaftsverlag NW, Verlag für neue Wissenschaft GmbH
Am Alten Hafen 113-115, D-2850 Bremerhaven 1
Impressum:
© 1985, International Labour Organization (ILO), Genf
Gesamtherstellung: Wirtschaftsverlag NW, Verlag für neue Wissenschaft GmbH,
Postfach 101110, D-2850 Bremerhaven 1, Tel. (04 71) 4 60 93-95
Printed in Germany 1985
ISBN 3-88314-264-9
Contents
page
Preface
Prefacio
9
1
"
SESSION I
1/1 J. A. Merchant
Coalworkers'pneumoconiosis surveillance in the United States
I/2 T. S. McLintock
The prevalence of pneumoconiosis in British coal miners, 1959-1977 . . .
I/3 G. Degueldre
Epidemiologie des pneumoconioses dans les charbonnages de la
campine belge
I/4 A. Minette
Peculiar aspects of the natural history of chronic bronchitis in
coal miners
I/5 M. Jacobsen
Dust exposure and pneumoconiosis at 10 British coal mines
13
37
51
63
89
SESSION II
11/1 M. Adrianza
Epidemiologia de la neumoconiosis en Venezuela
II/2 B. Méndez
An epidemiologic study of silicosis in Brazil, from a survey of patients in
tuberculosis hospitals
II/3 G. Cornea, A. Ghachem, A. Ben Kheder, Silvia Gabor, L. El Mekki
La silicose dans une mine de spathfluor de Tunisie
II/4 J. Prenafeta, G. Leyton M„ R. Sepulveda M.
Variability in the X-ray diagnosis of early silicosis
II/5 K. Chiyotani, Ken-ichi Saito
Excess lung cancer risk in silicotic cases under hospital care preliminary report
II/6 J. Prenafeta, A. Valenzuela, G. Leyton, S. Villagran
Epidemiological survey and prognostic evaluation in silicosis
111
161
163
177
179
181
SESSION III
III/1
B. Barhard
L' évaluation du risque coniotique sur les lieux du travail
185
Hl/2
III/3
IM/4
III/5
111/©
III/7
G. Cornea, A. Ghachem, A. Ben Kheder, M. Maalej, J. Daghfous,
H. Bou-Acha, L. El Mekki
La pneumoconiose dans une mine de fer de Tunisie: aspects
radio-cliniques et fonctionnes
199
C. E. Rossiter, J. C. Wagner
Man-made minerai fibres: Joint European medical research project . . . .209
D. F. Goldsmith, N. Stroup, J. F. Gamble, C. M. Shy
Chronic lung disease in the furniture industry: An epidemiologic study
design
219
M. L H. Flindt
Pulmonary disease due to proteolytic enzymes
237
S. M. Rab, Zakaullah Beg, Abu Zafar
Work-related diseases in Pakistan
249
C. Cornea, L. El Mekki, B. El Gharbi, A. Ben Kheder, Silvia Gabor
Une nouvelle pneumoconiose végétale: le poumon de Neffa
251
SESSION IV
IV/1
S. H. Zaidi
Recent progress in etiopathogenesis of pneumoconioses
IV/2 T. Sano, I. Ebihara
Considerations on pathology, pathogenesis and etiology of
pneumoconiosis
IV/3 L. Le Bouffant, H. Daniel, J. C. Martin
Nowite variable des poussières de silice selon leur origine: Influence
de certains minéraux d'accompagnement
IV/4 E. Quinot, C. Cavelier, M. O. Merceron
Chimie de surface et cytotoxicité de silice
IV/5 W. Weiler
New aspects in the etiopathogenesis of silicotic and anthracosilicotic
lesions
IV/6 H. Hayashi
Mineralogical analysis of lung dusts in pneumoconiosis with an analytical
electron miscroscope
267
303
313
327
345
355
SESSION V
V/1
V/2
V/3
M. Espinoza
Neumoconiosis en el Peru
369
G. Mowé, Egil Phus, B. Gylseth
Asbestos fibre content in lung tissue in relation to asbestos exposure and
causes of death
383
N. V. Vallyathan, J. E. Craighead
Silica dust-associated pulmonary lesions in granite workers lacking
radiologic evidence of disease
397
V/4 J. A. Dick
The role of pulmonary tuberculosis in the causation of progressive
massive fibrosis in coal workers in Great Britain
V/5 T. L Guidotti
The higher oxides of nitrogen: A role in altering pulmonary response
to injury
V/6 J. Rosmanith, R. Leonardt, D. Prajsnar, H. Breining, W. Ehm
The effect of the combined application of cadmium and lead sulfide and
coal dust on the development of lung fibrosis in rats
V77 D. Prajsnar, H. Breining, J. Rosmanith
Lung fibrosis in rats after lead sulfide application
V/8 H. Breining, J. Rosmanith, D. Prajsnar
Lung fibrosis in rats after cadmium sulfide application
409
423
435
447
455
SESSION VI
VI/1
Y. Hosoda, N. Saito, T. Kono, H. Ohtake, Y. Chiba
Epidemiology of asbestos-induced pleural thickening
465
VI/2
M. L. Newhouse
Asbestos-related diseases in relation to type of occupation
475
VI/3
Ruth Lilis, J. Selikoff
Asbestos disease in maintenance workers of the chemical industry
S. F. McCullagh
Biological effects of asbestos-the unresolved matters
W. Weiler
Biological effects of asbestos-quartz dust-mixtures
VI/4
VI/5
VI/6
. . . .479
501
511
L. M. Lacquet, L. Van der Linden, J. Lepoutre
Prevalence of lung changes, and mortality in a Belgian asbestos-cement
factory
A. Hirsch, L Di Menza, M. Mangold, J. Bignon
Rigidité diaphragmatique et exposition à l'amiante: correlation
radiologique et chirurgicale dans 47 thoracotomies
555
VI/8 J. M. C. Davis, R. E. Bolton
The pathological effects of asbestos cloud of different fibre dimensions
on the lungs of rats
571
VI/7
525
SESSION VII
VII/1
P. Sadoul, D. Teculescu
Epreuves fonctionnelles dans le diagnostic précoce et la réadaptation
des pneumoconioses
587
VII/2
L. Maldonado T, M. Martha Méndez, J. A. Legapsi V, A. Conzález Z.
The value of studying pulmonary function with a view to the early
diagnosis of silicosis
599
VII/3
K. Wilson, R. Richie, P. Stevens, B. Valley
Effect of chronic amorphous silica exposure on sequential pulmonary
function
609
VII/4
VII/5
P. García-Herreros, G. Scano, L. Stendarti, S. Degré, R. Sergysels,
A. de Coster L'adaptation cardiopulmonaire à l'effort chez les
mineurs de charbon
J. E. Diem, R. N. Jones, J. C. Gilson, H. Glindmeyer, H. Weill
The influence of asbestos exposure on radiographie progression and
functional decline: A preliminary report
615
625
SESSION Vili
VIII/1
VIII/2
VIM/3
VIII/4
VIII/5
VIM/6
VIM/7
VIII/8
VIM/9
W. T. Ulmer
Biological and functional tests in early diagnosis of pneumoconiosis and
rehabilitation
M. Adrianza, C. Ernould, Y. Sanchez
Pulmonary function of smoking workers esposed to inorganic dust . . . .
Richard R. Martin, J. J. Gautheir, C. Bernard
Exploration fonctionnelle dans le diagnostique précoce de l'asbestose . .
K.Nobutomo
Air pollution and cytological changes in sputum
M. L. H. Flindt
Identification of illness from allergenic dusts
T. Mattsson, Matti S, Huuskonen, A. Zitting
Correlation between radiographic and physiological
findings in asbestosis
T. Mattsson, P. L. Kalliomäki, O. Korhonen, V. Vaaranen
Lung contamination among workers exposed to dust with
an iron component
T. L. Guidotti
Arc welders pneumoconiosis: Studies with advanced techniques of
scanning electron microscopy and microprobe analysis
H. Shida, K. Chiyotani, Y. Saito
Application of the four-fold magnified selective alveolobronchography to
pneumoconiosis
641
653
661
691
693
705
719
733
747
SESSION IX
IX/1
K. Robock, U. Teichert
Techniques, strategies and results of dust measurements in the asbestos
industries
755
IX/2
P. H. Cooper, J. E. Day, C. A. Kennedy, H. C. Lewinsohn
Dust control in a conventional asbestos textile factory
775
IX/3 A.A.Cross
Progress in the control of asbestos dust in the work place
793
1X74 A.Gibbs
The environmetal data base for prevention studies in Quebec
807
IX/5 A.Schütz
Protection against quartz and asbestos dust exposures at workplaces
..815
IX/6 B. Carton, E. Kauffer, J. C. Vigneron, M. Villa
Comparaisons des différentes techniques de comptage des fibres
d'amiante
823
IX/7 A. Degoumois
Cas d'application de la convention de l'OIT (N° 139) sur le cancer
professionnel, 1974, en relation avec le flocage à l'amiante des structures
métalliques et des tuyauteries d'un immeuble en construction à Genève. . 833
SESSION X
X/1
D.Ascarrunz
Factores medio-ambientales y silicosis en Bolivia
X/2 V. V. Tkatchev
Two-stage gravimetric method of dust concentration measurement
and its application in ore mines
X/3 C.Amoudru
Problèmes méthodologiques actuels de la lutte contre les
pneumoconioses dans les charbonnages français
X/4 N. Wiles, F. Fairclough
The prevention and prevalence of pneumoconiosis in New South Wales
coalmining
X/5 V. S. Nikitin
Modern methods of dust control in open-pit mines in the Soviet Union.
839
851
865
871
. 885
SESSION XI
XI/1
A. Bulmer
Developments in dust control and dust suppression in mining,
tunnelling and quarrying, engineering control, organisational aspects,
medical prevention
XI/2 L. Le Bouffant, J. C. Martin, H. Daniel
Effet des aerosols de sels d'aluminium pour la prévention
et le traitement de la silicose
XI/3 M. L. H. Flindt
Prevention of illness due to allergenic dusts
897
911
929
**^«¿:f
XI/4 W. T. Ulmer
Coal workers'pneumoconiosis long-time treatment and its outcome
XI/5 D. Else, N. Caro
Problems associated with the use of half-mask respirators in dusty
environments of developing countries
. . . 939
949
Working Group No. 1
working Group No. 2
963
967
List of Participants
971
P R E F A C E
Vth International Pneumoconiosis Conference
Caracas, Venezuela, 29 October to 3 November 1978
The International Labour Office in co-operation with a number of
national institutions and agencies has conducted up to now a series of
International Pneumoconiosis Conferences. The first of these was presented
in Johannesburg in 1930, the others in Geneva (1938), Sydney (1950) and
Bucharest (1971). The fifth Conference on occupational lung diseases was
organised in 1978 in Caracas, Venezuela. Since then the Vlth International
Pneumoconiosis Conference was held in Bochum in 1983; the Vllth International
Pneumoconiosis Conference is in preparation.
The Vth International Pneumoconiosis Conference held in Caracas in 1978
was of high importance. Four hundred and sixty-three participants were
assembled. Among them 160 scientists, practitioners, physicians, government
officials, employers and workers representing 40 foreign countries. Seventytwo scientific papers were presented in twelve sessions. Three panel
discussions dealt with the subjects: Occupational risk due to exposure to
asbestos and methods of its prevention; Synergic effects of combined exposure
to dust and other occupational hazards at the workplace; How to improve the
conditions of man at .work. Two working groups were convened, dealing with
the revision of the international radiographic classification of pneumoconioses,
and with safe limits of exposure to mineral and vegetable dust in the working
environment, respectively. Moreover, parallel to the sittings of the Conference,
four postgraduate courses of 10 hours each were held on basic diagnosis of
pneumoconioses, on cardiopulmonary physiopathology, on safety and health
inspection and on dust monitoring.Two courses of 20 hours each were conducted
on industrial toxicology and on organisation of occupational health services
in enterprises. These courses were attended by 260 participants.
Unfortunately, due to a number of obstacles, it was not possible to publish
the proceedings of the Vth International Pneumoconiosis Conference immediately
after this event. In doing so now, we will not only fill the gap in the series
9
2.
of the published proceedings of all ILO International Pneumoconiosis
Conferences, but in particular will pay tribute to the science and
practice of occupational health. Important research results were
reported which would not reach the scientific community without publication.
Some of the observations and ideas expressed may be outdated, nevertheless
they remain valuable as documentation of steps in the history of
occupational medicine.
The papers have been reprinted in the original form without
editorial changes. Reports of the two working groups are included
in the publication.
The objective of publishing this material is to make it available
to scientists and the occupational health practice through libraries
of the ILO and scientific institutions. Moreover, copies can also
be ordered directly from the publisher.
We wish to express our thanks to the Organising Committee of
the Vth International Pneumoconiosis Conference, and in particular
to the President of the Confernece, Dr. Manuel Adrianza whose untiring
enthusiasm resulted in a most successful meeting.
Occupational lung diseases remain the major occupational health
problem to workers. This publication will help to stimulate worldwide
efforts for the prevention and the control of dust-related respiratory
diseases.
August 1985
International Labour Office
10
P R E F A C I O
V Conferencia Internacional de Heumoconiosla
Caracas, Venezuela; 29 octubre al 3 de noviembre de 1978
La Oficina Internacional del Trabajo en cooperación con varias
Agencias e Instituciones nacionales ha dirigido hasta ahora las
series relacionadas con las Conferencias Internacionales sobre
neumoconiosis. La primera de ellas celebrada en Johannesburgo en
1930, las otras en Ginebra (1938), Sidney (I95O) y Bucarest (197D.
La quinta Conferencia sobre enfermedades pulmonares del trabajo
fué organizada en 1978 en Caracas, Venezuela. La sexta Conferencia
Internacional de Neumoconiosis se realizó en Bochum en 1983. La
séptima se encuentra en preparación.
La quinta Conferencia Internacional de Neumoconiosis celebrada
en Caracas en 1978, fué de gran importancia: 463 participantes se
reunieron, entre ellos 16O científicos, practicantes, médicos,
representantes oficiales, empleadores y trabajadores de Uo países.
Setenta y dos trabajos científicos se presentaron en 12 sesiones.
Tres paneles de discusión se condujeron sobre los temas: los
riesgos del trabajo debidos a la exposición al asbesto y los métodos
para su prevención'; efectos sinérgicos de la exposición combinada
a polvos y a otros' riesgos en el sitio de trabajo; cómo incrementar las condiciones del hombre al trabajo. Dos grupos de trabajo
fueron formados para intervenir sobre la revisión de la Clasificación
Internacional de Radiografías de Neumoconiosis y con los limites
de exposición seguros a polvos minerales y vegetales en el ambiente
de trabajo respectivamente. Mas aún, paralelo a la realización
de la Conferencia, cuatro cursos de postgrado de 10 horas fueron
impartidos sobre las bases diagnósticas de la neumoconiosis, la
fisiopatologia cardiopulmonar, la inspección de la seguridad e
higiene y el monitoreo de los polvos. Dos cursos de 20 horas cada
uno se llevaron a cabo sobre toxicología industrial y sobre la
organización de los servicios de salud en las empresas, a estos
cursos asistieron 260 participantes.
11
2.
Desafortunadamente, por un gran nùmero de obstáculos no ha
sido posible la publicación de los trabajos de la V Conferencia
Internacional de Neumoconiosis inmediatamente después del evento.
Por ahora, no quisiéramos dejar incompleta la publicación de los
artículos de esta serie de las Conferencias Internacionales de
la OIT sobre Neumoconiosis, en particular quisiéramos pagar un
tributo a la ciencia y a la práctica de la salud en el trabajo.
Fueron reportados resultados importantes de investigaciones
que no quisiéramos dejarlos sin publicar para la Comunidad Científica. Algunas de las observaciones e ideas que se expresaron
posiblemente no sean vigentes, sin embargo harían falta como una
documentación valiosa sobre las etapas que ha tenido la historia
de la Medicina del Trabajo.
Los trabajos han sido reimpresos en su forma original, sin
cambios editoriales. Los reportes de los dos grupos de trabajo
han sido también incluidos en la publicación.
El objetivo de publicar este material es ponerlo a disposición
de los hombres de ciencia que practican la salud en el trabajo, a
través de las librerías de la Organización Internacional del Trabajo
y de las Instituciones Científicas. Copias aparte que se deseen,
pueden ser ordenadas directamente al editor.
Expresamos nuestro agradecimiento al Comité Organizador de
la V Conferencia Internacional de Neumoconiosis, en particular
a su Presidente Dr.Manuel Adrianza, quien por su inagotable entusiasmo hizo que los resultados de esta reunión fueran prósperos.
Las enfermedades pulmonares del trabajo, persisten como uno de los
mayores problemas de salud de los trabajadores. Esta publicación
ayudará a estimular en todo el mundo, los esfuerzos para prevenir
y controlar las enfermedades respiratorias ocasionadas por los
polvos.
Agosto de 1985
Oficina Internacional del Trabajo
12
I N D I C E
S E S S I O N
"I
J.A.merchant.
Coal Workors' Pneumoconiosis Surveillance in the United States
JfS.fflcL intock.
The Prevalence of Pneumoconiosis In British Coal Winers, 1959-1977
C.Dequeldre
Cpldemiologle des Pneumoconioses dang les charbonnages de la campin
belge.
A.minette
Peculiar aspects of the natural history of chronic bronchitis in
coal miners.
CI.Jacobson.
Dust Exposure and Pneumoconiosis at 10 british coal mines.
13
COAL WORKERS' PNEUMOCONIOSIS SURVEILLANCE
in the '
UNITED STATES
J. A. Merchant,
Division of Respiratory Disease Studies,
Appalachian Laboratory for Occupational Safety and Health,
National Institute for Occupational Safety and Health, USA
The Coal Mine Health and Safety Act of 1969 was landmark legislation which mandated, among many health and safety provisions, a res.
pirable coal mine dust standard of 2.0 mg/m , a vigorous mine inspection and enforcement program (Mine Enforcement and Safety Administration), coal mine safety and health research, and routine medical
examinations of underground coal miners in the United States.
Despite this legislative emphasis on mine safety, the latest available fatality rates per 1,000 full-time workers (1976) revealed a
job-related fatality rate of 0.49 for the mining industry group
as opposed to the agriculture, forestry, and fishing industry group
which had the second high job-related fatality rate of 0.28 (Figure
1).
In the area of dust control, great strides have been made
since 1969.
Table 1 reviews
Mining Safety and Health Administra-
tion (MSHA), formerly the Mine Enforcement and Safety Administration
(MESA), data which compares operator and MSHA mean respirable dust
levels from July-December of 1972 through January-June of 1978.
Although operator-generated dust levels tended to be somewhat
higher in earlier years, over the first half of 1978 there was
good agreement on a mean dust level of 0.5 mg/m . Dust control
has also been generally achieved in underground mines (Table 2)
15
where there has been steady Improvement since 1972 and good agreement between operator and MSHA samples with the
overall mean dust
level of 1.2 rag/m for the period January through June of 1978.
The ability of the U.S. coal mining industry to maintain the re*
latlvely good dust control mandated by the Act is attributable to
major Improvements in mine ventilation, predominant use of room
and pillar mining techniquesf and the lack of significant use of
diesel powered equipment in underground coal mines. Although a
mean respirable dust level 1.2 mg/m
Is well under the standard
of 2.0 mg/m , not all sections of all mines meet a 2.0 mg/m
standard.
This is particularly true for long-wall operations.
In Table 3, data from a 1969 MSHA survey of 28 mines is compared
to all MSHA data collected for the years 1973, 1976 and 1977.
The improvement in dust control from 1968-69 is clear.
This data,
however, points out marginal dust control for jacksetters and longwall operations.
An important provision of the Federal Coal Mine Health and
Safety Act of 1969, and which was reiterated in the Federal Mine
Safety and Health Act of 1977, was for medical examinations of
underground coal miners. As reviewed in Table 4, the Act calls
upon NIOSH to administer this health surveillance program, for
coal mine
operators to pay for these examinations, for the re-
sults of these medical examinations to be
submitted to the De-
partment of Labor (MSHA), which In turn notifies the miner of any
rights and benefits which may include transfer without loss of
pay to a less dusty area of the mine (under 1 mg/m ) should the
miner's chest radiograph show evidence of coal workers' pneumoconiosis.
In order to administer this program, NIOSH through
16
its Appalachian Laboratory for Occupational Safety and Health
(ALOSH) has certified a large number of coal mine operator
examination plans and examination facilities throughout the
coal fields of the United States (Table 5).
It is the responsi-
bility of the coal mine operator to arrange for
periodic exami-
nations (no less than every five years and more frequently for
new miners) of his miners through development of a Mine Operator
Plan, approved by ALOSH, for examinations at a conveniently located
facility.
In order to qualify, the facility must be able to pro-
vide satisfactory radiographic equipment, technicians and physicians all meeting minimum qualifications set forth under regulations for administration of this program (42 Code of Federal Regulations, Part 37). The medical examination currently consists
of a brief occupational history questionnaire and a posteroanterior chest radiograph.
The radiograph is initially interpre-
ted using the ILO U/C 1971 classification*' ' by a physician who
may be either an "A" reader or "B" reader.
"A" readers are those
so designated because they have attended a training course on the
radiographic interpretation of the pneumoconioses provided by the
American College of Radiology under contract with NIOSH, or by
correctly classifying six radiographs of pneumoconiosis of their
own choosing.
The film is then sent to ALOSH for processing and
re-reading by a "B" reader, so designated because he or she has
passed a proficiency examination on radiographic interpretation of
the pneumoconioses developed by John Hopkins University.
If the
initial reader and "B" reader agree within a minor category (ILO
U/C 1971 classification), the film is classified by the "B" read-
17
ing and the miner provided this information plus information on
rights and benefits through the Department of Labor.
Should the
first two readings not agree, a further "B" reading is obtained.
Ultimately, the film may be sent to a panel of readers for resolution of differences in interpretation.
Results are now available for two rounds of this programs
Round One from August 18, 1970 to July 27, 1973, and Round Two
from July 27, 1973 to July 28, 1978. Table 6 summarizes the
prevalence of coal workers' pneumoconiosis (CWP) by region.
Although it has not been possible to determine the'exact proportion of underground miners participating in each round, it is
thought to be close to sixty per cent for each round.
Therefore,
the increased number of miners examined in round two is largely
a reflection of new miners coming into the industry since the
beginning of Round Two.
There is an apparent trend toward a
lower prevalence of CWP in western states as compared to the Midwest and especially Appalachia in both rounds. There is also an
apparent reduction in CWP prevalence (10% to 6%) between Round
One and Round Two. However, when one examines the distribution
of miners in each Round by years underground (Table 7), there
has clearly been a major shift in the
miner population and thus
accumulated underground dust exposure between rounds.
The avail-
ability of federally funded compensation for lung impairment
for coal miners, also a provision of the Federal Mine Health
and Safety Act of 1969, may well be a contributing factor in
explaining the lower number and proportion of men with greater
than ten years underground.
The explanation for the increase
18
tn new miners is largely attributable to the "energy crisis" of
1973 and the renewed emphasis on coal production In the United
States.
When CWP prevalence by duration of underground exposure specific rates are compared (Tables 8-10), there is no convincing
trend toward less CWP from Round One to Round Two.
Pneumoconiosis
observed among those with less than one year underground exposure
is thought to be
largely attributable to previous exposure to
pneumoconiosis producing dusts.
CWP prevalence among those ex-
posed underground from one to ten years is similar (Table 9), but
somewhat Increased in Round Two among those exposed for more than
ten years (Table 10).
Examination of Table 10 reveals that near-
ly all of the increase in prevalence occurs In radiographic
Category 1, while the prevalence of progressive massive fibrosis
(PMF) is reduced by half.
It is thought that some of the
increase
In CWP prevalence in Round Two is attributable to a change In
radiographic reading schemes (UlCC/Clncinnati 1968 In Round One
and ILO U/C 1971 In Round Two).
tations on the
Table 11 examines the interpre-
26,374 miners common to both rounds of examinations.
The expected variation in interpretation as well as evidence of a
higher prevalence of Category 1 CWP in Round Two is observed tn
these figures.
Further examination of the prevalence of CWP by
years underground in Round Two reveals a strong association between years underground and prevalence of CWP (Table 12).
This
data also reveals that nearly all Category 3 CWP and PMF occurs
among miners exposed underground for twenty years or longer, a
reflection of conditions preceding improved dust control.
19
Another element of health surveillance of coal miners is
periodic review of their mortality experience.
Recently a large
cohort (n= 22,998) of coal miners was studied by Rockette et al
(3)
v
under contract with NIOSH
. Major causes of death are review-
ed in Table 13. Although all causes of death did not differ from
the white male U.S. mortality experience, it is higher than rates
quoted for healthy working populations.
A number of respiratory
causes of death were found to be significantly increased - influenza,
emphysema, asthma, and tuberculosis.
Similarly, accidents, ill-
defined causes and all other causes were significantly increased
while a number of chronic disease categories revealed apparent
decreases-major cardiovascular diseases, diabetes mellitus, peptic
ulcer, and cirrhosis of the liver.
Although the standard mortality
ratio (SMR) for all neoplasms was not significantly different from
the standard population (Table 13), there were some individual
cause specific neoplasms which did increase (Table 14), most
notably stomach cancer and a modest but significant increase in
neoplasms of respiratory organs and lungs. Although an increase
in SMR's for stomach cancer among underground coal miners has
been found in several previously published reports,
' ' ' pre-
vious studies in regard to lung cancer are conflicting^ '
'.
The following conclusions are drawn from the data presented:
1.
By the most recent available figures, mining remains the
most hazardous major industry in regard to job-related
fatalities in the United States.
2.
Marked improvement in the control of respirable coal mine
dust has been achieved by the coal mining industry since
2o
passage of the Federal Coal Mine Health and Safety Act
of 1969.
Apparent declines In the prevalence of CWP are accounted
for by shifts in the mining work force toward miners with
fewer years underground.
No trend toward less CWP since dust control is yet
apparent after two rounds of examinations.
Recent mortality figures show continued excess mortality
non-malignant respiratory diseases and accidents, but
also excesses in lung cancer and particularly stomach
cancer which deserve further inquiry.
Job—Relatad Fatalities Due To Injurie» and Illnesses By Industry Group*
0.08
Private Sector
H H | 0.49
Agriculture, Forestry,
Fishing
0.28
0.25
Transportation,
Public Utilities
Manufacturing
0.19
pjffjj 0.06
0.05
Services
Wholesale and Retail
Trade
1
Finance, Insurance,
Real [state
!»
0.04
Fatoßty rates pe r 1.000
full—time works rs for 1976,
01
Bur•au ot labor Statistics.
21
TABLE 1
COMPARISON - OPERATOR AND MSHA SAMPLES
SURFACE (MG/M*)
OPERATOR
MUÍA
SÁMELES.
AYEBAfiE.
SÁMELES.
AYEBAGE.
1972
62,543
1973
75,527
1974
75,571
1975
95,679
1976
106,527
1977
93,564
0.7
0.5
0.5
0.5
0.7
0.4
12,749
0.5
1.2
1.1
0.8
0.7
0.5
48,018
0.5
5,214
0.5
JUL.-DEC.
3,927
2,265
2,258
2,946
5,701
JAN.-JUNE
1978
SOURCE:
MINING SAFETY S HEALTH ADMINISTRATION, 1978
22
TABLE 2
COMPARISON - OPERATOR AND MSHA SAMPLES UNDERGROUND (MG/M*)
OPERATOR
SÁMELES;A^EBASE.
MSHA
Í&EBASE.
SAMELEI
JULY-DEC
25,556
301,488
1.6
1.2
1.2
1.2
1.3
1.0
11,357
1.5
1.9
1.8
1.5
1.2
1.1
125,701
1.2
4,924
1.2
1972
187,618
1973
346,538
1971
317,872
1975
384,905
1976
395,432
1977
9,347
10,457
9,939
14,245
JAN-JUNE
1978
SOURCE:
MINING SAFETY & HEALTH ADMINISTRATION, 1978
23
TABLE 3
HIGH Ri!
1968-1969
1973
1976
1977
JACKSETTER
H.2
LONGWALL
2.6
2.1
2.1
1.8
2.7
1.9
1.8
1.3
1.1
1.2
1.2
1.9
2.2
1.3
1.2
1.1
1.3
CONTINUOUS MINER OPERATOR
ROOFBOLTER
CUTTER OPERATOR
LOADER OPERATOR
SOURCE:
6.5
3.9
5.9
6,0
MINING SAFETY & HEALTH ADMINISTRATION,
24
1978
TABLE 1
PROVISIONS OF THE
FEDERAL MINE SAFETY AND HEALTH ACT OF 1977
(1)
NIOSH ADMINISTER A COAL MINER HEALTH SURVEILLANCE
PROGRAM
(2)
COAL OPERATIONS PAY FOR
(3)
RESULTS OF EXAMS SUBMITTED TO DEPARTMENT OF LABOR
(4)
DEPARTMENT OF LABOR NOTIFY MINER OF RIGHTS AND BENEFITS
(5)
TRANSFER RIGHTS AND RATE RETENTION
EXAMINATIONS
25
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26
TABLE 6
PREVALENCE OF CWP B Y REGION
REGION
N
ROUND ONE
'%
MIDWEST
7,539
WEST
1,827
14
8
5
71,008
10
APPALACHIA
TOTAL
61,661
ROUND TWO
N
%
93,723
6
14,824
5
5,619
2
111,166
TABLE 7
DISTRIBUTION OF MINERS BY YEARS MINING
YEARS MINING
ROUND 1
N
ROUND 2
%
N
%
15,853 22.2
52,809 46.3
1 - 10
21,637 30.3
39,871 34.9
>10
34,023 47.5
21,486 18.8
<1
TOTALS
71,513
114,166
27
TABLE 8
CWP BY ROUND
<1
YEAR MINING EXPOSURE
RADIOGRAPHIC
CATEGORY
ROUND
ONE
ROUND
TWO
%
N
N
X
99.9
0.1.
0
1
2
3
PMF
15,755
99.3
52,772
79
15
0
4
0.5
0.1
31
2
0
1
TOTALS
15,853
0.6
-
52,809
28
-
0.1
TABLE 9
CWP BY ROUND
1-10
YEARS MINING EXPOSURE
RADIOGRAPHIC
CATEGORY
ROUND
ROUND
ONE
TWO
0
N
21,255
Z
98.2
N
39,171
Z_
98.2
1
340
1.6
638
1.6
2
35
0.2
37
0.1
3
2
-
2
5
-
23
0.1
39,871
1.8
PMF
TOTALS
21,637
1.8
29
TABLE 10
CWP BY ROUND
>10
YEARS MINING EXPOSURE
RADIOGRAPHIC
CATEGORY
N
26,574
4,716
1,857
TOTALS
ROUND
ROUND
ONE
TWO
Z
%
N
78.1
13.9
143
733
5.5
0.4
2.2
34,023
21.9
3o
15,626
4,473
1,043
72.7
20.8
114
230
4.9
0.5
1.1
21,486
27.3
CSI
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TABLE 12
ROUND TWO RADIOGRAPHIC CATEGORY
ÜfífÍG
O
N
1
m
%
N
2
3
m
PMF
%
N
%
N
%
N
-
19
%
3-9
90,520 99.3 585
0.6
35
-
-
10-19
7,316 87.1 973
11.6
83
1.0
4
0.1 22
0.3
20-29
5,192 72.2 1635
21.5 387
5.1
26
0.3 69
0.9
30-39
3,336 62.0 1167
27.3 428
8.0
61
1.2 88
1.6
905 56.0 485
30.2 149
9.2
20
1.2 56
3.5
107,569 94.2 5145
4.5 1082
0.9 116
0.1 254
0.2
40+
TOTAL
32
TABLE 13
STANDARD MORTALITY RATIOS FOR COAL MINERS
FOR SELECTED CAUSES OF DEATH
(N - 22,998)
SJÜR
CAUSE OF DEATH
101.6
ALL CAUSES
97.7
ALL MALIGNANT NEOPLASMS
95.2*
189.6*
MAJOR CARDIOVASCULAR DISEASES
INFLUENZA
ASTHMA
M3.7*
171.9*
TUBERCULOSIS
M5.5*
EMPHYSEMA
DIABETES MELLITUS
58.1*
PEPTIC ULCER
71.6*
CIRRHOSIS OF LIVER
61.0*
ACCIDENTS
1M.2*
ILL-DEFINED CAUSES
187.9*
ALL OTHER CAUSES
136.0*
*P¿.05
SOURCE:
ROCKETTE (3)
33
TABLE.14
STANDARDIZED MORTALITY RATIOS FOR COAL MINERS
WITH SELECTED NEOPLASMS
CAUSE OF DEATH
SUR
BUCCAL CAVITY AND PHARYNX
83.6
DIGESTIVE ORGANS AND PERITONEUM
97.8
138.2*
STOMACH
COLON
69.9*
OTHER DIGESTIVE CANCERS
96.4*
112.4*
RESPIRATORY ORGANS
113.7*
LUNG
OTHER RESPIRATORY CANCERS
93.7
82.6*
GENITAL ORGANS
*pé.05
SOURCE:
ROCKETTE (3)
34
REFERENCES
1.
ILO U/C International Classification of Radiographs of Pneumoconiosis.
Occup. Saf. Health Serv.(rev. 2 2 ) , International Labour Office,
Geneva, 1972.
2.
Morgan, R.H.: Decision processes and observer error in the diagnosis
of pneumoconiosis by chest roentgenography. Am. J. Roent., Rad.
Ther. & Nuc. Med.
3.
Rockette, H. : Mortality among coal miners covered by the UMWA
Health and Retirement Funds. DHEW (NIOSH) Publication No. 77-155,
1977.
4.
Stocks, P.: On the death rates from cancer of the stomach and
respiratory diseases in 1949-53 among coal miners and other male
residents in counties of England and Wales, 1962, Brit. J. Cancer,
16, 592-598.
5.
Enterline, P.E.: Mortality rates among coal miners, May, 1964,
Amer. J. Pub. Health, _54, 758768.
6.
Liddell, F.D.K.: Mortality of British Coal Miners in 1961,
1973, Brit. J. Ind. Med., .30, 1-14.
7.
Costello, et al: Mortality from Lung Cancer in U. S. Coal Miners,
Mar., 1974, Amer. J. Pub. Health, £ 4 , 222-4.
35
vip.ilancia de la neumoconiosis do los
mineros
del carbón en Estados Unidos
Informe introductorio por
A. Merchant, Estados Unidos
La Ley de 1969 sobre seguridad e higiene en las minas de
carbón establecía, entre otras muchas disposiciones en materia
de seguridad e higiene, que en Estados Unidos los mineros del
carbón fueran sometidos a exámenes médicos.
Esta ley fijaba
asimismo el nivel de las concentraciones respirables de polvillo
o
de carbón en 2 mg/m . Desde la entrada en vigor de esta legislación el Instituto Nacional de Seguridad e Higiene en el Trabajo,
a través de su Laboratorio de los Apalaches, ha llevado a término un programa de exámenes y de vigilancia radiográfica para
los mineros del carbón.
La organización del programa de exámenes y los métodos y
procedimientos para interpretar las radiografías serán objeto
de debate. Actualmente se han concluido dos series completas
de exámenes, con un total de más de 157000. Los resultados de
estas dos series se examinarán junto con datos sobre concentraciones de polvo de carbón reunidos y facilitados por la Administración de la Seguridad e Higiene en las Minas del Ministerio de Trabajo de Estados Unidos. Las repercusiones de estos
resultados en lo que atañe al control y prevención de la neumoconiosis de los mineros del carbón en Estados Unidos serán
objeto de debate.
36
il»
THE PREVALENCE OF PNEUMOCONIOSIS IN BRITISH COAL MINERS,
1959 - 1977
J. S. McLintock
National Coal Board, United Kingdom
Introduction
There are a number of geographically discrete coal-fields
in Great Britain (Fig.l) with distinctly different types of coal
and, it would appear, different risks of pneumoconiosis. When
the British coal-mining industry was nationalised in 1947, there
were approximately 750,000 miners.
It was recognised that there
was a major pneumoconiosis problem in the South Wales coal-field
but prevalence elsewhere was virtually unknown.
The few years after 1947 were devoted to the reconstruction
of the industry.
were
In the field of pneumoconiosis, dust standards
introduced! dust control began, research to establish appro-
priate dust standards was planned and investigations to measure the
pneumoconiosis problem in the
various coal-fields were started.
Because of the geographical spread of collieries which on
average employed about 1,000 miners - some coal-fields extended
over 150 to 200 kilometres - it was desirable to base any periodic
chest X-ray examination on mobile X-ray units.
Investigations,
comparing 70 mm miniature X-ray films with full-size, had shown
the former to be inadequate for the accurate diagnosis of pneumoconiosis.
At this time, some 25 years ago, there was very limited
experience of the operation of mobile X-ray units using large film
techniques.
Planning therefore occupied much of the 1950s, but
by the end of that decade a fleet of mobile X-ray units had been
built, staff recruited and trained and record systems devised.
37
THE COALFIELDS OF GREAT BRITAIN
LOCATION OF THE MAIN CLASSES OF COAL
KM m nu
3«
ftiMMM to Ww Nwtontf Ca* tOMl Hotel H
K.SWI —Mar Iff*
By 1959 a scheme offering a full-size chest X-ray to all miners
on a regular basis was fully operational.
Mobile units visited
each colliery in turn and examination was on a voluntary and confidential basis.
Because dust control measures had considerably reduced the
airborne dust levels in British mines, the radiographic appearances
of pneumoconiosis were slow to change and it was considered appropriate to set the interval between colliery visits at 5 years.
(By this time pulmonary tuberculosis was being brought under
control and the need for frequent X-ray surveys of the
population was beginning to disappear).
general
The objectives of this
Periodic Chest X-ray Scheme (P.X.R.) were«(a) To offer each mine worker the safeguard of a regular chest Xray, and
(b) To use the epidemiological data collected to assess the
efficacy of the dust control programme.
PREVALENCE - 1959
-
1963
This first round of surveys demonstrated the prevalence
of pneumoconiosis in the various coal-fields.
39
(Fig.2.)
fofi-2.
Prevalence of pneumoconiosis in British coal—fields,
1959 - 1963.
Key
.Coal-field
No. of men
.X-rayed
SCOTTISH
53,849
NORTHERN (N&C)
27,458
URHAM
YORKSHIRE
D
Prevalence
Cats. 2 & 3
^
w
m?%
101,001
32,587
EAST MIDLANDS
80,087
WEST MIDLANDS
34,551
SOUTH WESTERN
6o,286
SOOTH EASTERN
3,875
GREAT BRITAIN
462,999
P.M.P.
^
69,305
NORTH WESTERN
Cat. 1
mtm
m
^
mmi
^
0*
^
T
'%
'IO*
T
\%
Per cent of men X-rayed
»0
20fr
These coal-fields were using the same techniques and equipment; the men were virtually all British (a few Poles and even
fewer Hungarians had entered the industry, but the labour force
was almost 100% British) with much the same age structure in the
various mining areas.
Yet the difference in prevalence is marked
with South Wales highest and Scotland and Northumberland lowest.
The coals of South Wales are in general anthracite and high quality bituminous, while in Scotland and Northumberland they are of
distinctly lower quality.
It is therefore not to be expected that every country will
experience the same pneumoconiosis risk.
Much will depend on the
type of coal mined in addition to dust control measures adopted.
PREVALENCE 1959 - 1977
Between 1959 and 1977 four rounds of surveys have been
completed and the overall prevalence on each occasion is shown
in Fig. 3.
41
Fig.3.
Prevalence of pneumoconiosis in British miners 1959-1977«
1$
^
=. P.M.P.
////X/
= Cats. 2 & 3.
¥&M
= Cat.
1.
1964-68
1969-73
10$
TOTAL
PREVALENCE
1974-77
ss/ss
s
%
¿
536
o?S
42
Not only has the overall prevalence improved but the prevalence
in each age group shows a very satisfactory trend.
Figure 4, which illustrates this, is based on data from 219
collieries which were surveyed in each of the four rounds.
Pig. 4.
Prevalence of pneumoconiosis by age-group at 319 collieries surveyed in
305S _
1959-63, 1964-68, 1969-73 and in 1974-77.
1959-63
1964-68
1969-73
203Í -
1974-77
IO56 _
15-24
25-34
43
35-44
45-54
55-64
PROGRESSION 1964 - 77
In Britain, miners with pneumoconiosis are given a state
pension but are permitted to remain in the coal-mining industry
if they so wish.
Most choose so to do; naturally they are offer-
ed employment in particularly low dust conditions.
Nevertheless, it is possible that the changes in prevalence
shown above could be due to the selective departure of men with
pneumoconiosis. Various checks have failed to demonstrate such
an effect, but it was considered desirable to develop a further
indicator of change. This was done for each colliery by taking
two successive X-rays of all men working on the coal-face at
the time of the first of the two surveys and who remained at
that mine throughout the interval between the surveys. These
radiographs are categorised in the elaboration of the ILO
classification by at least two doctors specialising in this work.
(The elaboration was originally developed within the National
Coal Board specifically for this purpose.) The results are
expressed as the number of additional steps recorded in the
elaborated scale for 100 men in the sample.
Obviously, as only one chest radiograph was available in the
first round of surveys, it was not until the second
round of
surveys started in 1964 that the progression index for each
colliery could be determined.
Figure 5 shows the progression indices year by year from
1964 to 1977.
44
^
^
^
^
^
I-1
^
\
O
\ 0 B!
í
o
H
X\\\\\\\\\\\\\\\N
, \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ ' ^
x\\\\\\\\\^
X
\ \ \ \
\ \ \^
\\W\M
"q
xw^
^5
8
CHANGES IN PREVALENCE AND PROGRESSION
During the late 1950s and 1960s, oil became a major fuel In
Western Europe.
Çoal mining industries began to contract and in
Britain the number of miners decreased from some 750,000 to
approximately 250,000. However this reduction did not occur
because of the departure of older men especially those with
pneumoconiosis! rather it was the younger men who left the industry.
Thus the change in manpower was not calculated to have
any significant effect on prevalence.
However especially in the 1950s and 1960s major technical
changes were taking place.
In the first decade the long-wall
coal face was established as the principal method of coal-getting
in Britain and at the same time great improvements were made in
ventilation.
During the 1960s, mechanised methods of extracting,
loading and transporting coal were developed intensively.
These
new techniques in mechanisation presented new problems in dust
control and it took some time for our engineers to find solutions.
Thus, between 1959 and 1963 the prevalence of pneumoconiosis
in the various coal-fields was established.
When the results
from the second round of surveys became available between 1964
and 1968, a clear improvement in prevalence and progression could
be seen, but in the third round from 1969 to 1973 this improvement slowed down and at one stage appeared to be halted.
However in 1970 new gravimetric dust standards were introduced and a renewed drive on dust control began.
The results
began to appear in improved prevalence and progression data in
1973, and the results from the 1874-77 round of surveys are
46
very encouraging in all coal-fields.
CONSISTENCY OF DATA
The diagnosis and categorisation of pneumoconiosis on a chest
radiograph is to some extent a subjective judgement.
All subject-
ive judgements are liable to vary from person to person, and from
time to time in the same person.
This is certainly true in the
field of pneumoconiosis and in endeavouring to minimise this effect
within the Periodic Chest X-ray Scheme, particular attention is paid
toi
(a)
the consistency of X-ray film q u a l i t y .
(b) the consistency of radiological diagnosis.
We are fortunate in that the mobile X-ray units which provide
this service operate from only six centralised bases in the various
coal-fields.
The 15 radiographers who take the chest radiographs
and the 7 radiologists who interpret them, are engaged full-time
in this work and can therefore concentrate particularly on consistency of film quality and of diagnosis.
A code of practice is in force involving frequent checks on
generator output, film speed, cassettes and film screens, processing
chemicals and temperatures and archival permanence of the processed
film.
But more importantly a large sample (of
the order of 30%)
of radiographs from each X-ray base are examined for quality by
at least two radiologists from another base who of course report
their comments back.
In addition regular meetings are held of
radiographers and of radiologists to ensure that there is general
agreement on film quality and that all possible steps are taken to
maintain a consistently high level. Similarly the 7 radiologists
ft7
meet several times per year and in discussion concert their
diagnostic standards.
carried out regularly.
In addition several formal tests are
In one, each radiologist is required to
interpret 350 radiographs, 100 of which had been included in the
previous year's test and 250 of which are included for the first
time.
Figure 6 demonstrates the consistency of performance.
CONCLUSION
Dust control is rapidly reducing the pneumoconiosis problem
in British coal-mines, but to ensure that the results of radiographic surveys can be compared over the years.it is essential
that consistency of film quality and of diagnostic standards
be maintained, and formal systems to ensure such consistency
have been introduced.
*8
? s s? sr ? s ?
Ö
o
td ¡»
P
co
s
o
i
s
»9
E/2
PNEUMOCONIOSIS IN BRITISH COALHINERS, 1959-77
T.S. MoLintock (united Kingdom)
In 1959 a Periodic X-ray écheme was introduced for B r i t i s h miners.
Since then motile X-ray u n i t s , using large film teohniquea t have v i s i t e d
every c o l l i e r y on a regular basis» Almost 92 per cent of miners, both
surface and underground, have come forward for examination on a voluntary
b a s i s . In the f i r s t s e r i e s of surveys over 460,000 chest X-rays were
taken; because of the contraction of the coalmining industry in B r i t a i n
during the 1960s and e a r l y 1970s, the number had f a l l e n t o 200,000 i n
the most recent round.
This paper desoribes the prevalence of pneumoconiosis i n the various
c o a l f i e l d s of B r i t a i n and the changes «hieb have taken place over the years
as dust control becomes more e f f e c t i v e .
To ensure the comparability of the survey r e s u l t s over the y e a r s ,
emphasis has been l a i d on (a) the maintenance of high q u a l i t y of X-ray
films and (b) the consistency of interpretation- by the r a d i o l o g i s t s concerned. Both the systems developed are s e t out.
50
1/3
EPIDEMIOLOGIE DES PNEUMOCONIOSES DANS LES
CHARBONNAGES DE LA CAMPINE BELGE
G. Degueldre
I 'ìnsiti tut
d ' H v o i p n o rios f i n p s , M a s s a i t ,
Pe)ni nue.
INTRODUCTION
Le Bassin de Campine, situé dans le Nord de la Belgique,
exploite sous 500-600 m de morts terrains aquifères, un gisement de charbon industriel (essentiellement charbon à coke) comprenant surtout de6 couches du Westphalien A supérieur et du
Westphalien B inférieur, dont l'ouverture moyenne rarement l,50n.
La production du Bassin est de l'ordre de 7 millions de
tonnes nettes par an, réalisée dans des tailles chassantes en
piateures d'une longueur de 200 m environ.
Malgré leur faible puissance et leur profondeur (atteignant
parfois 1000 m), certains chantiers complètement mécanisés produisent de 1500 à 2000 tonnes nettes par jour, le rapport net/
brut ou propreté gravimêtrique moyenne des veines étant de 75 %.
Le débit d'air moyen par taille est généralement compris entre ROO et 900 vr d'air par minute.
A.
METHODES DE PRELEVEMENT ET D'ANALYSE DES POUSSIERES
1. La réglementation minière belge, toujours en vigueur,
a été imposée en 1965; elle a introduit le prélèvement pondéral c'est-à-dire que les résultats de la mesure sont ex»
primés en mg de poussières par nr d'air (mg/cr).
51
Etant donné le fait qu'à cette époque, on ne trouvait
pas sur le marché des appareils sélectifs fiables, autonomes
et d'emploi commode, les autorités minières ont adopté le
principe du prélèvement gravimêtrique total ou "gravimétrie
globale", la prise d'échantillon consistant à capter toutes
les particules en suspension dans l'air, (prélèvement quasi
isocinêtique).
Cette façon de procéder, apparemment simpliste, a eu des
effets bénéfiques certains, car tout chantier mis en exploitation sans prévention était irrémédiablement catalogué comme
dangereux.
2.
Les chantiers d'exploitation et ateliers souterrains des mines de bouille sont classés en fonction de la concentration en
poussières de leur atmosphère (mg/nr) et en fonction également
de la teneur en cendres de ces poussières ( % en poids).
Cet aspect qualitatif de la poussière (c.à.d. teneur en
cendres ou en stériles) se justifie pour des mesures de routine.
Dans un gisement donné, il existe en effet une relation statistique simple qui permet de connaître, en moyenne, la teneur en
silice libre ou quartz, à partir de la teneur en cendres, pour
autant que cette dernière ait été déterminée suivant un mode
d'analyse bien défini.
Sans entrer dans les détails des modes opératoires prescrits pour l'emplacement, la durée, la fréquence des prélèvements,
l'examen et l'analyse des poussières, le classement des chantiers
ou des ateliers s'opère en se référant à certaines limites (classes
I, II, III, etc,). Les travaux ne peuvent d'ailleurs actuellement
52
Otre poursuivis normalement que dans les chantiers ou ateliers
classés I ou II, A titre d'information, sont classas I les
chantiers dans lesquels les concentrations en poussières globales de toutes granulomêtries sont inférieures à 25 mg/ra*
lorsque la teneur en cendres de toutes les particules en suspension dans l'air atteint une valeur de 30 à 35 %•
3Il va sans dire que depuis l'introduction de cette législation, d'autres techniques de prélèvement et d'examen ont
été et sont utilisées dans les mines belges, pour mesurer notamment les poussières "dites respirables", l'échantillonnage
se faisant en l'occurrence au moyen d'appareils sélectifs munis
d'un êlutriateur ou d'un prôséparateur (appareils CPM-TBF-MREMPG).
Une comparaison établie par l'Institut d'Hygiène des Mines dans les chantiers d'abattage campinole, montre que pour
des particules charbonneuses & - 30 % de cendres, une concentration gravimêtrique globale de poussières respirables captées
au CPM ou TBF et à 5 mg/m* de poussières reaplrablBB captées
au MRE. (Cette comparaison ne vaut que dans la mesure ou elle
tient compte de la granulometrie moyenne des particules qu'on
obtient dans l'état actuel de la prévention des poussières pendant l'abattage).
PREVENTION TECHNIQUE DES POUSSIERES - RESULTATS
1.
L'importance de la lutte contre les poussières apparaît
immédiatement lorsqu'on se rend compte que les concentrations
mesurées dans les chantiers è hautes performances, mais sans
prévention, peuvent dépasser de plus de 10 fois les valeurslimites proposées.
53
Les procédés visant à éliminer la poussière(qu'ils soient
appliqués directement aux points de formation ou utilisés pour
lutter contre les poussières sêdimentêes ou entraînées par le
courant d'air) permettent heureusement, grâce à une combination
judicieuse, d'atteindre des taux d'élimination de 90 % et plus,
par rapport a ce qu'on mesurerait sans lutter contre les poussières.
2.
Les moyens mis en oeuvre dans les charbonnages belges sont
décrits régulièrement (°); on peut ainsi suivre et comparer d'année en année, l'évolution de la situation à cet égard. En ce qui
concerne les chantiers d'abattage, les procédés classiques repris
dans ces statistiques sont:
l'injection ou infusion d'eau en
(° ° ) , l'arrosage des fronts, le
tion de piqueurs à pulvérisation
de taille,... (éventuellement machines
pulvérisateurs).
vaine sous toutes ses formes
havage humide, l'utilisad'eau dans les extrémités
de creusement pourvues de
( °) Annales des Mines de Belgique - Revue de l'Institut d'hygiène des Mines.
(°°) Une variante de l'infusion d'eau en veine, dénommée "prétôlê-inject^on" a été développée en Campine depuis 1963. Elle
consiste a imprégner d'eau un panneau avant sa mise en exploitation en opérant à distance par sondages profonds
creusés à partir de stations extérieures au panneau considéré. Elle est de ce fait complètement indépendante des
cycles d'abattage; elle est susceptible par ailleurs de modifier dans un sens favorable la dêsorption du méthane au
moment où se produit l'abattage.
54
En plus de la pulvérisation d'eau appliquée systématiquement sur les engins d'abattage et les transporteurs en taille,
plus de 80 % de la production sont actuellement traités par
ces procédés classiques de prévention (combinés ou non).
3.
Les valeurs médianes des concentrations gravimétriques en
poussières mesurées dans toutes les tailles en début ou en fin
d'année, sont également communiquées régulièrement dans les revues précitées.
Des études statistiques faites sur près de 1.500 prélèvements (effectués en 1976-77 on Campine) montrent que les valeurs
médianes obtenues conduisent à des valeurs moyennes de l'empoussiêrage de l'air qui ne diffèrent pas significativement des moyennes arithmétriques annuelles ni même des valeurs moyennes pondérées de l'empouesiérags dans toutes les tailles. C'est ainsi que
les concentrations globales médianes 12,5 et 12,0 mg/m , trouvées
fin 1976 et fin 1977, correspondent è des valeurs moyennes de
16,0 et l/f,6 mg/m3, alors que les moyennes arithmétiques annuelles
sont: 17,5 et 16,7 mg/m3, les empoussiérages moyens pondérés s'élevant à 16,74 et 16,^9 mg/m3,
C'est pourquoi nous considérons que la concentration médiane (en fin d'année par exemple) est un bon indicateur de l'empoussiérage des chantiers.
Notons que compte tenu de la granulometrie et de la nature
des poussières, les empoussiérages moyens pondérés exprimés ciavant en gravimetria globale, correspondent à:
^ 3 , 5 mg/m3
et ^4,5 mg/m
3
de poussières "respirables CPM ou TBP'
de poussières "respirable MRE".
55
k.
L'évolution des concentrations (globales) médianes constatée en Campine depuis la mise en application de l'actuelle législation, est caractérisée par les valeurs suivantes:
33mg/n3 en 1965
15,5 mg/m 3 en 1975
21 mg/m 3 en 1970
12,2 mg/m 3 en 1977 (fin.] )
alors que la meilleure estimation donne pour I960 un empoussiêrage global médian de l'ordre de Zf5 mg/nr.
A la fin de 1977, on trouve moins de ZZ,5mg/m3 de poussières dans R5 % des postee d'abattage, la moyenne pondérée (qui
tient compte de la durée de vie des chantiers) s'êtablissant à
16,5 mg/nr de poussières de toutes granulometries. (c.a.d.
<.3?5 mg/m3 de poussières respirables CPM).
C-.
RESULTATS MEDICAUX DE LA PREVENTION ET PERSPECTIVES
1.
L'incontestable amélioriation des conditions de travail
qui s'est produite en Campine depuis plus de 15 ans, grâce à
la prévention technique, se traduit par une nette diminution
des prevalences et incidences pneumoconiotiques.
En particulier, les prévalences des pneumoconioses de ty<nes
M2.(2/29)et 112 .... exprimée en % de l'effectif inscrit-fond
dans chacune des classes d'ancienneté montrent que par rapport
à la situation des années 1959/60, le risque de présenter actuellement une image radiologique HZ, M2 +• ... est considérablement
réduit.
En 1976, par rapport à la situation des années 1959/60,le ris-r
que était 18 fois moindre pour ceux qui avaient 10 ans de fond
10 fois moindre pour ceux qui avaient 15 ans de fond
6,if fois moindre pour ceux qui avaient 20 ans de fond
et 4,5 fois moindre pour ceux qui avaient 25 ans de fond.(fin.?>
56
En d'autre termes,
ouvriers ayant 25 ans de
siêrages élevés en début
radiologique invalidante
1959/60.
en 1976, on constatait que 9»5 % des
fond (et ayant donc connu des empousde carrière) présentaient une image
de type M2, M2+ ..., au lieu de 1,3 % en
En 1959/60, environ 33% des ouvriers ayant 20 ans de fond
présentaient aussi la même image radiologique. Depuis 197^, moins
de P, % des ouvriers de môme ancienneté (5 % en 1976) ont la môme
image radiologique, le taux d'incidence des pneumoconioses de type
M2 et M2 • ...étant inférieur â 0,50 % pour les ouvriers mineurs
ayant.de 20 à 25 ans de fond en Campine (en 1976).
2.
L'ETUDE DES COURBES EPIDEMIOLOOJQUES PRESENTE UN AUTRE INTERET
PLUS IMPORTANT ENCORE POUR ORIENTER LA LUTTE CONTRE LES POUSSIERES.
En effet, si on admet que la probabilité d'apparition d'une
pneumoconiose est une fonction cumulative d'une certaine fonction
de l'empoussiêrage, il est possible de trouver une relation qui
lie le nombre de sujets restés sains (après X années d'exercice
de la profession) au nombre de sujets inscrits l'année zéro de
référence. On peut en déduire une formule (dite formule de prévalence) dans laquelle intervient l'empoussiêrage "historique"
c'est-à-dire l'empoussiêrage dans lequel les ouvriers sains l'année zéro de référence, ont eu à travailler pendant x années. Moyennant certaines hypothèses qui sont acceptables si la décroissance de l'empoussiêrage est linéaire (ce qui est le cas), et à
condition d'admettre que les empoussiêrages médians mesurés pendant l'abattage donnent une "image valable" de l'empoussiêrage
de la mine, on peut calculer l'empoussiêrage qu'il aurait fallu,
en moyenne, ne pas dépasser pendant x années soit inférieure à
une valeur donnée (°)
(°) Ganier, M. Méthode pour la détermination d'un seuil
d'empoussiêrage - R.I.M.- Mine, décembre.
57
Il est ainsi possible de fixer "une limite d'exposition aux
poussières" qui n'est toutefois valable en toute rigueur
que dans un gissement similaire.
3-
Compte tenu des empoussiêrages obtenus en Campine et en se basant
sur les courbes êpidêmiologiques tracées à partir des résultats de
tous les examens médicaux effectués depuis 1959/1960, on en arrive
à la conclusion quii aurait fallu ne pas dépasser en moyenne la
médiane 13,75 mg/m^ pendant 30 ans (avant 1974) pour que le risque
de présenter une image radiologique de type M2, M2 *•... ne dépasse
pas 5 % après 30 ans de fond.
On trouve par ailleurs que les empoussiêrages médians
atteints en Campine en 1976-77 ne devraient pas provoquer, en
moyenne, plus de 2,5 % d'images radiologlque
M2 et M2 •• ...
après 25 ans de fond (au lieu des 43 % de 1959/60 et des 9,5 %
constatés encore en 1976).
Ces empoussiêrages gravimêtriques globaux, traduits en
"poussières respirables CPM" correspondent à une concentration
moyenne de l'ordre de 3,4 mg/nr lorsque 5 prélèvements sur 6
donnent une valeur inférieure à 4,4 mg/nr.(dans les conditions
propres au gisement campinois).
Une telle "limite d'exposition aux poussières" pour 25
années de service entraînerait un risque pneumoconiotique 17 à
18 fois moindre que celui enregistré en 1959/60. On est même
presque en droit d'affirmer que le risque de contracter une pneumoconiose de type 112, M2 + ... sera nul dans 20 à 25 ans pour ceux
qui, indemnes au départ, ont commencé leur métier de mineur en 1976.
58
CONCLUSION
L'étude des courbes épidémiologiques et la confrontation
de certaines données techniques prouvent que les progrès accomplis en matière de lutte contre les poussières sont réels et
que les procédés adoptés sont efficaces, d'autant plus, il est
vrai, que l'évolution sociale conduit à une diminution de la durée d'exposition par réduction du nombre de Journées travaillées.
Il est maintenant possible de garantir la santé des futurs
travailleurs après un nombre raisonnable d'années de service au
fond (20 à 25 ans au moins) si, à l'avenir les empoussiêrages
ne dépassent pas ceux qui ont été obtenus en moyenne ces deux
dernières années, dans les conditions particulières du Bassin
de Campine.
59
fio
Pneumoconioses de catégories M2 et M3 + •••
"•/"o Prévalence
-50^
1950/60
40
30
1969/70
20
1974
1976
10
j... "*' courbef
. « cible
(objectif)
10
15
20
25
30
Years of service undorgroundÀnnées de travail au fond
Pie. 1 - Courbes épidémiologiques - Mineurs de
°harb0n
du B a s s
^ de Campine (Belgique)
61
Epidemiología de la n^umoconiosis en las
explotaciones de carbon de Campine. Belgica
G. Degueldre (Belgica)
El presente trabajo, después de presentar algunos
datos acerca del yacimiento explotado, describe brevemente los métodos de extracción y análisis de polvo utilizados habitualmente.
Teniendo en cuenta la concentración, la naturaleza y
la granulometria de las partículas captadas, se especifica el significado de esas determinaciones de la cantidad
de polvo en el aire comparándolas con los valores obtenidos
por medio de los diversos aparatos gravimétricos selectivos
empleados en las minas de Europa Occidental.
^Se hace una clasificación de las explotaciones subterráneas según las prescripciones reglamentarias vigentes y se describe la evolución de la prevención técnica
siguiendo las variaciones de las concentraciones medidas
en los tajos durante las operaciones de arranque desde
hace unos quince años.
Se describe más adelante el estado sanitario del
personal» la prevalencia e incidencia de la neumoconiosis
se expresan en çorcentajes del personal que trabaja en
el interior según las diferentes clases de antigüedad.
En relación a la situación en los años 1959/1960, se
comprueba que el riesgo de presentar una imagen radiológica de tipo nu, Enu..., es actualmente alrededor de
20 por ciento menor para quienes tienen diez años de
trabajo en el interior y cerca de cinco veces menor para
quienes tienen 25 años de trabajo en el interior.
Las perspectivas son, pues, tranquilizantes para el
futuro denlos jóvenes que, indemnes al comienzo, comienzan o están por comenzar el oficio de mineros.
62
PECULIAR ASPECTS OF THE NATURAL HISTORY OF
CHRONIC BRONCHITIS IN COAL MINERS
A. MINETTE
Institut d'Hygiène des Mines,
Hasselt, Belgium
The epidemiologists usually base the definition of chronic
bronchitis on a clinical entity characterized by chronic cough
and phlegm production, for more than 3 months a year for at least
2 years (6). In fact many pneumologists have insisted for many
years in different countries that the clinical evolution of the
disease is characterized in a not negligible number of cases by
dyspnea complaints or a broncho-obstructive pattern from the very
beginning of its evolution (3) (17) (34). Recently Fletcher et al
(15) published the results of a long-term longitudinal epidemiological survey supporting these views.
In miner's bronchitis a high frequency of dyspnea complaints
was described by several authors (1) (21) (24) (37) (38) (41).
However, the functional mechanism which may support these complaints
do not clearly appear in many cases of simple pneumoconiosis (1)
(29) (39) (42). On the other hand, one might express some doubts
on the reliability of the finding of an excess of dyspnea complaints
when the attention of the patients can be focused on their symptoms
for particular reasons.
Some authors advocate that financial moti-
vations could have an influence on the prevalence of dyspnea on
account of compensation preocupations (8) (10). Moreover, purely
psychological circumstances, as for instance the fixation of the
miners' relatives on the disability in this occupation, could also
provide an explanation for at least a part of this excess (38).
63
Nevertheless, we found previously in a group of 1234 coal miners
hospitalized with bronchitis complaints a definite excess of
dyspnea, in comparison with patients with chronic cough and
phlegm without dusty antecedents, even in the
absence of pro-
gressive massive fibrosis and of compensation problems (26). In
Great Britain, Morgan et al, studying 29,984 coal miners, also
pointed out the high prevalence of dyspnea in a large sample of
this population (31).
Otherwise, the bad prognostic value of the dyspnea complaints
is well known in the literature (22), whereas the aetiology of
this symptom remains unclear and is obviously not univocal in
coal miners.
It seemed therefore of great interest to proceed to a careful examination of the prevalences and causes of chronic cough,
sputum and dyspnea, in the coal miners in our country.
In this
paper, we summarize the results obtained in a study performed
in the coal mining area of Belgian Limburg where large numbers of
coal miners and matched controls employed in other dusty and nondusty occupations were compared (29).
MATERIAL AND METHODS
Two transversal surveys were conducted by the same team at
the St. Barbara Institute of Lanaken at a few years' interval
(27) (28).
In the first survey 204 representative cases of a group of
247 coal miners selected by alphabetic order on the population
registers of the village of Lanaken were compared to 197 other
€A
workmen matched for age and economic status, and who were representative of the different professions exercised in this
residence (part A of Table I).
Since the yearly pollution level
was on the average low in the different parts of the village no
bias could be expected from that point of view when matching the
coal miners with their controls. The estimation of the pollution
was made by using an SF apparatus according to the rules edicted by
the CEC (7). For SO, we took as upper limit for the low pollution
3
3
50/ig/m , and as lower l i m i t for the high pollution 100jug/m •
3
3
For smoke those limits were 20/ig/m and 50/jg/m . These limits
are more severe than the index of Douglas-Waller (14).
In the second survey (part B of Table I) we examined 1,060
representative coal miners regularly at work at the coal face in
two collieries situated in areas with low and high degree of atmospheric pollution! 599 of them were at work in the first area
and 461 in the second.
In both mines results of periodic dust
counts at the coal face were at disposal (13). They did not
differ in that regard (29).
During the same period we examined
all the workmen of two steel works who were exposed to the
same
low and high levels of pollution as the coal miners. This study
involved 1,284 workmen at work in the five divisions of the steel
works located in the area with low pollution, and 1,218 men in 3
divisions of the steel works situated in the high pollution area.
The technical aspects and standardization of the methods used
for the surveys had been discussed in detail before in an extensive
monograph (29). All the surveys were performed by using the short
65
questionnaire (12) of the European Coal and Steel Community (ECSC),
completed by measurements of vital capacity (VC), of one-second
forced expiratory volume (FEV.), and by chest X-rays (35 cm x
35 cm) in every subject.
The spirometrie measurements were done
according to the criteria of the ECSCi 3 measurements were performed in each subject, the highest value being taken as the real
value¡ the calculations of the expected values were done according to. the ECSC prediction formula (25)t The chest X-rays were
performed according to the prescriptions of the ILO (4). In the
first survey we also carried out provocation tests with acetylcholine, according to a
standardized method involving the inhala-
tion of a constant dose of acetylcholine by every subject (9) (30).
The coal miners were matched with their controls for age and
tobacco use.
For the matching by age we used 5-year categories.
For the smoking habits we choose a classification in 4 groups when
comparisons of symptoms were made.
Indeed, in previous standard-
ization studies we found that such a classification gives more
reproducible results than a ranking according to the number of
pack-years (29). Category I comprised all the non-smoking subjects.
They had either never smoked or only very occasionally but without
inhaling the smoke; in fact none of these subjects had smoked more
than 0.1 pack-year.
At the other end of the scale, Category 4
comprised all heavy smokers. These had smoked at least 10
cigarettes a day with inhalation for 10 years or more till the
moment of the examination, with a maximum tolerance of 1 month in
that respect.
Category 2 comprised all the subjects who always
smoked without inhaling, whatever the kind of product smoked
66
(cigarette, cigar, pipe).
In Category 3 we
ranged all the other
subjects i i.e# all the men who had smoked with inhalation, without
reaching the duration and intensity of the smoking habits characterizing Category 4.
For some particular comparisons involving linear
correlation studies between different factors we needed a
continuous
numerical scale for the smoking habits, and we used a pack-years
classification.
RESULTS
1.
ESTIMATED RISKS FOR RESPIRATORY SYMPTOMS IN COAL MINERS
AND CONTROLS
In Table II we give the estimated risks for chronic
cough,
sputum, dyspnea grade 2 and some characteristic grouping of these
complaints for all the coal miners aged 35 to 54 years from both
surveys.
The coal miners were matched case by case with steel
workers for their age, smoking habits, socio-economic status and
general pollution exposure. There was an important excess of dyspnea
complaints in coal miners. Moreover, in this group dyspnea appeared more frequently as an isolated symptom than in the controls.
2.
FACTORS INFLUENCING THE COMPLAINTS IN COAL MINERS
2.1.
Pneumoconiosis
Table III summarizes the relations observed between the
complaints and the grade of pneumoconiosis in the coal miners from
the village of Lanaken.
The mean smoking habits of the X-ray groups were similar.
They varied from 9.86 pack-years to 11.15 pack-years in the different X-ray
categories.
None of these small differences appeared .
67
to be significant when the categories were compared two by two.
The average weight was also practically similar in the different
X-ray groups.
The weight was expressed by reference to the expect-
ed value according to the formula of Lorenz (35), the expected
weight being equal to 50 + 0.75 (T - 150), where T represents the
height in cm.
The mean weights were 101%, 104%, 107%, 106%, 99%
of the expected values for the different X-ray categories going
from 0 to B + C.
None of these means differed significantly from
the others when compared two by two.
On the contrary, there were
some differences between the mean ages of some groups. The coal
miners in group B + C were on the average significantly older than
those of the other groups (54 years, p^-.05), whereas the ages weœ
comprised within a small range going from 37 years to 43.2 years in
the other groups: p>.05 when compared two by two.
Table II shows that the simple association of chronic productive cough without dyspnea was absent in the X-ray groups 0
and 0/1 aged 37 and 42.6 years respectively.
This association
appeared only in some cases in group 1 aged 37 years¡ its prevalence went down when pneumoconiosis progressed and became null when
massive fibrosis was present.
On the contrary, dyspnea as an iso-
lated symptom without cough or phlegm was already present in a
small proportion (12%) in group 0.
The prevalence of this symptom
increased abruptly at grade 0/1 and remained relatively stable
beyond this stage till the categories B + Ci only for grade 2 was
this percentage somewhat higher(50%), but this isolated result may
have been fortuitious.
The association of the 3 symptoms increased
while pneumoconiosis progressed, and its maximum prevalence was
reached in the group with massive fibrosis B + Ci on account of
68
the mean age and tobacco use in the different categories this could
not be explained by heavier smoking habits, but we cannot exclude
the influence of age.
Table IV gives the respective proportions of the different
complaints in the 200 coal miners aged 30 to 39 years examined at
the coal face in the second survey.
In this study, we did not ob-
serve X-ray categories higher than 2/2. However, here again, we
found a definite difference in prevalence of dyspnea, but not of
chronic productive cough between grade 0 and the onset of simple
pneumoconiosis.
2.2. Influence of cigarette smoking
Figure 1 gives a schematic representation of the effect»
of smoking by comparing 3 groups of coal miners i a first group
comprising only non-smokers living in a non-polluted area, another
group of heavy smokers in the same area and a third one of heavy
smokers living in a residential area with high pollution levels.
Figure 1 also gives the results of a similar comparison in steel
workers.
All groups were matched for age as indicated in the
methods i they comprised only subjects aged 30 to 44 years.
The general trend of the comparison is strongly suggestive
of a difference in prevalence of dyspnea complaints between nonsmoking coal miners and steel workers of the same age living in a
low pollution area.
Butthe prevalences for cough and chronic
phlegm production were not significantly different between these
groups.
Figure 1 clearly indicates that smoking habits have a
significant effect on cough and phlegm production in both coal
miners and steel workers.
But tobacco use had no effect on the
69
frequency of the dyspnea complaints.
Adding the influence of a
general pollution exposure to tobacco use produces a definite
higher prevalence of chronic productive cough and dyspnea in coal
miners.
But air pollution seemed to be without additional effect
in smoking steel workers.
2.3. Length of exposure at the coal face
For this study the subjects were divided into 4 agespecific categories and matched for their smoking habits. All
these groups were further subdivided into 5 categories according
to length of exposure at the coal facei 0-4 years i 5-9 years, 10-14
years, 15-19 years and >20 years.
Neither in the first nor in the second survey could we
find a significant relationship between this length of exposure
and the prevalences of chronic cough, chronic sputum or dyspnea.
In fact, we must point out that the numbers of subjects were too
small in the different sub-groups cited above to allow valid
comparisons to be made in that respect.
For instance, in the
second survey, which concerned the largest total numbers in this
investigation, the number of non-smokers from the low pollution
area were 16, 50, 39 and 21, respectively, in the 4 age categories.
In the heavy smokers groups those numbers were 15, 48, 52 and 37.
It is quite understandable that further division of those small
groups into 5 sub-categories according to length of exposure
would give too small figures for valid statistical evaluation.
3.
RELATIONSHIP BETWEEN SPIROMETRY AND BRONCHITIS SYMPTOMS
IN COAL MINERS
In the first survey, 64 coal miners from the 204 men of
7o
the whole group complained of Isolated dyspnea.
From these 64
cases, 10 (16%) had a FEV.,/VC ratio smaller than 60%. On the
contrary, we found In the whole group 21 coal miners with chronic
productive cough and dyspnea, 10 (48%) of them showing this bronchoobstruction pattern.
The difference in that respect was signifi-
cant (p < .01).
It is also interesting to stress that a similar trend
was found by analysing the results of the acetylcholine tests.
Of 21 subjects with chronic productive cough and dyspnea, 13
(62%) gave a positive response to this test, whereas this was
the case in only 12.5% of the 64 subjects with isolated dyspnea
(p<c .01).
DISCUSSION
The lack of relations found between the length of exposure at the coal face and the prevalence of bronchitis symptoms
disagrees with recent findings of British authors (33). However,
this contradiction could be only apparent.
Indeed, the mean age
of our coal miners groups was lower than in the British groups,
and we mentioned above results suggesting that age could play by
itself a role in the onset of bronchitis complaints.
On the other
hand, the size of our groups was perhaps too small to allow the
detection of an effect of chronic exposition to coal dust (23)
(36).
An interesting finding of our investigation is the abrupt
increase in the prevalence of dyspnea observed beyond stage 0 in
both surveys. This fact is strongly suggestive of an aetiological
role of pneumoconiosis in the onset of dyspnea complaints in coal
miners.
However, the constant prevalence of the complaints of
71
Isolated dyspnea beyond stage 1 to stages B + C In the first survey
could provide an argument against such aetiology.
It is interest-
ing to point out that chronic cough and phlegm production without
dyspnea do not seem to be influenced by the grade of pneumoconiosis.
But such relation seemed to be present when considering chronic
productive cough associated with dyspnea.
Those figures could
agree with the hypothesis that cough and expectoration are not
directly related to pneumoconiosis, but appear later than dyspnea,
frequently when the latter is already present.
In this way most
of the cases with cough and phlegm would at once be associated
with dyspnea, anyway more frequently than this is the case in
bronchitis from a non-dusty origin.
According to the results
mentioned in figure 1, we would suggest that smoking has a major
influence on the onset of cough and sputum.
In that respect, we
must also stress that in the first survey we did not observe
in the village of Lanaken any coal miner complaining of chronic
cough associated with phlegm production in the group of nonsmokers younger than 40 years.
Figure 1 seems to suggest that the
general pollution could intervene in coal miners by producing a
synergistic effect with tobacco use on the occurrence of these
symptoms.
Such synergism did not appear to exist in steel
workers.
These different pathogenic mechanisms could provide an
explanation for the natural history of the respiratory disability
resulting from chronic bronchitis in coal miners. They explain
three main facts i
72
the relatively low prevalence of the cases with productive
cough without dyspnea in the young coal miners under 40
years t
the relative constancy of the percentages of coal miners
with isolated dyspnea when simple pneumoconiosis and age
increase;
the frequency with which chronic cough, sputum and dyspnea
are present at once in association In coal miners at a relatively lower age than in subjects with bronchitis from a nondusty origin.
An explanation for the high prevalence of dyspnea complaints in coal miners from the initial stages of simple pneumoconiosis could be the diffuse focal emphysema of Gough (20) as
well as the high prevalence of diffuse stenotic and ectatic bronchiolitis lesions from the very beginning of the diseases (18) (19).
At more advanced
stages, above all in the case of condensations,
it is well known.that emphysema plays a major role in the causation
of shortness of breath.
Moreover, in our cases of massive fibrosis,
age and past smoking habits were higher» therefore we cannot exclude that the same mechanisms as those intervening in bronchitis
from a non-dusty origin have contributed by themselves to a further
increase of the dyspnea prevalence.
The lack of relationship between isolated dyspnea at the
first stages of simple pneumoconiosis and the spirometrie figures
is anyway an argument for a different pathogenesis for this clinical
type of dyspnea and the dyspnea complaints associated with productive
cough observed at higher age and when more pronounced smoking ante-
75
cedents are present.
Similarly, the lack of relationship between the frequency
of isolated dyspnea and the responses rate to acetylcholine as compared with the rate found in coal miners with productive cough, is
also an argument for a particular specific pathogenesis for this
symptom.
In that respect, it is interesting to add that the role
of the cigarette similarly appeared to be different when considering the isolated dyspnea and the whole of all the dyspnea complaints
inclusive those associated with chronic cough and expectoration.
Such discrepancy was strongly suggested by the results of the first
survey when making an age-specific comparison of the prevalence
of both types of symptomatology in light smokers and heavy smokers
(Table V ) .
The figures of this table clearly suggest that above
30 years of age tobacco could increase the prevalence of all
patterns of dyspnea, whereas this phenomenon was not observed
when considering only the cases with isolated dyspnea. However,
on account of the small number of cases, a valuable statistic
evaluation could not be performed.
Therefore, it seems reasonable to explain by specific
mechanisms most of the cases of isolated dyspnea at the initial
stages of pneumoconiosis.
Rasmussen et al suggested that lesions
of the small peripheral arteries in simple pneumoconiosis could
provide an explanation for this (37).' Other authors described an
alteration of the CO diffusion in pinhead and micronodular pneumoconiosis (2) (16). They explained these abnormalities by a reduction of the diffusion capacity and by a restriction of the
74
capillary bed.
Of course, small-airways obstruction due to
bronchiolitis, as suggested by increases in closing volume, or
changes in elastic properties due to fibrosis or emphysema could
also provide an explanation for the dyspnea.
More recently Smidt
emphasized that an increase of total lung volume may frequently
occur in workmen with long-lasting occupational antecedents in
dusty atmospheres (40). Similar facts were also reported by Morgan
et al (31). Such phenomena could explain an excess of dyspnea complaints at the early stages of pneumoconiosis.
However, one must point out that all the functional
abnormalities quoted above, are not systematically present in simple
pneumoconiosis.
On the other hand, when they are present they are
usually at an initial stage.
The evaluation of these hypotheses
would therefore remain difficult in the particular cases (32).
It is only by means of longitudinal surveys in large groups that a
reasonable approach to the necessary correlations could be performed.
75
LITERATURE
1.
BECKLAKE M.R., ZWI S. and LUTZ W. : Studies of the nature and
aetiology of respiratory disability in Witwatersrand gold-miners
free of radiological silicosis. - Brit. J. industr. Med., 1959,
16, 290-296.
2.
BILLIET L., van de WOESTIJNE K.P., PRIGNOT J. et GYSELEN A. :
La capacité de diffusion pulmonaire chez le silicotique. - Acta
tubero, pneumol. belg., 1964, 55_, 255-258.
3.
BRILLE D., KAUFFMANN F., ORIOL P. et QUERLEUX E. : Bronchite chronique obstructive : définitions, facteurs de risque et prévention.
- Rev. Epidém. et Santé Pubi,, 1976, 2jJ, 321-344.
4.
BUREAU INTERNATIONAL DU TRAVAIL : Réunion d'experts sur la classification internationale des radiographies de pneumoconioses. Sécurité et Hygiène du Travail, 1959, 9, 8 p.
5.
BUREAU INTERNATIONAL DU TRAVAIL : B.I.T. U/C. Classification
internationale des radiographies de pneumoconioses, 1971, 4 p.
6.
CIBA GUEST SYMPOSIUM : Terminology, definitions and classification
of chronic pulmonary emphysema and related conditions. - Thorax,
1959, 1±, 286-299.
7.
COMMISSION OF THE EUROPEAN COMMUNITIES : Aide-memoire on air pollution measurements within the framework of the epidemiological
survey on respiratory diseases in children. - Commission of the
European Communities, Health Protection Directorate, Environmental Research Programme, Document No. V/F/3370/74e.
8.
COMMUNAUTE EUROPEENNE DU CHARBON ET DE L'ACIER : Commission Bronchite-Emphysème. Ulmer W.T. Luxembourg, 7 février 1962.
9.
COMMUNAUTE EUROPEENNE DU CHARBON ET DE L'ACIER : Standardisation
des épreuves pharmacodynamiques. Etat de la question en matière
de tests irritatifs. - Minette A. Rapport présenté à la Commission
Bronchite-Emphysème. Luxembourg, 25 juin 1963.
76
15,
COMMUNAUTE EUROPEENNE DU CHARBON ET DE L'ACIER : Commission Bronchite-Emphysème. Jarry J.J. - Document C.E.C.A. nc 5188/66.
Luxembourg, 1966.
COMMUNAUTE EUROPEENNE DU CHARBON ET DE L'ACIER s Questionnaire
de la Haute Autorité de la C.E.C.A. pour l'étude de la bronchite
chronique et de l'emphysème pulmonaire. Edition 1967. Minette
A. (rapporteur). Brille D., Casula D., Lende R. van der, Smidt
U. - Luxembourg, 1967.
COMMUNAUTE EUROPEENNE DU CHARBON ET DE L'ACIER : Commentaires
relatifs au questionnaire pour l'étude de la bronchite chronique
et de l'emphysème pulmonaire. Edition 1967. Minette A. (rapporteur), Brille D., Casula D., Lende R. van der, Smidt U. Luxembourg, 1967.
DEGUELDRE G. : L'échantillonnage des poussières envisagé dans le
cadre d'une recherche épidémiologique sur la bronchite chronique.
- Acta tuberc. pneumol. belg., 1974, i<5£, 105-114.
DOUGLAS J.W.B. and WALLER R.E. : Air pollution and respiratory
infection in children. - Brit. J. prev. soc. Med., 1966, 20,
1-8.
FLETCHER C , PETO R., TINKER C. and SPEIZER F.E. : The natural
history of chronic bronchitis and emphysema. - Oxford University
Press, Oxford, New York, Toronto, 1976, 272 p.
FRANS A., VERITER C. and BRASSEUR L. t Pulmonary diffusing
capacity for carbon monoxide in simple coal worker's pneumoconiosis. - Bull. Physiopath. resp., 1975, !_!,. 479-502.
GALY P. : Anatomie pathologique des bronchites chroniques obstructives. - in : Monographie du collège de Médecine des Hôpitaux
de Paris. Ed. L'expansion scientifique française, 15, rue SaintBenoît, Paris Vie, 1970, 11-20.
GALY P. : Historique des rapports entre bronchite chronique et
emphysème. - Bull. Physiopath. resp., 1973, 9, 843-860.
HÄRTUNG W. and MULLER K.M. : Chronic bronchitis and focal dust
emphysema in low grade anthracosilicosis. - in : Pathologie et
nosologie de la bronchite chronique. Colloque de Lyon, 22 et
23 septembre 1970. Ed. Laboratoires Boehringer Ingelheim, rue
Emile Druart, Reims, 259-267.
77
20.
HEPPLESTON A.G. : The essential lesion of pneumok >niosi:; L i Jelsh
coal workers. - J. Path. Bact., 1947, 5£, 453-460.
21.
HIGGINS I.T.T., COCHRANE A.L., GILSON J.C. and WOOD C.H. : Population studies of chronic respiratory disease. A comparison of
miners, foundryworkers, and others in Staveley, Derbyshire. Brit. J. industr. Med., 1959, _16, 255-267.
22.
HIGGINS M.W. and KELLER J.B. : Predictors, of mortality in the
adult population of Tecumseh. Respiratory symptoms, chronic
respiratory disease, and ventilatory lung function. - Arch.
environm. Hlth, 1970, 21, 418-424.
23.
JACOBSEN M., RAE S., WALTON W.H. and ROGAN J.M. : The relation
between pneumoconiosis and dust-exposure in British coal mines.
in : Inhaled Particles III. Proc. of an International Symposium
organised by the British Occupational Hygiene Society in London,
14-23 September 1970. Surrey, England, W.H. Walton, Unwin
Brothers Ltd. The Gresham Press Old Working, 1971, 903-919.
24.
JAMES R.H. : Distribution of pulmonary ventilation in disabled
Southern West Virginia coal miners. - Amer. Rev. resp. Dis.,
1970, 101, 715-720.
25.
JOUASSET D. : Normalisation des épreuves fonctionnelles respiratoires dans les pays de la Communauté Européenne du Charbon et
de l'Acier. - Poumon, 1960, 16, 1145-1159.
26.
MINETTE A. : Rôle de 1'empoussiérage professionnel dans la production des bronchites chroniques des mineurs de charbon. - in :
Inhaled Particles III. Proc. of an International Symposium organised by the British Occupational Hygiene Society in London
14-23 September 1970. Surrey, England, W.H. Walton Unwin
Brothers Ltd. The Gresham Press Old Working, 1971, 873-881.
27.
MINETTE A. : Results of an epidemiological survey on bronchitic
symptoms in the male population of a Belgian mining community.
in : Ecology of chronic nonspecific respiratory diseases.
International Symposium, September 7-8, 1971, Warsaw, Poland,
Warszawa Panstwowy Zaklad Wydawnictw Lekarskich, 1972, 87-96.
28.
MINETTE A. : Contrat CECA N° 6244-0O/2/O34 : Enquête dans des
bassins industriels à forte densité de population sur les lieux
du travail et en dehors de ceux-ci. - Commission des Communautés
Européennes, rapport final, 1975.
78
MINETTE A. : Apport ôpldémiologique â l'étiologie de la bronchite
chronique des mineurs de charbon. - These pour l'obtention du
grade d'agrégé de l'enseignement supérieur. Université Catholique de Louvain, Faculte de Médecine, 1976, 203 p.
MINETTE A., MARCQ M. and GEPTS L. : Prognostic value of a positive
acetylcholine test regarding VC and FEV. in coal-miners with a
history of chronic bronchitis. - Bull, europ. Physiopath. resp.,
1978, 1^, 167-175.
MORGAN W.K.C., BÜRGESS D.B., LAPP N.L. and SEATON A. : Hyperinflation of the lungs in coal miners. - Thorax, 1971, 26,
585-590.
MORGAN W.K.C., LAPP N.L. and MORGAN E.J. : The early detection
of Occupational lung disease: - Brit. J. Dis. Chest, 1974,
68, 75-85.
MUIR D.C.F. : Pulmonary function in miners working in British
collieries : epidemiological investigations by the National Coal
Board. - Bull. Physiopath. resp., 1975, 1_1, 403-414.
ORIE N.G.M., SLUITER H.J., de VRIES K., TAMMELING G.J. and
WITKOP J. : The host factor in bronchitis. - in : Bronchitis.
An International Symposium. Groningen 27-29 April 1960. Assen
(Netherlands), VanGorcum, 1961, 43-59.
PERLEMUTER L. : Bilan métabolique d'une obésité. - in : Problèmes
actuels d'endocrinologie. - Paris, Ed. J. Hazard, Masson et Cie,
1973, 7-15.
RAE S., WALKER. D.D. and ATTFIELD M.D. : Chronic bronchitis and
dust exposure in British coalminers. - in : Inhaled Particles III.
Proc. of an International Symposium organised by the British
Occupational Hygiene Society in London 14-23 September 1970.
Surrey, England, Ed. W.H. Walton, Unwin Brothers Ltd., The Gresham Press, Old Working, 1971, 883-894.
RASMUSSEN D.L., LAQEUR W.A., FUTTERMAN P., WARREN H.D. and
NELSON C.W. : Pulmonary impairment in Southern West Virginia
coal miners. - Amer. rev. resp. Dis., 1968, ¿8, 658-667.
SLUIS-CREMER G.K., WALTERS L.G. and SICHEL H.S. : Chronic bronchitis in miners and non-miners : an epidemiological survey of
a community in the gold-mining area in the Transvaal. - Brit¿ J.
industr. Med., 1967, 24, 1-12.
79
39.
SLUIS-CREMER G.K., WALTERS L.G. and SICHEL H.S. : Ventilatory
function in relation to mining experience and smoking in a random
sample of miners and non-miners in a Witwatersrand town. - Brit.
J. industr. Med., 1967, 24, 13-25.
40.
SMIDT U. : Chronische Bronchitis und Lungenemphysem. Klinisch
epidemiologische Untersuchungen über die Bedeutung beruflicher
Staubexposition. - Thieme Copythek 1975. VIII. Stuttgart,
Thieme-Verlag, 198 p.
41.
ULMER W.T., REICHEL G. und WERNER U. : Die
Bronchitis des Bergmannes. Untersuchungen
Normalbevölkerung und bei Bergleuten. Die
belastung und der Einfluss des Rauchens. pa th. Gewerbehyg., 1968, 25, 75-98.
42.
WORTH G., MUYSERS K. and SIEHOFF F. : Derzeitiger Stand der
Kenntnisse über den Einfluss von Grubenstäuben auf die Funktion
des bronchopulmonalen Systems. - in : Symposium BronchitisEmphysem, Stresa, 21.-22. April 1966, Europäische Gemeinschaft
für Kohle und Stahl, Hohe Behörde, Schriftenreihe Arbeitshygiene
und Arbeitsmedizin Nr. 5, Luxemburg, 1967, 27-47.
8o
chronisch obstruktive
zur Häufigkeit bei der
Bedeutung der StaubInt. Arch. Gewerbe-
TABLE I
GROUPS OF THE FIRST :SURVEY
MINERS
TRANSPORT
MISCELLANEOUS
*
LISTED
RESPONSES
ELIMINATED*
247
112
101
222 (90%)
112 (100%)
90 (90%)
18
2
3
EXAMINED GROUPS **
204
110
87
The elimination occurred on account of heart diseases or X-ray
abnormalities of a non-pneumoconiotlc nature.
** The non-responders and eliminated persons did not differ statistically from this examined group.
B.
GROUPS OF THE SECOND SURVEY
I.
COLLIERIES! REPRESENTATIVE GROUPS OF COAL GETTERS IN TWO COMPANIES
1. In a low polluted colliery
2. In a highly polluted colliery
II.
t 676 listed workmen, 599* examined
(88%)
i 575 listed workmen, 461* examined
(80%)
STEEL WORKERS « ALL WORKERS OF TWO COMPANIES
1. In a low polluted steel works
i 1284 listed workmen, 1175* examined
(91%)
2. In a highly polluted steel worksil218 listed workmen, 1150* examined
(95%)
*
It has been established that the non-responders did not differ from
the others from the point of view of bronchitis.
81
TABLE III
PREVALENCE OF VARIOUS ASSOCIATIONS OF COMPLAINTS WITH
RESPECT TO PNEUMOCONIOSIS IN 204 COAL MINERS
LIVING IN A LOW POLLUTION AREA*
PREVALENCES OF
NUMBER OF CASES
BY RADIOLOGICAL
CLASS
MEAN
AGE
(YEARS)
ALL
COMPLAINTS
DYSPNEA
ALONE
COMPLAINTS
COUGH
PHLEGM
COUGH
PHLEGM
DYSPNEA
0
i 25
37
16%
12%
-
-
0/1
i 49
42.6
47%
35%
-
10%
1 (q.r)
i 49
37
41%
25%
8%
4%
2 (p.q.r) • 44
42.1
64%
50%
5%
7%
3 (p.qi r) i 27
43.2
56%
26%
4%
22%
30%
_
50%
B + C
*
i 10
80%
54
See text i Material and methods.
85
TABLE IV
RELATIONSHIP BETWEEN RADIOLOGICAL STAGE AND PREVALENCE OF COUGH,
PHLEGM AND STAGE 2 (ECCS) DYSPNEA IN 200 NON-SMOKING
COAL MINERS AGED 30-39 YEARS
RX stage 0
RX stage 0/1-2/2
NUMBER
OF CASES
WITHOUT
COMPLAINTS
142
80 (56%)
58
22 (3B%)
84
CHRONIC
COUGH
CHRONIC
PHLEGM
DYSPNEA 2
(7%)
14 (10%)
30 (21%)
6 (10%)
7 (12%)
25 (43%)
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86
Caracteres particulares de la bronquitis
crónica de los mineros de carbón.
A. Minette (Bélgica)
Las enfermedades pulmonares crónicas no específicas
de los mineros de carbon pueden deberse a diversos factores que actúen conjunta o suceslvamentei uso de tabaco,
edad, polvo, contaminación ambiental, factores constitucionales. El autor efectuó dos encuestas por sección transversal sobre esos problemas utilizando el cuestionarlo del
Medical Research Council y la Comunidad Europea del Carbón
y del Acero. En la primera encuesta examinó a 204 mineros
de carbón residentes en una zona de poca contaminación
(Lanaken, Bélgica) y seleccionados al azar por orden alfabético en los registros de población. Los comparó con una
muestra representativa de sus esposas y con 178 testigos
residentes en la misma ciudad y cuya edad y condición socioeconómica fueran paralelas a las de los sujetos estudiados.
En la segunda encuesta comparó 1.251 mineros de carbón que
trabajaran regularmente en el tajo con 2.502 obreros de fundición. Se efectuaron regularmente controles del polvo en
el lugar de trabajo, así como de la contaminación del medio
ambiente.
Se comprobó que el factor predominante para la aparición de tos productiva en los mineros de carbón era el hábito de fumar cigarrillos. Tratándose de sujetos menores
de 40 años, el autor no halló siquiera casos de tos productiva crónica entre los no fumadores, en ausencia de una fibrosis masiva u otra anormalidad toráxlca correlacionada.
La exposición crónica al polvo de carbón y la exposición
prolongada a niveles elevados de contaminación pueden tener
efectos sinergéticos con el consumo de cigarrillos sobre la
aparición de una tos crónica con expectoración. Según lo
observado, la contaminación no tiene efectos sobre los trabajadores de las fundiciones. La conclusión general es un
poderoso fundamento para la opinión de que la definición de
la bronquitis crónica basada únicamente en la presencia de
tos crónica y expectoración no abarca toda la gama de la
enfermedad. En muchos casos de bronquitis llamada "del minero de carbón", la disnea aparece ya en las fases precoces
de la enfermedad.
.87
\
DUST EXPOSURE AND PNEUMOCONIOSIS
AT 10 BRITISH COAL MINES
M. Jacobsen
Institute of Occupational Medicine, Edinburgh, United Kingdom
1. INTRODUCTION
A large scale prospective study of British coal miners was
begun 25 years ago.
The aim of this "Pneumoconiosis Field Re-
search" was to determine how much and what kinds of dust cause
(coal workers') pneumoconiosis, and to establish what environmental conditions should be maintained If mine workers are not
to be disabled by the dust they breathe.
An Interim answer to
the first of these questions ("how much dust causes pneumoconiosis") was provided in 1970.
That work,which was based on 10-
year periods of observation at 20 collieries, demonstrated a
correlation between the radiological changes observed at the
collieries and the colliery-average coal face dust concentrations
measured during the 10-year periods.
The results were used to
estimate long-term risks of developing coal workers' simple
pneumoconiosis In relation to different average dust concentrations, and this Information provided the scientific background
for decisions on new coal mine dust standards which were Introduced In Britain at that time. (Jacobsen et âl, 1970).
A further 10-year period of observation has now been completed at ten of the collieries included In the study.
Analyses
to date of the results have concentrated on seeking answers to two
questions i
( 1) Are the newly acquired data consistent with the
estimates of
îrm d u s t - r e l a t e d pneumoconiosis
89
- 2risks that were made ten years ago using results from
only 10-year periods of observation?
(11) Is there any evidence that the chance of developing
coal workers' simple pneumoconiosis Is Influenced by
the quartz content of the coal mine dust to which men
are exposed?
Preliminary results from this work are summarised here.
2.
2.1
METHODS
Dust exposures
Since the start of the project, records have been kept of
the time worked by each man In different occupational groups
at the collieries. The average dust concentrations associated with these occupational groups have been determined
from a programme of dust sampling close to the men at their
places of work and during travelling time underground.
Dust
concentration measurements during the first 10-year phase of
the studies were made with the Thermal Precipitator and were
expressed at the number of respirable particles per cubic
centimetre of sampled air. These measurements were con's
verted later into mass concentration units (mg/m ), as described by Dodgson et al. (1971).
A more intensive programme
of dust sampling has been pursued during the latter 10-year
9o
- 3period, using MRE gravimetric dust samplers. The sums of
products, 5(time worked In occupational group x average
concentration in occupational group), provide measures of
exposure to respirable dust for each individual during the
course of the research.
Additionally, exposures to dust before the research began
were estimated from occupational histories obtained at interviews with the men.
The number of years spent in any one of
six broad categories of coal mining activities, were converted
into working hours and were multiplied by the mean dust concentrations for occupational groups corresponding to these
activities, as determined in the first 10-year period of
measurement.
Thus there were available estimates of cumu-
lative exposure to respirable coal mine dust, from entry to
the industry up to the time of the latest medical surveys.
The exposure units are gram-hours per cubic metre of
sampled air (gh/m ).
2.2
RadioloRlcal data
The latest medical surveys included full-size (anteroposterior) chest x-rays of 2,600 miners who had been examined initially 20 years earlier.
Serial chest radiographs,
spanning the two consecutive 10-year intervals, were examined by each of five physicians experienced in the radio91
- 4 logy of pneumoconiosis. A H 7,800 films were classified separately^ independently and in random order by each reader, according to the ILO U/C International Classification of Radiographs of Pneumoconioses (ILO, l97l).
Additionally, each
reader classified the three possible pairs of films from each
man, side-by-side on the viewing box.
3.
RESULTS
Correlations between dust exposure and simple pneumoconiosis
Figure 1 shows the proportions of men with at least the earliest
signs of simple pneumoconiosis (category 0/1 or more), as determined from the five readers' average results, in relation to
cumulative dust exposures.
Both methods of assessing the radio-
graphs (independent classifications, and side-by-side readings
of film-pairs) demonstrate very similar relationships between
this measure of radiological response and the exposure index.
(Most of the results reported below are based on the independent, separate film classification).
Differences between readers, using the independent classifications, are illustrated in Figure 2 in terms of the proportions
of men whose radiographs were classified as showing category 2
or 3 of simple pneumoconiosis.
Evidently, the differences
between readers are greater than the differences between reading methods, but it is clear that each reader's results show
convincing correlations with dust exposures. High correlations
with dust exposure were obtained also with readers' radiological
scores averaged over men in various dust exposure ranges.
latter scores are semi-quantitative representations of the
92
(The
- 5"amount of pneumoconiosis" seen on a chest radiograph.
They
are based on the 12-point scale used for classifying the profusion of small rounded opacities).
The confirmation, in Figures 1 and 2, of the correlation between radiological signs and the measures of dust exposure as
determined in the Pneumoconiosis Field Research, is important
for several reasons.
(
1)
Earlier results (Jacobsen et al, 1971) were based on
only ten years' observation in a selected group of
coal face workers. The work reported now Is not
restricted to face workers and the period of research has doubled.
( li) Dust measurements made during the first 10-year
phase of the project were respirable particie-count
concentrations, which were converted retrospectively
to mass concentration units. All dust measurements
during the last ten years have been made directly
with gravimetric samplers.
(ill) The 1970 Interim study was confined to correlations
between radiological changes over 10-year periods
and average dust concentrations during those periods.
The cumulative dust exposures described above refer
to individuals and they include estimates of exposure before the research began.
3.2
Dust exposure and Incidence of simple pneumoconiosis
The correlations demonstrated In Figures 1 and 2 are between
radiological signs as observed at the latest medical surveys
95
- 6and cumulative exposure to dust since joining the industry.
The time periods during which these exposures were accumulated
varied. These measures of response cannot therefore be Interpreted as disease incidence rates, since such rates refer to
the new occurrence of events during a specified time Interval;
and it is incidence rates which are of interest when considering disease risks and hygiene standards.
The quotient obtained by dividing an individual's cumulative
dust exposure by the time period during which that exposure
was accumulated is a measure of the average dust concentration experienced by that individual.
This alternative index
of exposure was used in a series of analyses aimed at expressing pneumoconiosis risks as a function of both exposure
time and average dust concentration.
Efforts were made also
to take into account previously observed variations in risks
resulting from similar exposures to dust at different collieries (Walton et al, 1977).
Figure 3 illustrates one such equation. The curve describes
the estimated increases in the probability of developing
category 2/1 or more simple pneumoconiosis with exposure
to increasing mean concentration of respirable dust over
61,000 working-hours. This time period has been selected
to illustrate the relationship because it approximates to a
35-year working-life at the research collieries in the late
I960's.
Thus the new results made be compared approximately
94
- 7with those published previously (the dotted line In Figure 3,
from Jacobsen et al, 1970).
The latter estimates of 35-year
risks were derived from less comprehensive data, and using a
different mathematical approach (Jacobsen, 1975).
It appears
that the earlier predictions underestimated 35-year workinglife risks by one to two percentage probability units.
3.3
Differences between collieries
The equation Illustrated in Figure 3 makes provision for variations In probabilities at the same exposure depending on
whether a man worked at colliery T, at colliery Q, or at one
of the other eight collieries studied.
These variations are
large and they dwarf the differences between the two analyses
Illustrated In Figure 3.
At colliery T (now closed) pneumo-
coniosis risks were some five to six
times higher than the
average results shown on the graph) at another colliery (Q)
they were about l/9th of the average. Yet the mean concentration of airborne dust to which men were exposed In colliery T
(2.9 mg/m ) was lower than the corresponding figure for colllery Q (4.4 mg/m ). Moreover, the average quartz content
of the mixed dust exposures at colliery T was the same as that
for all 2,600 men considered (5.0%); at colliery Q however It
was higher (6.4%),
The analyses to date have failed to explain these marked
colliery-associated variations which have been considered
also In previous publications (Walton et al, 1977).
Atten-
tion Is drawn to them again now because of the Implicit
95
difficulty in generalising from average results obtained at
only ten collieries.
Quartz in mixed coal mine dust
Several attempts have been made in the past to determine
whether or not relatively small quantities of quartz in mixed
coal mine dust affect the
pneumoconiosis.
chance of developing coal workers'
Earlier studies of British data have failed
to reveal a clear-cut effect (Jacobsen et al, 1971; McLintock
et ali 1971 i Walton et al, 1977).
Similar negative findings
have been reported from the Ruhr coal field in Germany (Reisner, 1977).
Greatly improved information about the quartz content of dust
sampled in the research collieries has been obtained recently, using infrared spectroscopy.
The accumulated results
were therefore re-examined in detail.
In principle, it is conceivable that the relationships between radiological signs and mixed coal mine dust (Figures 1,
2 and 3) are merely reflections of an effect wholly or mainly
due to the quartz content of that dust.
(This hypothesis is
tenable a priori because,although percentage quartz in the
dusts varied, in general, high exposures to mixed coal mine
dust tended to be associated with high exposures to quartz
dust (r = 0.76).
In fact, such an Interpretation of the data
is contra-indicated.
Analyses similar to those summarised
above, but substituting quartz for mixed dust as a variable,
did not explain the responses satisfactorily.
This confirms
a previous generalisation from British epidemiological data
96
- 9which asserted that "the most Important single variable determining the incidence of simple pneumoconiosis is the cumulative
mass of the
respirable fraction of all airborne dust to which
individuals are exposed" (Jacobseni 1973).
The conclusion
refers, of course, to dust exposures of the kind observed at
the collieries. The quartz level in these exposures averaged
5% and rarely exceeded 10%.
Yet it is possible that varying levels of quartz in the dust,
even in this range, influences the pneumoconiosis risk in
addition to the effect of the main environmental factor exposure to mixed dust. This possibility was explored ex- .
tensively using the newly acquired data, by considering whether
or not variations in quartz exposures helped to explain the
residual variability in radiological results, unexplained by
the equation defined in the caption to Figure 3.
pattern emerged from these studies.
No sensible
Figure 4 illustrates one
such negative result.
However, there is evidence that some Individuals who were exposed to relatively high average quartz concentrations over
10-year periods did show unusual changes on their chest radiographs .
In addition to the 2,600 miners whose life-time exposures to
dust have been discussed above, there were 1,750 men who had
worked at the same collieries only during the latter 10-year
period.
Among the total of 4,350 men there were 46 who showed
two or more steps of radiological change on the 12-point simple
97
- 10 pneumoconiosis scale over the 10-year interval.
(This is based
on the concurring judgement of at least three of the five filmreaders, using side-by-side assessments of the film-pairs concerned).
It was possible to select a "control" miner to match
42 of these "cases". The "controls" showed no radiological
change over the same time interval and using the same radiological criterion. Matching factors were (a) colliery; (b)
whether the "case" was aged more or less than 35 years at the
start of the 10-year period) and (c) whether the "case's" initial radiograph had been classified as category 0/1 or higher
at the earlier survey. Subject to these constraints, "controls"
were selected so as to minimise the difference ("case" - "control")
in cumulative exposure to mixed dust up to the final medical
survey.
Figure 5 shows the distribution of differences ("case" - "control")
in the quartz content to which the men were exposed during the
10-year intervals. Two thirds of the miners with unusual radiological changes had been exposed to more quartz dust than the
men without radiological changes with whom they had been paired.
The asymetry of the distribution of differences (Figure 5) is
unlikely to be due to chance (P< 0.005).
4. CONCLUSIONS
The general correlation between coal mine dust exposure and
simple pneumoconiosis, which was first demonstrated eight years
ago, is confirmed unambiguously.
Long-term risks were probably underestimated in the earlier
98
- 11 work by one to two (percentage) probability units.
3
There are large variations between collieries in medical
responses to similar dust exposures.
They dwarf the differ-
ences between alternative statistical approaches to the data,
and they make it difficult to generalise safely from the results.
4
The variations in pneumoconiosis risks between collieries are
not explicable in terms of different quartz levels at the
collieries.
Nor is there any general pattern in the results
which might indicate that quartz exposures amounting to less
than ten percent of mixed coal mine dust affect the probability of developing coal workers' simple pneumoconiosis«
5
However, there is evidence from the data that a few men may
re-act unfavourably over relatively short (10-year) intervals to coal mine dust with a high quartz content.
The Penumoconiosis Field Research is financed by
the British National Coal Board. All involved in
this project thank the miners, their Unions, and
the Colliery Managers for their willing co-operation during the past 25 years. We are grateful
also to Drs. J.G.Bennett, J.Burns, J.A.Dick, D.J.
Thomas, and J.S.Washington who classified the radiographs. Mrs. E.H.Copland and Mr. J.F.Hurley did most
os the statistical work reported above.
99
-12-
REFERENCES
DODGSON, J., HADDEN, G.G., JONES, C O . and WALTON, W.U. (1971).
Characteristics of the airborne dust in British coal mines.
Inhaled Particles III.
Ed. tf.H. Walton, pp 757 - 76*1.
In:
Unwin,
Old Woking, Surrey.
ILO, 1.972.
ILO Ü/C International Classification of Radiographs of
Pneumoconioses, 1971.
^rev,^
ILO
Occupational Safety and Health Series No. 22
Geneva.
JACOBSEM, M. (1973).
Progression of coalworkers' pneumoconiosis in
Britain in relation to environmental conditions underground.
In:
Proceedings of the Conference on Technical Measures of Dust Prevention
and Suppression in Mines, Luxembourg 1972.
JACOBS EN, M. (1975).
PP 77 - 93.
CEC,Luxembourg.
Effects of some approximations in analyses of
radiological response to coalmine dust exposure.
In:
Recent Advances
in the Assessment of the Health Effects of Environmental Pollution.
_1_, 211 - 229.
CEC, Luxembourg.
JACOBSEN, M., RAE, S., WALTON, W.H. and ROGAN, J.M. (1970).
standards for British coal mines.
New dust
Nature (Lond.) 227, ^5
- '»'»7.
JACOBSEM, M., RAE, S., WALTON, W.H. and ROGAN, J.M. (1971).
The rclatisr.
between pneumoconiosis and dust exposure in British coal mines.
Inhaled Particles III. Vol. 2, pp 903 - 919.
In:
Ed. W.H. Walton.
Unwin, Old Woking, Surrey.
McLINTOCK, J.S., RAE, S. and JACOBSEN, M. (1971).
The attack rate of
Progressive Massive Fibrosis in British coalminera.
Particles III. Vol. 2, pp 933 - 952.
In:
Inhaled
Ed. W.H. Walton.
Unwin,
Old Woking, Surrey.
REISNER, M.T.R. (1977).
Erkenntnisse epidemiologischer Unter-
suchungen fUr den Schutz vor Stauberkrankunßen.
1oo
Glückauf,
113, ?1 - 26.
WALTON, W.U., DODGSON, J . , MADDEN, G.G. and JACOBSEN, M. ( 1 9 7 7 ) .
The e f f e c t of q u a r t z and o t h e r non-coal dusto i n c o a l w o r k e r s '
pneumoconiosis.
¿n:
I n h a l e d P a r t i c l e s IV. Vol. 2 , pp 669 - 690.
Ed. W.H. Walton, Pergamon, Oxford.
PAIRED
("SIDE-Bi-SIDE")
READINGS
PEROENTAOE
WITH CATB30KT 0 / 1
OB HTftHER
100
#
15?)
2 »
23>
Ï0Û
SEPARATE
( INDEPENDENT)
READINGS
r
350
FIGURE 1
CDITOLATIVE DDST EXPOSURE ( g V " )
FIGURE 1.
COMPARISON OF TWO READING METHODS
Average results from five film-readers'" classifications
of radiographs of 2 6OO coal miners, by mean of
cumulative exposures to mixed respiratile coalmine dust
from entry to coal mining to time of radiological
survey;
grouped data.
loi
FIGURE 2.
COMPARISON OF FIVE READERS« CLASSIFICATIONS
Separate (independent-randomised) classifications of
radiographs of 2 600 coal miners, by mean cumulative
exposures to mixed respiratile coalmine dust from entry
to coal mining to time of radiological survey;
grouped data.
•"> — t
PERCENTAGE WITH
SIMPLE PNEUMOCONIOSIS
CATEGORY 2 OB HIGHER
¿AVERASE OF
FIVE READERS'
IÜDEP5IIDEH7
CLASSIFICATIONS
CDMOLATIVE DOST EXPOSURE FROM ENTRY TO INDUSTRY TO TIME OF X-RAI
THOUSANDS OF HOURS
x
FTWTHE ?
a*,'»3)
1o2
ESTIMATES OF PROBABILITIES 0 7 DEVELOPIW CATHJOHT 2
OR MORE SIMPLE PNEUMOCONIOSIS OVER AN APPROXIMATELY
35-YEAR WOHKIÑO-LIFE AT THK COALFACE
Based on weighted averages of estimates for c o l l i e r i e s
T, Q, and the other eight c o l l i e r i e s considered a s a
group, with t a 60.9 thousand hours.
The equation of
the curve i s :
l o g i t (P) = -2<».6028 + 2.i»352 Cln(r)] - 1.9059 (Q)
• 2.3'»27 (T)
• f.3222 Cln(t)]
where x = mean dust concentration,
t a exposure time, in thousands of hours,
and Q, T are dummy variables representing colliery effects.
The above coefficients are averages of results from five
separate fits, by maximum likelihood, to data from five
film readers' independent-randomised classifications.
Weights used to obtain the curve illustrated were the
proportions of men from the collieries in the sample studied,
i.e., (161/2 600) for colliery T, (326/2 600) for colliery Q,
and (2 136/2 600) for the other eight collieries.
Based on statistical extrapolation of radiological change '
over 10 years;
from Jacobsen t£ al (1970: 1971)
1o3
PROBABILITY ( * )
OF DCTELOPIHO CATEBOHÏ
2 / 1 OH MORE
10
7
/
/
/
-
/
/
/
/
/
b
1
2
3
I
I
I
<t
5
6
7
MEAN OUST CONCENTRATION (mR/aT)
FIGORE ?
1o4
riaURI k.
DIFFERENCES (R) BETWEEN OBSEHVED AMD PREDICTED
PERCENTAGES OF MEN WITH CATEGORY ?. OR MORE SIMPLE
PNEUMOCONIOSIS, BY MEAN PERCENTAGE QUARTZ IN MIXED
COALMINE DUST EXPOSURE
Data grouped In order of percentage quarts; 130 aen
per group.
Observed percentages from average of
five readers' independent-randomised classifications.
Predicted percentages from equation defined in caption
to Figure 3.
(The absence of a systematic pattern in
the residuals (R) with respect to percentage quartz
indicates that percentage quartz is not nssociated with
residual variability unexplained by the equation.)
I- R («)
-*-+
10
•
KKAN PERCFimWE QUARTZ
IN DUST EXPOSURES
naoRB *
1o5
FIGURE 5.
DIFFERENCES ("Case" - "Control") IN PERCENTAGE QUARTZ
IN EXPOSURE TO MIXED COAIMNE DUST OVER TET! YEARS
"Cásea":
two or more positive steps of change over 10
years on the 12-point radiological scale;
"Controls": no radiological change over 10 years on
the 12-point radiological scale.
+7
QTFT>:SE"CS I»
P:-:3CSNTA':K
w m z
I « MIXED COALMINE DUST
KXKT.URK:
(CASE-CONTROL)
2 $ CASES HAD MORE
•5
% QUARTZ THAN
CUKTROLS
+1»
•3
+1
O
O
O
-1
o
•
•
•
o
o
ó
o
o
o
14 CASES HAD LESS %
QUARTZ THAN CONTROLS
-2
FK5URE 5
106
Exposición al polvo v neumoconlosla en diez
minas del carbon en Gran Bretaña
M. Jacobsen (Reino Unido)
Los recientes estudios médicos realizados por el Servicio Británico de Investigaciones en materia de Neumoconlosis comprendían exámenes radiológicos de 2.600 mineros
del^carbón, examinados inicialmente 20 años antes. Se calculó la exposición al polvo respirable en las minas de carbón durante intervalos de 20 años a partir de los registros
del tiempo trabajado por cada obrero en grupos profesionales en las diez minas examinadas y los promedios de concentraciones de polvo respirable medidas en esos grupos. La
exposición al polvo anterior al primer estudio fue calculada a partir de las historias profesionales, reconstituidas
mediante entrevistas con los interesados. Cinco médicos
experimentados en la utilización de la Clasificación Internacional de Radiografías de Neumoconlosis de la OIT/UICC
llevaron a cabo evaluaciones repetidas de las correspondientes radiografías.
Los primeros resultados de esos estudios revelan una
relación indudable entre las estimaciones de exposición cumulativa al polvo de carbón respirable y las distintas interpretaciones que cada uno de los cinco médicos ha hecho
de las radiografías llevadas a cabo en los estudios más recientes.
Se han hecho comparaciones entre los nuevos resultados
y los de un análisis realizado anteriormente de los resultados basados en^exposlciones medidas únicamente durante
diez años. Las últimas estimaciones específicas, basadas
en la dosis de polvo, de los riesgos de neumoconlosis del
carbón de categoría 2 o más simple que se va desarrollando
a lo largo de la vida de trabajo son 1 ó 2 por ciento (unidades de probabilidades) superiores a las predicciones anteriores. Esta diferencia es insignificante comparada con
las Inexplicables variaciones en la relación de dosis a efecto según las minas.
1o7
. I N D I C E
S E S S I O N
II
B»B»Basss993SS9Saltasffl38iiisi
I
Kl.Adr lenza
Rapporteur
II
B.Klendez
An Epidemiologic study of silicosis in Brazil, from a
survey of patients in tuberculosis hospitals.
III
G.Cornea., A.Chechen., A.9en Kheder., Silvia Gabor.,
I. El Rlekkl.
La silicose dans une mine de spath-fluor de Tunisie.
IV
J.Prenafeta., Clayton., and R.Sepulveda.
Variability in the X-Ray diagnosis of early Silicosis.
V
K.Chiyoteni., Ken-ichi Saito.
Excess lung cancer risk in silicotic cases, under hospital care-preliminary report.
VI
J.Prenafeta., A.Valenzuela., G.leyton., S.Vlllagran.
Epidemiological survey and prognostic evaluation in
Silicosis.
1o9
EVALUACIÓN EPIDEMIOLOGICA DE LAS NEUMOCONIOSIS Ï OTRAS
ENFERMEDADES RESPIRATORIAS DE NATURALEZA OCUPACIONAL
EN
VENEZUELA
Manuel Adrianza H. Ministerio de Sanidad y Asistencia Social (MSAS)
Amílkar Toçrealba. Ministerio del Trabajo (MT)
Erich Schmidt. Ministerio de Sanidad y Asistencia Social (MSAS)
Catherine Ernould. Conicit
Francisco Fuenmayor. Instituto Venezolano de los Seguros Sociales (IVSS)
Maximiliano Acosta. Ministerio del Trabajo (MT)
INTRODUCCIÓN:
Es obligatorio el abordaje epidemiolàgico de un problema
de salud ocupacional, toda vez que la epidemiología está definida como disciplina para el diagnóstico de la comunidad, y además, como
una de las ciencias que sirve para solucionar los problemas de la Salud Pública y de la Medicina Preventiva. ( H ) .
El análisis del riesgo de exposición del cual depende di
rectamente la morbilidad, puede ser simple o complejo según el pro-blema y las ciroustancias que lo rodean. En el caso de las neumoconiosis en nuestro país, el problema podría circunscribirse en una primera etapa a la silicosis y a la asbestosis para los polvos inor_
gánicos, a la bisinosis, a la bagazosis y otros síndromes respirato
rios de la hipersensibilidad reactiva parenquiraatoaa o bronquial p¿
ra las exposiciones orgánicas.
Cuando este estudio se enfrenta a un desarrollo industri,
al de carácter explosivo como el nuestro, y con una dinámica apreta
da a un lapso corto de 20 años aproximadamente y cuando el proceso
va acompañado del incipiente desarrollo simultáneo de los otros pro
cesos de organización del sistema, como por ejemplo los registros y
las estadísticas, teniendo estas que sufrir en sus comienzos de la
misma imperfección, generan obstáculos para el valor de las aproximaciones en las inferencias matemáticas.
111
El presante estudio se hizo con la aplicación de las metodologías de salud, clínica, radiología, exámenes funcionales del
pulmón, aplicadas al diagnóstico de neumoconiosis en primer lugar y, en segundo lugar y con bastante validez para el diagnóstico de £
tras perturbaciones respiratorias como la bronquitis crónica ocupacional, separada o no de los efectos del hábito de fumar, el asma bronquial y los síndromes obstructivos respiratorios además del enfisema pulmonar. (12)
Representa un corte transversal del diagnóstico de salud
respiratorio para los años 1977 y primer semestre de 1978, en áreas
industriales expuestas a los riesgos de asbesto y sílice entre los
polvos inorgánicos; bisinosis, bagazosis y otras patologías respira
torias de las industrias del tabaco y pulpa de papel entre los ries.
gos orgánicos. El programa continuará hasta la cobertura de todos los riesgos y de toda una muestra suficiente por clase de riesgo.
El estudio especial para la población minera subterránea, se realizará durante el primer trimestre del año 1979.
Representa el resultado del diagnóstico de salud aislado
del diagnóstico ambiental, por la imposibilidad de realizar el moni
toreo pulvígeno simultáneo a las investigaciones médicas en todas
las plantas estudiadas.
Analizando pues, todo el problema a través del conocimien
to de las limitaciones, restó solamente enfrentar la decisión del estudio y la misma se hizo, a sabiendas de las posibles fallas esta.
dísticas, con el objeto de obtenec a la mayor brevedad posible, un
punto de referencia epidemiológico para los programas de prevención
de hoy y del mañana.
El criterio para la selección de exámenes de esta evalua_
ción epidemiológica, siguió estas pautas: 1o) Evitar pérdida innece_
saria de tiempo. 2 o ) No ofrecer riesgos ni inconvenientes al sujeto
examinado.3?) Tener el valor de predicción para estadios tempranos.
í°) Bajo costo. 5o) Factibilidad de relacionarlo cuantitativamente
al daño de salud. 6 ) Alta validez, es decir, sensibilidad y especi
112
fieldad para reflejar la situación verdadera que se investiga, Apa£
te de estas consideraciones metodológicas, fue necesario adoptar cierta flexibilidad en las normas y pautas de acuerdo a las condiciones de terreno inherentes a toda investigación de campo con equi
pos electrónicos instalados en Unidades Móviles. Por ejemplo, prefe
rir el estudio del grupo de las concreteras de la zona metropolitana por las posibilidades de hacer todos los exámenes en nuestro sex
vicio con óptimas condiciones de operabilidad. La historia clínica,
y el examen físico especializado, salvo algunas excepciones, se reja
lizó por personal médico especializado y se utilizó, como orienta—
ción, la ficha para polvos orgánicos del Servicio de Empleados y
productividad del Reino Unido y las orientaciones del EMAS (15)
CHIEF EMPLOYER MEDICAL ADVISERS del Reino Unido, cortesía del Dr. M.
Greenberg y se revisaron además los barridos específicos de Medicina del Trabajo, del Plan de Higiene y Seguridad del Trabajo en Espa
ña.
Los exámenes de función pulmonar se realizaron con equipos Jaeger, especialmente instalados para las condiciones de terreno y fueron diariamente sometidos a calibraciones, despula de cada
traslado. Se practicaron determinaciones espirométricas, curva flujo-volumen y pruebas de difusión con monóxido de carbono en estado
de equilibrio y la realización e interpretación correspondió a personal médico y técnicos especializados.
Los estudios radiológicos se hicieron con placas 14x17 pulgadas en las instalaciones fijas hospitalarias para los casos de
la zona metropolitana y para la población testigo con placas 100x100
milímetros con cámara Odelca en una Unidad Móvil en las plantas industriales y explotaciones mineras del interior del país. La interpretación la hicieron con doble lectura en la gran mayoría de los casos, médicos y neumonólogos clínicos de larga experiencia. Se uti,
llzaron las técnicas y las recomendaciones de la Organización Internacional del Trabajo aprobadas en Bucarest, en el año 1971, con oca
alón de la IV Conferencia Internacional de Neunoconiosis, pero, se
simplificó el dato final en el estudio de las Neumoconiosis a cuatro (4) posibilidades: normal, sospechoso, positivo y otros diagnÓ£
ticos. Todo el estudio fluorofotográfico se hizo a "boca de fábrica",
113
excepto las empresas de la zona metropolitana. Para el diagnóstico
de las perturbaciones respiratorias se estudiaron otros signos radiológicos de sobredistensión pulmonar con o sin signos de enfisema imarcado. El proceso general de la Encuesta siguió los lineamieri
tos del Informe Técnico N° 528 de la Organización Mundial de la Sa.
lud (15) (1973) y las evaluaciones estadísticas se hicieron con el
asesoramlento de expertos de la Organización Internacional del Tra_
bajo y la Dirección de Estadística Laboral del Ministerio del Trabajo de Venezuela. Los recursos presupuestarios para la adquisición
y el mantenimiento del programa se obtuvieron del Departamento
de
Tuberculosis y Enfermedades Pulmonares de la Dirección de Salud Pií
blica del Ministerio de Sanidad y Asistencia Social; y con el apo.^
yo regional de las Comisionadurías de Salud de los estados'Aragua,
Carabobo, Yaracuy, Lara, Falcón y Miranda, se realizaron las opera
ciones de terreno en esas Entidades Federales.
PROCEDIMIENTO:
Por lo menos 7 cifras se deberían conocer en nuestro
medio para manejar la evaluación de los problemas respiratorios
ocupacionales y especialmente conióticos, al saber:
1)
Población trabajadora en general expuesta a todos los riesgos
laborales. (17) (Tabla 1-1). Figura 1-1.
2)
Población trabajadora expuesta a riesgos respiratorios. (Ta-bla 1-2). Figura 1-2.
3)
Población trabajadora expuesta a contraer neumoconiosis. (Tabla I-3) (xx y xxx). Figura 1-3.
4)
Población trabajadora expuesta a ciertos riesgos específicos
entre las neumoconiosis por actividades económicas. (Tabla
1-3y
Tabla 1-4). Figuras 1-3-1, 1-3-2, 1-3-3. 1-3-4. 1-3-5
y Figura 1-4. y Tablas 1-5 y 1-6.
5)
Población mayormente expuesta de acuerdo a las áreas d.ej. proceso de explotación o producción para separar obreros y emplesi
dos en una primera etapa.
114
No es aconsejable definir la población por puestos de riesgos debi
do a la intensa rotación de puestos de trabajo que ha caracterizado este proceso entre nosotros desde sus etapas iniciales.
6)
Ciaras del Universo de trabajadores y obreros de los primeros
grupos seleccionados y
7)
Cl£ra de la muestra examinada y de la morbilidad proveniente
del muestreo.
7-1 Morbilidad respiratoria.
7-2 Morbilidad neumoconiótica propiamente dicha.
Para mejor comprensión resumimos en las Tablas 1-5 y
1-6, renglones específicamente relacionados con el primer muestreo
de la encuesta.
DATOS DEMOGRÁFICOS DE LA POBLACIÓN TRABAJADORA;
La tabla y la figura 1.1 recoge los datos de la poblact
ón trabajadora en Venezuela desde los años 1968 al 1977 ambos i n —
cluídos.
La línea de puntos representa la curva de tendencias
con unas estimaciones para los años 1982 y 1987 de .... 4-. 565.324trabajadores y 5.560.990 trabajadores; respectivamente.
Estos mismos datos se representan en la Tabla 1.1..
Figura 1.1.
Es de hacer notar el gran incremento en la población
trabajadora en Venezuela por un aumento en el cuatrienio 1973-1977
de 678.857 un promedio anual de 169.7H.por año frente a un promedio anual de crecimiento en el quinquenio anterior 1968-1973 de
89.117 trabajadores. Es decir, el promedio anual de crecimiento de
la población trabajadora en el cuatritenio 1973-1977 es el doble que en el quinquenio anterior 1968-1973. De acuerdo con las estima
ciones anteriormente realizadas este promedio, anual pasará a ser de 172.265 en el quinquenio 1978-1973 y de 161.870 trabajadores en
cuatrienio 1983-1987 de seguir el mismo ritmo de crecimiento que el encontrado hasta ahora.
115
Tobia 1.1
POBLACIÓN TRABAJADORA
VENEZUELA
(*) C¿i*a.A
t¿t¿mada*
116
1-8
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117
i
Tibia
I.I
TOTAL POBLACIÓN TRABAJADORA EXPUESTA
A ENFERMEPAPES PROFESIONALES RESPIRATORIAS
AÑOS
TRABAJAPORES
1941
1970
1975
77
I9*tf
1915
C¿4*44
155.49$
M*.315
151.445
154.450
173.924
111.519
191.III
19*.114
- ¿SI.117
153.192 •
141.I9S *
144.445 *
141.712 •
199.417 •
itO.Oit *
541,592 •
. 3*5.941. •
511.244 *
'41t.US *
44t.SU *
atinada*
118
\
•z
I
i
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-i
-I
Ss
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•
-I
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S
-I
n
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-I
-I
3
9
o
- 00
8
o
ö
— 1 —
8
o
s
2
S
§
—r
S
s
119
Población trabajadora con riesgo profesional respiratorio. En la figura 1.2 se recogen los datos de los trabajadores int¿
grados en las treinta y tres (33) actividades económicas señaladas
anteriormente y que son propensas a padecer una afección respiratoria de causas profesional.
La línea de puntos representa la curva de tendencia con
las estimaciones para los años 1982 y 1987 de .... 320.011 trabajadores y 4-42.316 trabajadores respectivamente. Estos mismos datos se
representan en la Tabla 1.2. Figura 1.2.
Obteniéndose como promedio asociados de crecimiento para
la población afecta de riesgo profesional respiratorio para el quiíi
quenio 1968-1973 la cifra de 9.127 y en el trienio 1973-1976 la cifra de 16.529 y unas estimaciones para el quinquenio 1977-1982 y
1982-1987 de 5.364 por año y 24.461 por año respectivamente.
POBLACIÓN TRABAJADORA CON RIESGOS DE NEUM0C0NIOSIS:
En la Tabla 1.3. se recogen los datos de los trabajadores con riesgos de Neumoconiosis.
La línea de puntos representa la curva de tendencia con
las estimaciones para los quinquenios 1977-1982 y 1982-1987. Las c¿
fras estimadas para estos quinquenios pueden observarse en la Tabla
1.3. Figura 1.3.
De esta misma tabla podemos observar que los promedios anuales de crecimiento de la población trabajadora expuesta a la
Neumoconiosis para el período 1968-1973 es de 7.810 trabajadores y
de 15.234 para el período 1973-1976 y unas estimaciones para el quiri
quenio 1977-1982 de 15.453 trabajadores por año y para el quinquenio 1982-1987 de 21.732 trabajadores por año.
Desglozando el Capítulo anterior en los diferentes riesgos específicos obtenemos los siguientes datos.
12o
Tabla.
1.3
POBLACIÓN TRA6AJAP0RA EXPUESTA
A LAS NBUIWCOUIOSIS
S
A N O
196 1
9
197 0
1
t
3
4
197 5
6
7
I
f
•
>
"
TRABAJAP0RE5
'
0
1
f
S
4
Ml 5
6
7
114.til
133.2*7
143.493
14t.476
151.496
163.994
173.191
139.t96
Í09.60Í
tlO.403 «
ff S. 15« '
fSl.fS« '
tS3.60t
'
169..46*
fl7.«7f
306.903
$14.74S
144.5*1
371.437
SI*.555
'
'
'
<
'
'
'
Clfuu -ikXJ.ma.Atk
121
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9
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tal
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J
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-1 i l
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Ul
i
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-2
i 1
122
M
POBLACIÓN TRABAJADORA CON RIESGO DE SILICOSIS:
En la figura 1.3.1 se recogen los datos de la población
trabajadora con riesgos de silicosis y que han sido enumerados por
actividades económicas anteriormente (parágrafo A.2.1)
La línea de puntos representa la curva de tendencia con
las estimaciones para los años 1977-1987. Las estimaciones para
1982 y 1987 son de 209.398 y 300.136 trabajadores respectivamente.
Estos mismos datos pueden obtenerse en la tabla 1.3.1. figura 1.3.1
Obteniéndose como promedios anuales para la población
laboral afecta de riesgos de silicosis las cifras de 5.301 trabaj¿
dores por año para el quinquenio 1968-1973 y de H.623 trabajado—
res por año para el trienio 1973-1976 y unas estimaciones para el
quinquenio 1977-1982 de 12.661 trabajadores por año y para el quin
quenio 1982-1987 la estimación es de 18.197 trabajadores por año.
POBLACIÓN TRABAJADORA CON RIESGO DE TALCOSIS;
En la figura 1.3.3» se recogen datos de la población
trabajadora con riesgos de talcosis y que han sido enumerados por
actividades económicas anteriormente (parágrafo 1.2.1).
La línea de puntos representa la curva de tendencia de
las estimaciones para los años 1977-1987.
Las estimaciones para 1982 y 1987 son de 8.949 y 10.660
trabajadores respectivamente. Estos datos pueden observarse en la
tabla 1.3.3. Figura 1.3.3.
Obteniéndose como promedios anuales de crecimiento para
la población laboral afecta de riesgo de Talcosis las cifras de
3Aí trabajadores por año el quinquenio 1968-1973 y un crecimiento
negativo para el trienio 1973-1976. Estas cifras negativas resultan
del crecimiento negativo del año 1976 respecto al año 1973 ya que
en el primer caso la población con riesgos de talcosis es de 6.81¿
trabajadores y de 6.234 para 1976. Estas cifras no se contradicen
entre sí si tomamos en cuenta que ellas solo reflejan los trabaja-
123
14
Tabla
t.S.I
POUACJOU TRABAJADORA EXPUESTA
A LA SILICOSIS
TRA3AJ Avoues
AÑOS
1900
¿m
1970
11
11
73
14
1915
7«
77
71
7»
1910
II
00
tS
$4
/90S
ti
. *1
* CH>uu
10.440
1
/ICI
•7. 0)1
0{.507
9 1.19*
100.215
Í07.Í49
M f. 071
fff.701
IS 1.019
144.09Í •
IS 4.990 •
H 0.719 •
It I.JI5 •
190.051 •
to9.J90 •
ti 5.5t* •
u 1.050 •
(S9.000 *
ti 9.000 •
so 0.1Jé •
titlmadcu
124
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oc
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s
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ai
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111
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2
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125
Tabía
f.).3
POBLACtOH TKABAJAVORA EXPUESTA
A LA TALCOSÏS
AROS
TRABAJADORES
5. 095
•
5 514
5
m
6 411
é. 59«
i.
tu
1 59%
1 105
6 254
1 512
1 IZO
t 057
t 344
t 641
9 til
9 591
9 «Jf
10 f f j
10 060
C¿¿*<u
tttA.ma.dcu
126
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•
•
•
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127
dores existentes en las actividades afectas de riesgo y que por razones económicas y otr.as en 1976 bajó a la cifra mencionada.
Las estimaciones del crecimiento anual para el quinque-nio 1977-1982 son de 287 trabajadores por año y de 34-2 para el quin
quenio 1982-1987.
POBLACIÓN TRABAJADORA CON RIESGO DE BISIHOSIS;
En la figura 1.3.4 se recogen datos de la población trabajadora con riesgos de Bisinosis y que han sido enumerados por actividades económicas anteriormente (parágrafo A.2.1)
Las líneas de puntos representan la curva de tendencia con las estimaciones para los años 1977-1987. Las estimaciones para
1982 y 1987 son de 25.098 y 26.697 trabajadores respectivamente. Es
tos datos pueden observarse en la tabla 1.3.4. figura 1.3.4.
Obteniéndose como promedios anuales de crecimiento para
la población laboral afecta de riesgos de Bisinosis las cifras de 669 trabajadores por año para el quinquenio 1968-1973 y de 19 trabsi
jadores por año para el trienio 1973-1976 y unas estimaciones para
el quinquenio 1977-1982 de 624 trabajadores por año y para el quinquenio 1982-1987 la estimación es de 721 trabajadores por año.
POBLACIÓN TRABAJADORA CON RIESGO DE BAGAZOSIS:
En la figura 1.3.5. se recogen datos de la población tr¿
bajadora con riesgos de Bagazosis y que han sido enumerados por actividades económicas anteriormente (parágrafo A.2.1)
La línea de puntos representa la curva de tendencia con
las estimaciones para los años 1977-1987. Las estimaciones para
1982 y 1987 son de 15.698 y de 20.640 trabajadores respectivamente.
Estos datos pueden observarse en la tabla 1.3.5. figura 1.3.5.
Obteniéndose como promedios anuales de crecimiento para
la población laboral de riesgos de Bagazosis las cifras de 686 tra-
128
Tabla, 1.3.4
•
P08LACJ0U TKABAJAVORA EXPUESTA
A LA UJ$i:WS13
A H0 S
TKABAJAVCRLS
u 9t$
15 Ut
H. 9ét
lé. 0S4
It 541
11, ni
19 i$i
11. ut
11. tti
H r97i
ti. 544
ti 149
ir«m
tt 4tt
ts 19$
15 655
U 41t
ts m
ts 954
U 491
(UiJuu
129
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ui
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2
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bl
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tabla.
1.3.5
VOÔLACICH TRABAJADORA EXPUESTA
A LA SAGAZOSlS
* « O S
TRAEAJAVOP.tS
1961
«9
»970
71
7f
75
74
1975
7«
77
71
7t
1940
«I
II
15
1«
1915
14
«7
5.615
4.716
5.415
5.1*1
7.1*7
7.04«
7.rjt
4.411
«.44»
9*091
9;«47
10.71r
-17,««4
tt.tu
•
15.691
14.141
14.159
17.511
19.015
20.640
•
•
•••
•
•
•: -
* C^iMU tMtA.ma.dM
131
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132
TABLA 1-4
POBLACIÓN TRABAJADORA EXPUESTA A 1A
MOKIUUIS
CRONICA PROFESIONAL
ENFISEMA
ASMA ÛCtiPACICNAE V OTRAS AFECCIONES RESPIRATORIAS
AROS
TRABAJADORES
lut 1
11.043
ti.041
Ì4.UI
IS.«54
14.421
ti.átS
ff.930
I7.5t0
ti.509
tí.719
Í4.44I
U.tlS
«4.114
- 3<r.f53
3*.339
34.414
37.1»!
39.»94
4Í.7«
45.^91
é\1
I97Í >
71
7S
7¡\
H1
W Ji
11l
7íi
- H1
H1
191(i
11
11t
f. 1
H1
IUI i
»i\
1)r
C¿{4&4
133
tAtimadcLA
•
•
•
••
•
•
*.
•
•
•
Hb
¡ó.;:;:.
\.:rb: p!::\
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bajadores por año para el quinquenio 1968-1973 y de 341 trabajadores por año para el trienio 1973-1976 y unas estimaciones para el
quinquenio 1977-1982 de 921 trabajadores por año y para el quinqué
nio 1982-1987 la estimación es 1.388 trabajadores por año.
POBLACIÓN TRABAJADORA COH RIESGO DE BRONQUITIS CRONICA PROFESIONAL.
ENFISEMA. ASMA PROFESIONAL Y OTRAS AFECCIONES RESPIRATORIAS:
En la figura 1.4 se recogen datos de la población traba
jadora con riesgos de Bronquitis crónica profesional, enfisema, a¿
ma profesional y otras afecciones respiratorias y que han sido enu
meradas por actividades económicas anteriormente (parágrafo A.2.1)
La línea de puntos de esta figura representó la curva de tendencia con las estimaciones para los años 1977-1987. Las e,s
timaciones para 1982 y 1987 son de 32.339 y 45.891 trabajadores respectivamente.
Estos datos pueden observarse en la tabla 1.4. figura 1.4
Obteniéndose como promedios anuales de aumento para la
población laboral afecta de los riesgos mencionados las cifras de
1.316 trabajadores por año para el quinquenio 1968-1973 y de 1.295
trabajadores por año para el trienio 1973-1976 y unas estimaciones
para el quinquenio 1977-1982 de 1.910 trabajadores por año y para
el quinquenio 1982-1987 la estimación es de 2.710 trabajadores por
año.
RESUMEN DEL UNIVERSO A ESTUDIAR:
Todas las 42 actividades que aparecen en los cuadros de
los sectores públicos y privados con riesgos, en general ligados a
la inhalación de polvos orgánicos e inorgánicos en explotaciones minera e industriales, hacen un Universo de 309.382 trabajadores
(7Í de actividad lextractiva y el resto de actividad manufacturera)
en 6.817 establecimientos industriales de 5 o más trabajadores repartidos en dos grupos: uno de empleados, el cual totaliza 70.355,
135
o sea el 25? y el restante, el más numeroso y más expuesto formado
por 239.027 obreros. Así pues, el Universo circunscrito al mayor riesgo de exposición sería de 239.027 personas, repartidas 154.293
en el área inorgánica y 84.738 en el área orgánica. La población más expuesta del área inorgánica se agrupa en 21 actividades de ajn
bos sectores totalizando 71.716 personas y se reducen menos en el
índice de riesgo de exposición por la variedad de factores que están en juego en la producción de la respuesta respiratoria a estos
agentes (ver Tabla 1-5 y 1-6).
PLANTEAMIENTO DE LA ENCUESTA:
El muestreo seleccionado se hizo combinando la lógica
de la representación obligatoria de la actividad, agrupación, grii
po y subgrupo para los riesgos de mayor jerarquía en la salud pública venezolana para los sexos, edades, tiempo de exposición esp¿
cífica en individuos escogidos al azar, dentro de las agrupaciones
previamente hechas de acuerdo al riesgo específico. (18) (19)
La primera etapa de la encuesta seleccionó 14 actividades, nueve de ellas del área de polvos inorgánicos con un universo
de 2:.762 obreros y cinco del área de polvos
orgánicos con un
universo de 32.8.4 obreros. El total de ambas áreas es de 58.586
obreros de un grupo de 73.296 trabajadores. El total de obreros re
presenta el 80Í del total de trabajadores y el 25Í de todo el Universo Nacional y el 35? de los grupos seleccionados para todo el estudio. (Ver Tabla 1-6)
GRUPO CONTROL;
La escogencia del grupo control fue precedida de una ajn
plia discusión de todas las condiciones necesarias para condicionar la validez de las inferencias estadísticas para todos los para
metros de la investigación. La primera condición fue elegir un gru
po humano no sometido previamente a contaminación intramural o extra-mural. De acuerdo a esta condición la ciudad de Coro ofreció las mejores garantías, debido a que esa ciudad no tiene un desarro
136
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Ilo industrial. Pero, posteriormente, cuando el análisis de la nraes
tra de casos estudiados en Coro mostró una sorprendente cifra de
procesos obstructivos especialmente asmáticos al cual se asociaban
alteraciones frecuentes de la columna vertebral de tipo escoliosis,
fue necesario hacer otra muestra testigo y se escogió la población
de Caucagua en el estado Miranda, donde existían las mismas condicio
nes relativas a la ausencia de industrialización. Como hecho de importancia la población sana respiratoria de Caucagua se caracterizó
por presentar una aparente incidencia aumentada de procesos vasculares del pedículo aórtico en los estudios radiológicos especialmente.
ANÁLISIS DE.LOS RESULTADOS;
Tabla 4-1. Muestra de Obreros con Riesgos de Silicosis.
Se estudiaron un total de 64.O obreros expuestos en mayor
o menor grado al sílice libre, pertenecientes a 18 empresas cuyas at:
tividades incluían la extracción,, utilización y/o transformación de
minerales con un mayor o menor contenido de sílice. Se clasificaron
en cuatro grupos según el riesgo teórico.
Grupo I
Canteras y piedras con 92 obreros
Grupo II
Alfarería, loza y porcelana con 147 obreros
Grupo III Cemento con 189 obreros
Grupo IV
Vidrios y fundición con 212 obreros.
El último grupo con 212 obreros tiene la particularidad
de asociar el riesgo silicótico, dado por la utilización de arenas
de alto contenido de sílice, el gran stress térmico que caracteriza
a las industrias de vidrio y la fundición.
La proporción de fumadores varía en conjunto desde un 27?
a un 10% del número de obreros de cada empresa y el tiempo de exposjL
ción medio es superior a cinco años.
La Tabla 4.-1, expresa los resultados encontrados en el es_
tudio de esta muestra. El análisis de estos resultados y su compara-
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ción con el grupo testigo nos conduce a las siguientes conclusiones:
1) Mayor incidencia de los diagnósticos específicos (silicosis) en
los grupos con mayor riesgo teórico, canteras, piedras, vidrios
y fundición y recíprocamente mayor incidencia de diagnósticos inespecíficos e independientes del riesgo en los grupos II y III
de alfarerías, lozas, porcelanas y cemento.
2)
Las alteraciones funcionales tienen la misma significación en los cuatro grupos.
3)
En la exploración clínica nos encontramos los mismos resultados
que en el capítulo "diagnósticos", mayor incidencia de patología en los grupos con menos riesgos específicos, pero, asociado
a factores de microclima laboral.
4)
La radiología tampoco aporta especificidad a ninguno de los grupos entre sí pero sí en relación con la muestra testigo.
5)
Excepto para lo que se refiere a la exploración clínica, (afectada siempre de gran subjetividad por no ser el mismo médico en
todos los casos) y más concretamente a la exploración del área
ORL, las diferencias en los demás parámetros, entre los grupos
estudiados y el grupo testigo son altamente significativas
(prueba x 2 de Pearson).
Tabla A-2.
Influencia del Tiempo de Exposición
Para estudiar la influencia del tiempo de exposición
clasificamos la muestra de 637 trabajadores en tres grupos:
Grupo
I Tiempo de exposición menor de 1 año (123 casos)
Grupo II Tiempo de exposición entre 1 año y 10 años (345 casos)
Grupo III Tiempo de exposición mayor de 10 años (169 casos)
Los resultados obtenidos en este análisis nos permiten
concluir lo siguiente:
a) La morbilidad específica por silicosis aumenta significativamen
te cuando se incrementa el tiempo de exposición hasta alcanzar,
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el grupo de mayor tiempo de exposición, la importante cifra del
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Este incremento se manifiesta también en las alteraciones funcionales, la exploración clínica y la radiológica.
c) El análisis estadístico de estas diferencias demuestra que son
altamente significativas (p 0,01) excepto en la radiología en
donde el nivel de riesgo es menor del 5?.
d) Al comparar cualquiera de estos grupos con el grupo testigo las
diferencias son también altamente significativas (p 0,01).
b)
Tabla 4-3. Influencia del Hábito de Fumar
Las diferencias entre ambos grupos
te significativas (N.S.) y al compararlas con
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radiología.
Tabla 5-1. Estudio de una Muestra de Obrero con Riesgo de Talcosis
El Universo de la población obrera sometida a riesgo de
Talcosis se encuentra muy atomizado en pequeñas industrias del ramo
de la cosmética por lo que no se ha abordado en esta primera etapa
del Programa de Neumoconiosis. En la industria del caucho se estu-dió en una planta un grupo de 36 obreros con alto índice de exposición y los resultados obtenidos se muestran en la Tabla 5-1.
Se destaca en la Tabla anterior el gran número de diagnósticos positivos encontrados (17Í) de obreros con patología específica correlacionados con un incremento de alteraciones funcionales restrictivas. Las diferencias con la muestra testigo son altamente significativas (p 0,01).
Tabla 6-1. Análisis de una Muestra de Obreros de la Industria Química
Se han estudiado un total de UU obreros de dos plantas
de industrias químicas relacionados con la industria de pinturas y
la fabricación de pesticidas. Estos obreros no están expuestos a un
144
riesgo específico de Neumoconiosis, no obstante el adverso microcli
ma laboral en que se desenvuelve su actividad hace presumir la aparición de alteraciones en la esfera respiratoria.
Los valores encontrados se muestran en la Tabla 6-1, así
como la comparación con la muestra testigo, pudiéndose extraer las
siguientes conclusiones:
1)
2)
Aumento estadísticamente significativo (p 0,05) de las alteraciones respiratorias inespecíficas y
Aumento altamente significativo (p 0,01) de los hallazgos radio
lógicos.
ANALISIS DE LA MUESTRA DE OBREROS SOMETIDOS AL RIESGO DE POLVOS
ORGÁNICOS:
Dentro del Universo de 64.738 obreros que están expuestos
a riesgos de alteraciones respiratorias por polvos orgánicos, se han
estudiado en esta primera etapa un total de 223 obreros, elegidos al
azar dentro de los obreros de ocho empresas encuadradas en las s i guientes actividades:
Ingenios y refinerías de azúcar
Hilados.de tejidos
Industria del tabaco
Alimentación
Artículos de pulpa de madera
Enzimas Biológicas - detergentes y papel
En este grupo los riesgos específicos característicos
son: el algodón que produce la Bisinosis y el bagazo de la caña de
azúcar productor de la Bagazosis. Sim embargo, dada la naturaleza or
gánica de las materias primas utilizadas predominantemente por estas
industrias son bastante frecuentes las alteraciones respiratorias de
naturaleza inespecífica, consecuencia de una especial sensibilidad de algunos individuos. Además hoy se sabe que puede existir cierto
grado de contaminación con substancias inorgánicas.
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TABLA 3.2.
Significación estadística de las diferencias y niveles de riesgo al aplicar l a
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Tabla 3-1. Análisis de los Resultados
La Tabla 3-1» muestra los hallazgos encontrados en cada
uno de los tres grupos que hemos subdividido la muestra. Los diagnósticos específicos fueron 23 casos de Bisinosis (34Í del total
de expuestos) y 6 casos de Bagazosis (19Í). Se detectó también una
Asbestosis contraída por el obrero con anterioridad al ingreso en
la fábrica de alimentos en que se encontraba en la actualidad. En
este mismo grupo es de resaltar la alta morbilidad en el grupo de
las azucareras (81? de diagnósticos patológicos) con gran predominio en las alteraciones respiratorias inespecíficas (58Í). Así miji
mo una alta morbilidad asmática (12$) en el tercer grupo formado
por obreros de la industria del tabaco, de la alimentación y de eri
zimas biológicas.
En el conjunto de las alteraciones funcionales destacamos el aumento de las patologías restrictivas en el grupo de las a.
zucareras que se diferencian significativamente con los otros que permanecen sin diferencias entre ellos y sin diferencia con la mues
tra testigo.
En esta misma característica presenta en la exploración
clínica el grupo de azucareras, con un porcentaje muy alto de halla¿
gos patológicos (97Í) de forma análoga no existen diferencias significativas entre los grupos textil, inespecíficos y testigos.
En los diagnósticos radiológicos se modifica en parte
la situación anterior siendo las diferencias entre todos los grupos
estadísticamente significativas excepto al conparar el grupo textil
con el inespecífico.
Un resumen de lo anterior lo mostramos en la Tabla 3-2,
con la significación estadística de las diferencias encontradas al
aplicar la prueba x2 de Pearson.
La Tabla 3-3» muestra estos resultados al clasificar con
juntamente la muestra según el hábito de fumar, eligiendo como testigo el grupo de no fumadores de la muestra testigo anterior. No
existen diferencias estadísticamente significativas entre ambos gru
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pos (fumadores y no fumadores) y se hacen muy ostensibles las dife
ferencias entre cualquiera de estos grupos con el grupo testigo.
Por último la Tabla 3-i, presenta los resultados de esta muestra al disponer los grupos según el tiempo de exposición.
No siendo las diferencias entre el segundo y el tercer grupo estadísticamente significativas; y siendo naturalmente significativas
las diferencias entre cualquier grupo y el grupo control.
CONCLUSIONES GENERALES DEL ANÁLISIS DE LAS DOS MUESTRAS :
1)
Pese a que en la muestra testigo elegida había una gran incidencia de alteraciones respiratorias por la frecuencia del asma bronquial, es clara la diferencia entre esta muestra testigo y cualquiera de las poblaciones examinadas. Estas diferencias se acusan más en el diagnóstico integrado y en la radiografia que en la exploración funcional y clínica.
2)
El grupo de obreros que trabaja en azucareras se encuentra más
afectado que el grupo textil y el inespecífico siendo muy notable la presencia de Neumoconiosis específicas en los dos prjL
meros (37? y 19?) y de alteraciones inespecíficas en el tercero (67?). Este grupo lo formaron obreros de la industria del tabaco, artículo de pulpa de madera y papel de fabricación de
alimentos.
3)
La patología debida al clima laboral es más importante que la
del cigarrillo, al encontrarse dañado casi por igual el grupo
de fumadores y el de no fumadores. Ya vimos en el Volumen I
que en relación con el asbesto se incrementó la patología muy
especialmente al sumar tiempo de exposición y hábito de fumar.
Las estadísticas muestran mayor significación cuando se incluyen en el grupo de los no fumadores a los fumadores del grado
uno.
151
í)
Las alteraciones cauaadas por polvo organico son a diferencias
de los inorgánicos bastante independientes del tiempo de expos¿
ción.
ANÁLISIS ESTADÍSTICOS DE LOS RESULTADOS DEL PROGRAMA DE INVESTIGACIÓN
MEDICA EN LA MUESTRA DE TRABAJADORES CON RIESGO DE ASBESTOSIS
INTRODUCION:
El Volumen I contiene los detalles de la metodología,las
características de los grupos estudiados y los resultados individua^
les para cada grupo de los exámenes clínico, radiológico y funciona
les del pulmón. Las páginas siguientes contienen el análisis estadístico de toda la muestra en conjunto.
Para este estudio de asbestosis recordemos que fue sele£
clonada de un total de siete empresas con 1.500 trabajadores que utilizan asbesto como materia prima para la fabricación de bandas de
frenos y cloches como materiales de fricción, baldosas fibro-plásti
cas con asociación de asbesto y polivinil, materiales de fibro-ce —
mento para la industria de la construcción y, finalmente, materiales refractarios e hilados para ropas de protección contra incendio,
cintas, mecates, etc.
Se estudiaron un total de 253 obreros que dentro de un total de 1.500 fueron escogidos al azar dentro del grupo de exposición media de cada centro de trabajo. Para ello fue dividido el total de tiempo de exposición, es decir desde el comienzo del funcionamiento de la fábrica hasta el momento del estudio, en cuatro partes iguales y de las dos partes medias (que representa el 50Í del tiempo de exposición) se eligieron al azar los integrantes de la
muestra. Ver Tabla 2.
Los 253 obreros estudiados fueron clasificados de acuerdo con dos criterios, primero presencia o no de hábito de fumar,
152
segundo tiempo de exposición.
No se hizo la selección por puestos de riesgos debido a
la uniformidad ambiental de las plantas estudiadas lo cual quedó demostrado por las determinaciones del polvo en suspensión y fibras
de asbesto por encima de los niveles permisibles en todos los puestos de trabajo y segundo por la rotación intensa de los trabajadores dentro de las plantas.
En cuanto al primer criterio de clasificación la muestra
presentó un 80Í (202 casos) de no fumadores y un 20Í (53 casos) de
fumadores. Fueron considerados como no fumadores tanto los no fumadores propiamente dichos como los que fumaban menos de 10 cigarrillos al día por períodos cortos de tiempo y como fumadores los que
fuman más de 10 cigarrillos al día.
Para la clasificación con arreglo al segundo criterio
(tiempo de exposición) se han considerado tres grupos:
a) Grupo Cero:
Formado por aquellos trabajadores que llevan menos
de un año en la empresa.
Este grupo se ha adoptado como grupo control.
b) Grupo Uno : Formado por aquéllos trabajadores que llevan entre
uno y diez año en la empresa.
c) Grupo Dos : Formado por aquellos trabajadores que llevan más de
diez años en la empresa.
La distinta proporción de fumadores en estos tres grupos
fue del 13.5íí 22? y 20,6%.
Desde el punto de vista médico el estudio realizado i n cluye: anamnesis e interrogatorio con especial atención a las enfer_
medades respiratorias; segundo, conocimiento clínico del aparato
respiratorio; tercero, pruebas funcionales respiratorias; cuarto, radiología del tórax.
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RESULTADOS:
Resultados obtenidos para los grupos de no fumadores se
muestran en la Tabla 2.1. Es de señalar que tanto en las pruebas funcionales respiratorias como en la radiología de tórax, por fiif¿
cultades inherentes a todo estudio de este tipo, no se realizó a todos como sería de desear todas las pruebas; este hecho explica que únicamente se dispongan de 155 diagnósticos en los del grupo de no fumadores y 40 en el grupo de fumadores. Para la comparación
estadística entre ambos grupos se han considerado:
a) Diagnósticos totales
b) Alteraciones funcionales
c) Diagnósticos neumonológicos más específicos
d) Alteraciones clínicas
e) Alteraciones radiológicas.
Se reunieron en un mismo grupo los diagnósticos de as-bestosis y sospechosos de asbestosis que indudablemente represen-tan estadios precoces de la enfermedad.
La significación estadística de las diferencias encan—
tradas entre estos dos grupos se muestran en la Tabla 2.2.
En la Tabla 2.1, se muestran los datos obtenidos en los
tres grupos considerados al clasificar la muestra según el tiempo
de exposición.
Por último en la Tabla 2.2, se analizan las significaci^
nes estadísticas obtenidas entre los diferentes grupos.
CONCLUSIONES:
1) La inspección de las tablas 2.1 y 2.2, nos demuestran cómo el
hábito de fumar perjudica extraordinariamente a la salud del trabajador independientemente de las condiciones insalubres
que pueda tener el puesto de trabajo y que son indudables en el caso de la muestra estudiada.
156
157
2)
En cuanto a la patología específicamente laboral la inspección de las tablas 2.1 y 2.2, nos demuestra ese hecho
ya señalado de un incremento claro de la patología según
aumenta el tiempo de exposición.
3)
Utilizando los valores numéricos obtenidos en las pruebas
funcionales para capacidad vital forzada, índice de Tiffe
ñau, flujos expiratorios máximos, volumen residual y co cíente volumen residual a capacidad total, expresado en
porcentajes respecto al valor teórico para cada obrero,
así como los valores obtenidos para las presiones parciales de oxígeno y anhídrido carbónico e índice de difusión,
se realizaron estudios de correlación comparándolos con el
tiempo de exposición intentando encontrar tiempo de expos i.
ción crítica pero sin resultado positivo.
A)
Se compararon los resultados obtenidos en el estudio anterior con una muestra testigo de 135 personas alejadas del
medio industrial elegidas al azar con una composición siini
lar en cuanto al porcentaje de fumadores y promedio de
edad. El estudio comparativo entre esta muestra y el Grupo Cero (trabajadores con menos de un año de exposición)
no dio diferencias estadísticas significativas.
158
BIBLIOGRAFIA
1
Memoria V Congreso Venezolano de Salud Pública.
Octubre de 1976.
Caracas, Parque Central.
9-16
.2
Extracto de una.Encuesta Preliminar para determinar las Condiciones de Trabajo en
la Industria de Venezuela. Ing* Erich Schmith Smith y Sr. Carlos Ruiz Quintana.
19 - 25 de Noviembre de 1956.
3
Informe al Gobierno de Venezuela de la Misión Multidisciplinaria del PIACT, que visito al país del 8 - 2 9 Noviembre de 1976. PIACT/MDT/1. Oficina Internacional
del Trabajo. Ginebra. Abril 1977.
4
I Congreso de Ciencia y Tecnología.
5
Memoria VI Congreso de Tisiologia y Neumonología. Ciudad Bolívar. Junio - Julio
1969. Revista de Tisiologia y Neumonología. Volumen 11 Nos. 1 y 2. Junio Diciembre 1969. Instituto Nacional de Tuberculosis y Enfermedades Pulmonares.
El Algodonal - Caracas - Venezuela.
Caracas - Parque Central. 1975.
6
Memoria de la IV Reunión de la Comisión Nacional de Fisiopatologia Cardiopulmonar
Celebrada en Ciudad Bolívar. 4 - 5 Diciembre de 1970. Instituto Nncional de Tuberei!
loéis y Enfermedades Pulmonares. Publicacions "Fisiopatologia Cardiopulmonar.
Fl Algodonal - Caracas - Septiembre de 1971.
7
Gaceta Oficial de la República de Venezuela. Año C H I - Mes VII. Caracas: Junio
3 de Mayo de 1976. N" 30.972. Decreto N"1543 del 27 de Abril de 1976.
8
Informe Especial presentado al Ministerio' de Sanidad y Asistencia Social y Ministerio del Trabajo. Actividades Comité Nacional de Neumoconiosis desde 1968 hasta
1976.
9
Archivo Comité Nacional de Neumoconiosis. Informe del Asesor Técnico de la Dele
gación Gubernamental a la 61a. Reunión Internacional del Trabajo. Ginebra - Junio
1977.
10
Actas Provisionales N°22 de Vigésima Cuarta Sesión. Viernes 17 de Junio de/1977.
(Pueden consultarse Actas Provisionales 17 A y 17 B precedentes)'
11
Anteproyecto Ley Orgánica Sobre Condiciones y Medio Ambiente de Trabajo.
rio del Trabajo. 1978.
12
Encuesta Nacional. Volumen I. Ministerio del Trabajo. Comité Nacional de Neun»
coniosis. Decreto Presidencial 1543. Tipografía Mauro. Marzo 1978.
13
Memoria en preparación de la V Conferencia Internacional de Neumoconiosis.
vo Comité Nacional de Neumoconiosis).
14
Epidemiología. Segunda Edición. Dr. Anibal Osuna. Fondo Editorial de la Escuela
de Salud Pública. Universidad Central de Venezuela y Ministerio de Sanidad y Asie
tencia Social. Caracas 1973.
159
Ministe
(Archi
15
Evaluación de Programas de Higiene del Medio. Organización Mundial de la Salud.
Series de Informes Técnicos N°S28. Ginebra 1973.
16
Employment Medical Advisory Service.
Guidance. 1973.
17
Anuario de Estadísticas del Trabajo 1977.
nisterio del Trabajo.
18
Estadística para las Ciencias Administrativas.
Copyright. 194 by Me Graw Hill INC. Usa.
19
Metodología de Investigación. Tercera Edición.
nezuela. Hijos de Ramiro Paz. S.R.L. 1977.
Chieg Employment Medical Aviser'«. Notes of
160
Dirección de Estadística Laboral. Mi-
Segunda Edición.
Lincoln L. Chao
Carlos A. Sabino.
Impreso en Ve
F/9
LA SILICOSE AU BRESIL - ETUDE EPIDEMIOLOGICHE FONDEE
SUR UNE ANALYSE DES HOSPITALISATIONS DA'NS LES
ETABLISSEMENTS POUR TUBERCULEUX
R. Mendes
Brésil
On sait que la tuberculose pulmonaire complique souvent l'évolution dû la silicose, donnant lieu à une silicotuberculoee. Dans
le dessein d'élargir les connaissances actuelles sur l'épidémilogie
de la silicose au Brésil, l'auteur a anlysé de près les anamneses
de 3.'4^0 naïades adultes du sexe masculin hospitalisés pour tuberculoso dans 2.7 établissements spécialisés du sud-est du Brésil.
Les recherches effectuées sur des dossiers professionnels complets ont révêlé l'existence de 327 cas "suspects" de silicotuberculose (9i5 pour cent des enquêtes). Trois médecins possédant une
grande expérience des pneumoconioses (doux pneunalogistes et un
radiologiste) ont étudié les clichés thoraciques de ces malades
sans connaître leur dossier et san6 se consulter; dans 119 des cas
(3,5 pour cent), ils ont constaté dos signes positifs do pneumoconioses ou des images suspectes.
En appliquant ce taux de silicotuberculose à l'ensemble des
admissions d'adultes du sexe masculin enregistrées en 1977 et compte
tenu de la fréqr.onco de la fréquence de la tuberculose parmi les
silicotiques - elle est de 3,3 pour cent au Brésil -, on peut estimer a 30.000 environ le nombre des silicotiques au Brésil.
Ils ont présenté certaines des caractéristiques épidêniologiqueR dos 119 cas décèles: âge, lieu de naissance, lieu d'exposition a la silice, activités professionnelles, durée d'exposition.
En concluant, l'auteur relève l'importance de la silicose
en tant que problème de santé publique, et voyant une maladie
professionnelle à laquelle il convient qeu les organismes spécialisés du Brésil attachent une importance prioritaire.
161
n/3
I i\ STITronr nn,|C; II»T K-TMF n~ SOOTM-FI upr) OF Tllf'TSTF
r.rPRNFfl - A. r.unrMFTl - ft. RFM KMFnFR _ ST! VTA HAHOR
I.. Fl. Nr*Kl
Institut Hfi Pneumn-Phtisinlnnie de l'Ariana, Tunisie.
CRB dernières anníss, nnus avons nhsen/i un nombre important He silicose et si 1 icn-tuh.erculose a un stade avancé nrovenant d'une mine de spath-fluor. Par conséquent, nous avons
decidí d'entreorendre une enquête radio-clinique succossive
afin d'étudier et mieux connaître 1'étinnathooénie de ces formes nraves de silicose et silico-tuberculose.
La fluorine mi spath-fluor (Ca F«) est un minerai utilisé
dans une l a m e mesure dans l'industrie et notamment pour la
production de l'acide fluorhydrique.
Le contenu en silice libre (SiO_) de la roche mere varie
de.15 a 30 " suivant les qisements.
Les conditions de travail sont encore rudimentaires: sans
mécanisation suffisante et sans mesures efficaces de prévention.
L'abbatane se fait au marteau-piqueur et a sec. Il n'existe
jusqu'à Présent ni forane a l'eau, ni arrosaoe des déblais de
roche, ni ventilation mécanique efficace.
NATFRIFL FT HETH0DFS :
La mine concernée a un effectif rie 600 employés environ.
Nous avons effectué deux dépistaoes radioloninues successifs
a l'intervalle de deux ans sur des films de 10/10 cm. Tous les
suspects ont bénéficié d'une radiooraphie standard.
Certains d'ontre eux ont subi des explorations fonctionnelles (snirométrie simple), une na7ométria (un nombre réduit)
et pour SS cas, nous avons nratioué trois bacilloscnnies et
trois cultures D O U T r "
163
Parallèlement, nous avons entamé das sxpériences sur
des animaux da laboratoire avec la poussiere de galeries
récoltée de différents endroits.
RESULTATS ET COMMENTAIRES :
A l'occasion du premier dépistage (en 1976), nous avons
examiné 541 ouvriers, soit 90 % dea employas.
Il est a souligner que 70 % dos ouvriers examinés ont
l'âge antre 21 et 40 ans. Globalement le résultat radioloqique est le suivant:
(Suite) Tableau No. 1
164
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50/íi dB3 sujets ayant une imane thoracique normale nrésentent des calcifications hilaires, témoin d'une ancienne
primo-infection radioloqlquemsnt patente et 3,6 % des lésions séquellaires parenchymateuse3 ou pleurales. Ces constatations reflètent une certaine qravité do l'endémie tuhnrculRiise du milieu ambiant.
L'emphysnma sans autres sinnes de silicose représente
3,1 "*i. Etant donné le bas aoe des sujets atteints, il nous
semble otre au premier lieu la conséquence de l'empoussiéraoe professionnel.
Par contre, les anomalies de la si-
louette cardiaque ont été rencontrées dans la tranche d'ane
allant de 50 à 60 ans.
Finalement, 72 cas ont été retenus (13,3 %).
Ils ont
tous bénéficié d'une radiographie standard; 55 d'entre eux
de trois bacilloscopies et 3 cultures pour B.K.; 40 d'une
spirometrie simple et 8 d'une gazomôtrie.
A la lumiere de ces examens, ils se répartissent ainsi:
Tableau No.2:
72 CAS SUSPECTS DES 541 EXÁNIMES
SILIC0SILICOSE
SILICOSE TURERCULOSE SUSPECTEE
39
8,655
8
^
12
TUBERCULOSE
STABILISEE
10
2,2 %
1,B %
AUTRES
TOTAL
3
72
0,5 %
13,35«
!>''' ( Il (' ' t
Les cas do silicose et rie silicn-tuherculose sont analysé
par raoport a l'ane, a l'ancienneté au poste de travail et a
la situation familiale.
166
Tableau No. 3 : CAS OF SILICOSE: SELON LES STADES
RnnioLcninuEs,
AHE, ANCIENHETE ET NOMBRE D'ENFANTS
Silicose p
Silicose q
Silicose A
Silicotuberculose
15(31,9 %)
à (B,R ?,)
R (17 ?5)
NOFIRRE OE CAS
2n D (á?,55?)
Ane moyen/ans
39
AnciRnneté au
travai l/ans
8,2
Nombro d'enfants
à leur c h a m e
4,2
39,7
43,2
43,2
10
11,2
10,5
4,5
3,8
4,3
On constate tout d'abord que l'âge de9 mineurs atteints est
relativement bas (41 a n s ) . La durée d'exposition au risque est
assez courte (10 a n s ) .
Le taux de silico-tuberculosB éleva.-Une fois la silicose
installée et le mineur restant dans les mêmes conditions de
travail, l'évolution de la maladie sera plus rapide.
En dehors du terrain silicotique prédisposant le nourcentaqe
de silico-tuberculose élevé est beaucoup plus en relation avec
l'endémie tuberculeuse de la rénion.
Au point de vue ôpidémio-
looique, la silico-tuberculose représente 1,4 % du total des
mineurs examinés et 17 % des silicotiques.
Sur la plan fonctionnel, les résultats de la spirometrie
simple sont les suivants:
167
Tableau No. 4: LA SPIROMETRIE DE 40 CAS
SYNDROME
OBSTRUCTS
25 %
SYNDROME
RESTRICTIF
SYNDROME
PlIXTE
' NORMAL
30 %
5 «í
40 %
Il nous semble que celles-ci n'apprécie pas suffisamment
le degré ráel de la perturbation fonctionnelle respiratoire.
La majorité de sujets atteints (60 %) présentent un syndrome
mixte (30 %) et restristif (5 %) témoin d'une fibrose d'origine
professionnelle chez des sujets relativement jeunes.
Par contre, la gazométrie comparée a l'E.f.R. (exploration fonctionnelle respiratoire) nous paraît plus suggestive
quoique il s'agit d'un nombre limité des cas.
On note une baisse plus ou moins importante de la Pa 02
(soit 7/8 cas) au repos même en regard d'une E.F.R. normale.
A l'effort imposé (un équivalent de 40 U) ces sujets présentent une baisse notable de la Pa 02.
Malgré le nombre réduit des malades explorés, on constate
une Pertubation gazométrique sionificative s'installant déjà
dans des formes débutantes.
Apres deux ans,un deuxième dépistage intégral a été effectué (480 ouvriers examinés). On note une léoere diminution du
nombre de nouveaux 3ilicotique3 (33 cas soit 6,8 %), sans formes oravfis nt une chute appréciable de la filino tuberculose
(2 cas oour 33 silicoses soit 6 %).
168
T a b l e a u n° 5 : IA GAZQKETRIE DE 8 CAS AU JìEPOS ET A L'EFFORT (40 ff)
•
Pa 02 rrn Hg
N" COURANT
DE
MALADES
Pa C02 mu Hg
•
THORAX',
Repos
'.
Repos
Effort
52
:
Effort
1
27
42
C.V
117 X
V.M.M. . . . 119 X
V.E.M.S. . 79 X
Silicose
r
42
44
C.V
101 X
V.M.M. ... 32 X
V.E.M.S. ... 44 X
Silicose
A
1
78
1
E.F.R.
1
7Z
2
.
•
\
3
8S
82
40
37
C.V
V.M.M. ....
V.E.M.S. .
76 X
S3 X
48 X
Silicose
B, o
4
7S
77
4b
42
C.V
100 X
V.M.M. . . . 39 X
V.E.M.S. . 75 X
Silicose
p, 2
S
72
69
40
6
7
8
\
7S
70
82
80
90
.
54
36
'. 32, S
43,5
C.V
305 X
V.M.M. . . . 57 X Silicose
' V.E.M.S. . .. 63 X
'. 37
33,5
'. 46
169
r
' C.V
70 %
V.M.M. . . . 46 %
' V.E.M.S. . . 73 X
Silicose
A
' C.V
80 X
[ V.M.M. ... 54 X
'^V.E.M.S. . 57 S
Silicose
A
' C.V
V.M.M. . . .
V.E.M.S.
.
Silicose
p
102 X
99 X .
83 X
Parallèlement, des expiriences sur Hns animaux de laboratoire ont iti effectués ause la nnunsiam rio paierie. Cotte
poussiere de fluorine ainsi ricoltie:cootient 9,5 % de silice
libre (Sin?). Pn a utilisé des rats d'un noido moyen de 20^0.
La poussiere auec ries particules rie moins rie 5 microns de diametro n iti administrée par injections intra-trachiales a dose de oP mn/ml sérum physiolonique-animal. 15 animaux ont iti
ainsi emnoussierís et un lot timoin de 10 autres ont repu oar
la memo unie 1 ml de sirum physiologique.
Tous les animaux ont survaicu a 1'empoussiiraoe. flores
trois mois, tous ont été sacrifiis. On constate que:
1) le poids des poumons empoussiéris a aunmenti par
rapport au lot timoin;
2) aunmentation sipnificative du poids des nanqlions
trachéo-bronchiques traduisant un intense nettoyane
par voie lymphatique;
3) 1'hydroxyproline sionificativement aunmentie (intensification du processus de riticulisat.ion et de collaninose) - Tableau 1 A l'examen histolooique, le poumon prisante un important
processus inflamatoire a tendance nodulaire ipars et par ailleurs, des amas de cellules desquamatives lymphocytes et macrophages.
Pn note aussi (coloration HömfTri) une hyperplasia de9 structures riticulaires et une tendance a la formation des nodules.
Les risultats de ces expériences confirment une fois de
plus le risque nneumpcnni ot.i que élevé de la poussière de gnathfluor et concordent aven les observations cliniques.
17o
FN
cnrirLusTPr' :
n la suite fin l'étude effectuée, on trouve un taux élevé
r)R s.ilirnsn, rnpin'r>mRnt évolutive, entraînant uns invaliditi?
profRPsionfiRlle n un haï Ain (41 ans); un noiirc^ntane innulé—
tent rin si]ico-tuberculnse (17 'Í). f>s constatations sont
rattachées a plusieurs facteurs :
1)
les conditions de travail encorn rudimentaires sn-
2)
le taux elevi? de silice (Si 02) dans la poussiere de
trainnnt un empoussiérane massif;
naleries;
3)
le panqué de mesures de techniques de prévention;
à)
le role potentialisateur de la fluorine;
B)
ânfin, la pravità de l'endémie tuberculeuse dans
la rénion.
Notre expérience montre qu'une prévention médicale a vu
a elle seule renres9er le nombre et les complications de cette
redoutable maladie professionnelle.
171
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nifi, innre», M: i r
1) RARWtn C. - ROTARU L. - PETRESCU
"Recherches experimentales
histo-chimiques
sur les rmxcopolysacc1vnrid.ee
dans la
silicose"
Archives des Maladies Professionnelles
28,10/11 : 7G7-778 Oct; Nov. 67.
2) '. BARBAD' B.. - FSTRESCU L.
"Réaction physiologique
de l'appareil
respiratoire
sous l'influence
Poussières
chez les malades atteints
de
silicose"
Arch, des Mal. Prof. T. 23 N"4 (S p. 230-239 Avril 62
des
3) BRUCH J. :
"Lufthygiene
und silikoseforschnng
jahresberich,193Z,
seile
125.
4) J, ÇBAMPEJ et FOURIER P.
"Quatre cas a'ostéopathies
par intoxication
Ann. «ed. Leg. N" S •*• 1954 pp 1-7.
fluorée
chronique"
5) CBAMPEX J.
"Observations récentes
d'Osteoporose
fluorée
Arch. Kai. Prof. T. 21 - N"6 1966 - 357-361
professionnelle
6) CORNEA G. - EL GHARBI V. - L. EL MEKKI - M. ZBIBA
"Le profil
clinique
et radiologique
des moiades silicotiqves
à l'Institut
de Pneumo-Phtisiologie
de l'Ariana "
Congrès Maghrébin de Médecine - Mai 1975.
hospitalisés
7) CORNEA G. - GHACRFM A. - BEN KHEDER A. - EL MFXXI L. et BOVACHA H.
"H propos du dépistage
des pneumoconioses dans les mines de Tunisie"
ZVèmes Journées Nationales
de Médecine du Travail
Strasbourg - 10*13. Mai 1978
8) CRETEAUmi Gh - VRSULESCÜ GR -.K.
Congr, Nat; IT de Igiena,
IEREftTCWC. •* P. DVMITm, 7. PISLARU
Bucuresti
1968, P. 188.
9J LVTON et J. CBAMPEX ..
"Etude sur les pneumoconioses dans les gisements de
Ar de Mal. Prof. - T.12 N" S •* 1951 - pp 506^ 518.
spath-fluor"
10) EL MEKKI L; - CORNEA G. - EL GRARBI B. - HAMZA R. - ZBIBA M. - BEN KHEDER A.
"La silicose
pulmonaire
1971 - 75"
Tun. Med. N" 4 juillet
en Tunisie
à propos
de 114 cas observés
en 5 ans
Août 1976.
11) PESTIAVT ,T.L. - LOVSSAIEF M.L. - SANCHOU M.
"Le problème de la Silicose
dans une mine de fluorine
Tun. Med. Nov.- Dec. 74 p. 337.
en
Tunisie".
12) POÎ.TCARD et A. COLLET
"Recherches expérimentales
sur la nocivité
(fluorine) ".
Arch; Mal. Prof. T. 24 N" 2 - 1953.
173
des poussières
de
spath-fluor
La silicosis en una mina de espato-flúor
de Túnez.
G. Cornea, A. Ghachem, A. Ben Kheder, S. Gabor
y L. El Mekki (Túnez)
Hemos llevado a cabo en una mina de espato-flúor en
la que trabajan unos 600 obreros dos controles radiológicos sucesivos con un intervalo de dos años. Las condiciones de trabajo son todavía rudimentarias. La presencia de
SiO- (sílice) libre en el polvo de las galerías es de 9,5
por ciento.
En el primer control (1976), se descubrió que el 8,6
por ciento del personal sufría de silicosis, con formas
avanzadas en una cuarta parte de los casos.
La asociación con la tuberculosis (silicotuberculosis
- B.K. positivo) representaba el 17 por ciento. La edad
media de los enfermos era de 40 años, y la duración media
de exposición al riesgo, de 10 años.
La espirometría simple resulta perturbada en 60 por
ciento de los casos. La gasometría efectuada con 8 enfermos muestra una disminusion más o menos importante de la
Pa0?, incluso en descanso, pese a una exploración funcional normal.
Transcurridos dos años, se ha procedido a un segundo
control radiológico integral. Se observa una ligera disminución del número de víctimas de silicosis, sin formas
graves y con sólo dos casos de silicotuberculosis.
Paralelamente, se empolvó con polvo de las galerías
a animales de laboratorio que han sido sacrificados al cabo de tres meses. Se ha comprobado lo siguiente:
1) aumento del peso de los pulmones empolvados en relación con el grupo testigo;
2) aumento apreciable del peso de los ganglios tráqueobronquiales, lo que traduce una intensa limpieza por
vía linfática]
3) aumento significativo de la hidroxiprolina (intensificación del proceso de reticulización y de colagenosis).
174
Eh el examen histológico, el pulmón presenta un importante proceso inflamatorio con tendencia nodular dispersa y también aglomeraciones de cédulas descamativas,
linfocitos y macrofagos.
También se observa (coloración GSraöri) una hlperplasia de las estructuras reticulares y una tendencia a la
formación de nodulos.
Los resultados de estas experiencias confirman una
vez más el elevado riesgo de neumoconiosis que entraña el
polvo del espato-flúor y concuerdan con las constataciones
clínicas.
175
VARIABILITY IN THE X-RAY DIAGNOSIS OF EARLY SILICOSIS *
J. Prenafeta G., G. Leyton M. and R. Sepulveda M.
(Chile)
In 50 workers exposed to a silicotic hazard a posteroanterior chest radiograph was performed.
Everyone of these radiographs was read by 7 experienced
physicians.
In addition, 4 of them made a second reading of
the same films. So, each film was read 11 times.
The readers had to conclude on the existence or absence
of X-ray signs of silicosis.
No unconclusive diagnosis was
allowed.
Results showed that there was a diagnostic agreement in
72% of the cases, ranging between 50 and 90%. The standard
deviation was 9.2%.
Only 7 films were informed as negative for silicosis in
the 11 readings. On the other hand, there was no film informed
as positive for silicosis in the 11 instances.
*
Papers "in extenso" can be asked to the authors.
177
EXCESS LUNG CANCER RISK IN SILICOTIC CASES*
UNDER HOSPITAL CARE - PRELIMINARY REPORT
(Summary)
K. Chiyotanl, Ken-ichi Saito
Rosal Hospital for Silicosis Fujiwara, Tochigi, Japan
In the Rosal Hospital for Silicosis, a special hospital
for pneumoconiosis in Japan, 15 deaths in patients with silicosis complicated by lung cancer were observed In 1966-77.
The average age at death was 64.5 + 9.1.
While past surveys showed that the average death age
of silicotics as a whole In this hospital was 47.1 + 7.8
In the period 1950-54, becoming older year by year, recent
surveys demonstrated that the average death age did not reach
the age for cancer death quoted above, even in the period
1971-75.
Therefore, the relative risk of lung cancer In sili-
cotics was calculated from the data obtained after 1971.
This study showed that silicotics had a considerable
excess risk of lung cancer.
The necessity to shed more light on the relations between silicosis and lung cancer is stressed, though such a
relation has been rejected for several years.
* Paper "In extenso" to be asked to the authors.
199
Agravación del riesgo de cáncer de pulmón
en los enfermos de silicosis internados
en hospitales.
Informe preliminar
K. Chiyotani y Ken-ichi Saito (Japón)
En el Hospital Rosai para Silicosis de Japón se observaron 15 defunciones de enfermos de silicosis complicada con cáncer del pulmón entre 1966 y 1977, y el promedio de edad en el momento de la muerte era de 64,5 + 9,1.
Si bien las investigaciones anteriores muestran que
la edad promedio de muerte por silicosis en enfermos hospitalizados era 47,1 ± 7,8 en el período 1950-1954, y
que avanzaba anualmente, los estudios recientes de los
autores demuestran que la edad promedio de muerte no alcanza el nivel de los casos de muerte por cáncer mencionados ni siquiera en el período 1971-1975. Trataron, en
consecuencia, de calcular el riesgo relativo de cáncer
de pulmón en los enfermos de silicosis a partir de los
datos obtenidos después de 1971.
El presente estudio muestra que el riesgo latente de
cáncer de pulmón está muy aumentado en los enfermos de
silicosis.
Los autores desean subrayar la necesidad de insistir
en los problemas que plantea la correlación entre silicosis y cáncer de pulmón a pesar de que se los suele negar y de que su estudio fue abandonado durante varios
años.
18o
EPIDEMIOLOGICAL SURVEY AND PROGNOSTIC EVALUATION IN
SILICOSIS *
(Summary)
J. Prenafeta G., A. Valenzuela P.,
G. Leyton, Srta. S. Villagran 0. (Chile)
All cases of silicosis detected during the period 19621964 at the Chilean National Health Service were followed up.
The most favourable prognosis occurred in the earliest
forms of the disease in which the probability of deterioration
was 20.4/1,000 year-person and the rate of tuberculisation was
3.5 times that of the general adult population.
The prognosis in relation to the variables "stage of the
disease at the first diagnosis" and "over exposition" was analysed.
The probability of deterioration was analysed in relation
to the number of years after detection, and it was concluded
that the highest rates of deterioration occurred before the
seventh year, after which the probability persisted at a much
lower rate.
* The paper "in extenso" to be asked to the authors.
181
T N O i c c
III. !
III; II
S E S S I O N
TII
«.sai-hard.
L'évaluation du risque coniotlque sur les H P U X
du travail
C.Cornea., ft.Ghachem. , A.Sen Kheder., J.Daghfous.,
H.Bouacha., L.E1 Rlefckl.
La Pneumoconlose dan9 una mine de fer de Tunisie aspect9
radio-clinique et fonctionnel.
III. III
C.E.Rossiter., J.C.Wagner.
flan-Clade minerai fibres: joint Eurèpean medical research
project.
III. IV
0.F.Goldsmith. , J.r.Gamble., N.Stroup., C.m.Shy.
Chronic lung disease In the furniture industry: An
epidemiologic study design.
III. V
Hl.L.H. Flindt.
Pulmonary disease due to proteolytic anzymes.
III. VI
S.W.Rab., Zateoullah Beg and lï.Abu Zafar.
Work-Related diseases in Pakistan.
III. VII
Cornea G., El Ulehki U., El Charbi B., Ben Kheder ft.
Silvia G.
Une nouvelle Pneumoconiose vegetale
183
Le poumon de Neffa
III/l
L'EVALUATION DU RISQUE CONIOTIQUE SUR LES
LIEUX DU TRAVAIL
Dr. B.Barhard
Institut d'Hygiène et Santé publique - Bucarest
Roumanie.
L'extension continuelle des procédés technologiques engendrent des poussières et les limites relatives du rendement
des moyens techniques de lutte, l'augmentation progressive du
nombre des ouvriers exposés, le caractère invalidant et les
conséquences économiques-sociales des maladies dues aux poussières sont les principaux éléments qui justifient 1'approfondissement des relations "cause-effet" et "exposition-réponse.
Mais l'établissement de cette relation et surtout sa quantification se heurte encore à de nombreuses difficultés, qui touchent aux deux termes de la relation.
Des difficultés d'ordre théorique (scientifique) ont déterminé et entretiennent des difficultés d'ordre méthodologique,
concernant l'uniformisation et la standardisation des moyens en
vue de l'objectivisation (de la caractérisation) du risque, sur la
base des critères de sensibilité, de représentativité et de comparabili té; or ce sont justement ces instruments d'objectivisation
qui permettent en dernier ressort la quantification.
Comme on l'a remarqué, la sélection des méthodes et des instruments d'objectivisation de l'exposition darra s'adapter au niveau et à l'intensité de l'exposition. Quand la concentration de
la poussière est élevée, donc quand le degré d'exposition est
élevé lui aussi, le rôle de l'empoussiérage est déterminant, tandis que celui des autres facteurs est négligeable; dans cette
185
symétrie, la concentration des poussières de l'environnement,
la teneur en substances biologiquement actives et la durée de
l'exposition d'une part et l'importance des lésions pulmonaires
décelables à l'examen radiologique d'une autre part se trouvent
en bonne correlation (donc il y a une bonne correlation entre le
risque et la réponse). Quand les niveaux de l'exposition diminuent, à la suite de l'augmentation du rendement des moyens de
lutte contre les poussières, les autres variables (y compris
la sensibilité individuelle) gagent une importance toujours plus
grande et peuvent dominer la relation; dans ce cas il sera nécessaire de perfectionner les systèmes d'évaluation, tant sous le
rapport du stimule (l'agent spécifique), que de la réponse (réactivité) .
Mais les difficultés et les exigences se présentent quand
on pose le problème de l'adoption du système des concentrations
maximales admissibles, par lesquelles il faut assurer la protection de la population exposée su risque. Car les experts se sont
posé à juste titre la question: "Est-ce qu'on devra envisager
l'établissement de normes exprimées en unités d'exposition (mg,
h,m-5) ou en unités de concentration (mg/m-')"? Une réponse acceptée de façon unanime n'a pas été encore donnée et cela souligne
de nouveau la difficulté de la quantification du risque.
Dans ce contexte, nous nous proposons d'exposer une bilan
des connaissances accumulées dans l'approche du risque coniotique;
-
-
1» facteur ôtiologique - évalué par les caractéristiques
quantitatives et qualitatives, considérées de façon dynamique ;
1* facteur exposition - évalué par le nombre des ouvriers
exposés au risque et la durée de leur exposition et
186
-
le facteur biologique - la rôactivitê de l'individu
ou de la collectivité exposée, évaluée par des indicateurs de l'état de santé.
Pour ce qui est du au facteur étiologique, le risque coniotique, l'investigation réclame l'acceptation de certains
desiderata d'ordre méthodologique (techniques: de mesure - analyse - évaluation). Parmi les desiderata indispensables, mentionnons: la sélection des indicateurs de manière qu'ils soient
objectifs, pertinents, représentatifs; la sélection des méthodes
et des techniques afin d'objectiviser les indicateurs choisis;
l'uniformisation des techniques de prélèvement de mesure et d'analyse; l'adoption d'une méthode d'investigation appropriée au
but poursuivi; l'uniformité de l'interprétation de l'information.
La première étape consiste dans l'étude technique et du
procédé technologique depuis la matière première jusqu'au produit
fini, dans laquelle on observera les opérations du cycle de travail, la nature et le mode de génération des poussières, les moments où les dégagements sont le plus importants, les conditions
dans lesquelles ont lieu ces dégagements, le degré de mécanisations et le rythme de la production, l'existence et l'efficacité
des moyens techniques de lutte contre la poussière et le nombre
d'ouvriers exposés. Le chronogramme professionnel d'un nombre
représentatif de lieux de travail empoussiérés complète l'information dans cette première étape. Sur cette base on établit lee
lieux de travail à investiguer ainsi que la fréquence des mesures
et l'on élabore un programme pour les investigations de l'étape
ultérieure.
Quelques indices d'ordre général sont recommandés en fonction des niveaux d'empoussiérage connus et du degré de nocivité
des poussières: mesures continues sur la durée d'un cycle de
187
travail, plusieurs jours de la semaine (de façon différenciée
dans l'industrie extractive, l'industrie de surface,.l'industrie
textile etc.) et pendant au moins deux étapes annuelles selon le
niveau de la production et de la saison).
L'étape de mesure-évaluation tient compte de la caractérisation quantitative et qualitative des paramètres physiques
aussi bien que chimiques de la poussière de la zone de travail
en fonction de l'action biologique, de la durée de l'action sur
les sujets exposés et des caractéristiques du travail (régime de
travail, effort, mécanisation etc).
La concentration de masse de la poussière en suspension
(niveau de l'empoussiérage) est mesurée sur le lieu de travail
dans la zone respiratoire de l'ouvrier, par des déterminations
continues) (sur la durée d'un poste), l'évaluation se faisant
en deux degrés - poussière intégrale et fraction respirable.
Des progrès considérables ont été enregistrés en matière d'équipement de prélèvement ou de mesure (apports de la 5ème génération), mais aucune norme internationale n'a été adoptée.
L'analyse de la poussière concerne la détermination éléments constitutifs et surtout des éléments biologiquement actifs
de la poussière de suspension de la fraction respiratoire.
L'étape d'interprétation des résultats
consiste dans la synthèse de l'information recueillie, à des intervalles de temps déterminés, et les conclusions se rapportent
au système des valeurs de concentrations maximales admissibles.
Dans cet ordre d'idées on souligne l'importance de l'élaboration
d'un système d'informations unitaire centralisé pour le stockage
des données et leur traitement statistique-mathématique par des
techniques modernes. Ce système comprendra des informations tant
sur le niveau de l'exposition que sur sa durée.
188
La mise en valeur vise un seul but: l'efficacité de l'ensemble des mesures techniques et organisationnelles de lutte entre la poussière industrielle, efficacité exprimée en termes quantitatifs sans dépasser lee concentrations maximales admissibles.
Une seconde méthode d'évaluation du risque coniotique consiste dans les enquêtes êpidômiologiques. Cette méthode doit
être considérée en étroite liaison avec la première, autant par
rapport à leur objectif commun, que par rapport au fait que les
investigations du milieu offrent un critère pour la sélection de
la population - l'intensité de l'exposition au risque.
Les études épidémiologiques sur les pneumoconioses ont
deux objectifs:
- quantifier le niveau de la morbidité dans les populations industrielles exposées à diverses variétés de
poussières. De telles études visent des buts immédiates
(dépistage des sujets qui peuvent bénéficier de l'assistance médicale spécialisée), qu'informationnels et prognosi iquee, étant donné qu'elles constituent étant donni
qu'elles constituent les principaux moyens d'obtenir les
données nécessaires a l'évaluation du problème pour les
organismes des décisions médicaux.
-
mettre en évidence les principaux facteurs de risque et
leur variation sous l'influence des mesures de prévention,
qui se traduit dans une modification du niveau de la morbidité, indiquant l'efficacité sociale et économique des
programmes médicaux et techniques. Certains des problèmes
posés par ces études sont communs è toutes les études épidémiologiques, tandis que d'autres sont particuliers et
liés aux traits spécifiques de ces maladies.
189
Contrairement à la plupart des maladies chroniques, dans
le cas des pneumoconioses on connaît autant le facteur êtiologlque - la poussière contenant du SiO- libre, que les principaux
mécanismes pathogêniques.
Pourtant, la correlation entre l'exposition et la quantité de modifications pulmonaires attribuées à celle-ci, est réduite ou modifiée par l'intervention de nombreux facteurs secondaires dans la pathogénie de la maladie, et par les changements
répétés qui sont intervenus dans les techniques de prélèvement.
Les mesure6 et techniques de lutte contre les poussières
ont mené à des changements d'ordre qualitatif (physique et chimique) et quantitatif des particules de poussière et le degré
d'empoussiérage s'est réduit. La réduction concerne surtout les
particules ayant un contenu réduit en silice libre, et l'on a
constaté une modification de la dispersion des aérosols de poussière, soit une augmentation de 60 à 90 % de la proportion des
particules de petites dimensions (moins de 5 pm).
On rencontre une situation similaire quand on utilise les
données concernant les modifications radiologiques observées
dans les poumons, car les techniques de dépistage et les critères de diagnostic ont subi des changements importants. Cet état
de choses pose des problèmes pour tes enquêtes rétrospectives et
facilite en revanche les études transversales.
Il's'ensuit que le meilleur moyen d'évaluation de l'exposition individuelle dont nous disposions est le stage professionnel
dans les conditions de risque. C'est évidemment, une évaluation
qui manque de finesse, mais pour le moment c'est l'unique indicateur quantitatif et individuel à l'aide duquel on peut mettre en
évidence l'existence d'une relation entre l'exposition et la maladi'
19o
Lors de l'élaboration de la méthodologie,un autre problème qui
se pose est celui de la sélection des lieux de travail. Dans certaines industries, l'extraction des minerais par exemple, on ne
peut pratiquement pas parler de lieux stables. L'évaluation du
degré d'empoussiérage est rendue difficile aussi par l'utilisation dans la même mine de plusieurs techniques d'extraction en
associations variées et inconstantes, surtout lorsqu'on ne pratique qu'un nombre limité de prélèvements.
La population n'est pas homogène ni du point de vue biologique, ni du point de vue social ni en ce qui concerne le degré
d'exposition au risque des individus. Les niveaux moyens de l'exposition varient beaucoup par rapport à la technologie et aux moyens de lutte contre la poussière. L'exposition est donc difficile
à évaluer dans des termes quantitatifs.
Il est difficile aussi de recueillir des données sur l'exposition à d'autres facteurs de risque tels que l'usage du tabac
ou les maladies respiratoires antérieures. Les informations sont
obtenues par •interview",la personne interrogée doit pouvoir et
désirer comprendre les questions, reconnaître les symptômes et
donner des réponses exactes; l'ôpidêmiologie ne peut pas contrôler ses aspects, et les sujets diffèrent par leurs performances.
La nature des phénomènes étudiés (souvent les maladies respiratoires sont courtes et ne s'accompagnent pas de grandes souffrances ou d'inconvénients matériels pour le malade) et la motivation souvent insuffisante (le sujet n'est pas convaincu de l'utilité des informations dans la même mesure que les enquêteurs) expliquent l'imprécision assez grande des réponses.
Voyons maintenant quelques problèmes méthodologiques spéciaux liés à l'étude épidêmiologique des maladies provoquées par
certaines poussières.
191
La penumoconioee dee mineurs du charbon (PNC) est une
maladie spécifique qui fait partie des pneumoconioses. Le caractère spécifique est donné par l'étiopathogénie et par le
niveau des taux de morbidité • Les enquêtes épidêmiologiques
sur la PMC ont des caractérisques particuliers et impliquent
l'élaboration d'une méthodologie d'étude spécifique.
En Roumanie, l'intérêt pour la PMC s'explique par l'importance de l'industrie charbonnière qui emploie Un grand nombre de personnes et par la tendance à accroître eri permanence
la sécurité des travailleurs pendant toute leur activité professionnelle .
Une étude êpidêmiologique sur la PMC a été effectuée en
vue de:
- donner une description des conditions actuelles d'exposition des travailleurs, en d'autres termes d'établir
quels sont les.poussières et les niveaux moyens d'empoussiérage auquels se trouvent exposés les mineurs de
l'industrie du charbon;
- évaluer la fréquence des cas de maladie et de modifications radiologiques pulmonaires qui peuvent être attribués à l'exposition aux poussières et identifier les
principaux facteurs de risque.
On a conduit une enquête transversale qui offre une
image générale des effets des facteurs de risque au niveau de
la population.
Les hypothèses suivantes ont été testées:
- peut-on mettre en évidence la correlation entre l'exposition aux poussières et la morbidité respiratoire en
utilisant le stage professionnel pour estimer l'exposition ?
- l'âge est-il un déterminant biologique de la susceptibilité à la maladie (PMC)?
192
L'étude a commença par una analyse des conditions existant
dans les mines de la région afin de sélectionner l'unité qui, par
le nombre d'employés, la technologie utilisée et le niveau moyen
de l'empoussiérage, était représentative pour toute la région.
La population de mineurs sélectionnée pour l'étude a été
recensée et l'on a enregistré les caractéristiques biologiques
(âge) et professionnelles (stage professionnel), les habitudes
liés à l'usage du tabac et les maladies respiratoires passées
de chaque travailleur.
On a effectué le dépistage de la pneumoconlose par une méthodologie normalisée comprenant: une examination radiologique
(radiographie pulmonaire), l'étude de la ventilation pulmonaire
(capacité vitale, VEMS, index de perméabilité bronchique) suivies d'un examen clinique et de la recherche des symptômes respiratoires.
La réponse des poumons il l'exposition a des poussières variant en quantités et en qualité a été mesurée par la quantité
totale de modifications radiologiques constatées.
La plupart des mineurs (90 %) ont présenté des modifications pulmonaires minimes et 10 % ont présenté des modifications
importantes, ce qui confirme les données des études expérimentales sur l'aggressivité des poussières.
L'ftge biologique et le stage professionnel ont une influence
déterminante sur le niveau de la morbidité par PMC.
Dans le cas de l'amiante, les études épidémiologlques ont
pour but d'identifier les.effets pathologiques de l'exposition
sur l'état de santé de la population et de vérifier l'hypothèse
sur la correlation entre le risque de maladie et l'influence de
la poussière.
193
Les enquêtes êpidêmiologiques diffèrent des autres études
par le fait qu'elles concernent l'ensemble de la population car
non seulement l'exposition professionnelle mais aussi l'exposition dans l'environnement général peuvent être suivies des effets
pathologiques.
Les effets possibles sont les suivants: l'asbestose, associée ou non à des calcifications pleurales liées surtout à l'exposition professionnelle, le cancer bronchique et le mêsothêliome
pleural dont l'incidence a été associée surtout à l'exposition au
crocidolite, môme dans le cas de contacts mineurs et éloignés.
Les principaux problèmes liés à-la réalisation de ces études sont: l'identification et l'évaluation de l'exposition, la durée, le niveau et la nature du matériel utilisé ayant une très
grande importance pour la nature des effets ultérieurs.
L'étude statistique de la relation entre l'exposition et
la maladie (surtout le mêsothêliome) est modifiée par une série
de facteurs parmi lesquels on peut citer: les doutes liées au
diagnostic môme, les difficultés à reconstituer l'exposition et
l'intervalle très long entre l'interruption de l'exposition et
l'apparition de la maladie, période durant laquelle le sujet peut
changer de profession et de résidence.
Dans beaucoup de cas, l'identification des tumeurs qu'on
peut attribuer à l'effet de l'amiante est difficile parce que les
malades ont été exposés à d'autres agents nocifs, surtout le tabac
et la pollution atmosphérique, mais on peut admettre que le risque
est beaucoup plus élevé chez les fumeurs qui travaillent dans des
milieux pollués à l'amiante.
194
On peut conclure qu'à présent les enquêtes êpidômiologlques et surtout les enquêtes rétrospectives portant sur les
cas de maladie dépistés et admis dans les hôpitaux ou sur les
cas signalés dans lee zones polluées, peuvent fournir certaines
conclusions sur la relation entre l'exposition à l'amiante et la
maladie, de même que sur les facteurs de risque qui peuvent influer d'une manière caractéristique sur les taux de morbidité.
195
Evaluación del riesgo de neumoconlosls
en los lugares de trabajo.
Informe preliminar
B. Barhad (Rumania)
Para el especialista en medicina del trabajo, el
riesgo de neumoconlosls comprende el conjunto de peligros
para la salud que se manifiestan en forma de cuadros
clínicos específicos provocados por la exposición profesional al polvo«
La evaluación de ese riesgo puede llevarse a cabo de
dos maneras i vigilando la exposición al polvo en el lugar de trabajo, o mediante un examen médico sistemático
para detectar las enfermedades que puedan imputarse a dicha exposición,
Los criterios de evaluación de la intensidad del
riesgo de neumoconlosls se presentan por medio de la vigilancia de los lugares de trabajo (identificación de las
fuentes de emisión, vigilancia de la presencia de otros
riesgos, estudio dinámico del nivel y de la composición
del polvo^en suspensión en la atmósfera, evaluación de la
ventilación pulmonar externa durante el trabajo, etc.).
A fin de asegurar la comparabllidad de los resultados es preciso optar por metodologías y técnicas de análisis uniformizadas.
El estudio de los efectos en la población de la
exposición conocida desde el punto de vista cualitativo
y cuantitativo constituye un medio de evaluación de la
intensidad del riesgo de neumoconiosis, y al mismo tiempo ofrece la posibilidad de verificar los conocimientos
adquiridos acerca de la agresividad del polvo por medio
de la observación en los lugares de trabajo y de los estudios experimentales realizados en laboratorio.
Las encuestas epidemiológicas ofrecen Informaciones
sobre las relaciones existentes entre los efectos de la
exposición profesional y los siguientes parámetros i
agresividad del polvo i concentración de polvo en la
atmósfera del lugar de trabajo, y duración de la permanencia profesional en ese medio.
196
Merced a esos estudios es posible Identificar la
Influencia de ciertos factores de riesgo (consumo de tabaco, endemia tuberculosa, residencia, etc.) que contribuyen a crear una "susceptibilidad Individual a la enfermedad" específica, lo cual explica las diferencias que
pueden registrarse entre las tasas de morbilidad observadas en las poblaciones estudiadas y las previstas de
acuerdo con estudios anteriores.
En la práctica se utilizan simultáneamente esos dos
medios para evaluar el riesgo de neumoconiosis. Los resultados del estudio experimental "In vivo" e "in vitro"
del polvo de los lugares de trabajo aportan una valiosísima contribución en la labor de investigación de los riesgos.
Por último, se examina la necesidad de elaborar metodologías específicas de evaluación, adaptadas al estudio
de los riesgos que engendra la exposición a ciertos tipos
de polvo, como, por ejemplo, el polvo de mina y el amianto.
197
III/2
i. A PMCurincoNin^r DANS UNE PI I NE nr FER OE T U N I S I E
nsprr-rs R(\nTn-CLTMi'-iir FT FUMCTTP^NEL
n. rnrìMF/i - n.nnnnHEH - n. PEN KHEDER - .n.riAGHFDUS
ii.
nni.inrHA - i . EL PIEKKI
Institut de Pneumn-Phtisiloaie de l'Ariane
Tunisie.
Notre étude norte sur les données d'un depistane rarii.nloninue denn une mine de Fe. Le minerai exploité est soit do
l'hématite
fFpn ) , soit la siriérorite (FeCP,).
L'exploi-
tation du minerai se fait 9 0 ^ en profondeur et 1OrS a ciel
ouvert.
Le taux de Si n _ libre dans le minerai no dépasse
pas y~'< et dans la roche accomnaonante 7 a 8fî. Dans l'ensemble,
les conditions de travail sont satisfaisantes nar rao-
nnrt aux autres mines. Plais une amélioration de la ventilation et rie la mécanisation du travail sst souhaitable.
riATERIEL ET METHODES:
Lé depistane radioloninue concerne 1240 ouvriers,
snit plus de "p1"? des employés. Une premiere lecture des
films IP/IP cm a retenu 162 sujets suspects.
Chacun a bé-
néficié d'un cliché standard, d'un examen clinique complet
aipsi que d'une ennuete professionnelle portant sur lo poste
de travail et la durée d'exposition au risaun. Uinot-cinq
malades ont été hospitalisés Dour des explorations fonctionnelles plus poussées.
Le microclimat minier ainsi que la cnniométrie ne
font nas partie de nntrn trnvn.il.
199
PROFIL
_RaninLnnini)!:;
a - L'analyse'radioloçique des 162 cas retsnus (soit
13,25? d'ouvriers examinés) montre 1,2% de (pneumoconiose
confirmée 4,5^5 de cas suspects de pneumoconiose, l,lîî de
tuberculose eéquellaire et 0,08 % de tuberculose cavitaire.
Tableau 1
Lésions
Nombre de cas
PNEUMOCONIOSE CONFIRMEE
90
7,2
PNEUMOCONIOSE SUSPECTEE
57
4,5
TUBERCULOSE SEQUELLAIRE
14
1,1
1
TUBERCULOSE CAVITAIRE
0,08
.
TOTAL
...
!
162
L'asoect radiolorique prédominant dans les pneumoconioses confirmées est celui d'image en tete d'épinole, plus
ou moins denses, de répartition homogene, sans formes tumorales ni association avec la tuberculose. Dans l'ensemble
domine le stade ponctiforme.
2oo
T a b l e a u ">
STAOF Rnrnninni^nr
'''ombre fie Cas
Pnurcentane
n
SS
(in,l
n
30
33,3
r
5
5,5
b- DONNEES CL IN ICQ-PROFESSIONNELLES :
-
L'acie moyen des malades e s t de 4 5 , 7 ans
-
L'ancienneté au poste de travail est de 18,3 ans
-
La durée de travail au marteau piqueur est
de 12,2 ans
-
Le taux des fumeurs est de 86,5$
Priseurs de NEFFA (poudre de tabac a priser) :
13,9 %. Certains d'entre eux prisent et fument
en même temps.
La Symptomatologie clinique chez nos malades est
marquée dans la majorité des cas par une dyspnée a l'effort
(70 3 ) , une toux productive (64 %),
des arthraloies(54 <)
et des hémontvsies de oetite imoortance (14,4 Tí) sans explication nette.
2o1
Concernant 90 cas de pneumoconiose et 57 oas suspects de
pneumoconiose
Tableau 3
SYMPTOME
CLINIQUES
!
PNEUMOCONIOSE
CONFIRMEE
PNEUriOCONIOSE
SUSPECTEE
Dyspnée
70
4 3 , 7 •&
Toux
64,6 %
43,7 %
¡
'
Expectoration
64,4
r>
;
30
%
20
%
28
%
20
;0
j
Raies
B r o n c h i q ues
Arthralgies
Hémoptysie
33,3
%
i
*
!
54
14,4
%
1
En somme, du point de vue radio-clinique, il s'agit
d'une pneumoconiose d'apparition tardive (après 19 ans en
moyenne) sans formes graves, ni association avec la tuberculose. La Symptomatologie clinique, quoique présente dans
la majorité des cas, est quand même discrete et bien tolérée.
c - PROFIL FONCTIONNEL
25 malades ont subi des explorations fonctionnelles
plus poussées; 20 dossiers ont été retenus.
l) Une spirometrie simple par soironranhe GODARD.
- CU (capacité vitale) et nourc^ntaoe oar rarcort
à la valeur théorioue;
- UEMS et le raooort TIFFEMEAU
- UT'lt'1 (volume m i n u t e ) .
2o2
2) Une nn7nmÄfrin nu reno.i sur éphanti ). Inn artériel
nrélpv* 3D nivn.-iu 'In la f¿mpra.1 e (PaO-, PnTT-, P h ) .
70
rprnuun d'nffnrt trisnnut a j rn effectuée nn line
seule r.fi.anr.r, nur er^orycla par palier de 3fin et
ein durée dn 3 minutes, jusqu'à la tolérance maximale Mu sujet. flu cnurr, de la dernière minute, nn
effectue un nrél fn/onçnt. do sann artériel au niveau
de la radiale pour dosane den na? du sann (Pan ,
PaCOj, P h ) .
rMçnm T/iT_ri FT noiw^JTAinr^:
Au point de vue binloeique, nn note une tendance a la
nn.1vrlnbu.lie (envirnn 5 300 OPP) par rapport au reste de la
pnnulation.
La spirometrie mnotre chez certains un léper syndrome
obstructif (Tif.<6F> ^)»Tous sont ries fumeurs ou des priseurs
de NETTA (tabac a priser). On ne note pas d9 syndrome restrictif (tableau 4 ) .
La oazométrie au repos montre une logera perturbation
de la PaP,J
II s'anit d'une hvooxémie lécere qui ne s'accom-
panne pas d'h»nercapnie.
l'effort.
Une amélioration est constatée a
Ceci est vraisemblablement lié a 1'hyperventilation
et la modificatinn du rannnrt VA.
TT
l'énreuve d'effort révèle une diminution de la PriT
(nuissanco maximale tenue) (13P U nn moyenne).
marquée (I1
n
Cile est plus
'•') chez les malader, présentant une dvsnnée. Cette
limitatinn de l'effort chez nos malades ne s'explique nue partiellement par l'existence de svnrirome obstructif. (fio.]) et
de la nazomét-rin 1éoeremept perturbé-- au renos (fin.?).
2o5
L'handican constata a l'effort Quantifia ne concorde
pas avec les trouhlen fonctionnais ventilatnires enrsnistrés.
Ceci laisse prévoir des mécanismes ohysio^atholnoioues oui
se situent au delà de l'alvéole pulmonaires, vraisemblablement d'ordre vasculaire.
Des études histoloniques pourraient éventuellement
compléter ces observations.
En conclusion, des données radio-cliniques ainsi que
les constatations fonctionnelles plaident plutqt en faveur
d'une pneumoconiose non collagene a type de sidérose-silicose
d'aooarition tardive et d'évolution lente.
2o4
REFERENCES
1 ) AMTHOn'r.n. I.AMV.P.t
HE REN. H.; PRP.IIM,P.; CERVONI.P.;
PETIET. G.j„SCHJ.inRTJ.j_Jl.. et LAMAZE, R. :
"Lo nancnr bronchi quo rien mineurs de fer do Lorraine
(a nrnnns dn 270 nouveaux cas observés de 1964 a 1927)",
XVemes .Tournées Nationales de Médecine du Traviai!,
Strnsbnurn, 1(1-13 Hai 7R
7
)
E»EH, R.; SORS, 5. :
"La pneumoconiose des mineurs de fer".
Pressa Médicale, Mai 195B, 66 NS 46, 906-907
3
)
ENCYC. PlEOICflL - POUMON :
7.6D18 -
4
A 30
) nUILLERM, .1.; MACINOT
et SADOUL :
"Le!caractéristiques anatomiques de la pneuraoconiose
du mineur de fer et leurs conséquences fonctionnelles".
Archives des maladies professionnelles, Hanv. - Février
1960 - 21, 21 MO 1-2, 62
5) MOSINSER, M. et Eoli :
Archives des maladies professionnelles Danvier - Février 1968, NO 1 - 59-66
6) SAOOIIL, P.(1974) Sidérose pulmonaire in_ : Encyclopédie de
médecine, d'hyniene et de sécurité du travail, vol II,
pp. 1495-96. Bureau international du Travail, Heneve.
7
) SADOUL, P. ET COLL. :
Rapport : "Les pneumoconioses dans l'Est de la France",
Xl/ëmes Tournées Nationales de Médecines du Travail,
Strasbourg, 10-13 Mai 1978.
2o5
La neumoconiosis en una mina de hierro
de Tunez.
Aspectos clinicor-radiológicos v funcionales.
G. Cornea, A. Ghachem, A. Ben Kheder, M. Maalej,
J. Daghfous, H. Bou-Acha y L. El Mekki (Túnez)
En una mina de hierro se ha llevado a cabo un control
radiológico íntegro, habiéndose examinado a 1.240 obreros.
Se han descubierto 90 casos de neumoconiosis. lo que representa el 7,2 por ciento del conjunto de los obreros y
el 11,2 de los mineros de fondo. La proporción de S10» en
el mineral no excede del 3 por ciento.
La edad media de los enfermos es de 45 añosi la antigüedad en el puesto de trabajo, de 18 años, y la duración
del trabajo en el martillo neumático, de 12 años. Los fumadores constituyen el 86 por ciento del total y los adictos al NEFFA (polvo de tabaco) el 13 por ciento.
En el plano clínico se observa la presencia de la disnea en 70 por ciento de los casos, de tos blanda en el 64
por ciento, de broncoespasmos en el 33 por ciento, de la
artralgia en el 54 por ciento y de la hemoptisis en el 14
por ciento (sin explicación clara).
En el plano radiológico se observan imágenes puntiformes, finas y apretadas en la mayoría de los casos (fase
p 60,1 por ciento;. Incluso en las formas micronodulares
(fase o, 33,3 por ciento) y nodulares (fase r 5,5 por ciento), el aspecto es denso pero sin tendencia a la confluencia; no existe asociación con la tuberculosis ni cáncer
pulmonar entre los mineros examinados.
A 25 de ellos se les ha sometido a exploraciones funcionales más completasi espirograffa simple, gasometría
en descanso y prueba de esfuerzo triangular con gasometría
durante el esfuerzo.
Resultados«
Se advierte una ligera poliglobulla (5.300.000) con
respecto al resto de la población. Una espirografía al límite fisiológico (sin obstrucción bronquial importante).
La prueba durante el esfuerzo muestra una baja relati-
2o6
va de la PMS (potencia máxima sostenida)» Soportaron como
promedio 130 W. La disminución de la PMS es más manifiesta
entre los neumoconlótlcos dlsnelcos (110-W), si bien la
espirometría y la gasometría no revelan anomalía alguna
en reposo ni durante el esfuerzo.
En conclusión, el aspecto cllnlcorradlológlco y el
perfil funcional permiten prever más bien una neumoconlosls no colágena del tipo de slderosls o slderoslllcosis.
2o7
Man-made mineral fibres» Joint European Medical Research Project
C. E. Rossiter, J. C. Wagner
MRC Pneumoconiosis Unit, Penarth, United Kingdom
J. Dodgson
Institute of Occupational Medicine, Edinburgh, United Kingdom
R. Saracci
International Agency for Research on Cancer, Lyon, France
It is now just 100 years since the commercial mining of
asbestos was started, and its hazards to human health and life
are well known.
The hazards were thought to be due to some proper-
ty in asbestos which was unlikely to be present in other mineral
fibres.
However, animal experiments with fibres of different
sizes and diameters (Wagner, 1966i Stanton Sc Wrench, 1972« Pott &
Friedrichs, 1972) suggested that all fibres which are rigid rather
than curly, fine (less than 3¿jm in diameter) and long (at least 10
/um) are likely to have dangerous biological activity.
Follow-up
studies resulting from the report from Turkey (Baris et al, 1978)
suggest that fibres other than asbestos may be dangerous to humans,
as well as experimental animals.
With the thought that fibre morphology may be more important
than chemical composition, it is natural for interest to focus on
the possible hazards of fibrous materials used as replacements for
asbestos, such as calcium silicate, ceramic fibres and man-made
mineral fibres (glass fibre, glass wool, rock wool and slag wool).
Particularly following the report by Stanton and Wrench
(1972) of mesotheliomas being induced in rats by the intrapleural
implantation of a wide range of fibres, the manufacturers of manmade mineral fibres in Europe and in the United States of America,
2o9
decided to support research into possible respiratory health hazards
occurring during the production of these fibres.
Current information on health hazards of man-made mineral fibres
Man-made mineral fibres have many uses.
For textiles and
for reinforcement of plastics the fibres are produced by drawing
molten glass and hence they have a relatively narrow range of diameters, about 10-25/jm.
For insulation purposes the fibre wool is
created by a combination of blowing and centrifugal force with a
target diameter of about (yum, but there may be a proportion of respiratale
fibres present.
For some lightweight and acoustical insu-
lation purposes, the nominal diameter may be less than 2um.
Pro-
duction for other specialised purposes makes up about l%-2% of
total output.
However despite the many years of production of these fibres,
very little evidence of human disease has been
that of the dust acting as a skin irritant.
publised apart from
Hill (1977) has re-
viewed the literature and reports only 9 cases of respiratory
disease in any way attributed to exposure to man-made mineral
fibres.
Upper respiratory tract irritation also occurs occasional-
ly but none with lung involvement.
In 8 detailed epidemiological studies in U.S.A., Sweden and
U.K. no evidence of human disease was reported, except that in
one study there were 3 retirements due to bronchitis, compared
to 0.5 expected, and in a second there was an excess of nonmalignant respiratory deaths, excluding pneumonia and influenza.
However, this latter study has been criticised because the expected
21o
number of deaths for the industrial group was based on all white
male Caucasians in U.S.A. including the country dwellers.
Several animal experiments have been carried out, and although a few have shown that inhalation or intratracheal injection of man-made mineral fibres does sometimes cause minimal
fibrosis, the general
concensus has been that these fibres are
biologically inert, with the reaction being one of macrophage
mobilisation.
However, in the Intrapleural implantation studies by Stanton
and Wrench (1972) and Pott and Friedrichs (1972), it was found
that glass fibres, as for all tested fibres, produced mesothelioma
in rats if the fibres were fine enough and long enough.
More
recent studies have confirmed these findings.
The European Medical Research Project
Cameron (1977) has described the formation of the Joint
European Medical Research Board following the decision by two
trade associations* within the man-made mineral fibre industry
to support medical research into possible health risks. After
consultations with interested scientists, it was agreed that any
research programme had to be independent of the industry.
Thus the contracts with the International Agency for Research
on Cancer, the Institute of Occupational Medicine and the British
Medical Research Council provide for the payment of agreed amounts
to these institutions as contributions towards the cost of the research to be carried out and for the findings to be published with
complete scientific freedom.
To coordinate the research programme
* Glass Fibre Producers' Group of the Comité International de la
Rayonne et des Fibres Synthétiques.
European Insulation Manufacturers' Association.
211
there Is a scientific committee with representatives from the three
research teams, an independent chairman and a trade union medical
adviser, who reports to the International Confederation of Free
Trade Unions.
Epidemiological studies
The research team from the International Agency for Research
on Cancer have visited very nearly all the 72 man-made mineral fibre
production plants in Europei
For the historical follow-up mortality
studies, 13 of these plants with a total population of about 10,000
have been chosed which satisfy four criteria for inclusioni
1.
duration of manufacture at least 20 years i
2.
diameter of some fibres known to be less than 6LUK;
3.
complete intact records of exposed personnel;
4.
only man-made mineral fibres produced.
Nominal rolls of past and present employees at these plants
are currently being prepared, so that death records may be obtained.
Each nominal roll will be sent, where possible, to an investigator
with access to national death records who will prepare the necessary
data for the complete mortality analyses. Personal identification
data will not be sent across national boundaries.
These mortality
analyses are expected to be complete by the end of 1981.
In most countries, the national investigator is a member of
a national death or cancer registry or a University epidemiologist
with access to death records. However, one French company to be
studied has very good personnel records, but French regulations
do not currently permit access to national death records. This is
a problem which has also prevented the inclusion of plants in some
other European countries into *"v,~ •»«»-•!•«i.ed studies. The increasing
212
need for international studies of the health hazards of a wide range
of products and materials should be used to persuade all countries
to provide access to death certificates for bona fide research
purposes.
As experience from the visits to the various plants has
developed, the research team has been preparing a standard form
of personnel record including the minimum data required for further
prospective studies, should these be required.
All companies are
being recommended to collect this minimum set of data for each
current and new employee.
Environmental studies
At the Institute of Occupational Medicine, techniques for
the environmental sampling of airborne dust in man -made mineral
fibre production plants are being developed as part of their continuing
research programme.
For routine sampling in factories,
a standard method to assess full shift dust exposure using personal membrane filter samplers has been recommended for adoption
by all the European plants.
This method is a modification of that
commonly used for asbestos monitoring and provides fibre number and
total mass concentrations over an 8-hour period.
The environmental monitoring team will eventually have
visited all 13 plants included in the epidemiological studies and
a further 3 to extend knowledge about dust levels relative to type
of fibre manufactured and age of plant.
Preliminary visits are made
to each plant to discuss openly with management and union representatives why sampling is to be undertaken and to ask for the cooperation of the workers.
For the actual sampling, workers within each
213
production zone are selected at random to wear the personal samplers,
and large volume static samplers are set up at pre-determined positions to permit comparisons between plants.
Sampling continues
for up to 3 weeks, with about 200 samples being taken.
Usually
within 4 weeks a preliminary report on the results is sent back to
be made available to everybody in the plant, and a final report
is sent when all the analyses have been completed.
The dust analyses are expected to be completed during 1980
when technical reports and the results of collaborative studies
with various national environmental sampling groups will be published.
The results will also, of course, be made available to the epi-
demiologists so that estimates of dose-response relations may be
made.
Animal experimental studies
As part of its general interest in the biological effects of
fibres, the MRC Pneumoconiosis Unit is carrying out inhalation and
intrapleural
implantation studies of man-made fibres using rats.
In the implantation studies 20mg samples of glass wool, rock wool
or slag wool with and without resin coating, and glass fibre, each
suspended in saline, have been injected into the right pleural
cavity and the rats are being allowed to live out their lives.
Comparisons of the results of concomitant studies of chrysotile
asbestos and saline alone will be
made.
This experiment started
in December 1976, and as the rats may survive over 3 years, the resulti
are expected sometime in 1980.
The inhalation studies are being carried out cooperatively
with the National Institute of Environmental Health Sciences, U.S.A.
Similar dusting chambers are being used with rats from the same
214
source and with certain dusts in common so that direct comparisons
may be made.
At the MRC Pneumoconiosis Unit exposure will be for
one year to equal respirable mass concentrations of glass fibre,
glass wool with and
exposed controls.
without resin coating or rock wool, with un-
From this it will be possible to determine the
amount of dust deposited and
the fibrogenic effects.
retained over definite periods and
In addition, by sacrificing some animals
after 3 months exposure, at the
end of exposure and 12 months later,
it will be possible to indicate whether any fibrosis is progressive.
The majority of the animals will be allowed to survive their full
lifespan.
At death they will all receive detailed examination and
the findings will be recorded, including all tumours, whether or not
associated with the exposure.
Comparisons will be made with parallel
studies of asbestos-exposed animals. These experiments started in
October 1977, so that exposure has just finished.
Final results
are not expected for at least two years.
Outside the research support by the Joint European Medical
Research Board, cell biology studies are being directed towards
the development of in vitro tests for cytotoxicity and fibrogenicity
of mineral fibres, whether man-made or naturally occurring. Considerable progress in the cytotoxicity tests has been made using
techniques for adding mineral fibres to cell cultures of Chinese
hamster lung cells (V79-4), and in the
fibrogenicity tests by
studying the selective release of lysosomal enzymes from exposed
macrophages.
Comments
Past evidence of adverse human response to exposure to airborne
215
man-made mineral fibres is essentially negative.
This could
perhaps be because the sizes of fibres being produced thirty
or more years ago were generally too coarse for many to be respiratale, or indeed because man-made mineral fibres do not in fact
present a hazard to man when inhaled.
However, it is now in-
cumbent upon industry to ensure that its products are safe before
they are shown to be otherwise.
Thus the man-made mineral fibre
production industry decided to support independent research into
possible health hazards on a pan-European basis. This is probably the first time that such a large international independent
research programme has been undertaken without prior evidence
of human disease.
216
' References
BARIS, Y.I., SAHIN, A.A., OZESMI, M., KERSE, I., OZEN, E.,
, KOLACAN, B., ALTINORS, M., and GÖKTEPELI, A. (1978) An
outbreak of pleural mesothelioma and chronic fibrosing
pleurisy in the village of Karain/Ürgüp in Anatolia.
Thorax, 33., 181-192
CAMERON, J.D. (1977) Man-made mineral fibres: medical research
- CIRFS/EURIMA initiative.
Annals of occupational Hygiene,
£0, 149-152.
HILL, J.W. (1977) Health aspects of man-made mineral fibres.
A review.
Annals of occupational Hygiene, 20, 161-173.
POTT, F. and FRIEDRICHS, K.H, (1972).
Tumoren der Ratte nach
i.p. Injektion faserförmiger St'áube Naturwissenschaften, 59,
318.
STANTON, M.F. and WRENCH, C. (1972).
Mechanisms of mesothelioma
induction with asbestos and fibrous glass.
Journal of the
Rational Cancer Institute, 48, 797-821.
WAGNER, J.C. (1966).
The induction of tumours by the intrapleural
inoculations of various types of asbestos dust.
In: Lung Tumours in
Animals. Proceedings of the Third Quadrennial International
Conference on Cancer, Perugia, June 1965. (ed: SEVERI, L.)
University of Perugia.Division of Cancer Research, Perugia.
589-606.
217
Fibras sintéticas i provecto médico europeo
de investigación.
C. E. Rossiter (Reino Unido), J. Dodgson (Reino Unido),
R. Saracci (Francia) y J. C. Wagner (Reino Unido)
Se ha establecido un programa de investigaciones sobre los riesgos para la salud que puede presentar la fabricación de fibras sintéticas. Ese programa cuenta con
el auspicio de dos importantes empresas de esa industria,
la cual, por otra parte, no ejerce ningún control sobre
los detalles de las decisiones y la publicación de los
resultados de los trabajos.
El grupo de especialistas en epidemiología visitó
prácticamente todas las plantas europeas de fabricación
antes de seleccionar a trece, que reúnen los criterios
necesarios para una investigación continuada. Dichos establecimientos están siendo estudiados en colaboración
con los registros de cáncer y las oficinas nacionales de
estadísticas. Se presentan algunos problemas en los
países que no permiten consultar los certificados de defunción.
En las mismas plantas están reuniéndose muestras
a fin de evaluar los niveles de exposición que permitan
establecer estimaciones de la relación dosis-respuesta.
Se ha recomendado una técnica uniforme de muestreo para
su utilización en todas las plantas de producción de fibras sintéticas de Europa.
Se han iniciado también estudios complementarios de
experimentación sobre animales acerca de los efectos de
la inhalación y la inoculación intrapleural de fibras
sintéticas, así como un programa para desarrollar pruebas
"in vitro" para determinar los efectos fibrogénicos, cancerígenos y mutagénicos de las fibras.
Se estima que ésta es la primera vez que se inicia
una investigación de esta magnitud sobre un posible
riesgo para la salud sin que exista prueba concreta de
efectos en los seres humanos.
218
4>
CHRONIC LUNG DISEASE IN THE FURNITURE INDUSTRYt
AN EPIDEMIOLOGIC STUDY DESIGN
1. D.F. Goldsmith,
Department of Epidemiology,
University of North Carolina
Chapel Hill, North Carolina
U.S.A.
2. J.F. Gamble
National Institute of Occupational Safety and Health
Morgantown, West Virginia
U.S.A.
3. N. Stroup
Department of Epidemiology,
Havard School of Public Health
Boston, Massachusetts
U.S.A.
4. C M . Shy
Department of Epidemiology,
University of North Carolina
Chapel Hill, North Carolina
U.S.A.
INTRODUCTION
Employment in the furniture and wood products industries is
associated with several chronic diseases) nasal cancer (1,2),
Hodgkin's disease (3), prostate cancer (4), occupational asthma (5,
6), dermatitis (7), and physical disabilities resulting from forestry
accidents (8). In this paper we will review the epidemiologic methods
to be used in a study of
respiratory disease (asthma, bronchitis,
and emphysema) as a result of employment in the furniture industry.
The same methodological considerations would apply to other chronic
diseases such as nasal cancer or Hodgkin's disease.
It is hypothesized that exposure to wood dust is of etiologic
significance in the occurrence of respiratory disease and other
chronic illnesses, particularly nasal cancer.
In this regard the
wood dusts must be evaluated for both types of wood (either soft
or hard) and particle size, greater than 5 microns and less than
5 microns (respirable size).
This study is important for two
major reasons i 1) there have been no thorough epidemiologic
studies of chronic disease from exposure to wood dusts in the
United States; and 2) the U.S. government agencies responsible for
safeguarding workers' health are evaluating the present wood dust
219
Standard to judge whether a stricter one Is warranted on the basts
of present epidemiologic findings.
Previous Findings
A review of the literature indicated three basic areas of research on wood dust i respiratory effects, nasal cancer, and measurements of exposure to dusts in the furniture industry.
Respiratory Effects
Early findings of respiratory effects from wood dust were limited to case reports.
In 1949 Ordman reported that the symptoms
of rhinitis and asthma varied according to the wood used by a cabinet
maker (10).
His symptoms appeared after substitution of western
red cedar, kejatt, iroko, "Congo hardwood" and panga panga in his
wood working.
Sosman (1969) described the asthmatic symptoms of
four woodworkers (11). One patient showed a markedly reduced forced
vital capacity (FVC) and expiratory flow rates when exposed to oak
dust or its alcohol extract.
A second patient had a broncho-spastic
reaction to mahogany dust, characterized by a reduced lung capacity
and wheezing.
The other two workers reacted to cedar dust. The
author suggested that an hypersensitivity reaction was responsible
for the findings in all four patients.
Booth et al., and Mitchell reported pulmonary hypersensitivity
among workers exposed to a abiruana dust and western red cedar,
respectively (12, 13). In the case report by Mitchell, the patient's
forced expiratory volume (FEV) was reduced by 53% within five minutes
in a bronchial challenge test with western red cedar.
The patient's
asthma attacks subsided after occupational exposure to western red
cedar dust stopped.
22o
Woodworkers' asthma has been reported in relation to 9 species
of tree including oak, western red cedar, cedar of Lebanon, mahogany and California redwood.
The allergic responses have been both
immediate and delayed hypersensitivity reactions.
In many cases
the results of skin scratch tests and intradermal injections were
equivocal.
Although measurements of lung function often showed
precipitous decrements, these effects appeared to be transitory,
and normal function returned after the workers were removed from
the wood dust exposure. However, no lengthy follow-up has been
conducted on any population of woodworkers.
Nasal Cancer
The pioneering work by Acheson led to the finding of a strong
association between furniture making and adenocarcinoma of nasal
sinuses.
His findings centred on the chair-making industry in
High Wycombe area near Oxford, England (l).
Subsequent findings
have confirmed this association in many countries including the
United States, Holland, Germany, Belgium, France, Denmark, Australia and Italy (14-22).
The work histories of the chair-makers from High Wycombe
suggested a mean latency period from first exposure to diagnosis
to be 40-49 years (1). The time of greatest risk was from the
1920's up to at least World War II. Occupational exposure to
hard woods was strongly
suspected of being the
etiologic agent
in most reports. These woods are beech, elm, mahogany, walnut in
England and teak in Denmark.
Subsequent research has turned up a further observation concerning wood dust. Those who are exposed had impaired mucociliary
clearance mechanisms, that is, these workers had a significantly
221
longer nasal clearance time than controls not occupâtionally exposed to wood dust (23). In addition, many of these men had
squamous metaplastic cells when cytologic exams were conduced
of the middle turbinates (24).
Concentrations of Wood Dust
It is of considerable interest that there is a sizeable
fraction of wood dust in the respirable range, less than five
microns.
Hounam and Williams conducted personal and area samplings
in several machining operations in High Wycombe (25)., They reported that average wood dust concentrations, measured by personal
samplers, of less than 6 mg/m
for the following operations:
band or circular sawing, planing, routing, spindle-turning, and
furniture assembly.
The average was greater than 6 mg/m
sanding jobs and in the turning operations.
overall average was 20.1 mg/m
in the
Using area samples the
near the sawing areas, while lower
concentrations were recorded In the other operations.
About 25%
of the dust from area samplers was smaller than five microns in
diameter.
The finest dust was collected in the sanding and assembly
jobs while the coarsest was found in the sawing operations.
Anderson (2) conducted a parallel investigation of particle
sizes with a cohort of 68 furniture workers in Denmark.
From high
volume area samplers he reported that 33% of the dust measured
less than 5yum In diameter.
Thirty-seven percent of the personal
3
"Î
samples were less than 5 mg/m and 63% were greater than 5 mg/m .
The average for the sanding jobs (by hand or machine) was 14.3 mg/m ,
while the drilling, planing, and sawing jobs had an average dust
3
level of 5.2 mg/m .
222
The Danish workers were divided into two groups exposed to an
average of greater or less than 5 mg/m
dust mostly teak.
of several types of wood
Those exposed to the higher dust levels report-
ed greater prevalence of the
following symptoms» sinusitis, pro-
longed colds, asthma, nose bleeds, frequent sneezing, and nasal
itching and nasal obstruction.
The proportion of workers with
middle ear inflammation was significantly higher among those exposed to the higher dust concentrations.
FEV and FEV25-75% did not
differ between the two groups. However, Anderson et al did not
conduct pre- and post-work day measures of FEV.
They measured
mucociliary transport by placing a blue-stained particle of saccharin
in the nose on the turbinate.
Normal clearance was judged to be the
appearance of blue in the oropharynx within forty minutes. There
was a clear inverse gradient indicating that those exposed to the
greatest concentrations of wood dust had the poorest levels of nasal
clearance.
It should be noted that six out of nine workers with
mucostasis had normal clearance when away from work for the weekend.
Table I summarizes the present knowledge about respiratory
disease and wood dusts. Wood dusts are associated with occupational
asthma and hypersensitivity, particularly western red cedar. Exposure to dusts from some hard woods (such as beech and teak) used
in furniture-making is a strong factor in the cause of adenocarcinoma
of the nasal sinuses.
Respiratory function and mucociliary clearance
are reduced in workers exposed to higher concentrations often
in sanding and finishing work.
found
Prior studies have indicated that
as much as one-third of the dust generated may be in the respirable
fraction of 5um or less.
223
Study Design Alternatives
In order to assess the risk of respiratory disease from exposure
to wood dust there are three possible methods i a prospective model,
a retrospective model and a cross-sectional or prevalence study.
The prospective model is seen in Table 2.
It begins by sampling
a group of exposed and unexposed workers who are healthy, and who,
it is thought, represent the whole population of furniture workers.
These individuals are then followed for a period from time To to
time T.
At the close of the study T., the investigators examine
the morbidity and or mortality of both groups for the proportion
diseased conditional on exposure.
If exposure to wood dust is a
true causal factor then the incidence of the disease will be higher
in the exposed group that in the unexposed one.
One can then calcu-
late a relative risk with appropriate confidence intervals to test
for significance.
A major drawback to this study is the loss of
subjects whose health status cannot be determined.
In general,
this model is slow and can be very costly in time and money.
Table 3 shows an alternative approach, the retrospective or
case-control study, which is generally cheaper and less wasteful
of resources.
It starts with participants whose disease state is
known and compares their past exposure to that of a control group of
individuals without disease.
This is the opposite of the prospective
model in that it calculates exposure conditional on disease status.
Utilizing Bayes' Theorem, one then calculates the odds ratio and
attendent confidence intervals to determine whether the result is
statistically significant.
Table 3 also illustrates the cross-sectional or prevalence
study.
In this study one calculates a prevalence ratio, that is
224
the prevalence of diseased individuals given exposure compared to
the ratio of diseased subjects who lack the exposure. However, there
are two major difficulties with this method.
The investigator may
be dealing with a sample of surviving workers who have neither left
the industry because of health problems nor been disabled.
Also in
a eross-sectional study one is unsure whether the exposure preceded
or followed the disease.
For example, a researcher may find that obese
individuals use saccharin more than normal weight persons.
Is
saccharin used to help lose weight or as a palliative to justify
not reducing calories?
Four Ma jor Obstacles
In testing the null hypothesis of no association between wood
dust and chronic respiratory disease there are four major obstacles
to an appropriate study design. They are seen in Table 4i
1)
access to a large and stable population of furniture
workers with accurate personnel records, the necessary
follow-up information such as death certificates for a
mortality study or hospital or clinic records for a morbidity studys
2)
selection of an appropriate set of controls who lack
the disease of interest, but have an equal probability
of exposure.
In this example, a case group of asthmatics
would require a control group of non-respiratory cancers
or perhaps healthy Individuals!
3)
adjustment for the likely confounding by the presence of
other factors which may be associated with the exposure,
and are independent risk factors for the disease. Some
225
of these are race, age, smoking habits, alcohol consumption, previous occupations, length of employment in the
furniture industry, and off-the-job hobbies. The list
should also include genetic susciptibility and a history
of other allergies.
If these are uncontrolled they may
lead to a biased estimate of risk¡ and
4)
in measurements of exposure to wood dust, both the types
of wood and partitele sizes are necessary for accurate risk
assessment.
The investigator may have to rely on surrogate
measures of exposure such as work histories or production
records which supply the dates when stocks were introduced
and discontinued.
Furthermore, a leap of faith must be
made in assuming present measurements are equivalent to
exposures occurring ten or twenty years before.
These limitations for accurate study design also apply to any
research on occupational cancer in the wood industry.
In addition it
is unlikely that a sufficient number of cases of nasal cancer could
be found to conduct a prospective or retrospective study of this
tumour.
Study Design Selected
The primary question isi is wood dust associated with respiratory disease?
There are four "branches" of the industry we wish to
evaluate which are characterized by wood type and particle sizei
1) small particle, hard wood) 2) small particle, soft woodt 3) large
particle, hard wood¡ and 4) large particle, soft wood.
It may not
be possible to obtain large cohorts of workers with homogenous
exposures, so that mixed exposures may be necessary.
226
In each
eligible plant we wish to do two things.
First, we wish to conduct a retrospective case-control study
of mortality from chronic lung disease (bronchitis, asthma, and
emphysema) comparing work histories of these men with those who
died from other diseases, excluding lung cancer and other pneumoconioses.
Our goal is to see if these men had a higher likelihood
of working in the sanding jobs than the controls. Adjustment must
be made for the confounding factors previously mentioned.
Those
types of data must be obtained by questioning relatives and personal
physicians.
Secondly, we will conduct lung function tests, specifically
volumes and flows from forced expiratory measures such as FEV, FVC,
and FEF 50%. This is a prevalence or crass-sectional study, and
will be conducted before work and after completion of the workshift to measure change over the course of the working day.
These
data will be correlated with environmental samples of wood dust and
volatiles used in painting, glueing, and varnishing.
The lung
function tests will be accompanied by a modified MRC questionnaire
and an extensive questionnaire to measure the confounding variables
previously noted.
The questionnaire will also ask about acute
symptomatology or other respiratory diseases (such as difficulty
of breathing when walking with peers).
It is expected that 200
individuals from each wood dust exposure group will be compared with
two control groups composed of finish applyers, i.e. painters and
varnishers, and nonproduction employees such as transportation or
supervisory personnel.
If wood dust is a factor, in changes in
pulmonary function these tests might provide an early indication of
227
susceptibility so that abnormal changes may be reversed.
If this
is the case, this may provide dose-response information on which
to base a new dust standard.
228
BIBLIOGRAPHY
Aohoson, E.D., R.H. Cowdell, E.Hadfield, R.O. Macbeth', 1968.
Nasal cancer in woodworkers in the furniture industry. Br. lied.
J. 2:587-596
Andersen, H C l . Andersen, J. Solgaard. 1977.' Nasal cancer«, symptoms
and upper airway function in woodworkers. Br. J. Ind. Med, 34:201-07
Peterson, G.R., S. Hilham, Jr. 1974. Brief communication—
Hodgkirr's disease mortality and occupational exposure to wood.
J. Natl. Cancer Inst. 53:957-58
Hilham, S'. Jr. 1976. Neoplasia in the wood and pulp industry. Ann. NY.
Acad. Sci. 271:294-300
Hilham, S'. 1976. Occupational Mortality in Washington State,
1950-1971. Vol 1-3. U.S. Department of Health, Education, and
Welfare (Public Health Service), Washington, B.C. U.S. Government
Printing Offico, I976
Gandevia, B., J. Milne. 1970. Occupational asthma and rhinitis due to
Western red cedar (Thu'ja plicata), with special reference to bronchial
reactivity. Br. J. Ind. Med. 27:235-44
Suskind R.R. I967. Dermatitis in the forest produot industries.
Arch. Environ, Health 15:322-26
Social Security Administration, 1967. Occupational Characteristics
of Disabled Workers, by Disabling Condition. U.S. Government Printing
Office, Washington, D.C. 307 pp.
U.S. Department of Health,' Education, and Welfare, Public Health Center
for Disease Control, 197°. NIOSH' Criteria for a Recommended Standard.
Occupational Exposure to Wood Dust, (first draft) U.S. Department of
Health, Education, and Welfare, Washington, B.C. June 23, 1978
Ordman, D.' 1949. Bronchial asthma caused by the inhalation of wood
dust. Ann. Allergy 7:492-96,505
Sosman A.J., D.P. Sclueter, J'.N. Fink, J.J'. Barboriak. 1969»
Hypersensitivity to wood dust. N. Engl. J. lied. 281:977-80
Booth, B. H-., R. H. LePoldt,'E. H. Hoffitt. 1976. Wood dust hypersensitivity, J. Allergy Clin. Immunol. 57:352-357
229
*
M i t c h e l l , C. 1970. Occupational' asthma due t o Western or Canadian
red cedar (Thuja p l i c a t a ) . Med. J , Aust. 2:233-35
B r i n t o n , L. A . , W.J. B l o t t , B . J . S t o n e s , J . P . Fraumeni J r . 1977.
A death c e r t i f i c a t e a n a l y s i s of n a s a l cancer among f u r n i t u r e workers
in North C a r o l i n a . Cancer Res. 37:3473-74
Delemarre, J . P . I ! . , H.H.' Themans. 197L Adenocarcinoma of t h e n a s a l
c a v i t i e s . * Ned. T i j d s h r , Geneeskd 115:668-90
L o f f l e r , P. 1972. Adenocarcinomas i n t h e nose and paranasal s i n u s e s .
MonatsschrOhrahoilkde Laryngo Rhinol 106:529-31
Debois, J.II. 1969.' Tumors of t h e nasal c a v i t y i n woodworkers..
T i j d s c h r . Geneeskd. 25:92-93
Leroux-Robert, J'. 1974. Cancer of the n a s a l c a v i t y in woodworkers.
B u l l . Acad. N a t l . Med. P a r i s . 158:53-59
Gignous M. , ' P . Bernard. 1972. Malignant tumors of t h e ethmoid among
woodworkers. J . Med. Lyon. 50:731-36
Mosbach, J , , and E.D. Achesoh. 1971= Nasal cancer i n f u r n i t u r e makers in Benmark. Dan. Med. B u l l . 18:34-35
I r o n s i d e P. and J . Matthews, 1975. Adenocarcinoma of t h e nose and
paranasal s i n u s e s in woodworkers i n tho s t a t e of V i c t o r i a , A u s t r a l i a ,
Cancer (Brussels) 36:1115-21
D i g i e s i V. 1972. Bronchiolar ( a l v e o l a r cfcll) carcinoma complicated
by spontaneous pneumothorx i n a woodworker. Prog. Med. (Rome)
28:614-19
Black, A'., J . C . ' Evans, E.H. Hadfield, R.G. Macbeth, A. Morgan,
M. Walsh. 1974. Impairment of nasal' mucociliary c l e a r a n c e i n
woodworkers i n t h e f u r n i t u r e i n d u s t r y . B r . J . I n d . Med. 31:10-17
Hadfield, E, H. 1970. A study of adenocarcinoma of the p a r a n a s a l
s i n u s e s i n woodworkers i n t h e f u r n i t u r e i n d u s t r y . Ann. R. C o l l . Surg.
Engl. 46:301-19
Hounam P . R . , and J . Williams. 1974. Levels of a i r b o r n e dust i n
f u r n i t u r e making f a c t o r i e s in the High Wycombe a r e a . B r . J . I n d . Med.
31:1-9.
230
TABLE 1 - SUMMARY OF LITERATURE ON RESPIRATORY DISEASE AND WOOD
DUST
1)
Associated with respiratory asthma and bronchial hypersensitivity, particularly exposyre to wester red cedar.
Reaction may be due to immune response.
2)
Exposure to hard woods, such as beech, used in furniture
making is strongly
associated with adenocarcinoma of the
nasal sinuses.
3)
Respiratory function and mucociliary clearance appear to be
affected by elevated dust concentrations found in sanding
and finishing jobs.
4)
Studies suggest that as much as one-third of the dust may be
in the respirable fraction of fyan or less.
231
TABLE 3 -ASSESSING DISEASE RISK IN A RETROSPECTIVE CASE/CONTROL STUDY
Exposed E/D
Case D
Unexposed S/D
Representative
of PAR?
Exposed E/5
Control D
Odds Ratio (OR) =
(from Bayes Theorem)
(E/D) X (Ë/D)
(S/D) X (E/D)
Unexposed Ë/5
Tl
To
TABLE 2 - ASSESSING DISEASE RISK IN A PROSPECTIVE STUDY
Diseased u/E
Exposed (E)
Populatioi
a t Risk
(PAR)
Healthy 5/E
Diseased D/S
R e l a t i v e Risk (RR)=
D/E
(P/E) + (5/E)
Unexposed (§)
Healthy D/f
T
l
232
D/Ë
(D/S) + (5/Ë)
TABLE 4 -
POUR IIAJOR OBSTACLES TO APPROPRIATE STUDY SESIÓN
1)
Access to a large and stable population of furniture workers with death
certificates or hospital records for accurate follow-up of vital status
2)
Selection of appropriate set of controls
3)
Adjustment for probable confounding variables which are associated with
exposure and a risk factor for respiratory disease
4)
a)
age
e) prior occupations, such as
coal mining or asbestos exposure
b)
race
f) length of employment in the
furniture industry
c)
smoking h a b i t s
g)
d)
alcohol consumption
o f f - t h e - j o b hobbies such as
furniture refinishing.
Measurements of exposure t o wood dust
a)
types of woods
b)
c o n c e n t r a t i o n s of d u s t - t h e proportion < 5jjm
c)
type of o p e r a t i o n such as Banding or sawing
d)
s u r r o g a t e measures of exposure such a s work h i s t o r i e s
233
Enfermedades pulmonares crónicas en
la industria del mueble i estudio
epidemiolop.ico .
Goldsmith, D. F., N. Stroup, J. F. Gamble
y C. M. Shy (Estados Unidos)
Se sospecha que el polvo de madera es un carcinógeno
de los senos nasales. Ciertos polvos de madera pueden
provocar ataques asmáticos e hipersensibilidad pulmonar.
Los trabajadores de la madera corren mayor riesgo de cáncer del sistema linfático y hematopoiético y de tuberculosis.
Los trabajadores del mueble expuestos a diversos
niveles de polvo de madera presentan altas tasas de tos y
expectoración, resfríos comunes, estornudos, irritación
de la mucosa nasal, sinusitis y conjuntivitis.
La finalidad de este estudio es presentar una reseña
de la literatura existente sobre los efectos del polvo de
madera sobre la función pulmonar y describir los métodos
epidemiológicos de evaluación de los riesgos de neuraopatías crónicas en la industria del mueble.
La literatura existente revela claramente que en el
proceso de fabricación de muebles, el aserrado, lijado, cepillado y taladro producen polvos de madera respirables
(5>üm).
Se consider» la neuropatía crónica como una con-
secuencia de la exposición múltiple al polvo de madera,
humo, los productos de acabado (pinturas, barnices, lacas
234
y dlluyentes) y el alcohol• y de los trabajos anteriormente
desempeñados•
El propósito de este estudio es identificar en la industria del mueble los sectores de mayor riesgo> mediante
una estrategia epidemiológica multifacéticaí
1) evaluar
la mortalidad por neumopatfas crónicas en los condados de
Estados Unidos en que predomina la industria del muebleí
2)
identificar los sectores laborales que se sospecha pre-
sentan mayores riesgos mediante un estudio retrospectivo
de control de casos dentro de una fabrica de muebles i
3)
emprender un test de la función pulmonar entre los tra-
bajadores en actividad comparándolos con muestras ambientales de polvo de madera y de productos de acabado.
Un
descenso en elVEFj al cabo de un turno de ocho horas puede indicar un futuro riesgo de enfermedad crónica.
235
PULMONARY DISEASE DUE TO PROTEOLYTIC ENZYMES
M. L. H. Flindt
United Kingdom
I will first bring up to date the story in respect of the
"detergent enzymes" before referring to the newer problems of
the meat tenderisers.
My initial work(l) showed that workers could become sensitised
to, and develop allergic illness from, detergent enzyme powders
and that the responsible allergen was in the enzyme component of
the commercial preparations used.
By skin prick-tests following
inactivation of the enzyme, it was also shown that this allergenic
effect was independent of proteolytic activity.
There was no
evidence that the viable spores of Bacillus subtilis, which at
that time were contaminating the commercial preparations, were in
themselves a source of illness, whether infection or allergy, it
being thought that the weak prick-test reactions to spore extracts
were probably due to the enzyme itself, as this was produced by,
and inseparable from, our spore cultures.
It was not thought likely that there was a problem of autosensitisation following tissue damage by the proteases, but it
was considered that, as well as being capable of causing allergic
illness, these powders could cause primary irritant effects on
the respiratory tract, the clinical manifestations being throat
and chest pain, haemoptysis and epistaxis.
At the time, the possibility that there might be problems,
independently or in association, from the various other ingredients of detergent enzyme powders was also considered.
My ex-
perience, over several years, had been that the detergents'and
257
additives in themselves did not appear to cause asthma or other
allergic respiratory effects, although the non-soap detergents
could cause primary irritant effects, including epistaxis.
Whether or not adjuvant effects were occurring, these could
not have been an essential factor leading to illness, as sensitisation and asthma had also occurred in development workers who had
handled the enzyme material prior to the incorporation of additives.
However, it is interesting to note that research has confirmed(2)
that detergents can indeed act as immunological adjuvants, potentially capable of enhancing the allergenic consequences of enzyme
inhalation.
As regards the immunological mechanisms causing the symptoms,
the case histories of asthma, and the immediate reactions to skin
prick-tests, later confirmed by RAST tests for specific IgE(3),
made it seem probable that reagin-mediated type I responses of
Gell and Coombs(4) were occurring.
What was not conclusively
demonstrated in the early work by myself, and by Professor Pepys
and his colleagues at the Brompton Hospital, was the nature of the
late responses, occurring in some of the workers a few hours after
exposure to the enzymes, and causing the dual response in challenge
tests(5).
There was understandable concern in the early days that
these late responses might be due to type III precipitin-mediated reactions of Gell and Coombs.
Such reactions, while capable of causing
an acute alveolitis within a few hours of exposure to an allergen,
can also lead to delayed fibrotic lung changes(6) causing impaired
gas transfer.
This consequence is not confined to those who have
had clinical illness, but may occur insidiously following repeated
238
smaller exposures to antigen(7).
In addition to the late reactions which were occurring
under factory conditions, and on challenge tests, others as
well as myself have obtained, in a small number of individuals,
late reactions to prick-tests which, in appearance and timing,
seemed indistinguishable from the so-called Arthus reaction,
a manifestation of type III allergy.
However, these late re-
actions followed on from typical immediate reactions and may
also have been primarily due to IgE-mediated type I mechanisms,
as has been postulated in another context(8).
In my original cases it had been possible to demonstrate
precipitins when enzyme solutions were tested against the sera
of some of the affected detergent workers. This might have
supported the possibility that type III reactions were occurring,
but the finding of similar reactions in the sera of a similar
proportion of unexposed control individuals reduced, but did
not exclude, the likelihood.
In addition, the absence of conclu-
sive radiological changes in the chests of the affected workers
was against the likelihood of type III effects, although this did
not wholly preclude them because few individuals were X-rayed
during their acute illnesses, and transitory radiopacity from
cellular infiltration might have been missed.
It is now thought likely that the precipitins demonstrated
were not due to immunological interaction between the enzyme as
an antigen and antibodies in the serum, but to interaction between
the enzyme as a protease and serum antiproteases(3).
It cannot be said that type III reactions do not and cannot
239
occur following inhalation of B. subtilis proteases, for IgG
antibodies have been demonstrated, but the predominant problem
appears to have been due to IgE-mediated asthma.
In the majority
of cases removal from exposure has led to complete resolution of
obstructive pulmonary effects, but this has sometimes taken
several months. The reduced lung gas transfer found in some of
the cases does not necessarily indicate an alveolitis, as it may
represent the small airway component of an obstructive condition,
Although, by taking stringent precautions, those who continue
to use the material have substantially reduced the incidence of
overt illness, it is important not to become complacent about it.
Some of the initial fears were allayed, not on account of its
harmlessness, but on account of the precautions taken.
treshold limit value(9) of 0.00006 mg/m
The ACGIH
gives some indication of
the care required, the figure approaching the limit of detectability and going some way towards the nil level hypothetically indicated. Measures such as screening out atopic workers, and removing from exposure those who develop symptoms, combined with using
encapsulated material to reduce dustiness, have tended to mask the
effects that would have developed had the industry continued to use
the enzyme in its original fine-powder form.
In addition, too much reliance must not be placed on skin
prick-tests to exclude enzyme-related disease.
Not only can
direct non-allergic effects occur, but I have shown by challenge
tests that the material can cause asthma despite negative skin
prick-tests(lO).
24o
The early fears that the B.subtllis protease might cause direct
destructive effects leading to emphysema, had support from the fact
that papain, another protease, causes emphysema in experimental animals when administered by aerosol inhalâtion(11) or Intratracheal
injection(12).
I have mentioned that some of the enzyme-affected
patients had developed impairment of gas transfer, sometimes lasting
for several weeks after an episode of chest illness but, although
this may well have Indicated effects at the small airway, or alveolar
level, its recovery made it unlikely that emphysema had been caused.
Gandevia, in Australia, reported loss of elastic recoil in some of
the enzyme-affected patients(13), which might have been an indication of emphysema, but from more than 100 papers that have followed
my initial contribution on this topic, one does not get the impression
that the material has been a significant cause of emphysema.
That the B.subtilis protease is less likely to cause emphysema
that papain has been shown experimentally.
In New York, Drs.
Goldring, Ratner and Greenberg(13) repeated with the B.subtilis protease the inhalation and intratracheal experiments In hamsters which,
with papain, had led to emphysema.
It was found that, when B.subtilis
protease was administered, some of the animals died from severe
haemorrhage into their respiratory tracts but, unlike the animals
exposed to papain, those animals which recovered from the Initial
haemorrhage did not develop emphysema.
Now, as to the problem of the other protease, papain, I have
mentioned papain in the context of its capacity to cause emphysema
in experimental animals. There is also the consideration of allergy.
241
On theoretical grounds, enzymes as proteins, with large molecular
weights, are potential
case
allergens and, as I was able to show in the
of the subtilopeptidase used in detergent enzymes, this
allergenic capacity could be independent of its proteolytic capacity.
Thus, the inhalation of powdered papain might also be capable of
causing sensitisation and respiratory allergic symptoms.
Papain has several industrial and commercial uses, two important
ones being, in the brewing industry, the treatment of beer so that
precipitates are not formed on chilling! and, in the food industry,
as a meat tenderiser, either by injection into animals before
slaughter, or by treating meat afterwards.
There are widely-marketed
preparations of "meat tenderiser" for use by the consumer, who is
instructed to shake the powder on to the meat before cooking.
In recent years, by use of such techniques as spray-drying,
papain preparations of high potency in fine-powder form have become
available, and with them the increased liability of atmospheric
contamination of workplaces where papain is handled, processed, or
packed.
I had been experimenting with papain solutions during my research into the effects of detergent enzymes and had found that '
the prick-test reactions to the subtilopeptidase were specific, and
not shared with other protease such as papain.
Consequently, when
asked to see a patient who developed asthma while working at a
factory where papain was packed as a meat tenderiser, I already
knew that, at certain strengths, solutions of papain did not give
irritant or other skin prick-test reactions in unexposed control
242
individuals whether or not they were atopic or were sensitised to
B.subtilis enzyme.
The patient was a warehouse fork-lift truck driver, but in his
early time at the factory he had helped in the papain packing room.
He developed attacks of asthma for the first time while working
at the factory, on one occasion being off work for two weeks.
These attacks came while he was working in the warehouse, on the
days on which papain meat-tenderiser was being packed in the next
room.
He gave no history of atopy, confirmed by negative skin
prick-test reactions to solutions of common allergens. However,
he gave positive prick-test reactions to solutions of papain at
strengths 10 times and 100 times weaker than had given no reactions
in unexposed control individuals, whether or not they were atopic(15).
This supported the likelihood that the death of a young man at
another factory, in a severe attack of asthma which developed
shortly after a workmate 10 metres away from him had tipped about
a kilogram of papain powder into a protein hydrolysis tank, was due
to papain allergy.
Subsequent investigation at another factory where spraydryed powder was packed for breweries and meat-tenderising firms,
revealed that several workers both atopic and non-atopic, from
the factory floor, laboratories, and adjacent offices had experienced nasal and asthmatic symptoms following papain handling,
and they gave positive prick-test reactions to papain solutions
at strengths weaker than gave no reaction in control individuals
243
not exposed to papain.
Thus it was confirmed that papain could
sensitise and cause allergic illness, a finding that has received
support from the work of Tarlo and his colleagues(16 ), who reported
positive skin prick-tests, as well as RAST tests for Ige antibody,
in their patients.
In view of experimental work that has shown that intratracheal
or aerosol inhalation of papain can cause emphysema, it was also
thought important to find out if there was any evidence of emphysema
in these workers. This might well be independent of whether or not
the exposed individuals had become sensitised.
Consequently I
arranged a wide range of lung function tests, chest X-rays and
serological tests in addition to tests relating to allergy.
It seemed important to include, in the serological tests,
assay of o •> -antitrypsin, in view of the vulnerability of homozygotes with very low oí.-antitrypsin levels to emphysema in early
lifei believed due to impaired protection against the action on
the lung tissue of naturally occurring proteases from
and bacteria.
leucocytes
There was also the possibility that those with inter-
mediate low levels - the
heterozygotes - might be more than nor-
mally vulnerable to the relatively gross exposure to protease
from the inhalation of papain powder at work.
I am not yet in a position to give full results of this work
as the survey is not complete.
One factory-floor worker, who
had had the heaviest exposure to the high-activity papain powder,
showed radiological evidence of large bullae in both upper lung
fields and the upper part of the left lower lobe. We have not
so far been able to exclude the possibility that this unusual
condition was caused by papain, but investigations continue.
244
Fortunately, I think that whether or not it is confirmed
that significant proteolytic lung damage can be caused by papain
in humans, the safety measures recommended as necessary to
pre-
vent the allergic hazard(l7) should also suffice to prevent direct
effects from the material.
2*5
REFERENCES
FLINDT, M.L.H. LANCET (1969) 1, 1177
THORAX (1976) 31, 621
HOW, M.J., Goodwin, B.J.F., Juniper, C.P. & Kinshott, A.E.
Clinical Allergy (1978) 8, 347.
GELL, P.G.H. and Coombs, R.R.A., in Clinical Aspects of
Immunology. Oxford, 1968.
PEPYS. J., Longbottom, J.L., Faux, J. Lancet (1969) ¿. 1181
BRITISH MEDICAL JOURNAL (1967) iii, 691
HARGREAVE, F.E., Pepys, J., Longbottom, J.L., Wraith, D.G.
Lancet (1966) i_, 445.
DOLOVICH, J., Hargreave, F.E., Chalmers, R., Shier, K.J.
Gauldie, J., and Bienenstock, J, Journal of Allergy and
Clinical Immunology (1973) 52 No. 1, 30.
American Conference of Governmental Industrial Hygienists,
Documentation of the Threshold^ Limit Values for Substances
in Workroom Air¡ Cincinnati, Ohio, 1976.
FLINDT,- M.L.H. Revista de Tisiologia y Neumonologfa
(1974) 13 No. 1, 115.
GOLDRING, I., Greenberg, L., Ratner, I. Archives of
Environmental Health (1968) 16, 59.
GROSS P., Pfitzer, Emil A., Tolker, E., Babyak, M.A.
Karschak, M. Archives of Environmental Health (1965), ii,
50.
GANDEVIA, B., Mitchell, C. Medical Journal of Australia
(1971) 1, 1031.
GOLDRING, I.P., Ratner, I.M. Greenberg, L. Science (1970)
170. 73.
FLINDT, M.L.H. Lancet (1978) 1, 430.
TARLO, S.M.' Shaikh, W., Bell, B., Cliff, M., Davies, G.M.,
Dolo.vich, J. and Hargreave, F.E. Clinical Allergy (1978)
8, 207.
FLINDT, M.L.H. Proceas Biochemistry (1978) 13 No. 8, 3.
246
Enfermedades pulmonares causadas
por enzimas proteolítlcas.
M. L. H. Fllndt (Reino Unido)
Los trabajadores expuestos a polvos de enzimas proteolfticas procedentes del bacillus subtllls. que se utilizan
en la fabricación de polvos biológicos de lavar, pueden
provocar asma alérgica« Las reacciones positivas "inmediatas" a la puntura cutánea, a los tests R.A.S.T. para un
IgE especffico indican que se están produciendo reacciones
de tipo 1 (Gell y Coombs). Las precipitinas encontradas
parecían deberse a reacciones proteasas-antiproteasas, y no
a reacciones inmonológicas de tipo III, cuya presencia no
ha sido establecida en forma certera, pese a reacciones
pulmonares demoradas en algunos individuos, y a un pequeño
número de reacciones "tardías" a la puntura cutánea. La
mayorfa de los individuos afectados se recobran completamente al cesar la exposición, y seoonocen pocos casos de
secuelas de larga duración, tales como la fibrosis que puede presentarse a consecuancla de tipo III, o una destrucción del pulmón atrlbulble a efectos proteolítlcos directos.
Recientemente se ha podido ver que a veces los trabajadores que manipulan otra enzima proteolítica, la papaína,
se sensibilizan y desarrollan asma. En experiencias animales, la papaína causa enfisema, y se están realizando estudios para ver si también puede producirse en los seres
humanos. No obstante, los riesgos alergénlcos de la papafna
son tales que no se justifica esperar los resultados de
esos estudios para tomar enérgicas medidas para Impedir la
Inhalación de polvo de papaína.
24?
WORK-RELATED DISEASES IN PAKISTAN*
(Summary)
S.M. Rab, Zakaullah Beg and M. Abu
Zafar (Pakistan)
The Interaction between man and his work environment may
lead to 111 health.
Developing countries are becoming Industrial-
ised, with the appearance of new chemical, physical and psychosocial hazards.
There are also traditional cottage industries
where ignorance prevails. A survey showed a substantial number
of cases hitherto unsuspected, as followst
1.
21% Incidence of byssinosis in the cotton industry,
the largest industry in Pakistan.
2.
40% pneumoconiosis amongst knife grinders and stone
crushers.
3.
Asbestosis ,in the shipping and motor Industry.
4.
14% barltosis in the barium sulphate mines.
5.
Barltosis was found to be the most benign of these.
*
The paper "in extenso" to be asked to the authors.
249
Enfermedades del trabaio en Pakistan.
S. M. Rab, M. Sakaullah
y Mohd Abu Zafar (Pakistán)
La acción del medio ambiente de trabajo puede llevar
al hombre a enfermarse. Los países en desarrollo se van
industrializando con lo cual se añaden nuevos riesgos de
índole químicat física y psicosocial. También existen las
industrias rurales tradicionales donde prevalece la ignorancia, En una encuesta, los autores descubrieron un importante número de casos hasta entonces insospechados t
1.
incidencia de 21 por ciento de la bisinosis en la industria del algodón, que es la más grande el Pakistani
2.
40 por ciento de neumoconiosis entre los afiladores de
cuchillos y los picapedreros»
3.
asbestosis en la Industria naviera y de motorest
4.
14 por ciento de baratosis en las minas de sulfato de
bario.
De todas ellas la baratosis resultó ser la más benigna.
25o
HI/7
UNE MPUVELI E Pf-JFrunocnMTO.SF \ / r r r T A L E
LE POI.IHPN or
MFFFA
rORMEA H. - Fl. PEKKT !.. - r|_ CHARBT P. - PFM KHFOFR A.
STLVTfl n.
Tnr.hit.ut rlR Pneumn-Phtis.i nlnnie de l'Ariana,
Tunisie.
Mous avons été frannés "ar la relative fréquence des
bronchnoneumopathies chroninues obstructives chez la femme
tunisienne ruralR nui ne fume absolument ñas. Notre attention a été retenue par l'existence, chez certaines d'entre
elles, d'une habitude particulière : celle de priser, c'està-dire d'aspirer car le nez une poudre de tabac appelée
"Neffa".
Cette toxicomanie est larqement répandue en milieu rural.
De même, elle touche les hommes et est fréquemment retrouvée
chez les mineurs (13 % dans une mine de Fe).
Un ori'seur (ou priseuse) acharné inhale en moyenne 100
a 300 n de poudre de Neffa par mois ce qui fait 1 a 3Ko par
an, traduisent ainsi un véritable emooussiérape. Deux espèces
de tabac sont cultivées en Tunisie : Nicotiana tabacum, le tabac a fumer et Nicotiana rustica le tabac a priser. Ce dernier
est caractérisé par une teneur importante en nicotine et constitue la matière premiere de base de la Neffa.
MATERIEL FT METHODES:
Le travail a été fait a l'institut de Pneumo-phtisinlnpie
de l'Ariana avec la collaboration du laboratoire de l'Institut
d'Hvniene et de Santé Pub.linii" de Clu.i - Roumanie, Le nombre
de cas observés depuis J974 dépasse la centaine. Notre étude
actuelle norte sur PO dossiers.
251
"ti s'anit i;n n(5n*r-il H» ruraux, en majority dRS fnromos
- 37 femmqg - snit 61 "* du total
— 23 hommes — snit 39 ,p' du total
t.'ane moyen de nos malades sç situe environ de 5Í3 ans
(57,? pour 1 R S femmes at Fin,7 pour 1 R S homn-es.
La duri™ ri * i r
nrimation tabanique est dn 23 ans pour 1 R S fpmmes et dp 31
nos nour 1 R S hommes.
nnnnrrc; rLTMTcn-RflnTni.pni^iiE :
a - Mode de recrutement : les malades ont Ät<5 hospitalisés onur des raisons diverses
Tableau
1; l»10TTF D'HOSPITALISATION
Nombre
Pourcentaoe
Hfimontsie
20 cas
33,3
însufisance Respiratoire
14 cas
23,3
CflHSF.
9 cas
15
Raisons diverses (Silicose, Tuberculose, Min,etc.)
9 cas
15
Pneumopathie banale
8 cos
13
Bronchite Chronique
T P T n L
60 ras
252
ion %
!
CI inique :
Sur le plan clinique, es sont les phénomènes des
bronchopneumopathies chroniques qui dominent dans la
majorité des can. L'hémoptysie, en nénéral de petite
importance, est presento daps 1/.3 des cas suivie de
| 'insuffisance respiratoire dans 1/4 des cas.
fl l'examen objectif, on retient une triade caractéristique :
- un facies tabanique a divers degrés
- une distension thoracique a divers daqrés
- une altération de l'état général plus ou moins
marquée avec amaiqrissement notable.
Cette triade clinique evocatrice est plus fréquente
chez les femmes (78,3 %) que chez les hommes (65,2$).
L'auscultation révèle la présence des raies bronohiques a prédominance de sibilanta dans 71,6 % des cas.
Le.retentissement cardiaque a type de tachycardie
sinusale et d'hépatoméqalie est retrouvé dans 43,2 % des
cas pour les femmes et de 26 % pour les hommes.
Radiologie :
Sur le plan radiolooique, on constate au début une
réticulomicronodulation intéressant la moitié inférieure
des deux poumons. A un stadR plus avancé, l'image réticulomicro-nodulaire peut intéresser même la totalité des deux
poumons respectant dans une certaine mesure les ommets.
253
A un starla ultime (la starlo de compi i cations ), nn observe en plus, sur un Fond emphysémateux des imanes fibrokystiques (en nid d'abeilles) essentiellement au niveau
de la moitié inférieure das poumons. Les premieres anomalies radioloqiques apparaissent après 10 a 15 ans de
tabagisme (prise de Neffa).
d -fliolonie:
A l'examen de laboratoire de routine, on note simplement
une Uw 3» moyenne élevée qui se situe a 47 mm/h.
e - L'Exploration fonctionnelle :
Elle montre une perturbation de type obstructif importante dans la majorité des cas (Tiffeneau 60 %).
f - La bronchoscopie pratiquée dans la plupart de cas décrit
un aspect inflammatoire particulier (rouoe framboise),une
hypersécrétion, une fragilité excessive de la muqueuse qui
saione au moindre contact du bronchoscope.
L'ANALYSE DE LA POUDRE DE MEFFA :
Ellea mis en évidence la présenco ds silice libre (SICU)
en proportion de 2,8 % et aussi en quantité semblable du Ca,Al
et Fe.
Le taux de nicotine de Meffa tunisienne varie entre 2%
et 2,B %.
La nranulométrie donne les résultats suivants :
- 66 % des particules ont un diamètre inférieur a 3Wm.
- 10 •' inférieurs a 9 Um.
- 24 )', supérieurs a 10 (Um.
rione la majorité des particules peuvent penetrar jusqu'au
fond des alvéoles plumonaires.
254
FXPFRjFfirrs sin nrs ArJIIWIX DF LARPRATOIRF:
I'PS nxneriencep ont été faites nur ries souris blanches
d'un nnids movrn dn IST a 2P0 n. La voie transtranhéable a
été utilisée pniir Rnnniiss.i érnr les animaux.
Une dosn do F¡0 mo
de nnudre nar animal dans l ml de sérum physiolonique a iti
administran a un premier lot de AO animaux. flores un mois,
? seulement ont survécu.
Les lésinns anatomn-patholoniques
observées sur les animaux sacrifiés sont d'un typB tres particulier : "Pneumopathie nodulaire oranulomateuse oinantncellu.la.ire a corps étranqer".
Une réaction fibreuse peri-focale
et une infiltration lymphocvtaire ont été observées.(V.V.
Paoillian).
Suivant la même méthode une deuxième 9érie d'expériences
(sur 7P animaux) a été faite.
Deux lots d'animaux sont empotis-
siérés a des doses de 10 et de 5 mn et un 3ème lot témoin est
installé avec du serum physiolonique (lml).
Les résultats histopatholopiques et biochimiques obtenus
après 4 mois de survie sont les suivants:
Les composants biochimiques du parenchyme pulmonaire ne subissent aucune mndification significative, y compris le surfactant
alvéolaire.
Fn revanche, on note une nette diminution du nombre des
macronhanes nar rapport au lot témoin avec altération importante
de leur viabilité a la dose de 10 mo.
L'examen macroscopique ohiactive une dissémination nodulaire narench"Piateuse, L'histopatholoni.p montre divers asoects:
- rarement des nndules lvmohocvtaires interstitiels;
- fréquemment des nndules avec cellules qéantes rote- •
nant un matériel amorphe éosinoohyle et entourés des
1vmphocytes;
255
- des nodules encapsulés par uno fibrose;
- ries nodules fibreux.
Ces asnects sont la traduction histopatholonique d'un
même processus a divers stades évolutifs.
EXAMEN ANnTOWn-PflTHClLnninilE :
Une étude anatomopatholooique a été faite sur du matériel humain prélevé soit par biopsie bronchique (2 cas),soit
par biopsie pulmonaire (4 cas).
Les fragments bronchiques montrent: "une fragmentation
intense et une dégénérescence oedémateuse et fibrinoide du
tissu conjonctif sous-épithélial et en particulier des fibres
élastiques" (M. KAP10UN).
Les biopsies pulmonaires (4 cas) montrent une architecture pulmonaire profondement remaniée lesquelles Intéressent essentiellement les alvéoles, les cloisons inter-alvéolaires, les bronchioles et les petits vaisseaux.
Les fragments pulmonaires des 4 malades biopsies ont
été respectivement examinés par trois laboratoires différents
l?.r cas : Y.B. 63 ans hospitalisé pour bronchite chronique, hémoptysie, lésions réticulo-micro-nodulaires.
Habitudes : priseur rie Meffa a raison rie paquet(lOn)
pour 2 à 3 jours depuis 25 ans.Riopsie pulmonaire
le 26.7.76.
Histo : 10.9.63
Biopsie nulmonaire (linnula) montrant un certain degré d'anthracose orincipalement autour ries arteriole
Par ailleurs, les cloisons inter-alvéolaires sont so
vnnt le sienn d'une hystinn»tnsR 1RS épaississant ri'
facon inénale., constituant des aman col lui aires rie
taille variable, réduisant parfois considêra'ulenent
la lumière des alvéoles.
256
In cvtoolasme da ces hi stincvtes Bst tatoué d'un pinment brun.
Dans certaines D I S H G S ces histiocytes s'allonoent nour prendre
un aspect f ihrnh.lastinue. Peaucouo plus rarement, ces histiocytes semblent occuper la lumiere des alvéoles (pr.A.Chedly Tunis),
2eJT8 caá L.A.«, 65 ans, hospitalisée a plusieurs reprises pour
bronchite chronique obstructive. Dernièrement, l'imane radinlogique évonue une collanénose (réticulomicronodulation).
Habitudes : priseuse de Meffa depuis 30 ans environ a raison
d'un paquet (lOn) par 3 jours.
Avril 1976, Biopsie pulmonaire (O.PITERS)
Protocole hintopatholonioue:
-La préparation histopathologique comporta 3 tranches da parenchyme
pulmonaire fortement remanié présentant uns lobulation tràs accentuée.
Les lobules .pulmonaires contenant des bronches dont la lumiere élarnie a un contour festonné irrénulier.
La plupart de
ces brennhes sont libres; quelques-unes sont toutefois remplies
de mucus; leur muqueuse est tapissée par un epithelium cylindrique cilié relativement haut ppurvu de quelques cellules mucipares. Les bronchioles ont une lumiere encore plus irréauliere et
leur epithelium de recouvrement est localement métaplasique.
Dans la lumiere, pn observe souvent du mucus et des histiocytes
tandis que dans leur paroi existe un infiltrat
lymphocytaire
avec des amas lymphoides au niveau du parenchyme alvéolaire.
La structure pulmonaire est peu reconnaissable.
Les al-
vénles sont souvent bordées d'un epithelium cubo-cylindrique;
leurs lumières rarement libres contiennent des histiocytes dont
le cytoplasme a un aspect spumeux.
Les septas alvéolaires cen-
sidérablement épaissis par de la fibrose sont parsemés de cellules inflammatoires a prédominance lymphocytaire et plasmocytaire einsi que d'histypeytes
alareis de oranulation de pous-
siere noire non cristalli nés nt part5.cul.es biréf rinrentes (Prt
F. P^FRSSmnn - Univ. dn Louvain).
257
- 3ome Cas : Z.B.A, : 67 ans, hronchite chronique depuis 7 ans
\ predominance hivernale. Dennis un an, expectoration mucopurulente avec quelques himnptysias. A la rariin, imanes
réticulo-micro-noriiilaires, fibrokystiques au niueau des bases.
Habitudes : Priseuse de Neffa a raison d'un paquet (lOq)tous
les deux jours, nu 3. Le 8 novembre, 1977, biopsie pulmonaire. Compte rendu histopatholoqique.
Description: Aspect de fibrn-nranulnmatnse pulmonaire tres
organisée avec bronchiolectasies micro-micro-kystiques,tres
nombreux dépots anthracoldes biréfringents parsemant le prélèvement, images d'anqoite des arterioles pré-capillaires
et de moyen calibre, microgranulomes avec assez nombreux
plasmocytes. L'ensemble peut faire évoquer des phénomènes
d'hypersensibilité au sens le plus larqe du terme, mais le
fait dominant est l'existence d'un empoussiéraqe majeur par
de nombreux dépots biréfringents (Pr. 3. CHRETIEN et Dr. L.
DANEL - Hôpital Laennec,Paris).
- 4eme Cas : ß.S..., 41 ans, ouvrier de fond (charqeur) dans
une mine de phosphates pendant fi ans. Depuis 8 mois, travaille au jour. A la suite d'un depistane radio-photo au
mois de mai 1977, on constate : image réticuln-micro-nodulaire
du tiers inférieur des deux poumons avec anomalie Hu diaphragme droit (imane en brioche correspondant a un kyste hydatique
rlu foie extrait par thoraco-phréno-lanaratnmie droite le 2
Janvier 1978).
Habitudes : Hon fumeur, mais il nrise de la Meffa a raison
d'un paquet (10 o) tous les deux a trois iours depuis 20 ans.
Biopsie pulmonaire droite.
258
"Fn conclusion: fihrnse pulmonaire debutante ause bronchectnsiRs micro-kystiques et tres nombreux dépots anthracoides contenant quelques rares particules biréfrinnentes
tatouant le prélèvement, associées a des imanes d'endartérito fihrousfî des arterioles précapillaires avec dédoublement dans certaines zones des limitantes élastiques
internes". (Pr. .1. CHRETIEN et Dr.. Cl. DftUEL - Hôpital
Laennec - Paris).
CONCLUSIONS :
Jusqu'à nos jours, le neste de priser est considérer
anodin par l'ensemble de la population.
La Neffa prend memo
le relais de la cinarette chez les orands fumeurs (moyen de
sevraoe souvent pratiqué).
CettB toxicomanie est largement répandue en Tunisie,
mais aussi dans toute l'Afriqua du Nord.
La patholoqie induits par la Neffa se présente cliniquement comme une bronchopneumopathie chronique obstructive
apparemment banale.
Par contre, l'aspect radiolopique dans les cas typiques
est celui d'une pneumoconiose.
tardive.
Son apparition est relativement
Elle entraîne un remaniement de l'architecture pulmo-
naire a la rone d'échanne avec toutes les conséquences fonctionnelles.
Quand ce type de tabanisme touche les mineurs, cela ne
fait qu'intrinuer et compliquer la patholnnie professionnelle.
259
Mous pensons que cette nouvelle entità fit innathn^ínique ORut se ranner parmi 1er; pneumoconioses x/n'oßtales. L'appellation "poumon de Meffa" nous semble justifia.
Nos remerciements au Docteur GUY PIETERS qui nous a airie dans
ce travail.
f nt'i-Clés : Tabac a priser "floffa" - Pneumncnni nsp. vanitalo
Pnumnn de rief fa. (Key-unrds).
26o
flTnl i M'ÍTí'PHir
1) BOUSQUET J. - GAÏRAUD J. P. '" MICHEL F.B.
:
*^
"Physiopathologie
des alvéolites
allergiques
Poumon et Coeur - Tome XXXIV - N" 2, 1978 p.
extrinsèques".
157-169
2) CHRETIEN .T.
"L'appareil
respiratoire
face aux nuisances de
l'environnement"
La NouV. Presse Med. Nov. 76, 5, N" 40, p . 2687-83
3) CBRETIEN .T:
:
"Un objectif
prioritaire
La Nouv. Presse Med.,
4) CHRETIEN J.
c la lutte contre le
tabagisme".
11 Dec. 76, S, N" 42, p.
2851-52.
;
"Les risques
aéro-écologiques"
Les Act. Pharmac. T N" 332 - fivr. 1977.
p.
19-25.
5) CORNEA ff. - EL MEKXI L. ~ EL ÇHARBI B. - BEN KHEDER A, et SILVIA QfiBOR
"Poumon de Neffa" (Une Pnenmoconiose
Tunisie Méd. N" 3 Mai-Juin
76.
6) MAIER A, - BMTZENSQHLAGEB. A.-.et
Végétale
?).
S.. ORION :
"Thrombarthériopathie
pulmonaire
professionnelles
de poussières
Arch. Mal. Profes. -Med.
Trav,
allergique
au cours
d'Inhalations
organiques".
et Sociale - 1974 T. 35 N" 10-11 p.
875
7) POPA 7. - GAVRILESCU N. - PREDA ff. - TECVLESCV D. - PLECIAS M. et CIHSTEA M.
"Etude de l'allergie
dans la byssinose
: sensibilisation
de coton, de chanvre, de lin et de jute"
Brit, J. Industr.
Med. av. 1969, 26,
101-108..
261
aux
antigênes
Una nueva neumoconíosis vegetal.
El pulmón de Neffa.
G. Cornea, L. El Mekkl, B. El Gharbl,
A. Ben Kheder y S. Gabor (Túnez)
Se trata de una neumoconíosis observada en Túnez y
provocada por la aspiración por la nariz de un polvo de
tabaco llamado "NEFFA". Este tipo de tabaquismo se encuentra muy generalizado en el medio rural y sobre todo entre
las mujeres. Afecta también a los menores (13 por ciento
en una mina de hierro), agredidos ya por otros polvos. El
adicto Inhala entre 109 y 300 gramos de polvo de NEFFA por
mes, lo que representa de 1 a 3 kilos por año - un verdadero empolvamiento.
En la mayorfa de los casos, el cuadro clfnico se caracteriza por fenómenos de bronquitis crónica obstructiva
con todas las consecuencias funcionales (enfisema, insuficiencia respiratoria, trastornos de transferencia, etc.).
En el plano radiológico, se observa al principio una
reticulomicronodulación que interesa la mitad inferior de
los dos pulmones. En una fase más avanzada, la Imagen reticulomicronodular puede llegar a interesar la totalidad de
los dos pulmones, salvo en cierta medida las vértices. En
la fase final (fase de complicaciones) se observan además,
sobre un fondo enfisematoso, imágenes fibroqufsticas (imagen en nidos de abejas), principalmente a nivel de la mitad inferior de los pulmones. Las primeras imágenes radiológicas aparecen tras un período de tabaquismo (Inhalación
de NEFFA) de 10 a 15 años.
El análisis de este polvo ha puesto en evidencia la
presencia de Si0 2 (sílice) libre con una concentración de
2,8 por ciento y también, en cantidades análogas, de Ca,
Al y Fe. La granulometria da los siguientes resultados i
el 66 por ciento de las partículas tienen un diámetro inferior a 3 micrones; el 10 por ciento, inferior a 10 micrones, y el 24 por ciento, superior a 10 micrones. Por
consiguiente, la mayoría de las partpiculas pueden penetrar
hasta el fondo de los alvéolos pulmonares.
Las experiencias efectuadas con animales de laboratorio
262
(empolvados por^vía intracraqueal a una dosis de 50 mg
en sérum fisiológico) muestran lesiones de un tipo Darticular "neumopatía nodular granulomatosa gigantocelular con
cuerpos extraños. Se han observado una reacción fibrosa
perifocal y una infiltración linfocitosa".
Las biopsias pulmonares hechas a personas enfermas
(cuatro casos) muestran una arquitectura pulmonar profundamente modificada, en lo tocante sobre todo a los alvéolos, las paredes interalveolares, los bronquiolos y los
pequeños vasos sanguíneos (angeitis de las arteriolas precapilares y de calibre medio). Se produce un espesamiento
de los tabiques, infiltrados por montones de histiocitos
cuyo citoplasma está inundado de un pigmento negro no cristalino y de raras partículas cristalinas birrefringentes.
El hábito del NEFFA se halla muy generalizado en Túnez,
pero también en todo el Norte de Africa; cuando este tipo
de tabaquismo afecta a los menores, la patología profesional se complica.
263
I N D I C E
S E S S I O N
IV
5.H, 7aldi
..
Recent proqress in etiopathogene9Ì9 of Pneumoconioses
Tatsuo Sano and Isamu Ebihara
Considerations on pathology, pathogenesis and etiology
of pneumoconiosis.
I.Le Bouffant., H.Daniel., J.C.Martin
Nocivité variable des poussières de silice selon leur
origine. Influence de certains minéraux
Quinot t.,
d'accompaqnememt
Cavelier C , Ulerearon m.O.
Chimie de surface et cytôtôxiclte de la Silice.
W.Uleller.
New aspects in the etlopathogenBSÌ9 of silicotic and
anthracosilicotic lesions
Hisato Hayashi.
Nineralogical analysis of lung dusts in pneumoconiosis
with an analytical electron microscope.
265
RECENT PROGRESS IN ETIOPATHOGENESIS OF PNEUMOCONIOSES
S.H. Zaidi (India)
Industrial Toxicology Research Centre
Lucknow - India
One of the earliest reports on the etiopathology of the
miners lung was made by Agricola (1494 - 1555) who mentioned
ulceration of the wind pipe due to dust inhalation.
Ramazzini
(Padua 1700) later described in detail the pathology of the
miners' lung and commented "when the bodies of such workers are
dissected the lungs are found to be stuffed with small stones".
Greenhow (1865) observed drifts and deposits of sand in the lung
tissue and from the lungs of one worker
he isolated about 30
grammes of this so-called sand. A year later Zenker gave a detailed description of the pathology of the lung due to inhalation
of iron dust. The autopsy showed "a brick-red pigmentation so
intense that all blood and tissue colouring was almost entirely
obscured
Several large cavities and numerous firm fibrous
nodules were scattered throughout both lungs", and these lungs
contained a total of 22 grammes of iron oxide.
Some pieces of
lung specimen obtained from Prof. Zenker by Dr. Greenhow are
still preserved in the Middlesex hospital( London.
Earlier Craig (1834) evolved the technique of large tissue
sections of miners' lung.
He wrote "the best manner of ascertain-
ing the exact situation of the black matter in such cases is by
inflating the lung-slightly, drying it thoroughly, and then cutting
it into slices in various directions
be distinctly seen
i the air cells can
the exact situation of the black matter
267
may easily be ascertained."
In recent times this technique has
created much interest and the large tissue section technique contributed by Gough and Wentworth (1948) has helped in the study
of pathology of miners' disease.
The end of the nineteenth cen-
tury, however, saw unanimous agreement that lung disease of the
miners was due to the inhalation of dust and that dusty lung was
more prone to tuberculosis.
Another approach to the study of the etiopathology of
miners disease is experimental pathology.
The research of Claude
Bernard (1887) is perhaps the first of great significance in the
field of experimental pneumoconiosis.
Bernard tied a bladder
containing sufficiently large quantities of coal dust around the
neck of rabbits. With each movement the dust stirred up and rabbits
breathed the dust cloud. At the end of several days, no black
pigmentation was seen in the lungs. The failure of Bernard's
experiments could be attributed obviously to the limitations of
his technique.
At the same time Arnold (1885) evolved a technique
in which he blew air through a tube or hopper of dust which was
vibrated or stirred, over a period extending to 10 years to rabbits
and dogs.
He succeeded in producing lesions which consisted of
dust deposits in the alveoli and lymph nodes. This technique
has formed the basis of present day dusting techniques in the
field of experimental pneumoconioses.
The world-wide industrial revolution of the present century
frequently made work in dusty atmospheres unavoidable, so extensive
experimental studies on the problem of pneumoconiosis have been
undertaken.
Now highly sophisticated dust chambers in which dust
clouds, temperature and humidity can be controlled are available to
268
the scientist for work in the field of occupational health.
SILICOSIS
Recent research has put at our command a vast body of facts
concerning the pathogenesis of silicosis, but there are still many
hiatuses in our knowledge.
Although attempts to produce experimen-
tal silicotic nodules have been successful, we still do not know
precisely the manner in which the human lesions develop. This
has given rise to over fifty theories which are based on physical,
chemical and biological principles.
The earliest physical theory was put forward by Zenkerk
(1866) who postulated that it was the sharp and angular edges of
quartz particles which produced fibrosis in the lung.
Heffernan
(1953) advanced the hypothesis that freshly fractured silica
particles had unsatisfied valencies on their surfaces which were
reactive and directly responsible for biological action. The
piezo-electric effect was propagated by Velicogna (1946) and
later by Evans (1948).
They showed that fibrosis was produced
because of piezo-electric properties of dust. A negative charge
theory was initiated by Hounan (1952, 1954) who thought that
silica particles were pathogenic due to the presence of negative
charge on the surface inciting interaction between the positive
charged protoplasm of the cell.
The crystallinity theory was put
forward by King (1953) and later it was shown by Zaidi et al (1956)
that there was a relationship between the crystallinity of silica and
fibrogenecity because fused silica was least fibrogenic while quartz,
cristobalite and tridymite in that order were increasingly more
fibrogenic.
Such relationship has not been established in man.
269
Scheel et al (1954) put forward the surface absorption theory
that quartz absorbs protein.
The theory of critical particle
size was also put forward by King (1953) and later by Zaidi et al
(1956), who determined the most pathogenic particle size of silica
dust.
Research on human silicosis and extensive experimental investigations have pointed out that there is a range of maximally fibrogenic particle sizes. The probable upper limit of pathogenic
particle size is 10 microns (although many believe it to be about
five microns) and the lower limit of pathogenic particle size is
probably 0.002 micron.
All the dust particles found in silicotic
lungs are less than 2 micron in diameter, and most are less than
one microni overwhelming experimental evidence supports clinical
findings that the optimum size of the silica particles (the size
which is most pathogenic) is in that range.
ly been emphasized by Vitums et al (1977).
This aspect has recentThe significance of
animal experiments and human autopsy findings for studies of the
fibrogenic activity of a particular particle size in man in still
open for further investigation.
The chemical theories are based on the hypothesis that
chemical interaction between silica and the tissue occurs. The
solubility theory was described by Kettle (1926, 1934) and King
and Belts (1938).
On the basis of animal experiments they observed
that the fine particles of stone dust which get into the lungs
were pathogenic because silicic acid dissolved out from their
surface.
Further the pathogenicity of any stone dust was related
to the rate at which it released silicic acid into the solution.
Holt (1957) observed that in the cytoplasm of quartz-laden phagocytes a collagen precursor was formed, which had the ability to
27o
collect the monosllicic acid as It was liberated from the surface
of the particles and to store it so that this acid could polymerise
and act as a factor which would change procollagen to collagen.
This modified silica solubility theory gives only an outline of
the process of silicosis and suggests that the basic solubility
theory can still be taken as a guide for further experiments on
the problem of silicosis.
Other chemical theories include the sericite theory of Jones
(1933), Edge (1934) theory of microinclusions of liquid carbon
dioxide in quartz, formation of alkali as a result of hydrolysis
of mineral silicates by Briscoe (1936), and the theory of Holzapfel
(1942, 1949) that fibrogenesis depended on the
acid«
acidity of silicic
The view of "mineral shift" of Schepers (1960) related to
the silicotic process still needs clarification.
Thomas (1965)
has shown that contact of the cell with SiO, tetrahydron groups
and transferable groups attached to them is a prerequisite for
fibrogenic action.
Brieger and Gross (1966,1967 a,b) further
confirmed this hypothesis and
suggested that the structure, and
not the dissolution of silica, was of significance in the production of fibrosis.
Vigliani et al (1950) suggested an immunological hypothesis
for silicosis based on the observation that in patients there was
an increase of gamma globulin and since antibodies belong mostly
to the gamma globulin fractioni the increase may be an expression of
antibody production.
It
was suggested that, if silicosis has an
immunological pathogenesis, the free silica may provoke or increase
271
the formation
of antigens and subsequently of antibodies.
Silica
may also act as a booster of heteroantigens or liberate autoantigens
directly by killing a comparatively large number of cells. This work
from the laboratory of Vigliani formed the basis for further investigations which have been reviewed by Zaidi (1969).
Evidence was also collected showing that the immunological
hypothesis does not satisfy several of the criteria required for a
disease on an established immunological basis. Klosterkötter (1955)
found that the increase in gamma globulins in silicosis is a nonspecific reaction.
Antweiler and Hirsch (1956) while doing animal
experiments on the formation of antibodies in the development of
silicosis could not get encouraging results.
and Voisin
Collet et al (1961)
et al (1964) also observed that silica does not act
as an antigen.
Licht (1960) found that the hyaline substances of
the silicotic nodule were devoid of any antigen.
According to Vigliani and Pernis (1962) "the final observation
is that silicosis is not an immunological disease but a disease
with strong immunological components.
The immunological phenomena
of silicosis do not develop from a specific antigen produced by
quartz but they consist of accumulation, in the developing silicotic nodule, of many antigens unknown at present, and in their
ability to stimulate locally the production of
the corresponding
antibodies by the adjuvant action of the quartz". The
immunolo-
gical hypothesis outlined needs more precise verification, chiefly
with regard to the possible mechanism or the formation of autoantigens capable of inducing active production of autoantibodies.
272
Recent research has again shown a shift in favour of a basis
of immunological hypothesis of silicosis.
Immunological response
is associated with lymphocytes, one population of which, known as
T-lymphocytes, is stimulated to maturation by the thymus and the
other, B-lymphocytes, has its origin in bone marrow.
The cellular
immunity which is T-cell dependent has assumed great significance
in regard to lymph nodes and the respiratory tissue. Two groups
of workers, Nash and Hoil (1973) and Kaltreider and Salmon (1973),
have shown that both T and B cell systems of the lung are capable
of being stimulated when an antigen comes in contact with the respiratory tissue through inhalation«
In the light of these recent
findings the immune response of the
lung due to contact with
antigen presents a fruitful field for further research.
Electron miscroscopic studies have been made on the fate of
silica particles after inhalation which have given useful information on the pathogenesis of silicosis.
Pernis et al(1960) and
Allison (1967) have demonstrated that the silica particles were
first engulfed by phagocytes and taken up into phagosomes which
then fused with, lysosomes to form phagolysosomes. The particles
chemically damaged the membrane of phagolysosomes and the hydrolytic enzymes were released into the cytoplasm.
became rounded due to the
tually died.
The phagocytes
action of hydrolytic enzymes and even-
Schlipkötter (1955) suggested that inactivation of
the particles of cytoplasm led to the lack of function of the
cells.
Further, Schlipkötter and Linder (1959) observed, after
nine months of intratracheal injection of quartz in to rats,
concentric lamellated membranous structures in the nodule which
later led to the initiation of the fibrotic process.
273
Similar
detailed studies of the interaction of silica particles and the
cytoplasm of macrophages have since been extensively reported.
ASBESTOSIS
Asbestos which is a magnesium silicate, has been mined and its
fiber made into fire resistant linen several centuries before Christ.
Today, in industry asbestos is a mineral of a thousand uses like
heat-resistant insulators, cements, furnace and hot pipe coverings,
filter medium, fire-proofing gloves, clothing and brake lining.
Since the comprehensive report of Merewether and Price (1931) it
has been established that asbestos dust is harmful per se and causes
asbetosis among asbestos workers who have a high morbidity and mortality (Elmes et al 1976i and Peto et al 1977).
are in progress in many parts of the world.
Studies on this aspect
The chemical, physio-
chemical and biological properties of asbestos have been reviewed
by Warwick (1973), Lewinsohn (1974), Harington et al (1975) and
Snyder (1977), and pathology described by Meyer (1976).
The follow-
ing are some of the recent views on the pathogenesis of asbestosisi
1.
Interstitial fibrosis of the lung (asbestosis)i
Two views on
the mode of development of asbestosis have_ been put forward. Accordi
ing to one, asbestosis is a chemical process and according to the
other it is a mechanical effect of the asbestos particles. Recently an immunological basis for asbestosis has also been described.
The problem of particle size in relation to fibrosis is still open
for further investigations.
However, particles of less than 5
micron diameter are supposed to be harmless (Gross,1977).
The
current knowledge will be advanced if more experiments are designed
to investigate the role of the size and shape of asbestos dust in
relation to fibrosis. Hammond and Selikoff (1973) have observed
that radiologically evident pulmonary fibrosis is also enhanced by
274
cigarette smoking.
2.
Asbestos bodies: These bodies are formed because of the in-
corporation on the fibers of a protein layer containing iron. They
are also known as ferruginous bodies. The formation of asbestos
bodies has been reviewed by Das et al (1978).
They may also be found
in the lungs of the population which is not exposed to asbestos,
but in workers handling asbestos they are found in large quantities
(Doniach et al 1975).
It is now possible to characterise and
differentiate asbestos fibers from other bodies by electron diffraction and electron probe microanalysis (Berry et al 1976¡ Langer et
al 1973¡ Auerbach et al 1977).
3.
Heural plaques i The pleural plaques are formed due to the
thickening of pleura which often gets calcified, and occasionally
there is hyalinisation.
Their formation has been attributed to
asbestos inhalation as well as to other previous pleural diseases
(British Thorax and Tuberculosis Assoc, and N.R.C. Pneumoconiosis
Unit, 19721 Navratil and Trippe 1972; Navratil and Dobias 1973¡
and Yazicioglu 1976).
4.
Lung caneen Increasing incidence of lung cancer has been re-
ported in asbestos workers (Doll, 1955; and Buchman, 1963).
The
cause of the cancer so far is unknown, but its occurrence is
affected by factors like inheritance, race and co-factors like
cigarette smoking (Selikoff et al, 1968).
Although the latent
period for the development of cancer may be many years, its appearance in the lung is detected at a comparatively late stage when
treatment is not very effective.
5.
Gastrointestinal and laryngeal tumoursi
Asbestos has been
suspected to cause an increase in the incidence of these tumours
275
(Enterllne and Henderson, 1973, and Stell and McGill, 1973).
A
relationship between asbestos, smoking and laryngeal cancer has
also been described (Shettigara and Morgan, 1975; Saracci, 1977
and Gross, 1977).
6.
Diffuse mesotheliomai
Wagner et al (1960) reported the asso-
ciation of mesothelioma with asbestos workers, and subsequent reports have shown that it
is associated with the crocidolite variety
or a mixture of different kinds of asbestos dusts«
Only a few fatal
cases of mesothelioma have been reported from amosite and none in
antophyllite asbestos mining.
pleura and in the abbomen.
These tumours occur both in the
The etiology of mesothelioma due to
inhalation of asbestos fibers still remains uncertain.
Animal ex-
periments with asbestos inhalation exposure or intratracheal injection have not led to the development of mesothelioma.
Wagner et al
(1969) demonstrated that it was intrapleural injection alone which
gave rise to the formation of this type of tumour.
No association has
been demonstrated between cigarette smoking and mesothelioma.
Harington (1965) demonstrated that tumours developed both with
untreated asbestos and the samples from which hydrocarbons were extracted.
He suggested that a critical proportion of Ferric (Fe )
+2
and Ferrous (Fe ) forms of iron in the fiber may be carcinogenic.
Experiments from Gross's laboratory indicate that contamination by
nickel or the chrysotile dust during the hammering process produced
lung cancer in rats exposed to high concentration of that dust
(Gross et al, 1967).
Animal experiments designed so far to test
the importance of waxes and oils as contributory factors in the production of mesothelioma have shown these contaminants unlikely to
be relevant, also there were no good clues suggesting that trace
276
elements were likely to be a major factor In the production of
asbestos cancer (I.A.R.C, 1973).
The question of the significance
of structure therefore assumes more importance than the physiochemical properties.
According to Gross (1977) lung cancer developed only in those
asbestos workers who were heavily exposed to this dust, and he
suggested that there was a dose-response relationship between the
dust exposure and disease.
Efforts should therefore be made to
restrict the use of asbestos by substitution and imposing restrictions under which asbestos is processed.
SILICATE PNEUMOCONIOSES
In recent years, the harmfulness of the inhaled silicate dusts
like talc, fiber glass, kaolin has been recognised.
The pneumoco-
niosis caused by silicate is termed "silicatosis".
Talcosls
Pneumoconiosis caused by the inhalation of talc dust has been
called "talcosis".
In their review on talcosisf Alivisatos et al
(1955) observed that the disease is a definite clinical entity, a
type of "Fibrotic pneumoconiosis accompanied by functional disturbances".
In New York disabling pneumoconiosis from talc has been
reported in 14,5 percent of the workers exposed (Hunter 1964),.
Messite et al (1960) pointed out that workers exposed to both
fibrous and non fibrous varieties of talc suffered from pulmonary
fibrosis.
Italian workers are, however, of the opinion that the
inhalation of pure talc does not bring about significant pulmonary
fibrotic lesions even if inhaled over a long period (Scansetti et
277
al, 1963| Tronzano et al, 1963; Ghemi et al, 1963; Rubino et al, 1963;
Pettinati et al, 1964, and Dettori et al, 1964), but Rubino et al
(1976) has recently described mortality in talc miners.
McLaughlin et al (1949) who described the first case of talcosis
concluded that "without doubt the fibrosis in the lung was associated
with the presence of the particles of talc dust". Later Biasi (1937)
noted the absence of quartz in the lung while Hunt (1956) showed
less than 0.5 percent quartz in the lung residue in cases of talcosis.
Schepers and Durkan (1955) described the fundamental pulmonary talc
reaction, which
was comprised of multiple irregular shaped foci 1-3 mm
in diameter consisting of macrophages arranged in a stellate manner
around medium-sized and smaller blood vessels. Seeler et al (1959)
and Kleinfeld et al (1963) noted diffuse pulmonary fibrosis, cystic
spaces, and asbestos-like bodies in talcosis.
Experimental studies have also shown that the initial reaction
to talc dust in various tissues of different laboratory animals is
mild (Zaidi, 1969).
Schepers and Durkan (1955) and Luechtrath and
Schmidt (1959) observed that the divergent reports on the fibrogenic
activity of talc dust were due to impurity in the talc.
Lords (1978)
who has, however, extensively reviewed the available literature on
talc, concluded that with talc there is a fibrotic response which is
dependent on the dose administered, and certain levels of
are tolerable.
exposures
Although no neoplasia has been observed with talc
inhalation, it may be suggested that the fibrous contents of talc
may pose a possible occupational carcinogenic hazard, and an open
mind has to be maintained on the matter (Blejer et al, 1973).
278
Fiber Glass
Glass in the form of the fine fibers is used in increasing quantities
in industry.
During preparation of "fiber glass" very small glass
fibers are released into the air and the atmosphere may shimmer with
them.
Roche (1946) observed that glass wool "fiber glass" did not
cause any pulmonary fibrosis which was confirmed by Dhers et al (1946).
Kahlau (1947) noted occasional cases in which the inhalation of glass
wool dust was claimed to be a contributing cause of pulmonary disease.
Barsi (1964 a,b) noted prevalence of chronic bronchitis and Murphy
(1961) described haemorrhagic bronchitis.
Pushkina (1965) observed
exudative and inflammatory response in the lung following glass wool
inhalation.
Post-mortem studies on workers exposed to dust for long
periods however failed to demonstrate any pathological lesions (Gross
et al, 1971).
Gardner (1942) observed that glass wool lacked the basic physiochemical properties that would produce fibrosis.
Schepers and Delhant
(1955) showed that inhalation experiments produce only focal areas of
dust collection but when introduced intratracheally into guinea pigs,
20 to 50 micron fibers provoked well defined fibrosis.
In inhalation
experiments short glass fibers of 6 micron and less in length produced
bronchial epithelioma hyperplasia.
This has been questioned by Gross
et al (1960) on the basis that spontaneous bronchial hyperplasia also
occurs frequently in stock animals. Gross et al (1960) studied the
biological effects of coarse glass dust (50-400 micron) and noted
the laying down of a few delicate collagen fibers. The lung reaction
to fine glass dust (1.1 micron) both in rats and guinea pigs for a period
of one year, consisted only of focal collections of alveolar dust cells
without fibrosis. Further inhalation studies conducted by Gross et
al (1974) with glass dust of average length of 10 micron in two species
279
also resulted only in macrophage reaction and no tumours were seen.
Kushner (1974) observed, by using intratracheal route instead of inhalation, that longer glass fibers of 20 micron length were associated with fibrosis of septal wall.
This data indicated that it was
the long fibers which may cause fibrosis.
In recent years, however, the animal experiments of Stanton and
Wrench (1972) and Wagner et al (1973) have indicated that, when glass
fibers or fibers of aluminium silicate of 0.5 micron diameter or less
and of a length of 10 to 20 micron or longer were injected by the
intrapleural route to rats, there was development of tumours.
The
experimental finding assumes significance in terms of the hypothesis
that these fibers when inhaled may also cause tumours in man.
Gross
et al (1977) observed that the dose of mineral fibers used in these
experiments was high and the animal species inappropriate. Nonfibrous and non-carcinogenic dust, e.g. barium sulphate or solids
such as plastic fibers, glass particles, cholesterol crystals, also
produce sarcomas but at a much lower incidence.
The extrapolation
to man of carcinogenesis induced by fibers in rats therefore appeared unwarranted.
Kaolin
Pneumoconiosis produced by kaolin is known as kaolinosis.
Recent references to industrial hazards arising from the inhalation
of kaolin have been concerned with the pottery, ceramics and refractory industries where kaolin is used in admixture with other
mineral powders, notably felspar and flint.
Lynch and Mclver
(1954) described that, in an autopsy on two cases of kaolinosis,
nodular fibrosis and emphysema were present.
Hale et al (1956)
observed in one case large amounts of pure kaolinite dust associated with massive fibrosis without evidence of tuberculosis, and in
28o
another large amounts of kaolin dust and excess amorphous silica
with a more nodular type of fibrosis and progressive tuberculosis.
Experimental work has shown that kaolin does not produce fibrotic
lesions in any way comparable with silicosis.
It has been suggested
that the fibrosis sometimes noted with kaolin results from the admixture of silica to kaolin.
This has been shown experimentally
by Rutter et al (1952), Policard and Collet (1954) and Schmidt and
Luechtrath (1958) who observed that particles of kaolin are always
accompanied by Silicat thus we are concerned not with kaolin alone,
but with kaolin-silica mixtures.
These difficulties explain the
differences in the conclusions drawn by various workers in the
field of kaolinosis.
The role of infection in producing massive
fibrosis is also significant (see pulmonary massive fibrosis).
The other two fibrous rocks are serecite and sillimanite.
Serecite has no commercial importance.
There is some evidence that
sillimanite may cause interstitial pulmonary fibrosis both in exposed workers and experimental animals (Jotten and Eickhoff, 1944,
Gardner and van Marwyck, 1947).
Fuller earth pneumoconiosis,
cement pneumoconiosis and mica pneumoconiosis which are benign,
have also been described.
In view of the recent recognition of the problem of pneumoconiosis due to silicates, the pneumoconiosis conference held at
Johannesburg (1959)* recommended "as observations on man with regard
to the pathogenicity of silicates are incomplete, it is desirable
that further observations on man and experiments on animals should
be carried out".
* Proceedings of the Pneumoconioses conference held at University
of Witwatersrand, Johannesburg 9-24 Feb.,1959, Orenstein, A.J.
(ed) J.C.A. Churchill (1960).
281
PNEUMOCONIOSES CAUSED BY COAL, INORGANIC AND OTHER DUSTS
In recent years the etlopathology of simple coal workers'
pneumoconiosis has been extensively described.
It has now been
shown that coal workers' pneumoconiosis consists of nodules which
are small, less firm and fibrotic than silicotic nodules and contain more dust.
They are surrounded by a zone of focal emphysema.
Numerous small discrete aggregations or drifts of coal dust and
sheaths of dust laden cells enmeshed in fine fibrous tissue, principally as cuffs around the respiratory bronchioles are also seen
(Heppleston, 1947,1951).
The particles size of the dust is 2-3
micron and ends at about 5 micron (Cartwright and Nagelschmidt,
1961).
The dilation of ensheathed bronchioles forms focal em-
physema which increases with the advance in age of the miners.
Both the focal and generalised varieties of emphysema may be found
(Gough, 1940, and Heppleston, 1947).
Heppleston's (1947) view regarding coal workers' pneumoconiosis
has been that it was the mechanical accumulation of dust irrespective of its nature which played a significant part in the pathogenesis of the dust lesions. Policard and Deyuns (1930) observed
that pulmonary anthracosis and fibrosis of the lungs of coal workers
were merely two phases of the same process.
The other view has been
that the disease is due to quartz but modified in appearance by
the large amount of coal.
ference with the
Cummins (1927) observed that the inter-
lymph drainage of the lung led to the retention
and accumulation of coal dust in the pulmonary tissue.
Belt and
Ferris (1942) noted that the fibrous tissue (reticulin) in these
foci was just sufficient to hold together the deposits of particles.
282
There is therefore no accepted view Inspite of extensive research
on the subject.
Simple coal workers' pneumoconiosis may be complicated
by
massive pulmonary fibrosis (see pulmonary massive fibrosis).
Among
the coal miners a condition known as "rheumatoid pneumoconiosis"
associated with rheumatoid arthritis has been recognised (Caplan,
1953).
The opacities in the lung may develop suddenly or coincide
with the onset of arthritis.
They often coalesce into large lesions.
Gough et al (1955) observed that the fully developed rheumatoid
nodule is bigger than the silicotic nodule and is composed of necrotic collagen separated by lines of dust accumulation and surrounded
by an inflammatory reaction.
recovered.
Tubercle bacilli have so far not been
Rheumatoid nodules may calcify, or the necrotic material
may be expectorated leaving behind a thin-walled cavity.
Other forms of carbon (graphite and lignite), metal (aluminium,
beryllium, iron, cadmium, tin, nickel) and a large number of inorganic dusts also give rise to a simple type of pneumoconiosis.
The inhalation of aluminium dust or the fumes from bauxite
smelting produces a pulmonary condition known as aluminosis or
"aluminum lung".
Goralewski (1939,1940,1941,1943) observed that
workers exposed to a high concentration of aluminium dust developed diffuse fibrosis with a tendency to spontaneous pneumothorax.
Shaver and Riddell (1947) and Shaver (1948) observed that the disease known as "Shaver's disease" was the result of the inhalation of
mixed fumes of very fine particles of silica and alumina.
From
Britain, investigations did not show any evidence of lung lesions
in workers exposed to aluminium or alumina dust (Meiklejohn and
Posner, 1957).
Again the pathological effects of aluminium dust
283
were reported on the basis of autopsy by Ueda et al (1958) Mitchell
(1959), and Mitchell et al (1961).
They observed characteristic
collections of large amounts of dust and intense generalised fibrosis and Swenson et al (1962) noted emphysematous bullae due to
aluminium dust. On the basis of these observations and experimental
evidence it has now been shown
that under certain conditions, alu-
minium and its various compounds can produce pneumoconiosis.
The
degree of fibrosis varies not only with the chemical structure, but
a positive correlation exists between alumina solubility and its
fibrogenic activity.
The results of experimental research with
aluminium and its compounds are so variable as to make it unjustifiable to apply them to man.
The mechanism of fibrosis induced by
aluminium and some of its compounds
therefore requires further in-
vestigation.
In recent years extensive use of beryllium has become an industrial hazard, for beryllium not only induces systemic toxicity but
also causes pulmonary granuloma.
Further beryllium produces pulmo-
nary cancer in experimental animals, which raises the possibility
that human subjects exposed to beryllium compounds may develop pulmonary carcinoma.
Further investigations on beryllium are therefore
required.
The inhalation of iron oxide
causes "siderosis". Haematite
miners usually develop a sidero-silicosis because haematite ores
usually occur along the quartz seams.
Electric arc welders also
show generalised reticular and nodular shadows in their chest Xrays but no fibrosis (Doig and McLaughin, 1936).
Workers finish-
ing or polishing silver articles inhale dust of powdered rouge
which contains iron oxide of high purity as well as silver particles;
284
they show an aggregate of dust under the pleura and pulmonary
vessels, but no fibrosis.
Iron oxide when inhaled along with
silica dust, for example by foundry workers and boiler scalers,
however, does cause fibrosis. There is evidence that iron and
steel workers suffer from cancer of all sites more than control
groups (McLaughin and Harding, 1956¡ Bonser et al, 1955¡ Faulds
1956).
It is now accepted that
among haematite miners there
was a notable predisposition to the development of tuberculosis
which often causes disability and death.
RARE EARTH PNEUMOCONIOSES
The "rare earth" elements include lanthanum, cerium, praseodymium, neodymium, europium, gadolinium, terbium, dysprosium,
holmium, erbium, germanium, thulium, ytterbium and lutecium.
Schepers et al (1955) observed radiological changes in the lungs
of workmen exposed to oxides and fluorides of certain rare earth
elements.
Inhalation and intratracheal injection experiments by
these workers did not produce fibrosis in guinea pigs, but a year
later vascular granulomata with a eosinophilic infiltration were
seen.
Schepers (1955) with a blend of rare earths with high fluor-
ide content noted pneumonitis, subacute bronchitis, and bronchiolitis associated with deposits of the dust.
Focal hypertrophic
emphysema was also seen but no fibrosis. Mogilevskaya (1961)
noted that the effect of mixtures was severer than the individual
components.
Mogilevskaya and Raikhlin (1963) and Mogilevskaya
and Roschina (1964) administered intratracheally the dust of
gadolinium oxide and confirmed its toxicity.
Ball and Gelder
(1966) also showed that inhalation of gadolinium oxide initiated
focal areas of interst
' "
"ckening around dust-laden macro285
phages, areas of calcification in the region of the alveolar
membrane) and elastic laminea of the small pulmonary vessels
in micet
It was concluded that gadolinium oxide caused only be-
nign lesions in the lungs of mice. Hoschek (1966) on the basis
of intratracheal injections to guinea pigs of cerium oxide and
fluoride observed that these effects of rare earth on pulmonary
tissue have however opened up a new field of research, the knowledge of which may be utilised with advantage in the prevention
of hazards caused by them,
The importance of many non-silicious dusts which cause benign pneomoconiosis is now being realised.
Under certain condi-
tions they may cause pulmonary impairment.
The effect on pulmo-
nary tissue of other substances like tin oxide, tungsten carbide,
barite, zircon, titanium oxide and calcium fluoride dusts has been
investigated, and some of the so-called "inert dusts" have been
shown to cause pulmonary damage and disfunction.
Combinations of different raw materials are also used in
industry today and, therefore, dust exposure from them may consist of a mixture of various substances, e.g. in certain ceramic
plants beryllium may be inhaled along with silica dust, and similarly quartz along with asbestos dust.
The combined effect of
many dusts with other inorganic dusts or other chemicals needs
further exploration.
NUTRITION AND PNEUMOCONIOSES
Study of the effect of a low protein diet similar to that
consumed by the mining population in India on the pulmonary
silicosis revealed that fibrosis and total collagen content of
the silicotic lungs was not significantly altered (Zaidi and
286
Kaw, 1970t Kaw and Zaidii 1970).
A synergistic action of low
protein diet on silicotic fibrogenesis appeared to be unlikely
(Zaidi and Kaw, 1970).
The progression of pulmonary silicosis in
subclinical ascorbic acid deficiency to guinea pigs took place in
almost a similar fashion as in those animals having an adequate
ascorbic acid intake (Kaw and Zaidi, 1969).
These studies suggest
that in miners, silicosis will probably develop uninfluenced by
the state of nutrition.
INFECTIVE PNEUMOCONIOSES
Infective pneumoconiosis has been defined as the modification in a dusty lung of the reaction to a chronic low-grade infection,
frequently tuberculosis, in the direction of increased fibrosis
(Simson et al, 1931).
Infective Silicosis
The hazards of the inhalation of silicious dusts have included
a high incidence of pulmonary tuberculosis among affected miners.
In infective silicosis necrosis and fibrosis proceed side by side,
with a preponderance of the latter.
The chronicity of the lesions
is possible due to the combined action of silica and tubercle
bacilli and often these factors were so closely blended that they
excercised a modifying influence on each other and the lesions produced were typical of neither.
In the presence of a chronic low-
grade tuberculosis infection and silica dust in the
lungs, the re-
action was modified and resulted in large areas of fibrosis.
Kettle (1932) however went so far as.to suggest that infective
287
silicosis was an example of chronic tuberculosis which was so modified by the presence of silica dust that a low-grade progressive
infection resulted which was accompanied by excessive fibrosis.
There are various views regarding the proliferation of tubercle bacilli in the presence of quartz. The necrosis produced by
quartz provided a suitable medium for the growth of tubercle bacilli.
Kettle (1930) and Price (1931) reported the enhancement of growth
of tubercle bacilli by silica In artificial media, but this could
not be substantiated by Vorwald et al (1954).
Eblna et al, (1960)
did not notice multiplication of BCG bacilli in the mononuclear
phagocytes ingesting dust particles, but observed that the dust
particles destroyed the phagocytes which may be one of the factors
to enhancing tuberculosis. Viglianl and Pernis (1959) produced
evidence that finely divided silica may enhance significantly
the
immunological response to bacteria, and therefore infective silicosis was a reciprocal non-specific enhancement of the Immunological response.
Goethe (1968) showed an influence on the transport
of quartz dust from the lung to lymph nodes, when the animals were
given BCG. The proliferation of tubercle bacilli and increased
fibrosis in infective silicosis however still requires further
investigations.
Infective Silicatosis
The term infective silicatosis has been used for the pneumoconiosis caused by silicates in which tuberculosis infection is
involved.
The relationship of tuberculous infection and experimental
kaolin pneumoconiosis has been extensively studied.
The fact that
a mixture of kaolin dust and tubercle bacilli produced an extensive
pulmonary fibrotic reaction in experimental animals has assumed
288
great significance in view of the recent clinical report of progressive massive fibrosis in workers exposed to heavy concentrations of kaolin dust (Lynch and Mclver, 1954)•
PULMONARY MASSIVE FIBROSIS
Pulmonary massive fibrosis was first reported in coal miners
from many parts of the world which on X-ray examination produced
opacities resembling a golf ball, a sausage or even a cricket ball.
The condition assumed greater importance because cases of pulmonary massive fibrosis have also been reported among workers exposed to other dusts like kaolin or haematite (Zaidi, 1969, 1977).
The etiology remained uncertain for several decades.
Earlier Belt
and Ferris (1942) suggested a sporadic factor "X" which caused this
type of pulmonary massive fibrosis. The nature of this factor has
been a subject of experimental investigations and recent views
are summarised below.
Silica hypothesis i It has been suggested that'pulmonary massive
fibrosis is due to the coalescence of silicotic nodule.
Classical
silicosis is however rare in coal miners. The other view is that
the coal macule is a modified silicotic nodule.
Extensive lung
dust residue analysis have shown that silica contents in the miners
are of the same order if not slightly more as that found in the
normal lung.
Total dust hypothesis i This theory is based on the assumption that
once a certain amount of dust has accumulated in the lungs a process
is started which is self-perpetuating.
This view appears to be un-
likely because the progress of disease is not influenced by further
dust exposure.
289
Immunological hypothesis i It has been suggested that pulmonary
massive fibrosis may be the result of an antigen and antibody reaction.
This is supported by the occurrence of the Caplan syndrome
(rheumatic pneumoconiosis) and lung autoantibodies.
Burrell (1973)
demonstrated that both types of IgA, secretory and serum are involved in the immune response, and such antibodies can be detected
in pneumocoriLctic nodules. This theory remains to be further investigated.
Infective Faeton
The concept that an infective factor was operative
gained importance in recent years because of the extensive experimental work done by Zaidi (1977).
James (1954) found bacteriolo-
gical and histological evidence of tuberculosis in 40% of cases of
pulmonary massive fibrosis.
Further the
discoveries of Mycobacte-
rium kansasil and the Scotochromogens in the sputum of miners were
other important factors in understanding the mechanism of pulmonary
massive fibrosis.
Zaidi et al (1955) showed that pulmonary massive fibrosis was
brought about by combined action of tubercle bacilli and coal mine
dust. Asymmetrical and irregular lesions in guinea pigs were produced by the combined effect of an isonized resistant strain of
Myco tuberculosis and coal mine dust, which persisted up to 300
days.
The failure to show any tendency to resolution is also seen
in coal
workers' lung.
They suggested that pulmonary massive
fibrosis was not brought about by an increase in the virulence of
the bacilli, and when fibrous tissue had formed the bacilli died
out.
It was therefore concluded that coal mine dust plus tuber-
culosis infection produced pulmonary massive fibrosis.
This aspect
was therefore re-investigated by several workers using different
29o
strains of Myco tuberculosis, and pulmonary massive fibrosis has
been produced (Zaidi, 1969).
To what extent a chronic low-grade infection other than tuberculosis along with different types of dust played a part in the
pathogenesis of these lesions remained obscure. This was, therefore,
investigated by Zaidi et al (1973) with asbestos dust along with a
low-virulence organism, namely Candida albicans. This organism
is capable of setting up a mild infective stimulus in the lungs
and is sometimes found in the normal physiological conditions of
miners.
Amosite dust was used in our experiments because animals
are more susceptible to this variety of asbestos.
The animals used
were Rhesus monkeys which possibly may have similar an immunological response to that of man and are therefore the best suited primate for experimental asbestosis.
From these investigations it
was concluded that Candida albicans can act synergistically with
amosite dust and produce more extensive pulmonary collagenous
fibrosis than caused by either the amosite dust or Candida albicans
alone.
Experiments were also undertaken to study the lesions, if any
caused by máznese dust, in the lungs of guinea pigs and their
modification by Candida albicans. The experiments showed that
manganese dioxide in the presence of infection produced more fibrosis and definite pneumoconiotlc lesions (Zaidi et al, 1973).
The role of organic dust and infection was also studied by
Zaidi et al (1971).
They investigated the disease of farmers known
as farmer's lung caused by the inhalation of mouldy clay.
The pa-
thological changes were caused by the combined action of hay dust
291
and thermophilic actlnomycetes.
Thermopolyspora polyspora regarded
as the causative factor was studied in guinea pigs.
The lung of
guinea pigs exposed to T. polyspora alone showed no discernible
connective tissue lesions. The lungs of animals,exposed to hay
dust alone produced lesions closely resembling those seen in actual
cases of farmer's lung. At the termination of the experiments at
180 days i both interalveolar and intra-alveolar fibrosis was observed with dust alone, but the lungs exposed to hay dust mixed
with organisms developed more extensive fibrosis.
Zaidi (1977) concluded that extensive pulmonary fibrosis, in
the presence of dust whether coal, asbestos, manganese or hay dust,
is not only related to tubercle bacilli, but also to other chronic
low-grade infestions which are found in the upper respiratory tract
of workers.
It may be inferred that extensive pulmonary fibrosis
is dependent possibly on the synergistic action between the dust
and the organism.
It was suggested that a regular check-up of any
acute or chronic respiratory infection of the workers and its early
eradication by prompt treatment may prevent extension of fibrosis.
Recent experimental and clinical investigations- have brought
to light the role of the infective factor, antinuclear anti-bodies
and rheumatoid factors in relation to the damaging action of a number
of industrial dusts.
The need for further research on the role of
these factors in the pathogenesis of dust disease can hardly be
overemphasized.
292
»Tricóla ( 1494-1 ">r",j ,ne ^5 Metallica Published (15%)
allvisatos.C.P., PontitaI:is,i.n., und Tersis.D (1953),!írit.J.Industr.
llod. ,12,43
<tllison,.t.C., Harrington, J.S., Mrbeck,!! and üasb.T (1*57) iníi„led
¡'articles and Vapours 11,121 edited by C.N.Duvles, tendon Perganon
Press.
vintwoiler.U and Hirscu.G (1956),Arch. Gcnerbepato,14,673
Auerbach,0., l!ocraond,£.C., Selitajif.I.J., Parks, V.R., Kaslow.il.D.,
and Garfintcel.L (1977) Environoental Hcsearcb.1,4.286
•Untold,J (IOCS) UntorsuehuiKren über Staubinhalation und Stauboctastase
Ulpzifl
Uall,n.<t., and von Gelder,3 (19ó¿),/irch.!^viroa.;'4}bli^,]¿«601
Barsi (1964u),noss.;ted.ïidastr.,^2,534
".arsi ( 1964b),!iass.*te<!.Iw¡uptr.,£Ü,6CíGelt.T.H., und Furris,«i.«'. (ICE) Tpcc. üept.Ser.ted. rUs.Coun.rond.,
rk> 1:43
"terry,¿.I'.,íteBoc,P.,5allo,P und Pariente,H (1976), The .recrican Journal
Of Patholo<jy,CG t«3,4::7
Diasi.r; (líi37),di lie<l.i*tt,J2,l2.14
GleJer.H.í'., und .irion.3 (1970),„ournul oí Occupational ridici ne, 13(2).92
Üonscr.G.fl., MaulUs.J.S,, und ntet.-urC,t.!.J(lÇ55), .«er. J.Clin. Peta.,
25,126
¡'ríeger onU "ross (1966),.reh. 'imMron. Ite»ltb.l3p38
Driver und r.ross (1967)«.*rch. ¡-«virón. Health. 14,.299
Qrioqor and Gross ( 19671}),.,rch. ¿n.-lron. lieu lth ,13*751
ariscoo,U.V.A., ¡'ölt,!'.!'., "atthews.-T.l.'., und Sanderson, P.1K 1936)
Trans.Inst..'"in. und retail. .46.291
British TTioruelc nd Tfoixr.-culosis -«ssociatien and Madicul iîesnareh
Council Pncfnoconiosis Cnit(1972),Environ,Res.,2,142
Ouchanun.K.n (1963). TTJO association of certain Victor with asbostosis
XTV Internationul Congress on Occupational Health,«adrid..«sterdan,
Excerpta Medica Foundation.
295
21.
Buriel!.R (1973), Oeeup. Lung. M M « * , Horgan,K.K.C., Seaton.A
R.B.Sonadera Coaçuny London,pò 46
32.
Caplaa.A (1983),1norax,g,29
23.
Cartwright,J und Nagelgehaidt.G (1961) Proceeding« of as International SjMçosiM 445-82.,467-81 C.N Oe«iea,edlter Hm York,
Kargenen rreei.
24.
Claude Bernard (1857) tocona.Sur.Les. Effet«, dea Suba Unce a,
«Btl<f»a e t ftedieaae»toasea,63 (ateta)
25.
OaIlei,A., »elain.G.A., Dania UMeaa tard.. aid
EBViVOI.HMltk,2*409
26.
Qralg.« (1034). 'idiab. •e4.Snrg.J.,|2 A 330
27.
CaaaUaa,S.L (1927),J.r*th.Du«t.,ab6lB
3B.
Dee.H.i.,Bolt,P,r and B m A C (MTB),!«, fedlela*. Del. Laro»,
Öfl.431
29.
Datteri,0., Seaaaettl.G., and Gribando,G ( 1964),«ed. Laroro,85,483
30.
Obere,V., Pelleret, J . , and aMbe.L ( 1946),Arca.nal. Prof. .7(11,19
31.
D»ig,A.T., and n«La«igni»,A. I.G (1936),Uaeet (Apr34),TTl
32.
Oall,R (19SB). » Oriti ah Journal ef Inösstrlol «edleine,12,81
33.
Donl.ckJ., SMtterhan.K.V., and Hntnom.N.K.S (1975),nrlt.J.Ind.Hed.
3¿,16
34.
libi no, T., 1akan«ahi,Y., and llet«ike,T (I960), <*»r.'tev.Reip.Dle,B¿¡j516
35.
Kdge.P (1934),Cfeoed.lln.J.,Qg,406
36.
Elnee.P.C and Slopaoa.H.J.C (1976),Orit. J.Ind.Ued.,^,174
37.
Entorllne.P.E and Ibnderson.V (1973), nrch.Environ.Hlth.,21,312
38.
Kvans.S.I (1948),J.Induatr,H)rg.1ajileol,aQ,3B3
39.
Faalda,S.J d956),J.PatB.Dact.,Z2*3S3
40.
Gardner.WU (1942),Report on the Sjemosiua held at the Saranae Lab.
Seranee Uke.N.Y.June 9
294
feillot.F
(1961). /»eh.
References
41.
Gartner.» and van Harwycft.C (1947), Deutseb.ited.!.,clinscl">r,7?,700
42.
Gheni.F,, Coscia,~.C and ParJgi,<i (1963),t.ted. <-uvoro,51,P,17
43.
GorulowsIil.G (1939), Arch. Gowsrbe path,2,676
44.
Gordlews!:l,G (1940),<trch. Geuorbepath,10,384
45.
GoralewsUl.G (1941),arch. Gewerbepath.ia.ini
46.
Corolewskl.G (1943)., Deutsches liberte -0 1 Jjj3
47.
Cough,J (19*0) 3. Path.Bact., 51,277
40.
Gcvtho.C.J (1960) Scand.J.ncsp.Des.49."27
49.
GoughtJ., ni ver S.D., ond Saol.R.H.G (1955) Tfcorax,lQ,9
50.
Cough,J., and Kentworth.J.E (1940) Proc. 9th Int.Cong.Industr.tled.,
n661.li»m!on
St.
51.
Grecnnon.E.H (1065),Traus.Path.5oc.(land),1¿,59
52.
Oross.P (1977), ¡ev. Environ. Health 2*167
53.
54.
iross.P.liarley.R.A.» Devis,J.M.G (1974) Transcript of Proceedings.
iyrçoslun on Occupational lùcposui« to Fibrous Glass Sponsored by
.. National Instituto Tor Occupational Safety und Health,Jene 27,1974
University COJlege,University of Uarylaud Ucntrc of .»duit riducati on
College Park, rw,20740 12,147
Cross,P., Ttna.J and deTreville.tt.T.P (1971), <trch. environ.Iloalth
22,67
55.
GrosB,P.,Nau,C.A (1967),Arcb.Euviron.neanh,il,450
56.
Gross,P., TJestrlctt.H.L., une! Hev*rnoy,3.H (I960), .«rch.Industr.
Health 21,10
57.
líalo,Uti.. ^urjb.J., uri Klng.li.J and Rarjelschnidt.G (1956) Brit.
J. Industr. »ed., 13,251
59.
Iluonond,::.C ond SelikofM.J (1973),iMolooical effect of Asbestos
I.A.R.C.312
60.
Harrington,J. S (1965). Aun.N.Y..lead.Sci., 122,31
295
Bpfereace«
61.
IlariDijton.J.S., *lllson,J.C aad UaAml.D.V (1975), .vdvun. Hturoaeol.
Cbonotter,12,291
62.
Hattanu» ( » 5 3 ) . l í b e n l a 31*246
63.
llappleatOD,A.G (1947), J. Patb.Baet.,82,453
64.
nappleatoa,<t.G (195l),*reb. Iaduatr.Hyg. Oeeup. Bed. ,1,270
66.
Hslt,P.F (1987) Paauaoeonloaia Industrial Diataaei of the Lung
Cenanti by Duet.Utnaon amarti Arnold.
66.
B»laaafel,L (1943)« Arbo!tanBd,21,T9
67.
Holaapfal.L (1949) nallold Z,UAil37
68.
Honnan.R.r (1982), A.M.A Arch. Indotti». "yo. Oeeup. Med.,5,375
69.
Uoanen,l.r (1984) A.N.A Arab. Induatr.n-fg. Ownp.ied.,J,284
70.
HeeaneM (1966) Zent. ¿«boltened. Arne 1 tésennos ]6JAi»l68
71.
Bnnt.A.C (1956),Tkorax,U,2S7
72.
fkintar,D (1964) Mceaee of Oocupationa.pOOS.londoni lb« Lngllab
tJnlreralt$»a Pratt Ud.
73.
JaaeatW.K.L (1964), Urlt.J «tbere.,4B,89
74.
*>n»e,».B (1933),J.Hyo., 33*307
78.
J o t t o B . M . , *nd Etekhoff.« (1944)« Generbepatb,l2i21¿:>3
76.
Knbles.G (1947), FMBkfurt.Ztwbi!.Patt.,¡&,143
77.
Kaltrelder.H.B and Salnen.S.B (1973), J. Clin, Inve«t.S£,22U
70
KaM.L and Zoidl.S.II (1969), «reb.^nvlronn. Ill tb,12,74
79.
&tt,J.L and Zuidl.S.D (1970), ¿«vlron-B. "«t.2,199
60.
kettki.E.H (1926),J.Iadua«r.qrg. Tbxlcol.^,491
81.
KeUta.E.H (1930).PrM.lto7.S0fl.MBd.2i,79
82.
Kettle.E.H (1932),J. Path.Oaet. ,35,395
296
References
03.
Itottle.E.Il (19"4),J.Fath.3 ct.,22,201
04.
King,E. J (1952-53) Silicosi», lectures on t e Scientific basis
of Dcdlclno.îi. l«ndon,.lthclone Prosr-
06.
Kino,E.J and Qelt.T.n (1938) Hiyslol. Bevs.. 10,329
87.
Klo Info Id , 0 . , ^lol.C.P., Hajoranowskl, J.F., and Hesslto.J (1963).
Arch.Environ. Helath,7,101
00. Kloste*otter,W (1965) Qeltr. Silikoseforsch.,34,17
89.
Kushner.B (1974), Transcript of Proceedings, Symposlua on Occup.
Exposure to Fibrous Class Sponsored by national Institut« for Occun.
Safety and Health, June 27,1974, university Golleqe, University
of dryland. Contro of adult education, Co liege Park.Ud 20740 Volli
31-38
90.
Lanrjer,.i.S and Ptoloj.F.D (1973), ^oloçlcal Effects of .tsbestos
119
91.
Uswlnsohn.II.C (1974) J. Soc. Occup. tied.,21,2
92.
Ucht (1960).iWch.ncW5rbopath, 18,327 U>str. In 0ull.llyg.,26j865(1961)
93.
lord.tG.ll (1970) '¿ololorjlcal effcots of talc In the expert Den tal
m i t a i s a literature review .EtI.Cusoct.Tbxl col.16.51
94.
Uieobtrdth.il and Schnidt.K.G (l959),Doltr.SU!koscforscb,6j,l
95.
Lynch ,K,a .ind UcIver.F.A (1954),.loar.J.Path,2^,1117
96.
Navratll.D and Trippe,F (1972),"uvlron.0os. 5*210
97.
UcLaughlin,A.I.G and nordlng,n.E.,a9S6),arch.Industr.nealth, 14,^50
98.
RcUwf!hlla,A.I.G., Rooers.E., and 0unnao,K.C(1949),artt.J Industr.
Uod.4,104
99.
HelkleJoh»,.» and toswr.E (1957),Crlt.J.Ind str.Kcd., 14J4J,229
100.
HerewothcT,li.P..A and Prlcn.C.W (1930) Beport on ¿ffocts of »sbestos
Dust on toe liw:s and Oust Suppression In the ¿sboscos Industry
H.M.S.O Iondoo.
101.
Hessite.noddln and Kleinfuld.U (1989).*rcb.Iiidustr.nealth,20,4o8
102.
Ueyer.A U976),Ar-h. Hal. Prof.,3^995
103.
Bltcboll.J (1999)., Drit.J .Indastr.Ood., 10,123
297
SBSSOMSA
104.
Micheli, J., Monnlao.G.O., B*lyaaux,H und Une.H.t: (1961).,
Urit.J.Induttr.Hod.,lS(l),10
105.
BogilevBkuyu.O.yi (1061),Gigleaa 1 c*nlt 2ÍU1B
106.
«oollerskuya.O.ya.end Baikblia.N.T (1963) z.l i vue 1'toa .editor
fesco« ( verified througb translation by Israel Program for
Seleatlflc Wsletloaa, Jerasalea (1967)pp 132-41
107.
Uogilevikaye.O.ja and Ro«alaa,T.A *1964) Bereshkoraya Mtt.,Akad
Utar. S.S.8 4ia>,108
108.
•arpkT,G.B.(jr(l96l)rircb.Bnrlron.BaaUh^U704
109.
Nuk ,0.1 aad Hoile,D (1973) Clio.Exp. taca» 1.,¿3,573
110.
NafnUl.ll aad Dabias.J (197S),ijrriroa.Bes. 6,455
111.
PLWIS.B.,
lia.
Rito«'.. tiBll.R «ad Hwar.S.V (1977) .Mt.J.lad. Bad.,24,169
113.
ftulaati.U* C»tala,G.C., Francia,* jnd Gbaat.F (1964),aed.U>voro
5âJM
114.
rolteard.fi and Gollet.A (19S4) .Sciurela 2bahr.<tllo.nith.,17,32n
116.
Pal learda and "evuaj.J (1930) Bull.J'iattol.rfppll .ue,l:122
116.
rrlos,a.H (193i).Proe.E)q>. BtaijbKi.,21,019
117.
rasMtim.I.IC (»6B). t i 0 .jfc. |Mf.äibol.,S,2fl
118.
Banaaatni.BtDC ..Morbus Artifleuai Diatriba Geneva (1713) Translated
by W.C Uright.Ualvenity of Ckleage Presi,diie*jo(194o)
119.
Roeh»,M1946)., Arcta.aal.Proif.,7JXL»W
120.
Rubino/;.P., Haraaaana.P., Bmlttatl,L „nd S«aasottl,G (1963),Ued.
Lavoro «24,496
121.
Vlgltaat,t.C . , and Uonaea.L (1960),*d.Lovaro,Sjl,3
ttublno,C.F.,Scun8ettl,n,Prolatte,n(i976),öortollty
•laars and ailiers J.O.I.,¿0,186
(tody of tale
122.
Ruttar.J.B., Bovet.P.. irAber.R and lUly.V (19S2) Naturvlsseaseliufton
(0,362
123.
Saraeel.R (1077),Intern,J Cancer,2(1,323
124.
<
*angettl,G.,[tos«tti,L., ind hen!,r,(1963).Jled.Uvoro,54,746
29R
i^feroncoa
125.
Scheel,L.D., ?blth,D., vun :ìlper,J.. ¿»nd FlelsiuT,S (1954),A.ïl..i
-ircli. Indus». Ilyn.Oceup. Mcd.1,29
126.
rcbcpcrs.C.K.n (1960),J.I»<!ustr. Bed. Surf)., 29(1), 326
127.
Schepera.O.K.l! und Uurfean.T.M (1953)., Arch. In. ustr.Ueulth,l2j317
12D.
Schepers.G.W.U (1955).Arch.Industr. Health 12*301
129.
Schepers.G.W.ll and Dolahant.a.B (I955),.trch.lndustr.lbaltb,12,276
ISO.
Schllpkötter.n.n (1955),Klln.t)och.,33( 74>,54
131.
Schllpk'rittor.n.N., and Under,E (1959) Ztschr.llyg.lnfcctlonslir.,
145(6),574
132.
Schmidt,K.G *cd Lnthtrath.K (lÇ5C),Gerup. Irvn..34(0).701
ir.3.
See 1er,A.C., Cryfxskl,\S., and tlacKafion.tl.E (1959), Arcb. Indurtr.
tilth. 12,392
134.
Sollkoff.I.J., Uaaaond.E.C., and Churrj.J (I960), J.,«er.Hed. ussoc.
204.106
135.
Shaver,C.G (194G),Cceup. Sled., 5_,7l0
136.
Shav»r,C.G an-1 Sldoell.á.!» (1947)., J.Industr. Ityj.Tbxlcol., 29(3)
145
137.
Shett<r;ari,P.T and Uorjan.n.W (1075).Arch.¿nvlron.Health.3Q.517
138.
SlaBon,F.K.,Strachan,.».S., and Irviue,L,C ( 1931 ),Proc.Trans. Min.
Bod. Officers, ASS., 10(110) Suppl.
139.
Synder.Il.B (1977), Bed.Bull.32,21
140.
Staoton.U.F and Kreuch,C (1972),J.Nat.Cancer. Intt.4£,797
14i.
Stell,H.H and BcGlll.T (1973) lancet. .HKJ25,416
142.
S*cnson,A., Nordenfelt.O., Forssnan,S., Lundgren,K.D and Otoñan
H.,(1962)., « d i , Cewròopath.1,131
143.
Tronzuno.L., Cose ¡a,'"..C., und Ca pe lluro, F (1963)., Sled Lavoro
£1,744
144.
Thoraas.K (1966) ,Beltr,SilikoBefoïsch.,6j21
145.
Ueda.a., BIEOI.Y., Hakl.Z., Kaeda.R., and Talada,H (1958)., Kobe.J
S»d. Scl.,4(2),91
146.
Velicogna..» (19'6). Hed.Uvwro,37,107
147.
Vlgy4lant,E.C.,0oseell!,A and Peeehlol.L (19r<0),Hed. Lavoro,¡LL.33
148.
Vlg/llani.E.C und Hernis.n (1959), J.Occup. Med.,1,319
299
149.
150.
Vigilimi,L.C uod fernii,B (1962)« ,trch.f*v*rbepath,12,507
Vltuna.V.C., £da«ras,H.J and Mata.N.R (1977),<trcn. Environ.
H»alta.,3¿,62
151.
Valaln.G.A.« Taullet.F and Voisin,) (1964),.tan.lnst.rastanr,iafc>353
ISS.
Vonmld.A.J., DaortkI.S., Pratt.P.C and Dalakaat^t.B (1954). w .
Re», Tunare., ¿£,766
153.
Wagner,J.C., Barry.G (19«), Orit.JMrnal of Canear,22,1,967
184.
Wngnor.a.C., Bcrry.C .nd tMmll.V (1973), Orlt. J. Cannar,}!, 173
188.
Uktnttr.J.C., Stegole.* Mi •arehaad,P (I960).. Brlt.J.IndJitr.
Ho«..17*960
186.
Vtanrlek.R.T (19T3), Biological Effnetf. of ¿atettas 2j&
187.
ïa»Iein<'lu,S (1976) ,Ckest 20,43
1BH.
Zatel.S.U (1969). IfcparUwnul Pnonooœnloili, Ike Joan Hopklna
Praia Baltlaaro
189.
«aidi.S.ll (1977) >mt. Ini. K«. Atao«.2aifc),239
160.
Zaldl.S.H., DBcra,n.K.S., banker.a and Chandra,S (1971) J.rata(]f&,41
161.
aldi,S.u., Uarrlsoo,C.V., Ua««i:.¿ «i* Hlt«htao*.Q..i (1955).
Drlt.a Eap. Fata. &G63
162.
Zai(«i,S.H und Kav.J.I. (1970) Brlt. i. Indiitr. »d..ZL250
163.
Zaldl.S.ll., Kiog.L.J., Barri•aa.C.t and Nagalietaldt.G (1956)
A.«.A ATCII. Iadurtr.lbdlttt.UylU
164.
Zaldl.S.ll., KlAj.i.J., Ifcrrtaon.C.V., und Naoolwidt.G (1956) «,*..*
«eh. Induate. Ulta.,12,133
168.
Zaldl.S.H., Shaaker.R., and UDora.E.K.s., (1973) ,Eavlroa.Rat,6j274
166.
Zsnkcr.F.A (l866),0Uet>. Arch.Kilo. tìed.,li6j2
3oo
Progresos recientes en la etiopatogénesls
de la neumoconlosls.
S. H. Zaidl (India)
El Informe presenta un breve historial de la etiopatología del pulmón del minero. Menciona sumariamente la
obra precursora realizada por Ramazzani, Greenhow y Zenker,
en la que se basan algunos de los conceptos actuales de la
etiopatología. Examina los sucesivos métodos experimentales, desde Claude Bernard hasta las cámaras de polvo perfeccionadas de nuestros días. Con respecto a la silicosis,
presenta trabajos recientes sobre diversas teorías i la
teoría de la partícula de sílice recién desprendida, la
teoría de la cristalinidad y la teoría del tamaño crítico
de las partículas. Esboza la teoría química, sus dificultades y modificaciones en estos últimos años y#la aparición de otras teorías conexas. Analiza la hipótesis inmunológica de la silicosis, las diversas dificultades con
que tropieza su aceptación y las ideas más recientes conocidas sobre la acción de los linfocitos T y B en la fibrosis del tejido pulmonar. Las investigaciones clínicas y
experimentales sobre la neumoconlosls debida al silicato
abarcan la neumoconiosis por el talco de los diversos problemas relacionados con la neumoconiosis por el vidrio y
el caolín. El informe señala el problema de las asbestosis
y la importancia de la estructura de la fibra. Indica la
importancia de las infecciones en la neumoconiosis, la fibrosis pulmonar masiva y los factores nutricionales.
3o1
CONSIDERATIONS ON PATHOLOGY, PATHOGENESIS AND ETIOLOGY
OF PNEUMOCONIOSIS
Tatsuo SANO and Isamu EBIHARA
Division of Work Environment and Occupational Disease,
Institute for Science of .Labour, Tokyo, Japan
Cooperative efforts In recent years (1948-1978) by clinicians,
radiologists and pathologists have evidenced the occurrence of
various pneumoconioses in Japan, namely, typical silicosis, atypical
silicosis, acutely developing silicosis, asbestosis and some other
silicatoses (talcosis, pyrophillite lung, bentonite pneumoconiosis,
diatomaceous earth pneumoconiosis, pyrite pneumoconiosis, metal
lung (welders lung or iron-oxide lung, metallic aluminium lung,
alumina lung, pyrite-cinder pneumoconiosis), carbonaceous dust
pneumoconioses!(carbon lung, graphite lung and activated carbon
lung), and organic dust pneumoconioses, (Joss-stick lung, cererai
dust pneumoconiosis), etc., and their diagnosis was confirmed by
autopsy.
I. Pathomorphology of pneumoconiosis.
The pneumoconiosis tissue changes by dust in the pulmonary
area are not only the fibrosis of dust foci, but the airway
affections (bronchitis, bronchiolitis, alveolar-wall changes and
emphysema) and .blood vessel changes due to the two former changes«
Pneumoconiosis can be classified into three types from the viewpoint of j.ts pathomorphological changes. (Table 1 ) .
1. .large nodule pneumoconiosis - only typical silicosisi
2.
small nodule pneumoconiosis - atypical silicosis (mixed-dust
silicosis), silicatosis, metal lung, carbonaceous dust
pneumoconiosis ;
3.
pneumoconiosis with bronchiolitis due to dust - asbestosis,
Joss-stick lung.
3o5
In the case of large nodule pneumoconiosis, nodules are usually sparsely scattered in the rather intact lung area, though the
fibrosis is strong in each lesion.
In the case of small nodule pneumoconiosis, on the contrary,
the density of nodules is usually high and the intact area of the
lung is far less than in the former, though the fibrosis is generally weak, and the bronchobronchiolar changes are stronger than the
former.
II.
Pathogenesis of pneumoconiosis.
Prudent histological investigation of about 650 cases of
various pneumoconioses and repeated animal experiments led the
author to the opinion that pneumoconiosis could be classified from
the viewpoint of pathogenesis into two types, namely, the interstitial type and the alveolar type. (Table 2)«
1.
Free silica dust or dust containing considerable amount of
free silica readily provokes strong collagenous fibrosis in the
dust foci, particularly in the pulmonary lymph nodes, and also
interstitial changes in the lung field to which the intra-alveolar
changes can gradually be added (pneumoconiosis of interstitial type).
2.
In the case of asbestosis, other silicatosis, metal lung,
'carbonaceous dust pneumoconiosis, organic dust pneumoconiosis, or
almost all other pneumoconioses, however, fibrosis is scarcely
or only little noticed in the lymph nodes, and the histological
changes in the alveoli resulting in fibrosis are dominant (pneumoconiosis of alveolar type).
Progression of pneumoconiotic changes is chiefly caused by
3o4
addition of intra-alveolar changes due to the increase of inhaled
dust.
The massive fibrosis of pneumoconiosis can be classified
from the viewpoint of its formation into two types, i.e. "conflation type by small atherectasis" and "filling up".
The former type is found in case of pneumoconiosis due to
long term inhalation of considerable amounts of dust, and dust foci
are predominantly located in the upper, rear part of the lung
(pneumoconiosis of the gradually developing type).
In the later type, which is usually provoked by excessive
dust inhalation in a short period, dust foci resulting in fibrosis
are found not only in the upper part, but also in the lower part
of the lung, accompanied with pleural thickening (pneumoconiosis
of the acutely developing type).
The above-mentioned course of formation is common to all types
of pneumoconiosis except asbestosis.
Asbestosis is usually characterised by homogenous distribution
of dust foci, continued bronchiolitis resulting in bronchioloectasis
in the lower part of the lung, due to long-fibered dust.
The distribution and nature of dust foci depend not only on
the quality as well as quantity of the dust and the duration of dust
inhalation and retention, but also on the condition of ventilation.
(Table 3).
III.
Definition and malignancy grade of pneumoconiosis.
The common histological changes of pneumoconiosis are not only
the fibrosis of dust foci, but also the various affections of airways and blood vessels.
Difference of pathological findings between
various pneumoconioses is the difference of grade.
Therefore, pneumoconiosis should be defined as follows
3o5
"pneumoconiosis Is the lung changes provoked by unsoluble or
scarcely soluble particulate matters that form the dust foci,
various airway affections and accompanying blood vessel changes"•
The conception that the malignancy of pneumoconiosis is related
with the potentiality of collagenous fibre production seems to be
a partial view paying attention only to one of the factors concerning malignancy.
The malignancy must be evaluated by factors which cause malfunction of the lung and pathological changes resulting in
earlier death, i.e. air-passage affections.
In Japan, permissible dust concentrations have been recommended from this viewpoint (1962).
IV.
Etiology of pneumoconiosis.
According to the autopsy findings and the results of repeated
animal experiments, excessive inhalation and sedimentation of
dust can provoke harmful pneumoconiosis of alveolar type.
(Table 4 ) .
From the viewpoint of pathomorphology and pathogenesis, it
is not rewarding to discriminate between organic and inorganic
dust.
Long-term inhalation of dust, organic or inorganic, and
its sustained deposition in alveoli can cause pneumoconiosis of
various types, if the dust is unsoluble or scarcely soluble.
The foreign-body reaction or inflammation is the process in
which the action of phagocytes and proliferation of cells including
the fibroblast and fibrocyte in the presence of excessive foreign
matters (dusts) occur, resulting in cell degeneration and fibrosis
of various grade.
In this sense, the fundamental and common cause of pneumoco-
3o6
niosis is the foreign body inflammation due to excessive dusts.
Consequently, every kind of dust is active and every pneumoconiosis is harmful. As earlier advocated, there is no inert
dust and no benign pneumoconiosis.
3o7
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Table. J
Btlmtkmikìp Between Pathological Findings and tat
Quantity and Period 0/ Inhal td Du ¡I
"——^^iàoTi of Pn.
( SINO)
Usual Pneumoconiosis
Acutely Developing Pn.
Quantity of Dust
large amount
extraordinary large amount
Period of Dust
Inhalation
relatively long
(10 years or more)
relatively short
(1-Syearsor within lOyears)
Distribution of
Dust Foci
massive fibrosis chiefly
in superior .posterior parts
M.F. in inferior parts
partial thickening in
endsuge
almost universal thickening
in early stage
Intraalveolar
Chance
addition to the
interstitial change
early outbreak in wide
lung area
Emphysema
remarkable in endsuge
Changes
""""
-—
neural Change
Table. 4
type
I
II
III
death by cor pulmonale or
complication of pneumonia or
tbc. before the dvelopment of
remarkable emphysema
three types of Dust Reaction in
Experiaental Pneumoconiosis
Fibrosis
in Lung
(•••)
(••)-(•••)
<•)
Substance
type of Pn.
Free S i l i c a
(quarg e t c . )
lyaphatic
Fib.in
Lymphnode
<•••)
(•)-(••)
(-)
(SANO)
Metalle
Alunlnua Aluala
Pyrophyllite e t c .
Asbest, Graphite
Carbon Black.
Organic dusts
31 o
alveolar
alveolar
Patología y patogénesis de la neumoconlosis.
T. Sano e I. Eblhara
(Japón)
De acuerdo con la atenta investigación histológica de
360 casos de diversas neumoconlosis y con repetidos experimentos en los animales, la neumoconiosis puede clasificarse en varios tipos desde el punto de vista de su patogénesis o de las modificaciones patomorfológicas.
I.
Desde el punto de vista de la patogénesist
1)
neumoconiosis de tipo linfático. Se produce una fuerte fibrosis colágena y los cambios intraalveolares se
suman gradualmente a los cambios intersticiales en la
zona pulmonar (sílice libre)t
2)
neumoconiosis de tipo alveolar. Se producen en los
alvéolos importantes cambios histológicos que acarrean
fibrosis, la cual, sin embargo, se encuentra rara vez
en los linfonódulos (asbestosis, aluminosis, talcosis,
neumoconiosis de tierra con diatomeas, neumoconiosis
de la pirofilita, pulmón de soldador, neumoconiosis de
la pirita, pulmón de minero del carbón, etc.).
II.
Desde el punto de vista de los cambios patoraorfológicosi
1)
neumoconiosis con grandes nodulos. Los nodulos están
bastantes desparramados en el tejido pulmonar relativamente intacto, pese a que la fibrosis es importante
en la lesión (silicosis clásica)»
2)
neumoconiosis con nodulos pequeños. La densidad de los
nodulos suele ser elevada y la parte intacta del pulmón
es mucho menos que en la primera forma, pese a que la
fibrosis es generalmente débil (silicosis con polvos
mixtos y casi todas las otras formas de neumoconiosis)i
3)
en la asbestosis y la neumoconiosis causada por polvos
orgánicos predominan la bronquiolectasia y el enfisema
por inflamación repetida en la zona inferior del pulmón.
311
lv/3
NOCIVITE VARIABLE DES POUSSIERES DE SILICE SELON
LEUR ORIGINE. INFLUENCE DE CERTAINS MINERAUX D'ACCOMPAGNEMENT
L. LE BOUFFANT, H. DANIEL, J.C. MARTIN
Centre d'Etudes et Recherches des Charbonnages de France,
Verneil-en-Halatte, France.
Introduction
En matière de toxicologie des poussières, une importance
particulière a toujours été accordée à la silice libre,
ou plus exactement au quartz présent dans les poussières d'une
grande variété de type6 d'exploitations minières. Aussi, la détermination du risque présenté par l'inhalation de ces poussières comporte-t-elle le plus souvent, soue une forme ou sous une
autre, l'appréciation de la quantité de silice libre contenue
dans les particules ihhalables. Cependant, jusqu'à présent,cette
appréciation ne prend pas en considérations l'éventualité d'une
différence de nocivité entre les silices de différentes origines.
Des observations déjà anciennes ont cependant fait apparaître
qu'il pouvait exister des différences importantes de risque de
silicose entre certaines mines et ceci pour des teneurs en quarts
équivalente. De notre cOté, nous avons constaté des écarts en
matière d'endémie pneumoconiotique entre les bassins houillère
français pour des teneurs en quartz comparables sans que ces
écarts semblent pouvoir être attribués à des différences marquées
dans les concentrations en poussières ou les granulométries des
particules (1).
Ces constatations couduisent à mettre en cause des variations possibles de la nocivité du quartz lui-même en fonction de
son origine ou de 6es transformations. Afin de tenter d'élucider
ce problème, nous avons entrepris d'étudier la nocivité des poussières de quartz provenent de divers horizons géologiques (quartz
contenu dans les poussières de mine de charbon) sous l'angle de
leurs propriétés fibrös
\-vis des tissus.
NOCIVITES COMPAREES DE POUSSIERES DE QUARTZ BRUT
Trois variétés de poussières de quartz <J>/*m, à savoir
du quarts de Madagascar,, du quartz synthétique et du sable de
Nemours ont été inoculés par injection intra-peritoneale à des
rats à la dose de 75 »g. Au bout de trois semaines, les animaux ont été sacrifiés et les lésions ont été examinées. Les
résultats, portés dans le tableau 1, montrent que le pouvoir
fibrosant de ces trois sortes de silice se classe en deux
groupes distincts : d'une part le quartz de Madagascar et le
quartz synthétique doués d'un pouvoir fibrosant élevé, d'autre
part le sable de Nemours faiblement nocif. Il apparaît en outre que la nocivité du quartz synthétique est aussi élevée que
celle du quartz de Madagascar, malgré une teneur en quarts,
mesurée par diffraction de rayons X, nettement inférieurs.
A partir de cette observation, deux hypothèses peuvent
être formulées sur les causes des différences de nocivité existant entre ces variétés de quartz:
1ère hypothèse:
2ème hypothèse:
leur nocivité propre est différente
il existe des modifications au niveau
de la surface des particules de quartz.
(Voir tableau 1.)
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RECHERCHE D'UNE DIFFERENCE DE NOCIVITE INTRINSEQUE DES QUARTZ
Dans un premier essai, la comparaison entre le quartz de
Madagascar et le sable de Nemours à été poursuivie afin d'étudier l'évolution de leur nocivité dans le temps. Pour cela,
ces deux variétés de poussières ont été injectées à des rats
par voie intratracheale. Les animaux ont été sacrifiés après
des délais d'évolution croissants et l'importance des lésions
a été appréciée en déterminant l'augmentation de poids des poumons et la quantité de collagène formé et en procédant à des
examens histologiques.
Les courbes'obtenues dans la(fiq.)montrant que le quartz ds
Madagascar possède un pouvoir fibrosant très important dès
les premiers mois. Au contraire, le sable de Nemours est presque sans effet pendant ce laps de temps, mais sa nocivité augmente progressivement lorsqu'on prolonge le délai d'évolution
et finalement la vitesse de formation de collagène rejoint
celle du quartz de Madagascar (2).
Dans un deuxième essai, des poussières de différentes
mines de charbon ont été incinérées et le quartz qu'elles contenaient a été extrait par attaque phosphorique. Les particules
ainsi obtenues ont été injectées a des rats et les lésions obtenues après trois mois ont été comparées à celles produites
par du sable de Nemours et du quartz de Madagascar ayant subi
le même traitement chimique.
Les résultats du tableau 2 montrent que les quarts ainsi
testés possèdent, quelle que soit leur origine, un pouvoir fibrosant elevé et comparable.
317
Tableau 2 - Nocivité comparée de quarts extraits
de poussières de mine, de sable de Nemours et de
quartz de Madagascar (Test I.T. 3 mois)
Origine du quartz
Poids des poumons
(g)
Poussières( Ostricourt
de
( la Houvre
mine
( Gardanne
Sable de Nemours
Quartz de Madagascar
Collagène formé
(mg)
2,55
2,63
2,92
12,8
13,5
16,6
3,25
13,4
3,05
18,1
De ce fait, ils tendent à infirmer l'hypothèse d'une différence de nocivité intrinsèque des quartz en fonction de leur
origine et accréditent au contraire l'hypothèse d'une inhibition
plus ou moins marquée mais passagère de la nocivité de certains
quartz.
MECANISME DE L'INHIBITION DE LA NOCIVITE DD QUARTZ
L'action toxique des poussières e'exerçant nécessairement
par leur surface externe qui se trouve au contact des cellules
et des tissus, il convenait de rechercher la cause de la modification de nocivité du quartz dans une transformation superficielle des grains de quartz, notamment sous l'action de certains
minéraux.
318
Pour cela, noue avons cherché a réduire artificiellement le pouvoir fibrosant du quartz de Madagascar en le mélangeant avec des poussières de mine de bharbon et, dans un
deuxième essai, avec les matières minérales extraites de ces
poussières. Les mélanges ainsi obtenus ont été testés par injection intratracheale sur des rats, et leur action comparée
à celle du quartz de Madagascar mélangé à des quantités égales de poussière inerte (oxyde de titane) afin qu'.il se présente dans le infime état de dilution.
Tableau 3 - Modification de la nocivité du quartz par
des matières minérales (Test I. T. 3 mois)
Poids des
poumons (g)
Collagène
formé (mg)
Quartz + inerte (TiO,)
¿
(7,5mg) (50mg)
3,33
28,6
Quartzt poussières de mine
(7,5mg) (50mg)
2,54
8,6
Quartz+ matières minérales
(7,5mg) (provenant de 50
mg de charbon)
2,05
10,0
Nature des poussières
Les résultats obtenus (tableau 3) montrent que les
poussières de charbon utilisées exercent sur le quartz un
effet inhibiteur important.
319
De plus, cet effet se montre localisé dans les matières minérales dont le pouvoir anti-quartz est comparable à celui des poussières totales. Il n'est pas provoqué par un simple effet de
dilution, car le quartz mélangé à une inerte demeure fortement
nocif.
Afin de rechercher si l'inhibition est produite par une
réaction moléculaire entre le quartz et certains constituants
solubles des matières minérales, une suspension aqueuse de ces
dernières a été dialysée contre une suspension de quartz et le
quartz ainsi traité a été testé sur l'animal selon la même méthode, et ses effets comparés à celui d'un quartz traité à l'eau
pendant le même temps.
Tableau k - Influence des produits de dissolution des
matières minérales de poussières de mine sur la nocivité
du quartz (Test I. T. 30 mg - 3 mois)
Nature des poussières
Poids des poumons
(s)
Quartz témoin
Collagène formé
(mg)
91,5
Quartz traité par dialyse
1,69
5,6
Les résultats du tableau k montrent qu'il existe bien un
transport de produits de dissolution des matières minérales vers
les particules de quartz se traduisant par une inhibition de la
nocivité du quartz, tout au moins pendant les trois premiers
mois de séjour des poussières dans le poumon (durée du test).
Il apparaît donc clairement qu'il s'est produit une modification de l'état superficiel du quartz.
32o
NATURE DES MINERAUX PROTECTEUR.
L'identification des minéraux capables d'exercer cette
action inhibitrice a pu être faite dane un certain nombre de
cas. Pour cela, nous avons entrepris l'étude systématique de
l'action anti-quartz des minéraux argileux rencontré dans les
poussières de mine. Bien que cette étude soit loin d'être achevée, il apparaît d* ores et déjà qu'il existe entre les argiles
des différences importantes d'efficacité.
Tableau (S)Effets protecteurs comparés de l'illite
et du koalin (Test I.P. 3 semaines)
Nature
du mélange
Poids des lésions
(g)
Collagene formé
par mg de quartz
(mg)
Quarts + illite
0,80
1,7
Quartz + kaolin
1,87
3,8
Témoin
(quartz
1,30
3,3
TiOp)
C'est ainsi que de l'illite dans la proportion de 50 % inhibe très fortement l'action fibrosante du quartz tandis que le
kaolin n'exerce aucun effet protecteur apparent mais ajoute au
contraire sa faible nocivité propre â celle du quartz (tableau 5 ) •
Divers autres minéraux argileux possèdent à des degrés divers un pouvoir inhibiteur de la fibrose silicotique. Parmi eux,
il convient de citer la inontmorillonite, dont l'analyse par diffraction de rayons X a révêlé la présence dans le 6able de Nemours
(2).
321
La formation d'une couche protectrice à la surface du
quartz peut être mise en évidence par des mesures do solubilité et par diffraction électronique sous incidence rasante (3).
De plus, une réaction colorée à l'aurine montre que les minéraux
argileux libèrent en milieu aqueux de l'aluminium dans des proportions d'autant plus grandes que le minéral exerce une protection plus forte. Il apparaît donc que l'effet protecteur des
argiles est dû à la formation d'une combinaison de l'aluminium
à la surface du quartz. Cependant comme nous l'avons vu précédemment dans la figure,la courbe de variation de la nocivité du sable de Nemours en fonction du temps montre que cette combinaison ne possède qu'une stabilité relative dans le temps et que
la couche superficielle du quartz est progressivement remise à
nu dans les milieux biologiques.
QUARTS ET SILICE AMORPHE
L'ensemble de ces résultats conduit par ailleurs à minimiser le rôle de l'état cristallin dans les variations que l'on
constate dans le pouvoir fibrosant de la silice libre et à rattacher davantage cette propriété à l'entité silice elle-même et
ses variations à un "masquage" plus ou moins accentué des groupements SiCs de la surface des grains par des combinaisons dues
à l'action de minéraux exogènes. A l'appui; de cette thèse, nous
avons montré (tableau 6) que l'état cristallin n'est nullement
indispensable pour que la silice manifeste des propriétés fibrosantes et que la silice citreuse possède pratiquement la même toxicité que le quartz de Madagascar ou le quartz synthétique, ces
deux derniers possédant eux-mêmes un pouvoir fibrosant identique
malgré des teneurs en quartz, déterminées par diffraction de rayons
X, nettement différentes. Des observations analogues ont été faites avec diverses silices amorphes obtenues par voie ignée ou
aqueuse (if,5).
322
Tableau 6 - Effet fibrosant de différentes forme de silice
!
Nature de la silice
Teneur
Si0 2
(56)
Quartz de Madagascar
env. 100
Quartz synthétique
env. 100
Silice vitreuse
env. 100
Teneur
en quarts
(56)
100
Colagène formé
par mg SiO,
(56)
2,60
2,64
0
2,30
CONCLUSION
Cette étude fait apparaître essentiellement que la nocivité propre du quartz ne varie pas de façon importante en fonction
de son origine, mais que les différentes constatées paraissent se
rattacher plutôt à des effets d'inhibition plus ou moins marqués
sous l'action de certains minéraux capables de libérer de l'aluminium en milieu aqueux. Ce phénomène peut avoir eu lieu au cours
des âges géologiques ou se produire seulement dans le milieu biologiques du poumon. Quoi qu'il en soit, cet effet inhibiteur, dû
à la formation d'un film protecteur à la surface des grains de
quartz, disparaît avec le temps lorsque ce film est solubilisé
ou que l'aluminium libérale de l'argile est épuisé.
323
BIBLIOGRAPHIE
(1) LE BOUFFANT, L.; MARTIN, J.C.; DANIEL,H. in: Lutte technique
contre les poussières de mine - Luxembourg 11-13 octobre 1972,
137-150.
(2) LE BOUFFANT, L; DANIEL, H.J MARTIN, J.C.; BRUYERE, S. (1977)
C.R.Acad. Se. Paris, Série D - 2£5_, 599-602
(3) LE BOUFFANT, L.; DANIEL- MOUSSARD, H.; MARTIN, J.C. CHARBONNIER, J.; LETROT, M.; POLICARD A. (1969) Arch. Mal. Prof.
¿0, 305-310.
(k)
CHARBONNIER, J. (1958) Die Staublungenerkrankungen, Ban 3,
215-220.
(5) STRECKER, F.J. (1955) Grundfragen Silikoseforach. I, 61-73.
524
L. Le Bouffant, H. Daniel y J. C. Martin (Francia)
Al estimar cl riesgo de silicosis que encierra la
inhalación de polvos de cuarzo sólo se tiene en cuenta
la intensidad de la exposición a los polvos, sin tomar
en consideración las posibles diferencias de nocividad
de la sílice inhalada. Sin embargo, según diversas constataciones. los efectos fibrosantes de las partículas
de cuarzo difieren claramente de acuerdo con su origen.
Así, con igual contenido de sílice, ciertos polvos de
cuarzo procedentes de filones son en extremo fibrosantes, mientras que otros, de naturaleza detrítica, parecen poco nocivos en los ensayos biológicos. De igual
modo, en las minas de carbón, los datos epidemiológicos
muestran que, con idéntico contenido de cuarzo, el riesgo de neumoconiosis puede variar considerablemente de un
yacimiento a otro.
Se han examinado dos hipótesis i por un lado, la
existencia de diferencias en el grado de nocividad propio de los cuarzos según su origen, y, por otro, la influencia de algunos otros minerales presentes que pueden
modificar la nocividad del cuarzo. Utilizando como referencia el elevadísimo poder fibrosante del cuarzo de
Madagascar, por medio de ensayos de larga duración realizados con animales, se demuestra que la nocividad de determinados cuarzos detríticos (arena de Nemours), inicialmente débil, aumenta progresivamente según el tiempo
transcurrido, hasta alcanzar por último la nocividad del
325
cuarzo de referencia. Asimismo, los cuarzos extraídos de
los polvos de las minas de carbón encierran en estado puro un poder fibrosante comparable al del cuarzo de referencia, cualquiera que sea el polvo de origen. Las diferencias de nocividad que puedan existir se deben en realidad a la acción protectora de ciertos minerales arcillosos que acompañan al cuarzo en la arena o en los polvos de mina, acción producida por una reacción superficial entre la arcilla y el grano de cuarzo. En los medios biológicos, el fenómeno no es permanente, y la nocividad propia del cuarzo reaparece progresivamente si no
se renueva la sustancia protectora.
De estas observaciones se extraen consecuencias
prácticas sobre la apreciación del riesgo y sobre una
terapéutica preventiva.
326
17/4
CHUCE DE SURFACE ET CYTOTOXICITE DE LA SILICE
QUINOT E., CAVELIER C ,
PIERCERON n.G.
Contre d'Etudes et de Recherches
des Charbonnaoa» de France
VERNEUIL - EN- HALATTE- FRANCE
Des études du CER CHAR ont montra que l'aluminium
était exoérimantalement un inhibiteur de la nocivité pulmonaire du quartz.
L'intérêt porté à de tels phénomRnes dfi
protection, mame transitoires, noua a conduits a envisager
un mode de fixation possible dR l'aluminium sur la charpente
du cristal et a rechercher si d*autre9 atomes pouvaient jouer
le même role.
Il serait alors légitime de poser comme hypo-
thèse de travail que certains da cea atomes puissent être empruntés aux composants organiques du cytoplasme et de la membrane cellulaire, phénomène en rapport avec la cytotoxicitô
du quartz.
GENERALITE
1 - Structure de3 complexes alumino-slllciques
L'aluminium est associé au silicium dans les composés
minéraloqiques naturels de deux façons différentes :
- soit comme cation isolé dans les silicates d'alumine.
Dans ce cas, Al assure la liaison des tétraèdres
Bt peut être remplacé par d'autres ccations.
l'aluminium est alors hexacoordonné.
327
[sioj
En général,"
VV '->
//
X
/•-'
\
^
• \
STRUCTURE D'UN TECTOSILICATE : LE QUARTZ B.T. (d'après BERRY et MASON,1959)
528
soit en particinant a l'édification das anions tetraédriquas AIO.
au lieu et place du silicium. Les orou-
r
pâmants SiO,
alumino-sllicates.
i5-
etIAlO
forment la charpente des
Dans ce ca3, l'aluminium est têtracoordonné. A ce nrnupe
anpartiennent les feldspaths et les zôolithes. Dana quelques
cas, l'aluminium joue un double role et le minéral est a la fois
un silicate d'alumine et un aluminosilicate. Il est donc possible que l'aluminium, inhibiteur de la cytotoxicité du quartz,
s'insère dans la charpente du cristal en se substituant, au silicium libéré, a la faveur du désordre superficiel qu'entraîne la
dissolution de SiO_.
S'il en est ainsi, des charges nôoatives apparaissent la
ou les atomes d'oxyqene sont liés d'une part a un atome de silicium, d'autre part a un atome d'aluminium. Il en résulte la formation d'un site acide au sens de BRONSTED (source de protons).
2- Acidité des catalyseurs alumino-slliclquea
L'acidité des catalyseurs industriels siliceux et aluminosiliciques se rattache e deux types :
-
d'une part celui des silanols qui forment l'ensemble
de la population des site9 acides de la silice hydratée.
A température ordinaire,.l'eau 9e condense sur les aitaa
conformément au schéma suivant:
-OH + H?Q
: ; > '
329
0
>Si
n
+ H.,0
L'ion hydroxonium (H,0)*rend compte du caractère acide
de ces cele avant calcination. Après chauffage a 600° C (20 h)
ces fonctions acides se raréfient; après chauffage â 900 °C (5 h)
elles ne sont plus détectables.
- d'autre part, celui dos sites qui confèrent aux catalyseurs de carcking du type zêolithe 1 acidité de BBÓNSTED.
Ils proviennent essentiellement du déficit de charge de
l'aluminium tetracoordonné dans le réseau mixte
Sil)^
*-
r ~i 5JAXOJ
A partir de 3O0P C, les sites de BROHSTED se transforment
en sites de LEWIS (accepteurs d'un doublet), tout en restant liés
a la structure mixte des tétraèdres ayant pour centre soit un atome
de silicium soit un atome d'aluminium. Les deux fonctions acides
coexistent aux environs de 500 »C. Après chauffage à 900 *C (5 h ) ,
elles ne sont plus détectables. Ce type de site acide peut être
mis en évidence au moyen des indicateurs colorés de HAMMET, par
exemple le p-dimpethyl-amino-azobenzène dans le benzène (mêthyl
jaune). La réaction est utilisée en pétrochimie pour déterminerla qualité de certains catalyseurs de craquage, connus sous le
nom de tamis moléculaires.
MATERIEL ET METHODES
FIXATION DE L'ALUMINIUM STO TA SILICE
1.- Nous avons recherché le comportement de différentes silices
ayant au non fixé des atomes d'aluminium, après calcination a 105° C
600° C et 900° vis-à-vis de l'indicateur nôthyl jaune, c'est-à-dire
recherche l'existence et la stabilité des sites acides.
500 mg de quartz fraîchement broyé â sec jusqu'à une dimension voisine du microjiitre sont mis on suspension dans l'eau distillée avec de l'alumine colloidale hydratée.
Après dour.e heures d'agitation la suspension est lavée, puis
séchée 20 heuren a 105° C. On applique ensuite lo te.ot au methyl
jaune dans le benzène. Le quartz prend alors la couleur
33o
{ouge caractéristique ds cet indicateur pour des pK inférieurs
e 3,3. Ou quartz agiti seul dans l'eau distillée ne fait pas
virer le réactif; il en est de même pour l'alumine hydratée
desséchée à 105» C.
Le quartz broyé, agité dans une suspension d'alumine
hydratée dans un tampon SORENSEN, ne donne une réaction positive, après séchage s 105B C que s'il a été soigneusement lavé à l'eau distillés pour éliminer les cations qui empoisonnent
le catalyseur alumino-silicique formé dans la couche de haute
solubilità. Si on nje pas opéré ce levage les sites acides apparaissent cependant a 6000 c.
Le quartz décapé de la couche de haute solubilité par
action a chaud d'une solution ION de soude et dialyse fixe
l'alumine en floculent. Desséché e 105D, il ne présente pas
de sites acides décelables au méthyl jaune, mais ceux-ci apparaissent après dessication a 6008 puis 9000.
En diminuant progressivement le quantité d'alumine mise
en présence du quartz, on peut observer le virage au roune de
l'indicateur Jusqu'à 1 à 2 mg d'alumine pour 500 mg de quartz.
La fixation de l'aluminium est largement indépendante
de l'accidité du milieu-aqueux dans lequel sont agitas quartz
broyé et alumine hydratée. L'alumine se fixe pour des pH compris entre 5 et 9.
Lorsque Si0_ et fll-0 sont en présence, la solubilité
de l'alumine est voisine de zéro pour des pH compris entre 4,5
et 11, tandis que celle de la silice est réduite elle-même à .
15 ppm au voisinage de la neutralité.
Un phénomène semblable se produit a la surface du quartz
dans la couche de haute solubilité. Plais l'alumino-silicate qui
se forme a la surface du quartz se distingue en partie par ea
résistance au cours d'un traitement thermique.
2.- Nous avons expérimenté sur un tamis moléculaire contenant
B7% de Si0.,13 % de A1.0-, obtenu par coprécipitation d'orthosilicete de soude et de sulfate d'aluminium. Le précipité s
été neutralisé par HCl puie traité a l'ammoniaque pour remplacer
per N H J les ions N a * neutralisant les sites acides.
Apres dialyse et calcination, on obtient par départ
d'amoniac, un tamis protonique (acidité de BR0NSTED) ouis par
deshydratation un' tamis acide uu sena de LCUIS.
331
Apres chauffage a 99fie C (5h) la réaction au méthyl
jaune est négative. (Tableaux 1 et 2).
Un dosane en retour par la butylamins permet de fixer
¿.'ordre de grandeur du nombre des sitas acides disoonibles
a la surface des différentes formes de silice ou des tamis
moléculaires étudiés. (Tableaux 3 et 4 ) .
RESULTATS
L'aluminium se fixB donc sur la quartz ou plus exactement dans la couche a haute solubilité, en s'insôrant dans
le système tridimensionnel tétraédrique, a caractère cryptocristallin dans sa partie profonde, hydraté et soluble dans
sa partie superficielle. Les différences de comportement a
haute température entre le quartz agité avec de l'alumine
et les composés silice-alumine laissent a penser qu'il se forme un voile zéolithique en surface mais qu'en profondeur l'aluminium est lié au réseau de tectosilicate du quartz; sinon,
on verrait disparaître au-delà de 600 0 C les sites acides
comme on le constate pour los tamis moléculaires.
Il semble bien que la structure du quartz ou même celle
de la couche crypto-cristalline confere uno solidité particuliere a la combinaison Si0_/ AI0O3 8 t traduit une affinité
spécifique de l'aluminium pour le rés,eau tétraédrique de la
silice, la ou les défauts lui permettent de l'aborder. Tette
affinité serait alors indépendante du système cristalina Elle
ne siqrtB pas non plus un simple phénomène d'épitaxie.
Nous sommes conduits a nous demander s'il existe d'autres atomes capables de donner, comme l'aluminium, des inns tétraédrinuns et si certains d'ontre eux ont In même dimension nue
1- -1,
r
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ll'ARTZ BROYE
(5 ECHANTILLONS)
z
o
SILICE H Y D R A T E E PRECIPITEE
.-i
- Tons susceptibles de s" suhritltuer au Silicium
La variété ries alumino-silicates montre que l'aluminium
se substitue facilement au silicium. Cela tient, outre son
abondance dans la lithosphère (8, 13 %);
- d'une nart a la orando différence d'électro-nérativitô
rie l'aluminium et dp l'oxygène au sens de PAULING
(1,74 et 3,50 respectivement), donc a l'énergie importante de la liaison ionique Al-0,
- d'autre part,, au moyen dB ..S*-qui permet la tétracoordinence de cet élément avec l'oxvqene, les anions
r
r
-|4-
Si04
et
is.
A10J
étant isométriques.
Ces deux caracteres de l'aluminium appartiennent a'
d'autres corps que l'on peut identifier a partir des regles
de substitution développées par GOLDSCHPIIOT sous le nom dB
renies de diadochie, en précisant la natura (covalsnce ou
électrovalence) et l'intensité de leur liaison avec l'oxygène.
Pour cela, il est commode da porter sur un diagramme
selon GOLDSCHPIIOT la dimensión at la charge ionique des éléments le plus coramment rencontrés (Fig.l).
A la lecture du diagramme dé GOLDSCHPIIDT on voit donc
que le nombre d'éléments capables d'une tétracoordinence avec
l'oxyoène ont restreint : Be 2 t , A l 3 * , G e 4 + , \JS*, As 5 , p5t Cr6*,
Se
, et peut-être quelques-uns de ceux qui sont a la limite
de la bande: re3*,
B 3 | Ca3'*' , Pln 4+ , Te 6 "*", S6*.
De plus, un élément pourra se substituer au silicium, si
.1 n rf.imrnsinn dp l'en.lon tétraértrique formé est isométrique de
337
338
ri 3 - r >- r >-•
r >
niO^
: r.p. nui est le can do
, IrranJ
VO^. I
>
nsCI
/J
Mais pour qu'un atome soit caoablo d'une telle substitution encore faut-il que l'énernie da liaison soit du même ordre de nrandeur que celle do la liaison Si-R.
Cela nous oon-
duit a rechercher lee éléments qui sont des formateurs de réseau (Network formera) capables par associations d'anions
tétraédriquea de donner'des éléments tridimensionnel;-, comme
dans les tectoailicates ou bidimensionnels comme dans lea phylosilicatas.
Voir:(tableau 5 ) .
La comparaison de l'ensemble de cea données conduit a
penser que les ions Al
, Ge
, J3
y—
et As'
peuvent se
substituer a Si dans le tétraèdre!-.- I " ou s'insérer dans
le réseau du quartz a la faveur de sa désorganisation superficielle.
INTERPRETATION ET COrWENTAIRES
"
Cytotoxicity de la silice et son Inhibition
Les théories qui tentent d'expliquer la cytotoxicité de
la silice se rattachent globalement a trois types.
Oans le
premier, les produits de disolution dispersés dans le solvant
sont responsables de la nocivité; dans le second, l'influence
du réseau cristallin sur le pouvoir fibroqene est fondamentale
et le troisième type est mixte.
La théorie de la solubilité a été abandonnée sous sa
forme orioinBlle.
339
TABLEAU 6 :TARLEAU DES Eí'ERHIES DE LIAISON AVEC L'OXYGENE
(EN kcal PAR LIAISON-GRAWIE D'APRES UN TRAWAIL
DE SUN CITE PAR PEYCHES.
MODIFICATEURS DE RESEAU
FORMATEURS DE RESEAU
104
Li
36
101
Na
20
P
111
K
13
\l
112
Rb
12
Ge
lOfl
Cs
ID
"7
fin
37
119
Ca
32
Sr
32
Rn
37
Si
Al
(coord 4)
fia
(coorti 3)
n
<
(cnord A)
09
34o
P.i.ßn que la nocivité de la silice varie avec 1 P
système de cristallisation, c l u t - c i ne peut seul rendre
compte des faits connus.
On pourrait résumer l'état actuel de la question
en reorenant les conclusions de CHARBONNIER et COLLET qui
admettent, hypothétiquement il est «rai, que "la toxicité
de la silice sa situe a sa surface, sous la forme probable
d'une couche de silice hydratée qui est le toxique cytoplasmique".
La couche responsable apparaît, a la limite de la
dissolution, comme désoroanisée tout en conservant une partie
profonde de cette couche, ou l'action du "Uartering" est encore peu sensible, qui est opérante dan3 la toxicité du quartz
décapé.
La localisation presque certaine de la cytotoxicité
ne présage en rien les mécanismes de son action, et plusieurs
théories ont été développées sur le sujet; une des premieres
voyait dans l'épitaxie sur la structure résiduelle du réseau,
l'oriqine d'un phénomène inductif.
Une théorie que l'on peut appeler catalytique a été
développée ensuite, en particulier par STOBER.
Pour cet au-
teur les silanols seraient responsables de l'état d'activation
de certaine» molécules organiques.
Outre que les silanols sont
présents a la surface de nombreux silicates naturels et des
tamis moléculaires silice-alumine, leur action catalytique
n'apparaît qu'a haute température et en milieux non aqueux.
De plus, le seul polymorphs da la silice ou le nombre de coordinence du silicium et de l'oxygène soit huit, la stishovite,
ne présente pas de cytotoxicité bien que sa solubilité soit peu
supérieure a celle du cristobalite.
5*1
Il est remarquable de constater que l'aluminium
qui se substitue facilement au silicium dans 1'assemblarle
A
tétraédrique des tectosilicates, est en même temps un excellent inhibiteur de la cytotoxicité du quartz.
Le pouvoir protecteur pourrait être associe a la
proprietà que possede l'aluminium de se substituer au sili?
cium dans le réseau tétraédrique ou l'environnement géométrique des atomes reste partiellement on place au cours de
la formation de la couchs hétôrooene de silice hydratée.
En effet, la ou se produit l'action cvtntoxique, on rencontre a la fois un réseau encore ordonné de tétraèdres et des
motifs détruits par dispersion de SiO_. L'aluminium capable de tétra-coordination prend la place des atomes de silicium disparus et donne des sites acides, fiais le germanium, le vanadium l'arsenic, le phophore, le soufre, pourraient peut-Btre jouer le mema role. Si l'aluminium an,it
comme inhibiteur de la cytotoxicité du quartz en comblant
un vide potentiel dans les tétraèdres en voie de dislocation, nn peut penser que cet élément interdit par cola même
une réaction du même type responsable de la toxicité mettant
en jeu un atome d'un des composés organiques du cytoplasme
ot riRR mnmhranes cellulaires.
r, cet titre, le nhosnhore pourrait jouer un role
particulier. Mous avons vu en effet que cet élément peut
se suhstituer au silicium cnmne l'aluminium. Il entre dans
la composition phnr.pholipidique des membranes cvtoplasmiques
nt on sait que la cytotoxicité de la silice débute par le
contact de la particule et d'une membrane, en particulier
celle des lysosomes.
342
CONCLUSION
L'étude rie la structure des composas aluminosiliciques naturals ou artificiels cnnduit a distinquer
un état de surface propre au quartz, en l'occurrence,
l'existence de vides dans le réseau tridimensionnel des
tétraèdres SiO..
L'aluminium inhibiteur connu de l'action cytotoxique du quartz peut s'insérer dans le roseau cristallin
a la place des atomes de silicium disparus. Il en résulte
l'apparition de sites acides dénombrables, stables a l'épreuve thermique.
Il ne s'agit donc pas d'un simple voile zénlithique de
surface mais d'une substitution d'etomes d'alumi-
nium en place de silicium dans le réseau cristallin préservé.
On peut montrer que d'autres atomes comme le soufre et surtout le phosphore sont susceptibles de se comporter comme
l'aluminium.
Il n'est pas interdit de penser que le pouvoir cytotoxique des quartz pourrait être en repport avec la captation par le cristal d'atomes constitutifs de la membrane
cellulaire.
3*3
Química de superficie v cicotoxicidad
de la silice.
E. Quinot, C. Cavelier, M. 0. Merceron (Francia)
Los estudios excelentemente resumidos y completados
por los investigadores del Centro de Estudios y de Investigación de Charbonnages de France han mostrado que el aluminio es experimentalmente un inhibidor de la nocividad
pulmonar del cuarzo. El interés despertado por tales fenómenos de protección nos ha llevado a estudiar un método que
permita fijar el aluminio en la estructura del cristal y a
tratar de ver si otros átomos pueden desempeñar el mismo
papel.
El estudio de la estructura de los compuestos aluminosilfcicos naturales o artificiales lleva a distinguir un
estado de superficie propio del cuarzo, o sea, en este caso,
la existencia de vacíos en la red tridimensional de los tetraedros ICIO». El aluminio, conocido inhibidor de la acción citotóxica del cuarzo, puede introducirse en la red
cristalina en lugar de los átomos de silicio desaparecidos.
Ello acarrea la aparición de puntos ácidos numerables, térmicamente estables.
No se trata pues de un simple velo zeolítico de superficie sino de una substitución del silicio por átomos de
aluminio dentro de la red cristalina preservada. Puede mostrarse que otros átomos como el azufre y, sobre todo, el
fósforo son capaces de comportarse como el aluminio.
Hasta cabría pensar que el poder citotóxico de los
cuarzos podría estar en relación con la captación por el
cristal de átomos constitutivos de la membrana celular. La
riqueza en puntos ácidos, térmicamente estables, descubiertos por contacto con el aluminio, sería entonces un factor
de evaluación del poder citotóxico de las diferentes formas
de cuarzo.
344
NEW ASPECTS IN THE ETIOPATHOGENESIS OF SILICOTIC
AND ANTHRACOSILICOTIC LESIONS
W. Weiler
Pneumoconiosis Research Institute, Bochum, Federal
Republic of Germany
Introduction
For experimental investigations on the effect of noxious dust
the inhalation test, particularly the long-term inhalation test,
certainly is the most appropriate method.
In order to obtain
more briefly comparable results injection tests, e.g. intratracheal
tests or intraperitoneal tests, are frequently applied.
The intra-
tracheal test, however, raises some problems i the anaesthesia
necessary for injections must not be too intense, permitting the
animals to breath normally after injection.
Shortly after waking
up some of the animals expectorate part of the injected liquid.
This leads to different initial values. Another problem is the
very various
distribution of dust quantities and the resulting
pneumoconiotic modifications in the lung.
It is important to know
that various local dust concentrations result from these different
distributions.
An additional factor is the pathological lung modi-
fications sometimes observed in rats, the animal species most
frequently used for experimental purposes. These modifications
are chronic respiratory diseases and alveolar lipoproteinosis.
We therefore preferred to use the intraperitoneal test.
In this
test dust particles can distribute freely in the peritoneal cavity.
Besides, a greater number of" organs for the evaluation of dust
effects is at disposal.
The test had the objective to define a quantitative measure
345
regarding the effect of quartz or coal-quartz-mixtures, respectively, dependent on dust dose, quartz proportion and test period.
The
intention was to use the obtained results as basis for the experimental test of coal mine dust containing relatively small amounts
of quartz only.
Methodology
The tests were performed with female SPF-Wistar rats under
SPF conditions (Weiler, 1972).
The animals were treated by intra-
peritoneal injections of 50 mg coal-quartz mixtures, the quartz
proportion ranging from 1 to 75%. Further to the investigation
of coal-quartz mixtures the isolated effect of the quartz quantities included in these mixtures was studied.
For control and
estimation purposes 2 animal groups received pure coal or pure
quartz injections of 50 mg dust/animal.
Each dust quantity was
included in 1 ml physiological saline solution.
The test duration
was up to 6 months. On each examination date 5 animals of each
group were examined.
Results
a) Quantitative measure for the effect of dust
With higher quartz proportions (10 - 75%) the following organ
weights showed a very good correlation to the quartz proportioni
omentum, lien, cranial mesenteric lymph nodes and lung lymph nodes.
Particularly the total omentum weight consisting of the actual
omentum weight and of modifications outside the omentum as well
as the total lymph node weight consisting of cranial mesenteric
346
lymph nodes and lung lymph nodes show a very good correlation to
the quartz dose (figure l)t
9
3 0 -,
d
'
lo, ,1
'
»"""tum
b) ToUt lymph n„J c: .
mg
500 - i
400 300
200 100 0
0
0
5U
0
«
5
110)
37.5 25
12.5 mg Coil
12.5 25 37.5 m9 Quarts
1251 1501 1751 °U Ouarti
in dust mistura
O Coal -quarti mistura
0 Quartz only
B
B
C M I only
Control
45 37.5
5
1ZS
1101 125)
25
25
(501
Q Coal - quartz mistura B
Q Quarti only
B
12.5 mg Coal
375 mg Ouartl
(751 •/. Ouarti
In dust miiturt
Coal only
Control
Fig. li Quantitative effect of coal-quartz mixtures compared to
the corresponding quartz proportion after a 6-month test
period. Intraperitoneal test, rats.
at Weights of the total omentum (actual omentum and modifications outside the omentum, at the peritoneum).
bi Weights of total lymph nodes (cranial mesenteric lymph
nodes and lung lymph nodes).
With small quartz proportions (1 - 8%) the weights for
total omentum and total lymph nodes were likewise determined.
Their dependence on the quartz content is shown in figure 2.
3^7
bl UWI t,muli noJc-i
i i Total omentum
1,1
1,5
LO-
100-
ft 5
\
0
0
O
<if>S
V)
<.8
<.;
<,o mg Coil
05
1,0
2,0
3,0
".,0 mg Quart;
11°/.) 12%) ( V U 141.1 18%) Quartz
in dust m i i t u r t
Coat • quartz mixtura B Coat o n t /
0
Quarti ont/
0
0
O
SO <,S>5
<.9
«9
1,7
<ii mg Coat
0
0,5
1.0
2,0
30
V 0 mg Quarti
11%) ( 2 % ) 14%) ( 6 % l 16%) Ouarti
m dust mixtura
Coat - quartz mixtura
B Coat ont)r
B
Quartz only
SO
0
•
Control
•
Control
Fig. 2: Quantitative effect of coal-quartz mixtures compared to the
corresponding quartz quantities, 6' months test period. Intraperitoneal test, rats.
a: total omentum weight
b: total lymph node weight.
It can be seen clearly that with small quartz proportions
the total lymph node weight shows a better correlation to the
dust or quartz proportion than the total omentum weight.
Lien
and liver show no dependence on the dust dose.
From these results it may be summarised that the total lymph
node weight consisting of cranial mesenteric lymph nodes and
lung lymph nodes represents a sensible criterion regarding the
quantitative effect of quartz or coal-quartz mixtures. The
same observation could be made regarding the effect of very
small quartz proportions. Thus, good conditions for the quantitative assessment of coal mine dusts are available.
An addi-
tional result of this study is the observation that the quanti-
348
tative effect depends on the quartz proportion only.
b)
Quantitative progression of contotic modifications
It is of great practical importance to know the extent, de-
pendent on dust composition and test period of the progression
of coniotic modifications.
After the total lymph node weights
have proved to be a sensible quantitative criterion, this problem
should be investigated in more detail considering the total lymph
node weights.
Based on these values a comparison between the
effect of coal-quartz mixtures and of the corresponding pure
quartz proportions, dependent on the test period, should be made.
This may be best achieved by virtue of net weights, i.e. the
weight of the coniotic modifications actually produced according
to figure 3.
Intraperitoneal test, rais
Totti lymph node
Ouartl injtctiort
mg
Coal qua
mg
500 -n
500
50 mg
«00
nttwttghts
-
ti nject on
Quarti
«00 - i
- o 37.5 mg
300
-
200
N> 12.5 mg
100
-
0
-
12.5 mg
25
25
300 "^o 25. mg
200
Coal
37.5 mg
"*o 5
1
1
(
3
1
6
mg
12.5 mg
5 mg
100 -
1
1
9
12 Mon
0
mg
mg
-
-
r
e
i
3
1
6
37.5 mg
«5 mg
1
9 Mon
Fig. 3i Chronological process of quantitative reaction after intraperitoneal injections of quartz or coal-quartz mixtures.
Net weights of total lymph nodes (cranial mesenteric lymph
nodes and lung lymph nodes), intraperitoneal test, rats.
349
Apart from minor differences the curves for the coal-quartz
mixtures and the pure quartz proportions of them are on the same
level.
This means that the quantitative reaction by coal addition
does not change even if time dependence is taken into account.
It may also be concluded that lymphotropism is not modified due
to the coal proportion.
Figure 3 shows for both groups that
low
quartz quantities or quartz proportions, respectively,cause a
higher relative effect, measured according to quantitative modifications.
This problem is discussed in detail in paragraph (c) t
of this study.
Regarding the progression of modifications it is important
to note that, after a rapid increase of coniotic modifications
during the first 3 months, both dust groups
after a 6 month
test period.
showed the maximum
Only after injections of 50 mg
pure quartz the maximum is reached after 9 months.
For the ratios
studied with small quartz admixtures (1 - 8%) similar pairs of
curves can be drawn. Here, however, the maximum quantitative reactions can be observed already after a 3-month test period.
The most important result is that a certain quartz quantity has
only a limited silicogenic potency and that there is no unlimited
progression.
c) Specific quantitative ouartz effect
Figure 3 shows regarding quantitative modifications that the
reaction to quartz is not linear.
In addition to organ weight
determinations, quartz quantity determinations by means of dust
recovery from the organs were made for the test series with large
quartz proportions (10 - 75%).
According to the organ net weights
consisting of the weight of the newly developed coniotic changes
and the quartz proportion in the corresponding organs,the ratio
35o
"mg net organ weight/1 mg quartz", i.e. the tissue quantity produced by 1 mg quartz, was defined and expressed as specific quantitative quartz effect.
Table 1 includes the values for various organs obtained in
the described way.
mg organ net weight/1 mg SiCU
Dust
Coal
Quartz
(mf>)
(mR)
45
37.5
25
12.5
-
-
5
12.5
25
37.5
Omen-
m
tum
Spleen
(10%)
(257.)
(507.)
(757.)
122
89
80
52
1724
1510
1390
127
48
47
56
2362
61
5
12.5
25
37.5
50
cranial
mesenteric
lvnroh nodes
lung
lymph
nodes
616
397
466
236
359
370
379
362
850
682
670
606
255
207
160
593
342
274
591
238
189
879
263.
Table li Net organ fresh weights in mg produced by 1 mg SiOo, in
the listed organs of the individual test groups (net organ
fresh weight = actual organ fresh weight - organ fresh
weight of the coal control group for the coal-quartz
series or - organ fresh weight of the normal control
group for the pure quartz series). Rats, intraperitoneal
test. 3 months test period.
A very interesting aspect is the different reaction of various
organs to certain quartz quantities.
In this regard as well as
regarding the orders of magnitude there are no differences between the coal-quartz series and the pure quartz series.
Basical-
ly, the examination of each organ listed shows comparative results,
though on various levels.
The supposed correlation according to
the quantitative results indicating that small quartz quantities
551
are relatively more efficient, can be seen from the results in
Table 1, except for the lung lymph node values in the coal-quartz
series.
In each presented organ small quartz quantities have a
much greater specific effect.
For the test series with higher quartz proportions (10 - 75%)
the specific quantitative effect was defined first.
From the organs
of the test series with small quartz proportions (1 - 8%) no quartz
was recovered so that precise value determinations regarding the
specific quantitative reaction were impossible.
In order to ob-
tain a comparison between these two test series,the developed
tissue modifications due to dust injections were correlated as
net organ fresh weight to the injected quartz quantities or quartz
proportions, respectively.
This is feasible under the condition
of a uniform dust distribution and a quartz concentration dependent on the total quartz quantity.
Figure 4 presents the calcu-
lated theoretical values for total lymph node weights.
Specific
quart?
effect
Total lymph nodes
Organ net weight / 1 mg quartz
— - •
Qu„ti
Co.I - Ou.rtl
352
Fig. 4« Specific quartz effect (mg net organ fresh weight/1 mg
SiO ? ) correlated to the absolute quartz quantity. Intraperitoneal test, rats. 3 months' test period. Specific
effect i theoretical calculation based on the set value
of the quartz injection and the net organ fresh weight
actually determined.
Here and in previous cases a uniform relation for both test
series can be observed.
There is no substantial difference between
the effect of quartz and the effect of coal-quartz mixtures.
From
this comparison it can be summarised that, as regards the quantitative effect, only quartz can be recognized as being the effective
principle.
It can also be inferred that the quantitative reaction
to quartz is not linear.
The principle of the decreasing specific
quantitative effect correlated to the increasing total quartz
quantity or quartz concentration, respectively, can be maintained
for very small as well as for greater quartz quantities.
Reference
Weller, W.
Long-term maintenance of SPF-rats under
"clean conditions".
Acta Pharmacol. Toxicol. 3_1, Supp. I,
1972.
353
Nuevos aspectos de la etiopatogénesis de las
lesiones silicoticas v antracosilicoticas.
W. Weiler (República Federal de Alemania)
En el presente estudio se ha tratado de saber si la
reacción coniótica depende exclusivamente del contenido en
cuarzo o si puede modificarse por la adición de polvo de
carbón. También se trataba de encontrar un parámetro cuantitativo correcto y más adecuado para evaluar la reacción
a pequeñas cantidades de cuarzo, Además de la protección
de cuarzo dentro del polvo total, había que estudiar la
reacción cuantitativa y la duración de la prueba.
En una prueba intraperitoneal de 12 meses con ratas,
se estudió el efecto de la mezcla de polvos de carbón y de
cuarzo. La porción de cuarzo iba de 1 a 75 por ciento.
Además de estas mezclas, se estudiaron los efectos de las
cantidades correspondientes de cuarzo puro.
Los resultados de los experimentos permiten formular
conclusiones respecto de los siguientes problemas « medida
cuantitativa de las lesiones conióticasi características
lineares de la reacción cuantitativa, según el contenido
en cuarzo i progresión de las alteraciones según el contenido en cuarzo y duración de la prueba. Podría elaborarse
un nuevo concepto de "reacción cuantitativa específica al
cuarzo".
354
V
MINERALÓGICA!, ANALYSIS OF LUNG DUSTS IN PNEUMOCONIOSIS WITH
AN ANALYTICAL ELECTRON MICROSCOPE
Hisato Hayashi
Rsearch Institute of Undergound Resources, Mining College,
Akita University, Akita 010, Japan
Introduction
In the past, there were no practical techniques available
for performing microanalysis; consequently, the compositional
determination of individual microparticles has been neglected.
Now, the detection and analysis of tile--characteristic X-ray can
be used to obtain qualitative and quantitative determination of
chemical compositions in individual microparticles.
There are
two different types of X-ray spectrometry technique in conjunction with the electron beam excitation.
One is the wavelength
dispersive spectrometry (WDS), using analyzing crystals. Although this method has an excellent energy resolution, it is
necessary for the surface of specimens to be flat. Moreover,
this system requires high beam currents to produce sufficient
X-ray emission to obtain good results. The analyzing crystal
of this system must be varied on the Rawland circle geometry
to make up one Bragg angle, and a spectrometer can detect the radiation of only one element at a time.
Thus the whole procedure
is rather tedious and time-consuming.
Chemical analysis by energy dispersive spectrometry (EDS)
is done by analyzing the primary or secondary Xrray emitted by
the elements in a sample according to their energy rather than
their wavelength, which is the procedure in traditional methods
of X-ray analysis. The method differs basically from wavelength
355
dispersive spectrometry (WDS).
It is possible to obtain and dis-
play on an oscilloscope screen the full X-ray energy spectrum of
an excited sample in a very short time, generally less than one
minute, using a solid-state detector.
Although the energy resolv-
ing power is about 50 times poorer than WDS, a considerably small
area can be analyzed by this system.
Solid-state detectors have
developed and their capabilities have improved considerably since
they were first introduced.
Today energy dispersive spectrometers
are used widely as analytical tools and are attached to electron
microprobes, scanning and transmission electron microscopes, X-ray
fluorescence intruments and powder diffractometers.
Recently a rapid and convenient procedure for semi-quantitative
chemical analysis of asbestos fibers and clay minerals with an
analytical electron microscope was proposed by the author and his
co-workers (1978).
This paper describes the technical details for
the application of the above-mentioned procedure to the study of
lung dusts in pneumoconiosis.
Materials and Methods
Lung specimens of two subjects with a clinically and histologically established diagnosis of asbestosis and silicosis were
examined.
As shown in Table 1, mineral compositions of the dust extracted from the lung tissues were previously studied in detail
by several analytical methods, such as X-ray diffraction analysis,
infrared absorption spectrometry and chemical analysis.
Sections of lung 5_/jm thick were cut from ordinary paraffin
blocks.
After deparaffinizing in xylene, the sections were pre-
356
pared for examination in the analytical electron microscope by
the carbon extraction technique.
The analytical electron microscope used in this study consists
of a transmission electron microscope (JEM-100 C ) , side entry
goniometer (SEG), scanning attachment (ASID), and energy dispersive
spectrometer (EDS).
Ultrastructures and sizes of materials are
clearly detected on both the conventional transmission electron
microscope (TEM) image and scanning transmission electron microscope (STEM) image. The selected area electron diffraction (SAED)
pattern is easily obtained from a microarea on the subject using
the SEG, and the chemical composition of the same area can also
be analyzed by the ASID and the EDS which is smaller than 200 Â
in size. This procedure can be carried out without any realignment of the electron microscope.
The isolated particles in the specimens on an electron microscope grid were selected on the STEM image. After taking the
photograph, they were examined by SAED, and then were analyzed
using the EDS. The time required for measuring the X-ray intensity was 100 to 200 seconds per position. The average values of
peak intensity and background intensity were determined from 5
to 10 measurements.
Chemical compositions of lung dusts were
analyzed quantitatively using the technique proposed by Hayashi
et al (1978).
Results and Discussion
Several random areas were analyzed from the lungs of 2 patients
with pneumoconiosis.
The identity of the mineral fibers and
357
particulate materials detected in the specimens was based upon
both the crystal structural analysis and the chemical analysis
of the various fibers and particulate analyzed.
Fig. 1 shows
a STEM image and the EDS spectra of particles extracted from the
lung with asbestosis. Particles 1 and 2 in Fig. 1 show a characteristic spectrum of talc.
Similarly, a typical spectrum of
actinolite, an amphibole type of asbestos, is shown in Fig. 1.
X-ray diffraction analyses of the mineral residue from this lung
tissue had already been studied, and indicated that the mineral
compositions of the lung dusts in this patient were talc, quartz,
illite, chrysotile and amphibole asbestos.
In Fig. 2 particles extracted from the silicotic lung specimen can be seen.
in Fig. 2.
The analysis of these particles is also given
It was determined by using
the energy dispersive
detector, and shows a characteristic spectrum for pyrophyllite
(particle 2), kaolin (particle 3), illite (particle 13), and
quartz (particles 11 and 12).
The X-ray diffraction analysis and
infrared analysis of these lung dusts had been examined previously
and revealed that there were quartz, trydimite, cristobalite,
pyrophyllite and kaolin in the mineral residue extracted from
the silicotic lung of a refractory worker,
Most of the minerals
detected by X-ray diffraction analysis were identified, and their
chemical compositions were estimated by the analytical electron
microscope.
Thus, the analytical electron microscope can be used to
detect the morphological, structural and chemical characteristics
of individual particulates in lung dust.
358
Recently Hayashi et al
(1978) proposed a rapid and convenient procedure for seml-quantltatlve analysis by using
an analytical electron microscope»
This
procedure applies to the chemical analysis of Individual particles
extracted from lungs with asbestosis and silicosis. The values
of K for talc, illlte (mica), kaolin mineral and pyrophyllite
are obtained after substractlng the water content from the ideal
compositions of these minerals. The K values of talc, illlte
(mica), kaolin mineral and pyrophyllite are 95.2, 95.5, 86.0, and
95.0, respectively.
In the same way, the K value of actinolite
is obtained from data of actinolite, Chester, Vermont (Weeks,
1956).
The results obtained from the study of dusts extracted
from lungs with asbestosis and
Table 3.
silicosis are given In Table 2 and
It can be seen In these tables that the EDS data of
Individual minerals extracted from lung tissues are In comparatively good agreement with the ideal compositions of each
mineral.
Furthermore, this technique permitted to identify
and determine some other minerals which could not be detected
by X-ray diffraction analysis.
The sensitivity of the X-ray
diffraction analysis for the detection of a small amount of a
particular mineral In a mixture depends a great deal on the
mineral concerned.
A well crystallized mineral can often be
detected at below the 1% level, whereas quite large concentrations of a poorly crystallized mineral cannot be detected.
Nevertheless, the studies using analytical electron microscopy
have been successful In Identifying minerals In the lungs.
A mineral can be said to be "determined" when we have
identified the crystal phase and have determined its chemical
359
composition.
These two kinds of information about a mineral may
be sought by several techniques. Today, these two informations
are obtained by the analytical electron microscope.
This micro-
scope has been developed for facilitating observations by the
transmission electron microscope, energy dispersive microanalysis
and selected area electron diffraction on the same microarea in
the specimen by instantaneous commutation.
Moreover, by applying
the procedure of semi-quantitative chemical analysis with the
analytical electron microscope, the chemical composition of
individual particles extracted from lung tissues with asbestosis
and silicosis can be determined together with their crystal phase,
This technique may contribute to obtain valuable information about
the relationship between lung dust and lung pathology in pneumoconiosis,
References
Hayashi, H., Aita, S., and Suzuki, M. (1978) Clays and Clay
Minerals, 26, 181. Weeks, W. F. (1956) Journ. Geol., 64, 456.
36o
3ju
e« aa.ai
Fig. 1.
co
Er* ao.Oi
Ct
aaoE toon
STEM image and EDS spectra of particulate
materials extracted from a lung with asbestos is.
361
\ KCa
Fe
»r. OD.Ol
C,
aoD-têoi*
Fig. 2. STEM Image and EDS spectra of particulate
materials extracted from a lung with silicosis.
362
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Table 2.
Minar«1«
Actinollta
Talc
Results of EDS analysis of p a r t i c u l a t e materials
extracted from the lung with asbestosis
Spaciaan
Mo.
6
7
810j
total
Iron
MgO
18.79
20.40
19.60
20.41
A1
CaO
Avaraga
Chaatar
53.80
58.71
56.25
55.26
9.05
4.79
6.92
6.30
11
63.29
1.98 28.43
-
4
3
5
1
2
65.06
65.38
65.62
65.93
67.57
65.48
63.5
1.02
1,08
0.86
0.82
29.12
29.81
29.57
28,17
26.76
28.64
31.7
-
41.37
47.04
51.74
46.71
1.61
10.04
5.44
5.70
5.73
1.91
2°3
16.00
13.74
14.87
12.07 2.23
*2°
0.10
oth
«r*
total
97.64
97.64
97.64
1.27 97.64
H20 a
otnera
Total
2.12
99.76
1.49 95.19
(ilo,)
Avaraga
Idaal
Comp.
Illita
8
10
9
Avaraga
Idaal
Camp.
45.2
1.43
0.48
95.20
95.19
95.19
95.18
95.19
0.25 95.19
95.2
34.29
20.08
30.57
28.32
18.23
95.50
12.62
95.50
3.86 2.43 95.47
11.58 0.80 95.50
38.5
11.8
364
95.5
4.8 100.0
4.5 100.0
Table 3.
Results of EDS analysis of particulate materials
extracted from the lung with silicosis.
UMItlt
•patüMB
M.
!K~-
2
Uolla
S5.U
M,0
Mt«l
2.51 3.25
95.00
1.S0
2.13
1.72
•6.5
39.5
ca.ll
«1.76
«.16
«.51
19.56
23.75
S2.66
25.32
1.06
0.55
10
95.0
1.15
«.»
COI
2.95
31.«
(3.76
63.5
•••
faul
5.0
100.0
lt.O
100.0
«.5
100.0
«.1
100.0
K.0D
•6.0
2.79
10.97
se.5
•5.2
UMI
9.0«
9.00
15.3«
11. U
95.50
95.«
95.»
95.«
11.1
95.5
95.20
31.7
95.2
COM..
9.5«
76.«
I
;
».16
96.33
51.75
5
IS
11
12
a
•llvary
nmtêl
«,0
6.65
1
U N I
llMTIl
C*0
2.17
21.3
Cav-
OMrti
utal
23.07
«0.50
«
S":"**"
Mao
«i,o,
35.75
u
Cálelas
•lllcat«
l.<8
)
ft*«ra«*
Tat«
tio
UHI
IdMl
Ml«
•IO,
InitMi
•o.
e
6.02
13.(2
5.U
0.69
99.99
1,58 c i - t . n 99.98
100.00
1.25
100.0
100.0
100.0
100.0
100.0
100.0
100.0
100.0
• 10,
!.«J
100.00
"•»
•
ci
«.55
6.51
1.01
-i
twal
77.(5
100.0
365
—
Análisis mineralógico de los polvos en el pulmón
en los casos de neumoconiosis. con un microscopio
electrónico analítico«
H. Hayashi
(Japón)
El microscopio electrónico analítico se compone de un
microscopio a transmisión electrónico, de un goniómetro
lateral con entrada lateral, de un accesorio de exploración y de un espectrómetro radiológico dispersor de energía. Los autores han propuesto recientemente un procedimiento rápido y sencillo para el análisis químico semicuantitativo de las fibras de amianto y minerales arcillosos con el microscopio electrónico analítico. Con este
procedimiento fue posible descrubir las características
morfológicas, estructurales y químicas de cada material
particulado por separado presentes en los pulmones sin necesidad de ajustar cada vez el objetivo. Se han estudiado
los materiales particulados presentes en los pulmones con
neumoconiosis tales como la asbestosis, talcosis, pirofilitosis, silicosis y neumoconiosis de polvos mezclados.
Los resultados de la dispersión de energía en cuanto a la
composición mirrerai de esos materiales particulados son
similares a los obtenidos por difracción por rayos X en
los polvos extraídos de los mismos tejidos pulmonares.
Además, los resultados de dispersión de energía de cada
material particulado coinciden con la exposición química
de algunos anfiboles asbestiforraes y los del talco ideal,
la pirofilita, caolinita y la ilita. Los estudios indican
claramente las vastas posibilidades del microscopio electrónico analítico para determinar la composición química
de las partículas finas, a la vez cualitativa y cuantitativamente.
366
T. N D 1 C r
I
S r S S T P N
V
ro.f-SDinoza
Reporter
II
Gunnar Mouie". , Egli Pphus., and fljorn Gylseth. ,
Asbestos fibre content In Idling tissue In relation to
Asbestos exposure and causes of death.
III
N.V.Vallyathan. , and JoNn r.Craighead
Silica dust-aS90ciated pulmonary lesions in granite workers
lacking Radiologic evidence of disease.
IV
J.A.Dick.
The role of pulmonary tuberculosis In the causation of
progressive massive fibrosis in coal workers in great britain
V
Tee L.Guldotti.
The higher oxides of nitrogen: A role In altering pulmonary
response to injury?
VI
J.Ro9manith., R.Leonardi., D.PrsJ9nar., H.Breining and
III.Ehm.
The effect of the combined application of cadmiun and lead
sulfide and côal dust of the development of lung fibrosis
in rats.
VII
D.PraJsna3., H.Breining., and J.Rosmanith.
Lung fibrosis In rats 8fter lead sulfide application.
VIII
H.Breinning., J.Rosmanith and D.PraJsnar.
Lung fibrosis In rat9 after cadmiun sulfide application.
367
NEUMOCONIOSIS EN EL PERU
Dr. Mario A. Espinoza M.
Lima •• Peril
Los conocimientos científicos sobre los efectos dañinos de
los polvos inorgánicos que causan las Neumoconiosis son de
época reciente. Sin embargo, se sabe que Plinio el Viejo, Hipaorates, Celso, Agrícola, Paracelso y otros habrían observado y
descrito mucho antes los efectos dañinos del polvo en los pulmones.
Estudios anatomopatológicos realizados por Diemerbrock en
1649 demostraron los efectos antes señalados por los hallazgos
de fibrosis, enfisema y depósito de polvo en el tejido pulmonar
examinado. Ramazzini en 1700, considerado como el padre de la
Medicina del Trabajo por sus brillantes observaciones clínicas
en este campo, describió también los efectos dañinos de dicho
elemento sobre el aparato respiratorio, muchos de ellos con efectos fatales.
Zenker fue el creador del término de Neumoconiosis y
Kussmaul demostré químicamente el efecto dañino del sílice
libre, siendo Visconti quién estableció el término de Silicosis.
Collis en 1915 haciendo una revisión de los conocimientos
sobre Neumoconiosis estableció la teoría del sílice libre como
responsable de la enfermedad, haciendo notar sobre la gran susceptibilidad de los enfermos de Silicosis a la Tuberculosis.
Gadner y Cummings de los Laboratorios de Saranac Lake realizaron estudios sobre la patología pulmonar en los trabajadores
de minas de hierro en Michigan y Wisconsin en los Estados Unidos,
obteniendo interesantes resultados y llegando a la conclusión
que la incidencia de patología pulmonar estaba en razón directa
con la exposición a polvos de cuarzo que como se sabe contiene
alto porcentaje de sílice libre.
En el Peni estudios sistemáticos sobre Neunoconiosis fueron
hechos a partir de 1948 cuando se creó el Departamento Nacional
de Higiene Industrial, hoy Instituto de Salud Ocupacional.
En Enero de 1935 dicha enfermedad fue declarada enfermedad
profesional sujeta a indemnización.
Conviene señalar que el término de Neumoconiosis se viene
utilizando en algunos países como sinónimo de Silicosis, a pesar
de que aquél es un termino genérico que agrupa a todas las entidades nosológicas causadas por el polvo, en tanto que Silicosis
es una Neumoconiosis Específica, entidad anátomo clínica, bien
definida.
369
En la Cuarta Conferencia Internacional de Neuinoconioais
llevada a cabo en Bucarest en Octubre de 1971, organizada por la
Oficina Internacional del Trabajo (OIT), se definii la Neumoconiosis como la acumulación de polvo en los pulmones y la reacción
del tejido en presencia de este material, definición simple que
prácticamente restablece la definición dada por Zenkor.
Entre las diversas Neumoconiosis, la Silicosis y la Asbestosis son las que causan "incapacidad" para el trabajo, mientras
que la siderosis, la antracosis, la baritosis, la estañosis y
otras causarían alteraciones mínimas del tejido pulmonar con
merma igualmente leve de la capacidad física para el trabajo.
Por eso las dos primeras suelen ser llamadas "Neumoconiosis Específicas" y las ultimas, "Inespecíficas".
La Beriliosis, neumopatía severa que se presenta entre los
que trabajan con sulfato de berilio es considerada,como una Neumoconiosis. La Bisinosis, la bagazosis y la tabacosis han sido
señaladas como causantes de procesos alérgicos pulmonares.
Los ingleses consideran a la antracosis como una Neumoconiosis
incapacitante, debido al enfisema que provoca, hecho que es discutido por algunos investigadores. Nosotros hemos encontrado muchos casos de antraco-silicosis en los que trabajan en minas de
carbón, creemos que en este caso los trastornos anatomo patológicos son debidos al sílice libre más que a las partículas de
carbón inhaladas, porquelas minas son de un alto poder silicógeno.
Los conocimientos actuales sobre Neumoconiosis están basados
generalmente en las investigaciones epidemiológicas sobre dicha
enfermedad cuyos resultados han permitido comprender e interpretar la relación que existe entre el agente (polvo), el ambiente
(lugar de trabajo) y el huésped (trabajador)i
Por esto; será motivo de un análisis breve cada una de estos
factores para poder comprender las características epidemiológicas de las Neumoconiosis,principalmente de la Silicosis en el
Pení, país eminentemente minero cuyos trabajadores que a pesar
de no ser muy numerosos contribuyen con más del 50$ de los ingresos de divisas para el país.
Características del Huésped
El minero peruano por lo general realiza inicialmente trabajos
mineros, además labores agrícolas.
El minero permanente resulta después de muchos intentos de
mantener este estatus de trabajo.
37o
Como la mayoría de los centros mineros están situados en
lugares superiores a los 3,000 metros sobre el nivel del mar, es
comprensible que los trabajadores sean personas que habitan en
la sierri o en lugares circunvecinos, cuyas características antropométricas corresponden al hombre andino, descrito por Monge y
Hurtado, en el Instituto de Biología Andina del Peru.
Edad
Los trabajos mineros por su naturaleza, requieren de hombres
sanos y resistentes, la edad mínima establecida por la legislación
peruana para realizar labores mineras, es 18 años. Algunos autores
consideraban que los jóvenes serían mas susceptibles de contraer
Neumoconiosis, pero estudios efectuados por el Instituto de Salud
Ocupacional han demostrado que la mayor prevalencia de Silicosis
en este grupo otario, era debido a que estaban expuestos a altas
concentraciones de polvos que contienen sílice libre.
El estudio referido ha demostrado casos de Silicosis temporana entre los trabajadores cuya edad estaba comprendido entre
los 20 y 24 años. Las ocupaciones que desempeñaban eran las
más expuestas al polvo, como las de perforistas, ayudantes y enraaderadores.
El estudio en referencia demostró que de 2,152 trabajadores expuestos a polvos que contienen sílice libre, 212 o sea el 98,5
por mil, adolecían de Silicosis, observándose que la provalencia
de dicha dolencia aumentaba paralelamente a la edad incrementándose
de 9.1 por mil en el grupo de 20-24 años a 353 por mil en el grupo
de 60 o más años, lo que demostraría lógicamente que el tiempo
de exposición (riesgo) se prolonga cuanto más es la edad del trabajador. Tabla No. 1
Analizando los casos de Silicosis en relación con el grado
de evolución se ve una relación directa entre tiempo de exposición
y grado de evolución de la enfermedad en los dos primeros estudios
SI y SII, no así en el tercer estudio (SUI), pues es de suponer
que en este período de evolución de la enfermedad, los obreros
abandonan el trabajo tanto por su edad, oomo por los efectos de la
enfermedad que le impide realizar trabajos que requieren gran esfuerzo físico, esto explicaría el hecho de que en el grupo de
edad, mayores de 60 años se encontró sólo 6 casos do Silicosis.
En cuanto a la SÍlico Tuberculosis, se observa un hecho importante
en relación a la edad del trabajador afecto de Silicosis y es que
hay una mayor incidencia de complicación cuanto más avanzado es
el grado de Silicosis.
371
Raza
Las afirmaciones hechas sobre la influencia de la raza en relación con la patogenia de la enfermedad no es un hecho comprobado ;
la existencia de una mayor prevalencia de Silicosis entre una
determinada raza se debe principalmente a que están mayormente
expuestos al agente como ocurrid en Sud Africa a cuyos trabajadores negros se les asignaban los trabajos en lugares con mayor concentración de polvo.
Nosotros no hemos encontrado ni observado una mayor predisposición ni en los naturales de la región ni en la raza mestiza,
pues ambas son igualmente susceptibles.
Sexo
La mayoría de trabajadores en lugares polvorientos son del
sexo masculino sin embargo, es digno de mencionar quealguas mujeres puedensufrir de Neumoconiosis (Silicosis) cuando trabajan
envasando detergentes domésticos como el sapoli u otros similares,
en cuya fabricación se emplean además del jabón,un material abrasivo como la tierra de infusorios.
La bisinosis es frecuente observar en las cardadoras en la
industria textil.
Afecciones del tracto respiratorio superior y de los pulmones.
Ciertas alteraciones bronco pulmonares y de las vías respiratorias superiores pueden ser causa de una mayor predisposición
para adquirir la enfermedad.
Es sabido que las personas que sufren de dsma bronquial, bronquitis crónica, desviación del tabique nasal tienen mayor riesgo
de trabajar expuestos a polvo por lo que debo evitarse asignarles
trabajos en lugares polvorientos.
Susceptibilidad Individual
Aunque no está plenamente comprobado, ciertas observaoiones
clínicas permiten juzgar que unos individuos son más propensos que
otros a contraer esta enfermedad. Así es como de un grupo de trabajadores quo laboran en las mismas condiciones ambientales expuestas a los mismos elementos contaminantes, unos adquieren la enfermedad, mientras que otros no la sufren, este hecho se explicaría
considerando el papel que juega la susceptibilidad individual.
372
Características del Agente
Debemos señalar lo siguiente:
a) La composición de polvo.
b) La concentración de las partículas.
c) El tamaño de las mismas y finalmente
d) El tiempo de exposición
Es un hecho comprobado que la Silicosis es debida a la inhalación de polvos que contienen sílice libre, las observaciones
clínicas y experimentales lo han demostrado así. Los trabajadores experimentales de Gye y Kettle empleando sílice coloidal ha
permitido observar la proliferación de tejido fibroso. Gardner
ha producido las mismas alteraciones en animales, en un periodo
corto de dos años, sometiéndolos a altas concentraciones de polvos de sílice.
Estos trabajos y otros permiten pensar que la sílice actúa
principalmente por acción química o inmunológiea y no por acción
mecánica como se creía anteriormente,
La exposición de animales de experimentación a polvos de diamante, carborundo y otros qua oon más duros que la sílice corroborarían esta tesis ya que el efecto no ha pasado de ser simplemente irritativo local.
La patogenia de la Silicosis sigue siendo aun desconocida,
la teoría química es muy discutida frente a los trabajos recientes
desarrollados en el campo de la inmunología y los estudios histoquímicoo de los componentes del nodulo silicótico.
Los pacientes estudiados realizados por Deny, Irwin y Robson
utilizando el aluminio con fines profilácticos y terapéuticos, no han
alcanzado los frutos que se esperaban.
Concentración de Partículas
La concentración de partículas de polvo en el ambiente de
trabajo juega gran papel en la etiopatogenia de la Silicosis, es
por eso que se han fijado en las industrias polvorientas ciertos
límites denominados "Concentraciones Máximas Permisibles" cuyos
valores han sido establecidos, teniendo en cuenta el contenido de
sílice libre, así polvos con un contenido mayor de 50f° de sílice
libre se considera permisible hasta cinco millones de partículas
por pie cúbico de aire; de 5 a 50$ veinte millones y por debajo
de 5$ cincuenta millones.
373
Se ha' obtenido una utilidad muy práctica de esto3 estudios,
aplicables a la patogenia y a la prevención de la Silicosis en
relación a la concentración de partículas de polvo, puás para
desarrollarse la enfermedad, la sílice debe estar presente en una
concentración tal, con uncontenido de BÍlice elevado y depositarse
en los pulmones en cantidad suficiente.
A bajas concentraciones de polvo, el peligro sería mínimo,
a pesar de una exposición prolongada. En esto está basado el concepto de "Concentración Máxima Permisible", cuyos valores varían
de acuerdo con la clase del contaminante atmosfèrico.
Dichos valoreB han sido establecidos para trabajos a nivel
del mar, por lo que en el Peni tendrían valor relativo por que
juegan además, otros factores condicionados por la altura a que
están situados los centros mineros. El análisis estadístico de
los datos obtenidos en ira estudios realizados, nos permitirá establecer dichos límites. • Otros factores tales como la temperatura,
humedad, ventilación, etc. influyen sobre la dinámica biofísicas
de las partículas de polvo.
Tamaño de las Partículas
En cuanto al tamaño de las partículas sabemos que las de tres
mieras o menores ganan fácilmente el nivel alveolar venciendo los
obstáculos que presenta el tracto respiratorio superior. Las
partículas de 10 mieras cúbicas o mayores precipitan fácilmente
y si Bon inhaladas son detenidas por el filtro naeal y el epitelio
ciliado del tracto superior siendo expulsadas con la expectoración
mediante la tos; en tanto que, las más pequeñas además de franquear
fácilmente dichas barreras, permanecen an-, suspensión mucho tiempo
en el ambiente de trabajo, con el peligro de ser inhaladas.
Estudios llevados a cabo por Hatch, hemdon, Landahl y otros
sobre retención o depósito de polvo inorgánico a nivel del sistema
respiratorio en relación al tamaño de las partículas han demostrado
que el porcentaje de retención disminuye de cerca de 100$ parapartículas mayores de 5 micrones a cerca de 25% para partículas de
1/4 de miera,
El tamaño de las partículas suspendidas en el ambiente de trabajo en las minas peruanas en promedio variaban entre 1 y 3 mieras
cúbicas en un alto porcentaje.
Tiempo de Exposición
El tiempo de exposición como factor en la patogenia de la Silicosis, por esto es importante establecer claramente mediante una
37*
historia ocupacional bien tomada, si la exposición a material
particulado fue prolongada y continua o esporádica, el análisis
ocupacional de 11,942 historias clínicas de trabajadores mineros,
QO los que 4,331 habían laborado exclusivamente en subsuelo y
7,611 en subsuelo y superficie, se encontró 461 trabajadores
10.6 pormil de casos de Silicosis en el primer grupo y 560 73.6 por mil en el grupo mixto, Los casos de Silicosis diagnosticados en trabajadores fuera de las galerías, tienen antecedentes de haber trabajado en labores de subsuelo.
El tiempo promedio de exposición para adquirir Silicosis
en primer grado de evolución fue 9.7 años; para el segundo grado
10.9 años y para el tercer grado 13.4 años, tiempos de exposición relativamente cortos que traducen un ambiente insalubre de
un gran valor epidemiológico para realizar acciones de prevención.
Merece subrayar que mientras en los estudios llevados a cabo
en el mismo centro de trabajo el tiempo de exposición guarda relación directa en el grado de evolución de la enfermedad, los datos obtenidos en el Departamento de Exámenes Médico-Periciales
de Lima son variables hasta cierto punto contradictorios como
puede verse en la Tabla No. 2,
Resulta que siendo el tiempo promedio de exposición para el
primer grado 10.8 años, para el segundo grado fue de 9.4 años,
lógicamente el tiempo debería ser mayor, tal discrepancia se explicaría teniendo en cuenta que, los datos o CU p ac i 0 nales referidos por
los trabajadores fueron inexactos. Habría que admitir en este caso
que los reclamantes de indemnización no refieren una historia veraz,
omitiendo tiempos de trabajos en otras compañías mineras, sabiendo
que en caso de sufrir de enfermedad ocupacional será responsable
del pagoÉ de la indemnización la ultima empresa que le tuvo a su
servicio. En la actualidad el pago de la Indemnización está a cargo
del Seguro contra Enfermedades y Accidentes del Trabajo.
Caracteres del Ambiente
Cada vez más la Ecología cobra actualidad, el concepto ecológico de salud y enfermedad en el campo de la Salud Ocupacional,
es muy importante ya que juega un papel preponderante el ambiente
de trabajo, especialmente en la patogenia de las Neumoconiosis.
Dijimos que las minas en el Peni están situadas en lugares que
sobrepasan los 3,000 metros sobre el nivel del mar, en los que la
demanda de oxígeno durante el esfuerzo físico es mayor, debido a la
bajo presión barométrica. Las minas en su mayoría son subterráneas, la perforación, voladura y otras actividados permiten la
dispersión del polvo en suspensión, aumentando cuando estas
375
operaciones se hacen en seco. La falta de ventilación, las galerías estrechas y los turnos de trabajo continuos no permiten en
muchas minas la dispersión del polvo que gañeran el mal.
Las limitadas facilidades de bienestar de que disponen los
trabajadores, especialmente en las pequeñas y medianas empresas,
la deficiente nutrición, el alcoholismo y la costumbre ancestral
de masticar hojas de coca, moman la ealud del trabajador minero
haciendo propicia el terreno para contraer enfermedades de diversos
orígenes especialmente la Neumoconiosis.
Los centros mineros del Perú, alejados de las poblaciones
con facilidades sanitarias constituyen verdaderos oasis poblacionales donde es posible hacer estudios epidemiológicos aplicando la Epidemiología Geográfica y principalmente desde el punto
de vista Ecológico.
Silicosis y Altura
El Perú productor de cobre, plata, plomo y otros minerales
afrontan con la acción adversa de la altura sobre la salud de sus
trabajadores. Estudios llevados a cabo por el Instituto de
Salud Ocupacional al respecto han-demostrado que existe una correlación entre Silicosis y altura, siendo mayor su prevalencía
cuanto mayor es la altura, especialmente sobre los 4,000 metros
sobre el nivel del mar. En el estudio efectuado en 32,498 trabajadores mineros se ha encontrado que las tasas de Silicosis suben
progresivamente de 4.2$ a los 1,000 metros Bobre el nivel del
mar a 61. 2# entre los 40001 - 5000 metroB de altura. Tabla No. 3.
La patogenia no está aun clara, pero se puede admitir que el
hombre de altura moviliza una mayor cantidad de aire para captar
la cantidad necesaria de oxígeno en comparación con los trabajadores de la costa, debido a la baja presión barométrica. Este
estado de hipoxia en el que vive y trabaja, hace que la cantidad
de hemoglobina y los hematíes se incrementen notablemente dando
una mayor densidad a la sangre y obligando al corazón a un mayor
trabajo, siendo la velocidad circulatoria más lenta, todo ello
causaría el fenómeno de lo que Monge del Peni llama encharcamiento, que a su juicio favorecía la presentación de Silicosis
en un tiempo menor al que se presentaría en los trabajadores de
la costa.
En el Cuadro No. 1 se hace un resumen de los factores patogénicos de la Silicosis, que han sido estudiados en cuatro minas
de cobre, situadas a diferentes niveles de altura sobre el nivel
del mar.
En las minas A,B,C y D, como se puede ver en la; Tabla se han
encontrado diferentes concentraciones de polvo en el ambiente,
siendo el más alto en la Mina C, un contenido de sílice libre
igualmente alto, con una incidencia de 8.4$ de Silicosis en un
tiempo de exposición relativamente corto de 8.7 años.
376
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O
CUADRO No. 1
RELACIÓN ENTRE SILICOSIS Y FACTORES AMBIENTALES
LIMA
-
PERU
MINA
A
B
C
Concentración
(millones por
p i e cúbico)
10.0
26.1
58.0
23.0
«5 de SÌO2
9.6
a
34.2
15
15,3
a
67.0
27
Promedio tamaño
de partículas *
(Me)
1.3
1.0
1.3
1.3
Tiempo promedio
de exposición
(en años)
12.1
8.0
8.7
13.6
0.3
16.0
8.4
13.7
Silicosis
*
Mieras ciíbicas
38o
PATOGENIA DE LAS NEUMOCONIOSIS
Dr. Mario Espinoza M.
Lima - Peru
Estudios llevados a cabo por el Instituto de Salud Ocupacional del Perú han demostrado que existen en el país diversos tipos de neumoconiosis, siendo los más importantes la sx
licosis y la antraco silicosis.
Se ha demostrado a través de los exámenes médicos realiz¿
dos en más de ¿0.000 trabajadores mineros y de estudios del
medio ambiente de trabajo, la existencia de una relación muy
estrecha entre la concentración de polvo en el ambiente de trabajo, contenido de sílice libre, tamaño de las partículas,
tiempo de exposición y neumoconiosis.
Que en el caso del Perú existe además, un factor muy impor,
tante, que es la altura. La mayoría de las minas están situa
das sobre los 3,500 metros sobre el nivel del mar donde la
presión atmosférica es menor, lo que obliga al trabajador a
una mayor movilización de aire durante la fase inspiratoria para captar la cantidad de 0 2 necesario que demanda el esfuej:
zo físico generado por el trabajo, hecho que no sucede a ni vel del mar.
Estos hechos y otros referidos a las características antro
pométricas del hombre andino han sido estudiados por Monge,
Hurtado y otros en el Instituto de Biología Andina del Perú.
Siendo la respiración más lenta y profunda en la altura hay
que admitir que el depósito de partículas en el aparato respiratorio sea mayor, lo que favorece la presentación de neumoco niosis en un tiempo corto.
Anualmente, estudios realizados por el Instituto de Salud
Ocupacional del Perú sobre la aplicación de "Concentración Máx^
381
2.
ma Permisible" establecida por los Higienistas Industriales
con relación al polvo ambiental para el control de las Neumoconiosis no es aplicable para niveles superiores a los 3.000 metros, porque se presentan casos de silicosis, aún
por debajo de dichos valores.
382
ASBESTOS FIBRE CONTENT IN LUNG TISSUE IN RELATION
TO ASBESTOS EXPOSURE AND CAUSES OF DEATH
Gunnar Mowé, Egli Ophus, and Bj(5rn Gylseth, Institute
of Occupational Health, Oslo, Norway
INTRODUCTION
Knowledge on the relationship between occupational asbestos
exposure, asbestos lung burden and different asbestos related
diseases is important for the evaluation of the health risk of
individual workers.
Evaluation of the occupational exposure
should include information on type of asbestos, intensity and
duration of the exposure and the lapsed period from onset of exposure.
Furthermore, other possible exposures should be record-
ed as well.
Several authors have determined the fibre concentration in
lung tissue using different microscopic techniques (1,2,10).
Lung tissue from persons who have died of asbestosis, mesothelioma and bronchial cancer has been studied in detail in order to
obtain an indicator of the asbestos lung burden.
Electron micro-
scopes fitted with an energy dispersive x-ray analyser have proved
to be valuable for the quantification and identification of asbestos
fibres in lung tissue (7).
The aim of the present investigation has been to study the
relationship between occupational exposure and asbestos lung burden
in different asbestos-related diseases.
MATERIAL AND METHODS
The fibre concentration in lung tissue samples obtained at
autopsy was determined by scanning electron microscopy (SEM).
Before the SEM investigation the samples were dried at 80°C for
385
48 hours and ashed in a low temperature plasma asher.
The fibres
were identified by morphological criteria and by energy dispersive
x-ray microanalysis.
Detailed methods will be described elsewhere
(3).
The material consists of samples of 23 cases which have been
classified into 3 exposure groups according to their occupational
histories.
Group I (high exposure) consists of 7 insulation workers who
have been exposed to both crocidolite and chrysotile asbestos.
The
exposure has been severe for some of them, and they have certainly
been exposed to man-made mineral fibres as well.
During insulation
work in refrigerator ships and plants, exposure to cork dust and
tar fumes also has occurred.
Group II (low exposure) consists of
3 workers who have been slightly exposed during handling and transport of asbestos products, but they have never been doing insulation work.
Group III consists of 13 persons with various occupa-
tions without known
occupational asbestos exposure.
Information on the occupational history was obtained from
several sources i The trade union of insulation workers, different
insurance files and through interviews with insulation workers who
participated in a recent epidemiological investigation.
RESULTS
In Group I the age at onset of exposure and the duration of
exposure show great variations.
1.
These results are given in table
The lapsed period from onset of exposure until death is very
long and rather constant.
The results in table 2 are presented as number of fibres per
381
gram of dry tissue. The fibre concentration in the lung tissue
and the proportion of fibres with positive asbestos identification are higher in group I than in group II and III. Lung tissue
in group I contained (2,2 - 36) • 10 6 , group II (0,3 - 2,4) • 10 6 ,
and group III (0,3 - 1,5) " 10
respectively.
fibres per gram of dry tissue ,
The proportion of fibres with positive asbestos
identification in group I was 79%, in group II 60%, and in group
III 23%, respectively.
Table 3 shows the number of coated fibres in relation to
the total fibre concentration.
are coated.
In group I only 9,6% of the fibres
Most fibres are shorter than 5jjm and thinner than Lum.
Table 4 shows the fibre concentration in relation to causes
of death.
The highest fibre concentration is found in the pleural
mesothelioma cases, in one of which asbestosis occurred.
The
fibre concentration in cases with asbestosis varies from (8,7 36,0) • 10
fibres per gram of dry tissue.
Owing to the small
sample it is impossible to determine the relationship between
fibre concentration and degree of lung fibrosis.
In one worker who died of mesothelioma (case No.2), 12%
of the total number of fibres and 47% of the coated fibres were
longer than lQjum.
Based on the x-ray spectra, 64% of the fibres
were identified as crocidolite, 15% as anthophyllite and 4% as
amosite.
No chrysotile fibres were identified.
Of the fibres
17% were difficult to identify.
The results for each case are shown in tables 5 and 6.
DISCUSSION
Occupational exposure and asbestos lunfi burden.
385
The present investigation shows that high occupational
asbestos exposure is associated with high fibre concentration in
lung tissue.
It is not, however, possible to distinguish cases
without occupational exposure from cases with low occupational
exposure. This may be due to that it is difficult to evaluate
the exact asbestos exposure in certain occupations.
The find-
ings are in consistence with other investigations (2).
Asbestos lung burden and health effects.
The concentration of fibres in lung tissue depends on
both the intensity and the duration of the exposure.
Further-
more, a minimum lapsed time from the first asbestos exposure,
i.e. the recidence time, is probably necessary for certain health
effects to occur.
Epidemiological studies (8) have shown that
long observation periods of 30 to 40 years are necessary to
study the health effects of asbestos exposure.
In the present
investigation all cases, even with high exposure, have a long
and rather constant lapsed period from the onset of exposure.
Ashcroft and Heppleston (l) found a long recidence time for
asbestos fibres in cases of mesothelioma .unrelated to the fibre
concentration and the grade of asbestosis.
Furthermore, Ashcroft and Heppleston (1,4), found a significant correlation between fibre concentration in lung tissue
and the grade of lung fibrosis in cases with slight and moderate
asbestosis.
However, no relationship between fibre concentra-
tion and the pathological changes of severe asbestosis were
found.
They therefore suggested that the changes of severe
asbestosis are due to the intervention of secondary pathological
386
processes as non-specific pulmonary infections.
Whitwell et al (10) found that the fibre concentration in
the lungs in cases of mesothelioma was closely related to the
occupational exposure.
Heppleston (5) suggests that the development of mesothelioma
appears to be unrelated to the concentration of coated and uncoated fibres in lung tissue, but
Bignon et al (2) found parti-
cularly high fibre concentrations in cases of mesothelioma associated with asbestosis.
The present investigation has shown that most fibres in
lung tissue found by scanning electron microscopy are uncoated,
shorter than fym and thinner than l^um. The results are in agreement with other investigations (1,2,4).
Furthermore, only amphi-
bole asbestos is identified in the lung tissue, which might be due
to chrysotile asbestos changing properties in the lung tissue
(5,6).
In our investigation we found the highest fibre concentration
in two cases of mesothelioma.
In one of these cases, without any
sign of lung fibrosis (case No.2), we found that 12% of the total
fibres and 47% of the coated fibres were longer than 10/um. This
is particularly interesting because experimental studies by Stanton
et al (9), have shown that fibre carcinogenicity probably depends
on fibre length and fibre durability.
They found that fibres
thinner than l,5un and longer than 8/um yielded the highest probability of pleural sarcomas.
Due to the limited size of the lung samples in this investigation, we have not been able to study the distribution of fibres
in different parts of the lung.
387
Our results must therefore be
regarded as approximate concentrations.
Furthermore, the material
is small, and therefore it has been impossible to study the relationship between asbestos burden and different asbestos-related
diseases.
Further studies on the quantity and the size distri-
bution of the fibres in lung tissue are necessary to evaluate
the relation between asbestos lung burden and health effects.
388
TABLE 1
OCCUPATIONAL EXPOSURE
GROUP
I
II
III
HIGH
EXPOSURE
LOW
.EXPOSURE
UNKNOWN
EXPOSURE
NUMBER OF CASES
7
3
ONSET OF EXPOSURE
1928 - 1 9 W
1935 - 1950
AGE AT ONSET
26 (15-33)
ill (33-53)
DURATION
19 (2 -35)
11 ( 2-28)
AGE AT DEATH
66 (58-75)
66 (51-78)
LAPSED PERIOD
FROM ONSET
37
28 (21-38)
(32-13)
ARITHMETIC MEAN AND RANGE
389
13
55 (11-78)
TABLE 2
FIBRE CONCENTRATION AND IDENTIFICATION
(FIBRES/G DRY TISSUE)
GROUP
I
HIGH
EXPOSURE
NUMBER OF CASES
FIBRE CONCENTRATION
10 6 FIBRES PER GRAM
OF DRY TISSUE
FIBRES WITH
POSITIVE ASBESTOS
IDENTIFICATION
% OF TOTAL NUMBER
II
LOW
EXPOSURE
7
18,0
(2,2 - 36,0)
79 %
3
13
1,0
0,7
(0,3 - 2,4)
60 %
(27 - 92)
(27 - 86)
ARITHMETIC MEAN AND RANGE
x) 6 CASES
39o
III
UNKNOWN
EXPOSURE
(0,3 - 1,5)
2 32
(8 - ¥0
TABLE 3
PROPORTION OF COATED FIBRES
SIZE DISTRIBUTION
GROUP
I
HIGH
EXPOSURE
NUMBER OF CASES
9,6 %
COATED FIBRES
% OF TOTAL NUMBER
FIBRELENGTH
7
< 5m
% OF TOTAL NUMBER
FIBRE DI AMETER <lm
Z OF TOTAL NUMBER
II
LOW
EXPOSURE
3
19,3 % X )
III
UNKNOWN
EXPOSURE
13
8,7 %
(6,8 - 17,6)
59.2
17 I
(38 - 71)
96.%
( 92-100)
ARITHMETIC MEAN AND RANGE
3 CASES
391
45 % x x )
(37 - 55)
89 %
91 %
(89 - 94)
TABLE 4
FIBRE CONCENTRATION AND CAUSES OF DEATH
FIBRE
CONCENTRATION
10 6 PER GRAM
OF DRY TISSUE
PLEURAL
FIBROSIS
LUNG
FIBROSIS
1
36,0
+
+
2
32,8
+ ,
3
28,0
+
+
4
9,4
+
+
6
9,3
7
2,2
+
?
5
8,7
+
+
UNCLASSIFIED
LUNG CANCER
8
2,1
EMPHYSEMA
9
0,3
10
0,3
CAUSE OF DEATH
CASE
NO,
MESOTHELIOMA
ASBESTOS IS
BRONCHIAL CANCER
' APOPLEXIA CEREBRI
392
?
TABLE
5
INDIVIDUAL RESULTS.
GROUP
ONSET OF EXPOSURE
AGE AT ONSET
DURATION
^VGE AT DEATH
^APSED PERIOD FROM
ONSET
FIBRE CONCENTRATION
10 6 FIBRES PER GRAM
DRY TISSUE
FIBRES WITH POSITIVE
ASBESTOS IDENTIFICATION
% OF TOTAL NUMBER
COATED FIBRES
% OF TOTAL NUMBER
FIBRE LENGTH<5 pm
% OF TOTAL NUMBER
£JBRE DIAMETER<1 ym
S*OF TOTAL NUMBER
I
i-i
CASE NUMBER
GROUP I AND II
2
1944 1939
3
II
4
5
6
7
8
1928 1935 1941 1934 1938
9
10
1949 1935 1950
43
25
75
19
17
58
15
2
58
27
35
66
31
3
67
29
16
71
30
35
66
33
4
54
38
28
66
53
2
78
32
39
43
40
36
37
36
21
38
25
36,0 32,8
28,0
9,4
8,7 . 9,3 . 2,2
2,4
0,3
0,3
27
27
86
68
_ 7,5 17,6
19,3
_
_
90
92
92
75
90
84
6,8
7,1
11,0
7,3
50
66
65
71
70
38
54
47
_
_
100
95
99
100
99
92
90
89
-
-
+
+
+
+
+
+
+
+
CAUSES OF DEATH
MESOTHELIOMA
ASBESTOSIS
BRONCHIAL CANCER
+
OTHER CANCERS
CHR. BRONCHITIS
WITH EMPHYSEMA
PLEURAL FIBROSIS
LUNG FIBROSIS
+
+
+
+
+
393
+
+
+
+
TABLE 6
INDIVIDUAL RESULTS.
CASE NUMBER
11
12
13
14
GROUP III
15 ! 16
17
18
19
20 ! 21
22
23
68
40
i
76
AGE AT DEATH
78
76
31
60
11
74
63 j 36
i1
FIBRE CONCENTRATION
1 0 6 FIBRES PER GRAM
OF DRY TISSUE
0,6 0,3 0,6 1,3 0,7 1,5 0,4 0,4 1,0 0,7 ;o,8 0,5 0,8
* FIBRES WITH
POSITIVE ASBESTOS
IDENTIFICATION
% OF TOTAL NUMBER
44
33
8
17
20
13
-
-
COATED FIBRES % OF
TOTAL NUMBER
FIBRE LENGTH<5 um
% OF TOTAL NUMBER
FIBRE DIAMETER<1 pm
% OF TOTAL NUMBER
j
i
8,7
i
43
37
55 ;
94~'
OCCUPATIONS
CORK WORKER
+
+
WELDER
+
INDUSTRIAL WORKERS
+
+
\
+
+
+
+
"TAXIDRIVER
+
HOUSEWIFE
+
SCHOOLGIRL
+
OTHER OCCUPATIONS
...
+
CAUSES OF DEATH
BRONCHIAL CANCER
+.
+
+
HEART DISEASE
+
+
+
+
ACCIDENTS
OTHER CAUSES
+
+
OTHER CANCERS
+
+
1
+
• 1-
39*
+
REFERENCES:
1.
Ashcroft, T. and Heppleston A.G.: The optical and
electron microscopic determination of pulmonary asbestos
fibre concentration and its relation to the human
pathological reaction.
J. Clin. Path. 26 (1973) 224-234.
2.
Blgnon, J., Sebastien, P., Fondimare, A, Bonnaud, G.,
Gaudichet, A., Janson, X. et Monchaux, G.: Etude quantitative et qualitative des fibres d'amiante dans
l'appareil respiratoire humain. Contribution a l'évaluation du risque cancérigène pour la population generale.
Rapport de Institut de Recherche Universitaire sur
l'Environnement, Paris 1978.
3.
Gylseth, B., Ophus, E.M. And Mowé, G.:
Determination of
fibres in human lung tissue by scanning electron microscopy. Submitted for publication in Scand. J. of Work
Environ » Health.
4.
Heppleston, A.G.: Correlation between the tissue response
and asbestos fibre content. Environ. Health Perspect. 9
(1974) 147-148.
5.
Jaurand, M.C., Bignon, J., Sebastien, P. and Goni, J.:
Leaching of chrysotile asbestos in human lungs.
Environ. Research , 14 (1977) 245-254.
6.
Pooley, F.D.: Electron microscope characteristics of
inhaled chrysotile asbestos fibre. Brit. J.of Ind.
Med. 29 (1972) 146-153.
7.
Pooley, F.D.: The identification of asbestos dust with an
electron microscopi microprobe analyser. Ann. Occup.
Hyg. 18 (1975) 181-186.
8.
Selikoff, I.J., Hammond, E.C. and Seidman, H.: Cancer
risk of insulation workers in the United States.
In P. Bogovski, V.Timbrell, J.C.Gilson and J.C.Wagner (eds).
Biological effects of asbestos. Proceedings of a Working
Conference held at the International Agency for Research
on Cancer, 2-6 October 1972. Lyon,France, 1973. pp 209-216.
395
?
Stanton, M.F., Layard, M., Tegeris, A., Miller, M.
and Kent, E.: Carcinogenicity of Fibrous Glass:
Pleural Response in the Rat in Relation to Fiber
Dimension. J. Natl. Cancer Inst. 58 (1977) 587-603.
Whitwell, F., Scott, J. and Grimshaw, M.:
Relationship between occupations and asbestos-fibre
content of lungs in patients with pleural mesothelioma,
lung cancer and other diseases. Thorax, 32 (1977)
377-386.
396
SILICA DUST-ASSOCIATED PULMONARY LESIONS IN GRANITE WORKERS
LACKING RADIOLOGIC EVIDENCE OF DISEASE
N. Vi Vallyathan, and John E. Craighead
Department of Pathology, University of Vermont
College of Medicine, Burlington, VT, USA
INTRODUCTION
Inhalation of particles containing silica results in silicosis
after prolonged periods of exposure. The disease is characterized
anatomically by diffuse fibrosis and the presence of discrete fibrotic nodular lesions located in proximity to the respiratory
bronchioles, arterioles, septae and pleura.
These nodules contain
loosely arranged, hyalinized collagen in the center and reticulin
fibers in the periphery.
In Vermont's granite industry, the widespread occurrence of
silicosis and an increased susceptibility to tuberculosis were the
scourge of workers during the early decades of this century.
Sub-
sequent to the institution of dust controls in 1937, a substantial
decrease in the prevalence of silicosis was documented in annual
chest roentgenogram surveys (Hosey et al., 1957).
This was
attributed to the lowering of environmental dust concentrations
to 10 million particles per cubic feet (mppcf) from an average of
60 mppcf before enforcement of controls (Hosey et al., 1957).
At present environmental dust concentrations, it has been
shows that prolonged exposure is necessary to induce changes in
chest radiograms and ventilatory function (Hosey et al., 1957|
Theriault et al., 1974b,c).
Since clinical expression of the
disease occurs only after an elapsed period of years, it is not
known whether subtle degrees of pulmonary fibrosis occur
397
in
workers lacking radiological abnormalities and clinical symptoms.
This investigation was undertaken to determine the extent and
severity of subclinical disease and its progression in the lungs
of workers employed in the Vermont granite industry since the
institution of controls in 1937.
It was designed to determine
whether or not current radiological and physiological techniques
are adequate to detect and monitor the development and progression
of cryptic disease.
MATERIALS AND METHODS
Samples of lung tissue from 15 workers who had been employed
in the Vermont granite industry since 1937 were studied.
Fourteen
of these specimens were obtained at autopsy and one by lung biopsy.
Occupational records were reviewed to confirm that none of the
cases had been employed in a dusty trade before 1937 and to determine the duration and type of industrial exposure.
For pur-
poses of comparison, studies also were carried out on autopsy tissue from four subjects who had been employed as granite workers for
varying periods of time both before and after 1937.
The Vermont Department of Occupational Health maintains health
and industrial dust exposure records on wotrkers employed in the
state's dusty trades.
Annual chest radiograms are available on
most of these workers, and the results of pulmonary function
studies and smoking histories are known on many.
The most recent
available chest radiogram on each of the cases was examined by a
member (B reader) of the panel of the UICC Committee who had no
knowledge of the origin of the x-ray.
Lifetime dust exposures
and dust years were calculated according to the method of Theriault
et al. (1974a).
Table I summarizes the available health and in-
dustrial exposure information and the primary cause of death.
398
Lung samples, either in paraffin blocks or formalin, were
processed for light microscopy, and 10 serial sections of 7 nm
thickness were prepared.
The first and tenth sections were
stained with hematoxylin and eosin and studied by light and
polarized light microscopy.
Adjacent serial sections 2 through
9 were used in scanning electron microscopic (SEM) studies employing secondary and backscattered imaging and mapping techniques.
Sections were placed on carbon planchets, deparaffinized,
carbon coated and examined by SEM.
Elemental analyses were made
according to the method of Brody et al. (1978).
Integrated x-ray
counts for Mg, Al, Si and Fe were made for 100 seconds and corrected
for background by the subtraction of calculated bremsstrahlung
derived by the channel averaging technique (Brody et al., 1978).
For these studies a JEOL JSM-35 SEM with a Kevex 5100 series x-ray
spectrometer were used.
Quantitative x-ray fluorometric analysis on lyophllized lung
tissue and x-ray crystallographic studies on tissue digestates
were made in those cases where tissue was available.
Particle
analyses on tissue digestates also were made when tissue was
available.
RESULTS
Table I summarizes exposure data and the results of clinical
and pathological findings on the 15 patients in this series.
As
can be seen, radiological abnormalities suggestive of either pulmonary fibrosis or silicosis were not evident in the lungs, and
pulmonary insufficiency was not prominent in functional tests.
Although 5 of the 15 had bronchogenic carcinomas, the series is
highly selective, and no conclusions regarding the possible car-
399
cinogenlc effect of silica exposure can be made.
Analysis of silicon in selected, localized fibrotic areas
of the lung by x-ray spectrometry demonstrated substantial concentrations of this element (Fig. 1). Interestingly enough, the
silicon in the tissues of individuals with long periods of
exposure (Table II) and overt silicosis was not substantially
greater than amounts found in the pulmonary tissue of the cases
comprising this series (Fig. 1 ) .
The lungs of each of the 15 patients exhibited varying degrees
of focal fibrosis (Figs. 2,3) and, in one case, localized nodular
lesions typical of silica dust exposure (Figs. 4,5). In none of
the patients was the fibrosis severe or confluent.
Crystalline
particulate matter was rarely found in these lesions by polarized
light microscopy, although it was readily demonstrable by backscattered scanning electron microscopy (Figs. 6-9). XES analysis
and x-ray mapping techniques were employed to further characterize
dust particles in these lesions and in tissue digestates (Figs. 10,
11).
These techniques proved essential in relating lesions to
silica dust deposition.
DISCUSSION
The prevalence of silicosis and silico-tuberculosis among
Vermont granite workers prompted a series of epidemiological investigations that resulted in the institution of dust control
measures in 1937 (Russell et al., 1929¡ Russell, 1941¡ Urban,
1939).
Russell et al., (1929) demonstrated a correlation between
exposure levels in different workplaces and the incidence of
silicosis.
These studies led to the conclusion that a safe
dust level in the granite industrv would be 9 to 20 mppcf.
4oo
After the institution of the present threshold limit value
of 10 mppcf In 1937, there was a considerable decrease in the
prevalence of silicosis, from a high of 43% before 1937, to a
low of 16% as monitored by chest radiograms (Hosey et al., 1957).
Further evaluations of workers employed in the industry for periods
of as long as 26 years since 1937 showed no silicosis by chest
roentgenograms (Ashe and Bergstrom, 1964).
However, recent
studies on the pulmonary function of granite workers have shown
a decrease of 2 ml/dust year after corrections were made for
ancillary contributing factors (Theriault et al., 1974b,e).
Nevertheless, an average of 32.5 dust years was found necessary
to affect the ventilatory function of 50% of workers and an average
of 46 years of dust exposure was associated with abnormalities in
50% of the x-rays (Theriault et al., 1974b,c).
It is evident
from these studies that the effects of dust on pulmonary function
seem to appear before radiological changes. Clearly, the clinical
expression of disease as reflected either in pulmonary ventilatory
function or radiological abnormalities is delayed due to the extended latency period of the disease.
Histopathological study of the lungs of our cases, with exposure histories ranging from 5 to 30 years, documented the presence
of subclinical disease. Analyses by XES suggest a rough correlation
between the severity of fibrosis and the concentration of silicon.
However, it was of interest to note that the amounts of silicon in
individual lesions often approximated the quantities demonstrated
in the lesions of lungs exhibiting classical silicosis. This observation supports the view that silicosis is a progressive process
resulting in the deposition of increasing amounts of fibrous tissue
with the passage of time. Thus, a reduction in dust exposure may
only reduce the number and distribution of discrete lesions which
4o1
ultimately develop in the lung.
Although histopathological studies showed extensive pulmonary fibrosis, polarized light microscopical studies usually
failed to detect dust particles in fibrotic lesions.
However,
when the same lesions were studied by scanning and backscattered
electron microscopy with x-ray microanalysis and x-ray mapping
techniques, it was possible to document the presence of crystalline
silica.
These modern approaches make possible cause and effect
associations that otherwise would not be possible.
ACKNOWLEDGMENTS
This work was supported by U.S. Public Health Service grant
#PHS 17292-04/3 to the Vermont Lung Center.
The contributions of
Drs. Jane Brisbane, Leonard Bristol, Arnold Brody, Roy Buttles,
Robert Christie, Peter Dietrich, Larry Fine and John Froines are
gratefully acknowledged.
Ms. Phyllis Alexander, Ms. Lena Bizzozero,
Ms. Judy Kessler, Ms. Marilyn White and Mr. Loren Hahn provided
excellent technical assistance.
4o2
REFERENCES
Ashe, H.B. and Bergstrom, D.E.: Twenty-six years' experience with
dust control in the Vermont granite industry. Industr. Med. Surg.
33:73-78, 1964.
Brody, A.R., Vallyathan, N.V. and Craighead, J.E.: Use of scanning
electron microscopy and x-ray energy spectrometry to determine
the elemental content of inclusions in human tissue lesions.
In : Scanning Electron Microscopy, Vol. II, SEM, Inc. (Johari,
0, ed.), Chicago, 1978, pp. 615-622.
Hosey, A.D., Trasko, V.M. and Ashe, H.B.: Control of silicosis in
Vermont granite industry. U.S. DHEW Pub. No. 557, 1957.
Russell, A.E.: The health of workers in dusty trades. VII. Restudy of a
group of granite workers. U.S. Govt. Printing Office, Public Health
Bulletin #269, Washington, 1941, p. 71.
Russell, A.E., Britten, R.H., Thompson, L.R. and Bloomfield, J.J.:
The health of workers in dusty trades. II. Exposures to siliceous
dust (Granite Industry). U.S. Govt. Printing Off., Public Health
Bulletin 187, Washington, 1929.
Theriault, G.P., Burgess, W.A., DiBerardinis, L.J. and Peters, J.M.:
Dust exposure in the Vermont granite sheds. Arch. Environ. Health
28:12-17, 1974a.
Theriault, G.P., Peters, J.M. and Fine, L.J.: Pulmonary function in
granite shed workers of Vermont. Arch. Environ. Health 28:18-22,
1974b.
Theriault, G.P., Peters, J.M. and Johnson, W.M. : Pulmonary function
and roentgenographic changes in granite dust exposure. Arch. Environ.
Health 28:23-27, 1974c.
Urban, E.C.J.: Ventilation in the granite industry. J. Ind. Hyg. Toxicol. 21:57-65, 1939.
4o3
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4o5
ABSTRACT
In Vermont's granite industry, the widespread occurrence of
silicosis and increased susceptibility to tuberculosis was the
scourge of workers prior to 1937.
Subsequent to the institution
of dust controls in 1937, a significant decrease in the incidence
of silicosis was documented by annual chest radiograms•
Since clinical expression of the disease occurs only after
prolonged exposures to dust, it is not known whether subtle degrees
of pulmonary fibrosis are occurring in workers lacking radiological
abnormalities and clinical symptoms.
This investigation was under-
taken to determine the extent and severity of fibrosis and concentrations of dust in the lungs of workers employed after 1937 and to
ascertain whether current radiological, physiological and histopathological techniques are adequate to diagnose and monitor the
development of cryptic disease.
Fifteen workers employed since 1937 and four who had worked
in the granite industry before 1937 were studied using light and
polarized light microscopy, scanning and backscattered electron
microscopy, x-ray energy and x-ray fluorescent spectrometry and xray crystallography.
Chest radiograms and pulmonary function tests
conducted on these subjects over a period of years prior to their
deaths were evaluated and dust exposure data was assessed.. These
correlative studies indicate that subtle dust-related fibrotlc
lesions are present in the lungs of granite workers who exhibited
no specific radiologic abnormalities and limited pulmonary function
disability premortem.
These findings suggest that the dust ex-
posure limits currently employed in the industry must be questioned.
4o6
Pruebas hlstopatolÓRlcas de la
prevalencta de silicosis asintomática
entre los trabajadores del granito.
N. V. Vallyathan y J. E. Craighead
(Estados Unidos)
En la industria del granito del Estado de Vermont,
hasta 1937 amenazaba a los trabajadores una silicosis generalizada y una gran susceptibilidad a la tuberculosis.
Gracias a la creación de controles de polvo en ese año,
las radiografías toráxlcas anuales revelaron un importante descenso en la incidencia de la silicosis.
Como la expresión clínica de la enfermedad sólo surge al cabo de una prolongada exposición al polvo, no se
sabe si entre los trabajadores que no presentan anormalidades radiológicas o síntomas clínicos no se está produciendo en grado sutil una fibrosis pulmonar. Esta investigación fue emprendida para determinar la extensión y la
gravedad de la fibrosis y las concentraciones despolvo en
los pulmones de los trabajadores empleados después de
1937, para verificar si las técnicas tradicionales radiológicas, fisiológicas e hlstopatológlcas son adecuadas
para diagnosticar y controlar el desarrollo de una enfermedad críptica.
Se examinaron 15 trabajadores que habían trabajado
desde 1937 y cuatro que habían trabajado en la Industria
del granito antes de esa fecha, utilizando la microscopía
óptica con luz polarizada, la microscopía electrónica por
centelleo y retroreflejo, la energía con rayos X, la espectrometría fluorescente con rayos X y la cristalografía
con rayos X. Se compararon las radiografías toráxlcas, la
función pulmonar y la exposición al polvo con la gravedad
de la fibrosis y las concentraciones de polvo. Se obtuvieron pruebas hlstopatológlcas y cuantitativas de la presencia de silicosis asintomática.
4o7
THE ROLE OF PULMONARY TUBERCULOSIS IN THE CAUSATION OF
PROGRESSIVE MASSIVE FIBROSIS IN COAL WORKERS IN GREAT
BRITAIN
J. A. Dick, United Kingdom
The National Coal Board of Great Britain set up Its
Periodic X-ray Service In 1958 with two principal objectives.
These were firstly to offer the Individual miner a chest xray at his working place and by achieving a high response rate
to establish the real national prevalence of Coal Workers'
Pneumoconiosis, the most Important occupational hazard In the
Industry, and secondly to use serial x-rays as a monitor of the
effectiveness of dust suppression.
Mobile x-ray units taking
full-size films visited every colliery In all coal fields and
employing suitable propaganda endeavoured to x-ray as many men
as possible.
Five years were required to complete the first
round of surveys. The scheme was entirely voluntary, but over
85 percent of men attended (current response Is 92 percent).
The films were classified for Coal Workers' Pneumoconiosis using
the ILO (1958) Classification of Radiographs of Pneumoconioses,
and it was thus possible to obtain the national and regional
prevalences of this condition In the British Coal Mining Industry.
It soon became clear, as Table 1 shows, that there was a
wide range In the prevalence of pneumoconiosis In the various
coal fields, and Table 2 Indicates that since 1959-63, although
there has been a significant decline in overall prevalence,
regional variations remain virtually unaltered.
4o9
TABLE li
Prevalence of Pneumoconiosis in the Coalfialds of Great Britain
1959 - 1963
AREA
HEN
X-RAYED
CAI 1
CAT 2
CAT 3
•iCTAL
SIMPLE
PNEUMOCONIOSIS
PMP
TOTAL
Soottisb
53,849
3.0
w
0.3
.5.4
0.3
5-7
North East
94,624
9*1.
2.5
O.4
11.9
0.8
I2.7
North Yorkshire
23,214
7.5
4.2
O.4
12.1
0.6
I2.7
Donoaster
23,092
8.0
3.9
0.5
I2.4
0.8
13.2
Barnsley
27,776
6.2
3.8
0.4
IO.4
1.0
II.4
South Yorkshire
26,91S
7.4
4.2
0.3
12.0
0.7
I2.7
North Derbyshire
23,143
3.4
2.1
0.4
3.9
0.3
6.2
North
Nottinghamshire
24,075
3.4
2.2
0.4
6.0
0.5
6.5
South
Nottinghamshire
21,760
3.1
1.9
0.2
5.1
0.2
5.3
South Midlands
18,421
2.7
1.3
0.1
4.0
0.2
4-2
Western
61,966
5.6
4.0
1.2
10.8
1.2
12.0
South Wales
60,286
14.O
5-9
I.7
2I.7
3.6
25.3
3,875
7.6
4-3
1.4
13.4
2.1
15.5
462,999
7.0
3.3
1 0.7
11.0
1.1
Kent
GREAT BRITAIN
12.1
1
4-1 o
TABLE 2: Pra/tilcnce of Pneumoconiosis in tho Coalfields of Great Britain
1974/75
AREA
Scottish
. 1
TOTAL
¡ PMP
SIMPLE
PNEUMOCONIOSIS ;
CAT 1
CAT 2
2.1
0.2
0.0 1 2.4
i
0.1
2-5
i
1
7.9
¡
0.3
8.2
CAT 3
TOTAL
PREVALENCE
North East
6.5
1.3
0.1
Forth Yorkshire
5.4
2.2.
0.1
7,
|
0.5
8.2
Donoaster
5.1
2.2
0.0
7.3
¡
O.4
7.8
Barnsley
4.7
1.6
0.2
6.4
0.6
7.0
South Yorkshire
4.4
1.5
0.1
6.0
0.3
6.3
North Derbyshire
4.8
1.1
0.0
5.9
0.2
6.1
North
Not t inghamshire
4.1
1.2
0.1
5-4
0.6
6.0
South
Not tineham3hire
4.0
0.7
0.0
4.7
0.2
4.9
South Midlands
2.6
0.3
0.1
3.0
0.2
3.2
Western
5.1
2.0
0.3
7.4
0.6
8.0
13.9
3.9
0.3
! 18.0
3.2
21.2
Kent
5.2
1.4
0.1
6.8
0.5
7.3
GREAT BRITAIN
5.9
1.7
0.1
7.7
0.7
8.4
South Wales
.
411
In planning the Perlodix X-ray Scheme It was recognised that
adequate records of surveys and of individual miners must be
maintained! and from the outset as much detail as possible has
been stored in computer tape at
Centre.
the National Coal Board Computer
Information for each miner who had a chest x-ray included
agef place of work, pneumoconiosis (recorded in category of the
ILO Classification) and the presence of other pathology.
As the
individual miner had successive chest x-rays so the national computer file was updated to include the latest information.
It was
thus possible to publish a yearly national prevalence (i.e. for
one fifth of the total population) and a quinquennial prevalence
for the entire industry.
As the programme developed it became evident that the Periodic
x-ray Service was accumulating a mass of data unlikely to be
available to other organisations involved in the problem of
Coal Workers' Pneumoconiosis, and for this reason it appeared to
be highly desirable to make use of periodic x-ray data in an
effort to make some contribution to the understanding of Coal
Workers' Pneumoconiosis.
It is generally agreed that, inter alia, there are two
principal problems in the field of pneumoconiosis for which, as
yet, no satisfactory explanation has been given. The first is What determines individual susceptibility to dust?
The second -
What causes the change from simple to complicated pneumoconiosis
in the individual miner?
It seems probable that from the data
available some contribution could be made to the problem of
complicated pneumoconiosis.
So far as is known a long-term
follow-up of Progressive Massive Fibrosis has not been made.
412
It was therefore, decided that an attempt should be made to
Identify all new attacks of Progressive Massive Fibrosis developing in the second survey period.
An attack of Progressive
Massive Fibrosis would be defined as the occurrence of categorisable complicated pneumoconiosis in an individual attending
for x-ray in the second round of surveys (1964-68) who had
also attended during the first round of surveys (1959-63) and
whose film then did not show complicated pneumoconiosis.
Having
identified such individuals! an effort would be made to establish,
as far as possible, the natural history of each man up to the
date of the investigations (1975-76), approximately ten years
later.
Method
In order to ensure as accurate a diagnosis as possible it was
decided to use data from epidemiological readings as this ensured
that two opinions were available for each pair of films.
Since the inception of the Periodic X-ray Scheme the coalmining population has changed drastically and, in theory, changes
in prevalence could be explained by the selective departure (or
retention if prevalence was static or increasing) of men with
pneumoconiosis. To overcome these difficulties of changing
populations a special study is made of men who have remained at
their own colliery throughout the interval between surveys. At
each colliery a sub-population is selected for special study.
These are men who were x-rayed on both the current and previous
surveys, and who were employed on the coalface at the time of
the earlier survey.
Each man's pair of films is assembled in
413
ten batches i corresponding to twice the number of doctors engaged
In film reading.
Two batches are sent to each doctor who, after
recording his assessments of pneumoconiosis on each pair of
films passes each batch to a different check reader, who does
the same.
From these readings an Index summarising the changes In
the x-ray films of the colliery sub-population Is obtained«
This
Index Is to be Interpreted only as a means of ranking the collieries
In terms of x-ray changes which are considered to reflect Increased
dust retention«
All attacks of Progressive Massive Fibrosis agreed by two
readers were automatically Included In the population to be studied«
Although agreement between readers on the diagnosis of Progressive
Massive Fibrosis Is generally very close, there Is Inevitable some
difference of opinion at the level of the lower limit of Category
A.
Those cases showing some disagreement were reviewed by all
the Board's readers and a majority consensus reading obtained«
If the consensus was In favour of Progressive Massive Fibrosis
the Individual concerned was Included In the study, If not he was
excluded«
The use of epidemiological data automatically reduced the
numbeis of men available for study«
However, of the sub-population
of 112,000 who had chest x-rays between 1959 and 1963 and again
five years later, 237 were selected on the basis noted above.
3 gives their distribution over the various coalfields In the
United Kingdom together with the prevalence In each coalfield
at that time.
414
Table
TABLE 3i Distribution, by coalfield and age group, of men selected
to be followed up, and prevalence at the time of the PMF
attack.
AGE CROUP (ACE AT DECEMBER 1976)
COALFIELD
UNDER
35 to
35
44
-
-
-
1
-
2
3.2
North East
1
7
18
32
62
13.0
Yorkshire
-
1
23
i 36
65
10.9
Scottish
45 to
54
65 to
74
55 to
64
75 and
above
TOTAL
TOTAL
PREVALENCE
1964-1963
i
Western
-
1
2
Î 18
24
9-7
East Midlands
-
2
5
i 11
19
5-3
South Wal«s
-
13
20
25
59
23.5
-
-
3
3
-
6
U.9
1
24
72
15
237
10.7
-
Kent
CHEAT BRITAIN
1 125
The precise stimulus for the change from simple to complicates
pneumoconiosis is not understood and It may be that there Is no
single stimulus common to all cases.
Nevertheless, It Is general-
ly accepted that the principal factor probably lies in one of the
following - pulmonary tuberculosis, silica, total dust exposure,
immunological reaction and finally other respiratory trauma such
as lung infection.
This paper reports the findings on the place
of pulmonary tuberculosis in the population studied.
The first step in the investigation was to establish whether
or not an Individual was still alive and if so his current address.
It will be seen that of the 237 subjects in the sample 184 were
415
still alive, but many had moved to parts of the country Inaccessible
to the Medical Service. Of the remainder still living without coalfield areas it was possible to personally interview 97 and to contact by postal questionnaire a further 43. Twenty-four men were
traced but could not be personally contacted and 20 could not be
traced.
Fifty-three men had died and details of death certificates
were available for 51. Thus of the total sample there were 21 men
for whom no information of any kind, other than their initial radiological appearance, was available. Analysis of these men did not
indicate any significant bias and they were therefore excluded from
the investigation, thus leaving a total of 216.
In addition to the clinical details available from completed
questionnaires, further information was obtained by scrutiny of
hospital and Pneumoconiosis Medical Panel records, which were
readily made available.
For this reason all results are expressed
as a percentage of the total sample (216).
Initial scrutiny of the data available indicated as Table 4
shows that there were 11 cases of positive sputum from 172 examined.
In addition there were 3 individuals who appeared to have some
suggestion of pulmonary tuberculosis although sputum was negative.
Therefore, there appeared to be 14 cases to be followed up clinically.
Despite considerable efforts it was not possible to obtain any
more information in one cases. Detailed examination of the clinical
records showed that of the 13 remaining 8 were sputum positive, a
further 2 were diagnosed firmly as tuberculosis on clinical and
radiological grounds and were treated by chemotherapy.
There were,
therefore, 10 cases in all which could be regarded as definitely
416
tuberculosis giving 4.2 percent of the total numbers followed up.
All 10 cases were treated with anti-tubérculous drugs.
In no case
did this have any beneficial effect on the extent of the PMF lesions i
on the contrary, in at least one case tuberculous cavitation took
place while the patient was on therapy.
The average age of those
who were known to be still alive was 63.5 years. Two men with
positive tuberculosis who were known to have died had an average
age of 64 years.
TABLE 4i Sputum « Examined directly and culture
COALFIELD
POSITIVE
CULTURE
DIRECT
NEGATIVE
NOT EXAMINE])
TOTAL
Scottish
-
-
-
2
2
North East
-
1
12
13
25
Yorkshire
1
2
24
39
64
-
7
3
Western
• -
15*
East Midlands
1
1
14
1
16
South Wales
-
3
24
21
45
Kent
1
•H
4
-
5
85
79
172*
_
GREAT BRITAIN
* Including 5 examinations without results
417
TABLE 5i
Distribution of the cases of active tuberculosis and
distribution of categories of pneumoconiosis.
— — — — — '
COALFIELD
NO.
CATEGORY C?
PKEOKOCOMZJSIS
Scottish
-
-
North East
i-i
IB q
Yorkshire
2
2B q
2B q
Testern
2
OA
3Í. q
East Midlands
1
IC q
South Wales
3
IC q
Kent
1
2A q
1C x
1A q
It is interesting to note that, with one exception, the small
opacities were all "q" type and that there were no "p" type opacities present in any of the casest
Numbers involved were so
small as to make it unlikely that the absence of "p" type opacities is of any significance.
In only one case had the Rheumatoid Arthritis Screening Test
(RAST.) been carried out and was negative.
In only one case
were the radiographic appearances considered to resemble Caplan
type change.
In summary, of 237 attacks of complicated pneumoconiosis,
10 were proved to have preceding or concommitant pulmonary
tuberculosis.
If clinical improvement resulted from anti-
mi 8
tuberculous therapy could be accepted as adequate evidence that
the lung lesion was In fact due to tuberculosis then this figure
could be Increased to 12 giving a percentage of 5.06.
Deaths
It is routine practice in the United Kingdom when a miner
dies and has, or is thought to have, pneumoconiosis that his death
is reported to the District Coroner.
Invariably a post-mortem is
carried out and on /'the basis of the pathologist's report the coroner
decides the cause of death.
lungs
In addition it is customary for the
of any deceased miner to be forwarded to the nearest Pneumo-
coniosis Medical Panel office where they are examined by Panel
pathologists.
It is the responsibility of the Panel to decide what
part, if any, pneumoconiosis played in the cause of death, and this
decision influences the payment of compensation to dependants.
From these two sources of information it is possible to obtain
accurate information on the causes of death and to decide what
contribution, if any, pneumoconiosis made to death.
Table 6 gives the primary cause of death for 54 men on whom
post mortems have been carried out, and it will be seen that in no
case was tuberculosis considered to be a primary cause of death
as stated in the death certificate. As it is possible that the
real cause of death may not be the primary cause of death, the death
certificates were re-examined and the results of the re-examinâtion
(see Table 7) once again shows that in no single case was tuberculosis considered to be a factor either primary or principal.
419
TABLE 61 Deaths - Various pathologies
CWP CARDIO
VENTRICULAR CIÎ2ST
' VASCULAR HÏPERTROFHÏ INFECTION
COALFIELD
Scottiah
1
"
_
North East
.- '
1
ÇA : PTB OTHERS ' NO
LUHG
1
RECORD
1
-
-
-
-
-
3
5
4
2
-
2 .
1
Yorkshire
-
4
1
2
1
-
5
j?
Eestern
1
3
1
2
-
-
2
-
East Midlands
2
-
-
-
2
-
-
-
louth Wales
2
-
-
1
-
3
-
Kent
1
.
2
-
-
-
-
-
-
CREAT BRITAIN
.
15
7
8
6
-
12
:1
!
TABLE 7,: Deaths - Pathology on Re-Examination
COALFIELD
cup !
CARDIO
1VASCULAR |
VENTRICULAR
HYPERTROPHY
cnnsT
CA
INFECTION
LUNG
PTB
1
-
-
-
-
North East
8
3
W
1
2
-
Yorkshire
f-i
5
-
1
1
Testern
3
3
-
1
-
East
Midlands
2
-
-
-
South Vales
1
2
-
-
Kent
1
-
r-l
-
! 16
I
"
2
"
1
5
f.
-
2
-
2
-
-
-
1
-
3
-
"
12
14
42o
NO
RECORD
Soottish
GREAT BRITAIN
OTHERS
It would apprear from this Investigation that pulmonary
tuberculosis Is not a principal factor In the causation of progressive massive fibrosis In British miners.
It may well be, how-
ever, that a ten-year follow-up Is not adequate. To Increase the
period of follow-up would present formidable epidemiological
problems because of the difficulty of tracing men and because
of the significant number likely to have died.
421
Función de la tuberculosis pulmonar como
causa de la fibrosis masiva progresiva en
los mineros del carbon.
J. A. Dick (Reino Unido)
No cabe duda de que la etiología de la evolución de
la fibrosis masiva progresiva sigue siendo uno de los
interrogantes, importantes en la historia natural de la
neumoconiosis. En diversas épocas se han intentado
explicaciones diferentes y tal vez la más difundida ha
sido que la tuberculosis pulmonar desempeña una importante función en la patogénesis de la fibrosis masiva.
En el presente trabajo se exponen las constataciones del
estudio a largo plazo de pacientes que han sufrido nuevos ataques de fibrosis masiva durante el período 19591963 a 1964-1968. Se describe el método utilizado para
seleccionar los casos al mismo tiempo que los problemas
que se presentaron para encontrar esas personas y obtener información de ellas. Se exponen las constataciones
clínicas con especial referencia a la tuberculosis pulmonar. Se llega a la conclusión de que la tuberculosis
pulmonar no desempeña una función preponderante como causa de la fibrosis masiva progresiva entre los mineros
británicos.
422
THE HIGHER OXIDES OF NITROGENI
A ROLE IN ALTERING PULMONARY RESPONSE TO INJURY?
Tee L. Guldottl,
Department of Environmental Health Science,
The Johns Hopkins School of Hygiene and Public Health,
Baltimore, Maryland, USA
In considering the pathophysiology of occupational lung
diseases, we customarily treat each exposure as a separate clinical entity.
Yet we know that this Is an oversimplification!
combined exposure Is probably the rule rather than the exception
In occupational settings»
With our rapidly developing state of
knowledge, we now have sophisticated concepts and techniques which
allow us to examine our previous simplifying assumptions. Among
these assumptions has been the concept that an occupational lung
disease, such a pneumoconiosis, consists of the specific tissue
response to a particular Inhaled agent. We are now In a position to
admit the possibility that the tissue reactions to Inhaled dusts
In the pneumoconioses may be altered by simultaneous exposure to
non-partlculate inhalants.
If It Is true that non-partlculate Inhaled agents may modify
the tissue response to particles, then an appropriate model for
this phenomenon would be nitrogen dioxide.
Nitrogen dioxide
(N02) and the other higher oxides of nitrogen may coexist with airborne particulates In a number of occupational settings.
In arc
welding, N0 ? may accumulate to high concentrations In enclosed
2 3
spaces.
In underground mining operations, N0 2 may be present
as a consequence of explosive detonation ' or in much lower quantities from diesel exhausts.
In agriculture occasional exposure
423
to NO? results in the well-recognized condition called silo
fillers' disease, and may coexist in the same worker with inhalation of organic dusts.
Most studies of particulate inhalation and toxic gas inhalation examine the effects of exposure to individual agents. This is
the first necessary step in understanding the process of tissue
injury and repair, but studies of individual exposure cannot adequately describe the common situation of sequential or simultaneous
inhalation of more than one potentially toxic inhalant.
The oxides
of nitrogen, particularly NO,, are now among the best understood
toxic gases, and a large body of work is available describing their
effects on the lung.
It seems appropriate to select NO, as a model
to explore the question of whether the pulmonary response to injury,
especially in the pneumoconioses, may be modified by a toxic gas.
Few studies have examined the effects of mixed exposures to
particulates and to NO,.
Some of these have investigated the role
of particles as vehicles for the deeper penetration of NO, into
the lung.
In the studies of Boren, respirable carbon particles
saturated with adsorbed NO, were inhaled by mice.
Compared to
animals inhaling either NOj or carbon particles alone, combined
exposure resulted in focal alveolar simplification associated with
carbon deposits and a reduction in infiltration by macrophages.
On the other hand, in the work of Furiosi, Crane and Freeman
simultaneous exposure to only 2 ppm of NO,, and to aerosolized
sodium chloride did not appear to produce a pattern different from
NO,
alone in mice.8
J
2
Another line of investigation has considered the possibility
of interactive or additive effects of combined exposure to NO,
424
and particles which are fibrogenic.
Studies by Daniel-Moussard
and Lewis and their colleagues bear on this question.9' 10
Rats exposed to both NOy and either anthracite or quartz dust had
a higher frequency of anthracotic and silicotic plaques after 5
q
to 8 weeks compared to animals inhaling the dusts alone.
After
3 months, the dry weight and the collagen content in lungs of rats
exposed to both NCK and quartz dust were higher than in lungs exposed to either alone, but the combined effect appeared roughly
q
additive.
Beagles chronically exposed to NO, and to ferric
3 11
oxide particles, a dust which is usually well tolerated,
developed increased airway resistance compared to animals chronically exposed to NCK alonei this suggest an interaction.
Gross et al, exposed guinea pigs intermittently to high doses
of NC>2 at variable concentrations, about 44 ppm for most of the experiment.
They followed this with intratracheal injection of
quartz, coal, or blast furnace stack dust, the latter containing
Fe2no, Situ, AljO-j, and carbon. They found a partially protective
effect, with the highest mortality in the group exposed to quartz
dust alonet there was no association between emphysematous changes
attributed to NO^, and the distribution of pneumoconlotie plaques.
12
It is difficult to interpret the results of this study because of
the unusual exposure pattern, the low incidence of emphysematous
changes compared to other studies, the use of both guinea pigs and
hamsters (the latter known to be relatively resistant to the effects
of NO2 ), and the use of water rather than normal saline as the
vehicle for intratracheal instillation of the dusts (hypotonicity
13
is known to disrupt macrophage activity ) . Nonetheless, this one
study offers tentative evidence for inhibitory interactions be-
425
tween N0 2 and flbrogenic dusts.
Lacking more definitive data on combined exposure, it may be
useful to examine the basic pathophysiology of NO2 In order to identify processes by which the handling of dusts may be disturbed.
In a set of experiments performed on dogs,
we adapted a
technique of unilateral bronchial intubation which had originally
been developed in 1930 by Van Allen for studies on collateral ventilation.
The technique involved intubating the anesthetized ani-
mal with a stainless steel cannula and then passing the cannula into
the left main bronchus (Figure 1).
This bronchial cannula had an
expandable head which sealed the bronchial lumen (Figure 2).
The
left lung could then be ventilated through the bronchial cannula
and the right lung could be ventilated through the intratracheal
cannula.
This system
has a number of practical advantages in
studies of acute toxic inhalation.
The clearance mechanisms of
the upper airway are bypassed, permitting delivery of a constant,
known concentration of gas to the lower respiratory tract. The
contralateral lung may be ventilated with room air or oxygen, and
serves both as a control and to support the animal through the experiment.
Using this system, we exposed 5 anesthetized beagles to 37.2
ppm NC>2 delivered to the left lung for 4 hours. The opposite lung
was ventilated with room air, containing no detectable N0 2 . We
measured oxygen uptake by each lung at intervals and at the
con-
clusion of the exposure sacrificed the animals with an intravenous
bolus of barbiturates and fixed the lungs by bronchial and intraarterial infusion of glutaraldehyde under physiological pressures.
We then examined the parenchymal tissue of both lungs by transmission electron microscopy and compared them using the morphometric techniques developed by Weibel and colleagues.16
426
We found an early, reversible decline in oxygen uptake in the
exposed (left) lung compared to the unexposed (right) lung, a difference best explained by induction of a ventilation-perfusion
inequality.
Morphologically and morphometrically, we found swell-
ing and increased numbers of pinocytotic vesicles in the capillary
endothelium of the exposed lung, associated with early interstitial
edema, with little visible epithelial damage (Figures 3 and 4 ) .
Morphometrically, the entire alveolar-capillary barrier was increased in volume and there was evidence for deformation of the
shape of the interstitium
(Figure 5 ) .
Combining this new data with the results obtained by other
workers, in particular Freeman, Evans, von Nieding, Kosmider,
Ehrlich, and Sherwin and their colleagues,
we proposed a schema
for the pathophysiology of NCU toxic inhalation.
rendering of this schema is giving in Figure 6.
A simplified
If this formulation
is acceptably close to the truth, we may identify certain
points
at which NOj at concentrations in the range of tolerable acute
occupational exposures may plausibly interfere with particle distribution and disposition, based on our present knowledge of the handl1 7-1 Q
ing of inhaled dusts i
1)
N 0 ? is a potent bronchospasm-inducing agent, so that inhalation
leads to an acute increase in airway resistance and a reduction in
i 20
airflow. '
This results in more turbulence and increasing nonuniformity of particle deposition, with a tendency for particles
to sediment more centrally and less in peripheral airways.
2)
N0 2 paralyzes ciliary activity in this concentration range
and thus would interfere with mucociliary clearance.
Some cilia
may be destroyed by chronic exposure so that this interference
might persist long after exposure ceased.
427
One would then expect
reduced clearance of dust by this mechanism.
3)
Alveolar macrophages appear to be particularly susceptible to
the toxic effects of N02«
experimental NCU exposure!
Phagocytosis is markedly inhibited after
Cell migration may also be impaired be-
cause NO, could deprive the cell of energy for motility by interfering with electron transport mechanisms.
4)
Alveolar macrophages injured by NOj may release locally pro-
teolytic enzymes resulting in focal alveolar destruction.
This
effect, which is known to occur in other conditions of macrophage
21-23
and neutrophil toxicity and inflammation.
might enhance
the "spillage" or secretion of lysosomal enzymes that normally
22
occurs with phagocytosis of indigestable particles.
The resulting local degradation of collagen may then stimulate fibro24
a s
blast activity,
or there may be a specific fibroblast-stimulating
factor released by the macrophage.25
5)
Acute, high-dose exposure to NO, produces an interstitial
edema and later interstitial fibrosis.
Both of these processes
are likely to affect lymphatic drainage and the interstitial
migration of particle-bearing macrophages. ,
These changes would
most probably impede clearance and favor local accumulation of
particles in plaques.
6)
Experimental exposure to NO, appears to reduce resistance to
pulmonary infection by both bacterial and viral pathogens.
This probably occurs as a result of impaired mucociliary clearance and reduced phagocytic function.
NOj also appears to inhibit
intracellular killing by the halogen peroxidase system and the secretion of interferon by macrophages. Thus, the NO?-exposed lung
428
may be more vulnerable to secondary Infection.
This In turn may
alter the response to inhaled particles by its own effects.
This approach to the problem of altered pulmonary responses is
not well documented
at present.
The mechanisms discussed above may
reasonably be expected to result in increased retention of particles
in the lung and increased damage and fibrosis, but these sequelae
have not been proven in studies to date.
In unusual circumstances,
a phenomenon of competing toxicity may act to reduce lung damage
by a fibrogenic dust. Aluminum metal powder is thought to inhibit
pulmonary fibrosis due to silicosis by competing with silicic acid
in toxicity to the alveolar macrophage or fibroblast. Although
both agents poison the electron transport chain in oxidative
phosphorylation at cytochrome c, the aluminum ion is less toxic
and appears to be a competitive inhibitor, resulting in a protect27
ive effect.
The same phenomenon might exist when exposure to
low concentrations of NCU accompanies inhalation of fibrogenic
dusts; this could explain the unexpected protective effect ob12
served by Gross et al.
and the lack of an increased tissue reaction to anthracite dust reported by Daniel-Moussard and colleagues.
q
This is speculation; the pertinent experiments remain to
be done.
These speculations on the possible role of N 0 2 in altering
the pulmonary response to inhaled particles derive from the small
number of directly applicable studies and inferences from the
known pathophysiology of toxic inhalation.
The question is ripe
3 18
for exploration using more sophisticated morphologic, '
429
morphometrio,
'
and functional
techniques that have be-
come available in the last few years. A systematic approach using
various concentrations of
gas and particles, comparing the effects
of different gases and different dusts, and using different species
with variations in lymphatic and vascular anatomy would add greatly to our understanding of the pathophysiology in actual occupational exposures.
In the meantime, reporting the results of
environmental monitoring for toxic gases as well as for particulates in the workplace may give us a more realistic picture of
occupational lung disease.
43o
References
1.
Gu1dott1 TL. 1978. The higher oxides of nitrogen:
Environ Res 15:443-472
2.
Jones GR, Prou dfoot AT, Hall J I . 1973. Pulmonary effects of acute exposure
to nitrous fumes. Thorax 28:61-65
Gu1dott1 TL, Abraham JL, DeNee PB, Smith JR. 1978. Arc welders' pneumoconiosis:
\Appl1cation of advanced scanning electron microscopy. Arch Environ
x
Hea th 33:117-124
3.
Inhalation toxicology.
4.
Kennedy MCS. 1972. Nitrous fumes and coal miners with emphysema.
Hyg 15:285-300
5.
Guldotti TL. 1978. Coal workers' pneumoconiosis and medical aspects of
coal mining. South Med J , 1n press
6.
Jorgensen H. 1970. Studies on pulmonary function and respiratory tract
symptoms of workers In an Iron ore mine where diesel trucks are
used underground. J Occup Med 12:348-354
7.
Boren HG. 1964. Carbon as a carrier mechanism for I r r i t a n t gases.
Arch Environ Health 8:119-124
Furiosi NJ, Crane SC, Freeman G. 1973. Mixed sodium chloride aerosol and
nitrogen dioxide in a i r . Arch Environ Health 27:405-408
8.
Ann Occup
9.
Daniel-Moussard H, Martin JC, Le Bouffant L. 1970. Etude expérimentale
de l'action des vapeurs nltreuses sur le poumon empoussléré. Poumon
Coeur 26:905-915
10.
Lewis TR, Campbell K l , Vaughan TR Jr. 1969. Effects on canine pulmonary
function via Induced N0? impairment, particulate Interaction, and
subsequent SO . Arch Environ Health 18:596-601
Gardner LU, McCrum DS. 1942. Effects of dally exposure to arc welding
fumes and gases upon normal and tuberculous animals. J Industr Hyg
Toxicol 24:173-182
Gross G, et a l . 1968. Experimental emphysema: Effect of chronic nitrogen
dioxide exposure and of papain on normal and pneumoconlotic lungs.
Arch Environ Health 16:51-58
Sachs DPL, et a l . 1978. Macrophage resistance to hypotonic. Intracellular
edema (Abstract). Am Rev Resp D1s 117Suppl.:389 (Presented to the
American Thoracic Society Annual Meeting, Boston, 16 May 1978.)
11.
12.
13.
14.
15.
van Allen CM, et a l . 1930. Gaseous interchange between adjacent lung
lobules. Yale J Biol Med 2:297-300
Gu1dotti TL, Llebow AA. 1977. Toxic inhalation of nitrogen dioxide In
canines. In Proceedings of the International Conference on Photochemical Oxidant Pollution and Its Control, Raleigh, North Carolina,
12-17 September 1976. US Environmental Protection Agency, Washington DC.
16.
Welbel ER, Kistler GS, Scherle WF. 1966. Practical stereologlcal methods
for morphometric cytology. J Cell B1ol 30:23-38
17.
Morgan WKC. 1975. The disposition and clearance of dust from the lungs.
In Occupational Lung Diseases, Ed. Morgan WKC, Seaton A. Philadelphia,
W.B. Saunders Co., pp. 20-28
431
18.
Sorokin SP, Brain JD. 1975. Pathways of clearance in mouse lungs exposed to
Iron oxide aerosols. Anat Record 181:581-626
19.
Guidotti TL. 1978. Breaching host defenses in the normal respiratory tract.
Bull Soc Pharmacol Environ Pathol, In press
20.
von Nieding G, et a l . 1970. Akute Wirkung von 5 ppm NO» auf die Lungenund Kreislauffunktion des gesunden Menschen. Int Arch Arbeitsmed
27:234-243
21.
Rynbrandt D, Kleinerman J . 1977. Nitrogen dioxide and pulmonary proteolytic
\enzymes. Arch Environ Health 32:165-172
22.
Unanue ER. 1976.
83:396-417
Secretory function of mononuclear phagocytes.
Am J Pathol
White RU, Lin HS, Kuhn C I I I . 1977. Elastase secretion by peritoneal
exudation and alveolar macrophages. J Exper Med 146:802-808
Postiethwalthe AE, Seyer JM, Kang AH. 1978. Chemotactic attraction of
human fibroblasts to type I , I I , and I I I collagens and collagen-derived
peptides. Proc Nat Acad Sci USA 75:871-875
25.
Leibovich SJ. 1978. Production of macrophage-dependent fibroblast-stlmulating
activity (M-FSA) by murine macrophages. Exper Cell Res 113:47-56
26.
Bergström R, Rylander R. 1977. Pulmonary injury and clearance of MnO,
particles. In Pulmonary Macrophages and Epithelial Cells (Proceeaings
of the 16th Annual Hanford Biology Symposium, Richland, Washington,
1976), Ed. Sanders CL et a l . Springfield, Virginia, National Technical
Information Service, No. 760927, pp. 523-532
27.
Guidotti TL. 1975. Pulmonary alumlnosls—A review. Bull Soc Pharmacol
Environ Pathol 3:16-18
Goldstein E, et a l . 1976. Methods for evaluating the toxicological effects
of gaseous and particulate contaminants on pulmonary microbial defense
mechanisms. Annual Rev Pharmacol Toxicol 16:447-463
28.
432
¿Desempeñan los óxidos elevados de nitrógeno
un papel en la alteración pulmonar como
consecuencia de la agresión?
T. L. Guidotti (Estados Unidos)
Las reacciones tisulares a los polvos Inhalados, que
constituyen la neumoconiosis. pueden modificarse considerablemente mediante una exposición simultánea a otros agentes inhalados no particulados. En las operaciones de soldadura, actividades agrícolas y el uso de explosivos en las
minas, se ha comprobado la exposición a los óxidos de nitrógeno y probablemente coexistan con la Inhalación de partículas. Los anteriores estudios de la exposición combinada en los animales hacen pensar que se produce un efecto
adicional con las partículas fibrógenas que acarrean la fibrosis pulmonar. En nuestros estudios, mediante una técnica experimental de intubación bronquial, se obtuvo la oxigenación unilateral con 37 ppm N02 en 5 perros. Comparando
el pulmón expuesto con el pulmón contralateral no expuesto
del mismo animal mediante técnicas fisiológicas y morfométrtcas se comprobó un ingreso reducido de oxigeno jy cambios
intersticiales y endotellales precoces en el pulmón expuesto. Estos cambios son de tal magnitud que pueden alterar
la disposición y la reacción del pulmón a las partículas
inhaladas. Se recomienda proseguir los estudios para descubrir la modificación de las reacciones pulmonares a las
partículas inhaladas de otros inhalantes exógenos.
433
The effect of the combined application
of cadmium and lead sulfide and coal
dust on the development of lung fibrosis In rats.
J. Rosmanlth, R. Leonardi, D. Prajsnar,
H. Brelning and W. Ehm
Abteilung Hygiene und Arbeltmedizin der
Rheinisch-Westfälischen Technischen
Hochschule Aachen and Institut für
Pathologie I der Bundesknappschaft am
Knappschaftskrankenhaus In Essen-Steel,
Federal Republic of Germany
Introduction
In experiments In which the rats were exposed to quartz
with coal dust, a decrease of the flbrogenlc effect of quartz
was observed (ref. 1,2). With the decrease of quartz content
In the coal, the duration of the protective effect of coal Increased (ref. 3). This effect of coal is first of all due to
argllaceous earth minerals (for Instance llllte) (ref. 3).
It Is known that coal Includes also pyrites, I.e. disulfides of some metals. The experimental results we have
hitherto, obtained Indicate the flbrogenlc effect of cadmium
sulfide as well as of lead sulfide In the animals (ref.4,5).
A synergistic reaction between cadmium and lead has been demonstrated (ref.6-10).
We will therefore test In experiments whether the slmulta'
neous application of cadmium and lead sulfide with or without
coal dust Involves an increasing flbrogenlc effect.
Methods
In the first series of experiments, 240 female Wlstar
rats with an average body weight of 200 g were administered
435
Single Intratracheal injections of cadmium sulfide and lead sulfide as suspensions in 0.5 ml saline solution separately or in
combination (see Fig. and Tables).
The various groups of ani-
mals were killed after 4, 8, 12 and 16 weeks. The typical parameters of the fibrogenie effect in the lungs and regional lymph
nodes i and the concentrations of cadmium and lead in these organs
were determined.
ly examined.
The lungs and lymph nodes were also histological-
The methods used are described in detail in other
papers (ref. 4.5).
Results
An increase in lead dose with an equal dose of' cadmium results in a decrease of the cadmium concentration in the animals'
lungs, with increasing cadmium doses at equal doses of lead a
decrease in lead concentration was observed (Table 1 ) .
After separate application of 50 mg CdS, the cadmium content in the lungs was found to be higher than after combined
administration of CdS and PbS. The cadmium concentration in
the regional lymph nodes was found to be higher.after combined
administration of CdS and PbS, than after separate administration of cadmium sulfide (Table 2).
The additional lead dose
seems to accelerate the elimination of cadmium from the lungs
into the lymph nodes. Lead increases the lymphotropism of
cadmium.
A similar influence was found for the lead concentration
in the lungs and lymph nodes of the animals; the additional
cadmium dose accelerated the elimination of lead from the lungs
into the lymph nodes (Table 2 ) .
436
The biological parameters of effect, such as wet weight of
lungs, dry weight of lymph nodes, content of oxiprolin and lipids
were influenced rather by the cadmium dose, however the differences after 12 weeks have not always been significant (Table 3).
The histological examination clearly showed an increased
fibrogenic effect of the administered dust mixture. After the
administration of 30 mg CdS and 15 mg PbS the lung fibrosis was
more distinctly and earlier detectable than after the
single
dose of 50 mg CdS. After a relatively short time a considerable
fibrogenic effect with the confluence of fibrous foci was observed
(Fig'. 1). The lung fibrosis occurs rather in a focus-like than
diffuse way and is also quite early detectable in the regional
lymph nodes (Fig. 2 and 3 ) .
In the second series of the experiment, the fibrogenic
effect of the two metal compounds was examined in the presence
of coal dustt
90 Wistar rats with an average body weight of 200 g were administered, by injection, single or repeated doses of
15 mg or
30 mg coal dust (anthracite coali 6,7% ash, 10,8% volatile Ingredients, 0,65% quartz) without or In combination with cadmium
sulfide and/or lead sulfide.
killed.
After 6 months all the animals were
The following examination was performed in a similar way
as in the first series.
The dry weight of regional lymph nodes increased, especially after simultaneous administration of cadmium sulfide and coal
dust (Table 4 ) .
The cadmium content in the lungs and lymph nodes depended on
437
the type of administration! when the various ingredients of the
mixture were applied successively in single doses (independent
of the order)i an increased elimination of cadmium from lungs
into regional lymph nodes was observed (Table 4).
The repeated
application of smaller doses increased the lymphotropism of the
mixture»
It was shown again that lead, even in the presence of
the coal dust, influences the lymphotropism of cadmium.
After combined application of coal dust and lead sulfide,
the lead content in the lungs was lower, when the two ingredients
were applied simultaneously (Table 4 ) .
The presence of coal seems
to disturb the influence of cadmium on the increasing elimination
of lead from the lungs. The behaviour of lead sulfide in the presence of coal is in any case quite different from that of cadmium
sulfide.
Neither the application of pure coal dust nor the simultaneous application of coal dust and lead sulfide led to fibrogenic
changes in the lungs or in the lymph nodes. Even after threefold repeated injection of 5 mg lead sulfide and subsequent application of 30 mg coal dust in 10 animals, a slight fibrosis in lung
parenchyma
was recognisable only in one case.
Otherwise after simultaneous application of 30 mg coal dust
and 15 mg cadmium sulfide, in all animals a slight focus-like
fibrosis in both lungs and lymph nodes was observed (Fig. 3 ) .
After intratracheal injections of 15 mg lead sulfide, 15 mg
cadmium sulfide and 15 mg coal dust, successively applied at
three days' intervals, a distinctly to heavily focus-like or
diffuse fibrosis in lung parenchyma was identified (Fig. 4 ) .
438
( 1)
Dolgner.R., rjchlipköter, H.V.". und Leiteritz,H. :
Tierversuche zur Bedeutung des Inkohlungsgrpdes
und Tonminerale für die Uewetsreaktion auf Quarz.
Silikose-Bericht Iiordrhfin-Westfalen, Bd 7,Bösmann-Verlag Detmold,1969, S.45-49.
( 2)
Martin, J.C., Daniel-Moussard,H., LeBouffant.L.
and Policard,A.: The role of quartz in the development of coal workers pneumoconiosis. Ann.N.Y,
Acad.Sci. 200, 127-141 (1972).
( 3)
LeBouffant,L., Daniel, H. und Martin,J.C.: Die
Rolle des Quarzes bei der Bildung pneumokoniotischer Läsionen beim Steinkohlenbergarbeiter. •
Kommission der EO, Schriftenreihe Arbeitshygiene und Arbeltsmedizin Nr 19, Luxembourg 1977.
( 4)
Breining,H|,-.J.Rosmanith und Prajsnar,D.: Lung
fibrosis in rats after cadmium sulfide application. Proceed. of the Vth Internat. Conference
on pneumoconioses, Oct. 29-Nov.,3, Caracas,
1978. .
( 5) Prajsnar,D.,Breitling,H. and Rosmanithjil*: Lung
fibrosis after lead sulfide application^. Proceed.
of The Vth Internat.Conference on Pneumoconioses,
Oct.,29 - Nov.,3, Caracas, 1978.
( 6)
Ferm, V.H.: The synteratogenic *i'feet- Vf lead
and cadmium. Experlentia 25 i 5 6 * 5 7 (1969).
( 7)
Chailop, R.S.: Role of cadmium in léatí poisoning.
New Engl.J.Med. 285, 970-971 (1971)¡i,
( 8)
Chisoìm, J.J.t Heavy metal exposurei toxicity
from metal-metal Interactions, and behavioral
effects. Pediatrics 53, 841-843 (1974).
( 9)
Rosmsnith, J., Elnbrodt, H.J. und Ehm, W.: Zu
Interaktionen zwischen Blei, Cadmium und Zink
bei Kindern aus einem Industriegebiet. StaubReinh.Luft 36, 55-62 (1976).
(10)
RosmanlthjJ., Pistorlus, D., PraJsnar,D. und
Ehm,W.: Darstellung von Interaktionen zwischen
Blei, Cadmium und Zink (Tierversuche). Wissenschaft und UmwfJiÜ?, 89-100 (1978).
*39
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Efecto de la aplicación combinada de sulfuro
de cadmio v de plomo v polvo de carbon en el
desarrollo de una fibrosis pulmonar
en las ratas.
J. Rosmanith, R. Leonardi y D. Prajsnar,
H. Breining y W. Ehm (República Federal de Alemania)
Se aplicaron simultáneamente por vía intratraqueal en
hembras de rata Wistar diferentes dosis de sulfuro de cadmio y de plomo en suspensiones. Este procedimiento provocó una fibrosis tanto en el parénquiraa pulmonar corao^en
los nodulos linfáticos de la region. El efecto fibrógeno
no dependía de la dosis total de sulfuro de cadmio y de
plomo. Una dosis inferior de una aplicación combinada de
CdS + PbS llevó a un efecto más fibrógeno que la dosis más
elevada de CdS o de PbS aplicadas separadamente. También
se descubrió la fibrogeneidad de ambos compuestos metálicos
en presencia de polvo de carbón, pero se observaba un efecto aumentado al aplicarse sucesivamente estos tres materiales.
445
LUNG FIBROSIS IN RATS AFTER LEAD SULFIDE
APPLICATION
D. Prajsnar, H. Brelning, and J. Rosmanith
Abteilung Hygiene und Arbeitsmedizin der
Rheinisch-Westfälischen Technischen Hochschule Aachen, Federal Republic of Germany
Introduction
Lead sulfide Is a constituent of some lead ores, copper
ores and of various types of coal (ref. 1-3). An Increased
content of lead was also found In the silicotic lungs of coalmlners as well as of dead lead ore miners with the Increase of
the S10 2 content (ref. 4-8).
To clarify the possibility of the fibrogenlc effect caused
by the compounds of lead (ref. 9-14), the effect of the lead
sulfide on the rats was examined.
Methods
60 Female Wlstar rats were divided into 3 groups i rats of
the first group were administered intratracheally a single injection of 15 mg PbS as suspension in 0,5 ml saline.
Rats of
the second and third groups, were similarly treated with 30 mg
PbS and 50 mg PbS, respectively.
After 12 weeks all the animals
were killed.
The lungs including the regional lymph nodes were removed.
The right upper lobe of the lung was examined histologically
after embedding in paraffin and stained with HE and EvG.
447
The
remaining lung tissue was chemically processed, and the following
components were quantitatively determinedi total content of oxiprolin (ref. 15), all lipids
both total and fractured
to this lead
(ref. 16), contents of phospholipids,
into lecithine (ref. 17-18).
In addition
was also quantitatively determined (ref. 19).
Results
It was found that the wet lung weight, the content of lead
and oxiproline in the lungs and the content of lecithine, total
lipids and total phospholipids (Table 1) increased with the PbS
dose.
The relative concentration of lead in the lungs remains
the same independent of the dose.
The content of oxiproline, total lecithine and total phospholipids found after12 weeks in the rats treated with 50 mg PbS
remains slightly lower compared to that after the application of
CdS (ref. 20)i on the other hand, the wet lung weight, the weight
of the lymph nodes and the content of total lipids were remarkable
lower than those found after application of CdS. The results of
the histological examination agree with the biochemical parameters!
12 weeks after the application of 15 mg or 30 mg PbS deposits of
the black-brown pigment (with a light foam reaction of the cells)
was recognised in the lungs, but no fibrosis was found.
12 Weeks after the application of 50 mg PbS, brown-black
pig-
ment was nodularly deposited showing partially tuberculoid reaction
and containing single giant cellst in addition the cells showed a
distinct fibrogenic effect with collagene fibres. The fibrosis of
the lungs is either nodular (Fig. 1) or diffuse (Fig. 2). Small
amounts of brown pigment without any cellular reaction were found
in the regional lymph nodes.
448
References
(1)
Baum, Ch.: Quantitative und qualitative Untersuchungen
zur Staubretentior. in den Lungen schwedischer ¡irzbergleute. Diss.-Arbeit, Medizin.Fak. RWTH Aachen, 1973.
(2)
Crable, J.V., Keenan, R.G..Wolowicz, F.R.,Knott,M.J.,
Holtz,J.H. & Gorski, C.H.: Metal and mineral concentrations in lungs of bituminous coal miners. Amer.Ind.
Kyg.Assoc.J. 29, 106-110 (1968)
(3)
Sorenson, J.R., Kober,T.H. & Petering,H.G.: The concentration of Cd, Cu, Fe, Ni, Pb and Zn in bituminous coals
from miners, with differing incidences of coal workers
pneumoconiosis. Amer. Ind.Hyg.Assoc.J. 35, 93-98(1974)
(4)
Thomas, R.W. & Cummins,S.L.; Acute silicosis in leadminers. Lancet 233, 1481-1484 (1937)
(5)
otbfen, D.: Die Rolle des Bleis in der Pathogenese der
Silikose. Arch. Hyg. 153, 478-482 (1969)
45o
( 6)
Knagge-Ruhe,B., Stecher, W. & Einbrodt,H.J.: Lungenveränderungen bei Arbeitern nach Bleierz- und Bleiexposition. Beitr. Silikose-Forsch.(Pneumokon.) 23,
156-171 (1971)
( 7)
Einbrodt,H.J., Kinny.H. & Kortemme.H.: Quantitative
Untersuchungen über den Lymphtransport von Blei aus
der menschlichen Lunge. Arch.Hyg. 153, 105-108 (1969)
( 8)
Kinny, H. & Einbrodt.H.J.: Quantitative Untersuchung
in den Lungen von Bergarbeitern mit Silikose. Arch.
Gewerhepath.^ewerbehyg. 25, 1-14 (1968)
,
( 9)
Eingham,E., Pfitzer.E.A., Barkley,V.". & Radford,2.P.:
Alveolar macrophages: reduced number in r ts £u"ter
prolonged inhalation oí lead sesquioxide. Science
162, 1297 (1968)
(10)
Glitz,E., Kinny,H. & Einbrodt.n.J.: Zur Erythrozytenschädigunc durch Jleistäuben. Int.Arch.Arbeitsirod.
26, 321-329 (1971)
(11)
Sanders,Ch..L.', ¿dee,«.it. U Jackson,T.A. : Fine structure
of alveolar areas in the lung following inhalation of
239FU0, particles.Arch.Environm.Health 22, 525-533
(1971r
(12)
Bruch,J., Brockhaus,A. & Dehnen,Y/.: Elektronenmikroskopische Beobachtungen an Rattenlungen nach Exposition mit partikelförmigem Blei. In: Environmental
Health Aspects of Lead. Proceedings of a symposium
held in Amsterdam ,0ct. 2-5 (1972), pp.221-229
(13)
Beck,E.G.,. Mano;)lovic,N. & Fischer,A.B. : Die Zytotoxizität von Blei. In: Environmental Aspects of
Lead. Proceedings of a symposium held in Amsterdam,
Oct. 2-5 (1972),pp. ¿451.
(14)
Kyono,H.,Homma, K., r¡agatani,T., Watanabe,T. & Kawai,
K.: Localization of inhaled lead particles in the
rat lung. Ind.Health (Jap.)12, 49-72 (1974)
(15)
Stegemann,H.: Mikrobestimmung von Hydroxyprolin mit
Chloramin-T und p-Dimethylamlnobenzaldehyd. HoppeSeyler's Z.physiol.Chem. 311, 41-45 (1958)
(16)
Folch,J., Lees,M.. & Sloane,S.: A simple method for
the isolation and purification of total lipids from
animal tissues. J.Biol.Chem. 226, 497-509 (1957)
(17)
Brockmann,U. & Gercker,E.: Quantitative eindimensionale Dünnschichtchromatographie der Erythrozytenphospholipide. Clin.Chim.Acta 23, 4S9-494 (1969)
(18)
Fiske,C.H. & Subbarov/,Y.: The colorimetrie determination of phosphorus. J.3iol.Chc:n. Co, 375-^0 0925)
451
(19)
Hachata,G. & Binder,R.: Bestimmung von Blei-,
Thalium-, Zink- und Cadmiumspuren in biologischem Material mittels flamraenloser Atomabsorption. Ztschr.Rechtsmedizin 73, 29-34 (1973)
(20)
Brelning,H., Rosmanith,J. & Prajsnar.D.: Lung
fibrosis in rats after cadmium sulphide application.
452
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e
Fibrosis pulmonar en las ratas previa
aplicación de sulfuro de plomo.
D. Prajsnar, H. Breining y J. Rosmanith
(República Federal de Alemania)
Se aplicaron por vía intracraqueal en hembras de rata
Wistar suspensiones de 15, 30 y 50 mg PbS. Este procedimiento llevó en 12 semanas a una fibrosis pulmonar dependiente de la dosis PbS. Se descubrió una estrecha relación entre la dosis y el aumento del peso húmedo del pulmón o del contenido del pulmón en oxiprolina. La lecitina,
los fosfolípidos totales y lípidos totales del pulmón de
las ratas aumentaron también con la dosis.
454
Lung fibrosis In rats after cadmium sulfide
application
H. Breining, J. Rosmanith and D. Prajsnar
Institut für Pathologie I der Bundesknappschaft am Knappschaftskrankenhaus in EssenSteele and Abteilung Hygiene und Arbeitsmedizin der Rheinlsch^WestfälIschen Technischen Hochschule Aachen. Federal Republic
of Germany
Material and Methods
72 Wistar rats with an average body weight of 200 g were
divided into 3 groups«
A dose of 15 mg cadmium sulfide sus-
pended in 0,5 ml saline solution was administered once by intratracheal injection to the first group of animals«
By the same
method, the animals of the second group received a single dose
of 30 mg, and the animals- of the third group a single dose of 50
mg of cadmium sulfide.
ether.
All animals had been anaesthetized with
The 24 animals of each group were killed 4 weeks, 8 weeks
and 12 weeks after administration of cadmium sulfide«
The lungs including the regional lymph nodes were removed.
The right upper lobe of the lung was examined histologically after
embedding in paraffin and stained with HE and EvG.
The remaining
lung tissue was chemically processed, and the following components
were quantitatively determinedi total content of hydroxyprolin,
all lipids, contents of phospholipids, both total and fractured
into lecithin.
In addition to this, cadmium was also quantitati-
vely determined.
Results
The results of this analysis are represented in Tables l-4i
455
Groups two and three, having received a dose of 30 mg and 50 mg
respectively, show a significant increase in the wet and dry
weights of their lungs dependent on dose and duration of experiment. An analogous trend is shown by the dry weight of the
regional lymph nodes. The total content of hydroxyprolin correlated more to the duration of the experiment that to the dose.
Not until after a period of 12 weeks a close correlation could
also be noticed to the dose of the administered cadmium sulfide.
The same was true with the total content of phospholipids and
the other lipid components of the lungs i 12 weeks after the beginning of the experiment a close correlation started to establish itself to the received cadmium dose.
length of the experiment, close
Independent of the
correlations existed between
the cadmium concentration of the lungs and the lymph nodes and
the weight of the lungs, as well as positive correlations between the cadmium concentration and the lecithin concentration
in the lungs of the animals.
The lungs of the animals showed abundants deposits of finegrained brown or black pigments.
In addition, an inflammatory
infiltration of varying degree, consisting mainly of leucocytes,
could be seen, especially in the
deposits.
neighborhood of the pigment
In some cases, the inflammation had caused distinct
confluence reducing the still functioning lung parenchyma to a
minimum.
Four weeks after the beginning of the experiment an
increase of collagen fibers could be
microscope.
noticed under the light
8 Weeks after administration of cadmium sulfide,
an increasing fibrosis of the lung parenchyma could be proven
456
Independent of the dose given. The fibrosis was distinctly
noticeable four weeks after administration of 30 mg of cadmium
sulfide.
8 Weeks after administration of 50 mg of cadmium
sulfide, the fibrosis of the
lungs was quite Intensive showing
sections of diffuse fibrous tissue. The collagen fibers showed
as broad bright red bands after staining with EvG without nucleus,
partly forming a network and in the net structures still showing
the described deposits of pigments (Fig. 1 ) . In some cases the
lung fibrosis was, even after a dose of 50 mg of cadmium sulfide,
more local or clrcumscript.
Some lungs presented groups of foam
cells, especially In the neighborhood of the pigment deposits.
No fibrogenic reaction was seen in any of the lymph nodes.
Our investigation has proved a distinct fibrogenic reaction
of the rat lung to the administration of cadmium sulfide dependent on the length of time of having been In the organism as well
as on the dose given.
457
Reforonces
(1)
Piske, C.H. and Subbarow,Y.: The colorimetrie determination of phosphorus. J. Biol. Chem. 66,375-400
(1925).
(2)
Folch,J., Less,M. and Sloane.S.: A simple method for
the isolation and purification of total lipids from
animal tissues. J.Biol.Chem. 226, 497-509 (1957)-
(3)
Grünspan,M., SchlLpköter,H.W. und Antweiler,H.:Ein
neues Kriterium für die biologische Wirkung von
quarzhaltigen Stäuben. Silikose-Bericht NRW,Bd 9,
137-140 (1973).
(4)
Kaw,J.L.,Gupta,G.S.D and Zaidi.S.H.: Lung lipids and
pulmonary silicosis in rats. Int.Arch.Gewerbepath.
Gewerbehyg. 27, 324-330{1971).
Kyselá,B., Jirakov4,D., Holusa,R. and Skoda,V.: The
influence of .the size of quartz dust particles on
the reaction of lung tissue. Ann.Occup.Hyg. 16,103109 (1973).
(5)
(6)
Löblich,H.J.: Quantitative Untersuchungen über die
Entwicklung der experimentellen Silikose. Beitr.
Silikose-Forsch., H.78, 1-18 (1963).
(7)
Hachata,G. und Binder,R.: Bestimmung von Blei?Thalium-,
Zink- und Cgdmiumspuren in biologischem Katerial
mittels flammenloser Atomabsorption.Zschr.ßechfcsmed.
73, 29-34 (1973).
(8)
Marks,G.S. and Karasas.L.W.: Change in the lung lipids
of rabbits and guinea-pigs exposed to the inhalation
of silica dust. Brit.J.industr.''ed. 17, 31-35 (1960).
(9)
Paterson.J.C: Studies on the to^icifcy of inhaled cadmium. J. Ind.Hyg.Toxicol. 29, 294-301 (1947).
(10) RosmanithjJ. und Breining,H.: Beschleunigung der Entstehung von experimentellen Lungenfibrosen nach intratrachealer Applikation von Cacimiumsulfid und Kohlenstaub. Beitr. Silikose-Forsch.(Pneumokon.) 27, 11-16
(1975).
(11) Stegemann,H.: Hikrobestimmung von Hydroxyprolin mit
Chloramin-T und p-Dimethylaminobenzaldehyd. HoppeSeyler's Zschr.Physiol.Chem.311,41-45 (1958).
458
Table 1. Wetweight of the lungs and dry weight of the regional
lymph nodes according exposure and dose
I
i
Lung
mg wet weiqht
Mean
Lymph nodes
mq dry weiqht
Mean
SD
1x15 mg CdS
1911.43
521.78
26.07
Application
9,57
1x30 mg' Cds
1698.75
342.03
22.69
7.79
1x50 mg CdS
2184.57
473.63
38.18
15.09
1x15 mg cas
2056.25
529.39
30.21
20.60
1x30 mg cas
2283.56
392.32
43.28
18.87
33.75
1x50 mg CdS
2277.50
376.93
54.99
1x15 mg CdS
2341.67 ,474.65
22.49
1x30 mg CdS
2904.75
461.78
46.87
19.35
1x50 mg CdS
413.80
479.27
65.92
26.44
459
6.95.
Table 2. Concentration of cadmium in the lungs and in the lymph
nodes according exposure and dose
I
Application
Lung
(mg Cd/g dry
weight)
Mean
SO
Lymph nodes
(mg Cd/g dry
weiqht)
Mean
SD
1x15 mg CdS
16,02
5,37
9,72
3,49
1x30 mg CdS
45.29
27.24
15.96
11.14
1x50 mg CdS
31.62
16.17
4.03
2.03
1x15 mg CdS
14.46
10.15
10.80
12.76
1x30 mg CdS
25.74
12.93
25.47
17.36
1x50 mg CdS
36.40
24.41
39.88
20.28
1x15 mg CdS
13.48
5.38
10.03
3.36
1x30 mg CdS
29.72
5.43
41.87
15.12
1x50 mg CdS
43.21
6.89
51.18
14.57
Table 3. Hydroxiprolin and lecithin content in the lung of rats
according exposure and dose
Application
Hydroxiprolin
(mg/lung)
Lecithine
(uMol P/lung)
Mean
SD
Mean
1x15 mg CdS
3,84
0.14
19.37
4.94
1x30 mg CdS
3.46
0.68
19.70
6.61
1x50 mg CdS
4.79
1.61
26.88
11.61
1x15 mg CdS
4.82
1.37
15.11
4.95
1x30 mg CdS
4.97
1.27
17.49
5.83
1x50 mg CdS
4.71
1.39
18.38
3.86
1x15 mg CdS
6.18
2.24
13.37
4.44
1x30 mg CdS
8.05
1.20
18.84
4.05
1x50 ng CdS
9.10
1.77
27.09
6.74
46o
SD
Table 4. Total phospholipids and total lipids in the lung
of rats according sxposure and dose
H
c
Application
Phospholipids
fyuMol
P/lung)
Total lipids
(jUMol P/lung)
1x15 mg CdS
35.77
73.46
16.16
1x30 mg CdS
35.73
12.31
57.38
14.25
1x50 mg CdS
45.80
13.80
75.70
21.27
7.50.
1x15 mg CdS
30.23
8.55
50.62
13.58
1x30 mg CdS
33.56
9.37
81.47
26.06
1x50 mg CdS
33.10
6.32
65.87
13.37
1x15 mg CdS
29.76
13.85
57.74
18.59
1x30 mg CdS
37.64
5.86
67.98
9.30
1x50 mg CdS
62.27
9.75
80.11
14.12
461
Fibrosis pulmonar en las ratas previa
aplicación de sulfuro de cadmio.
H. Breining, J. Rosmanith y D. Prajsnar
(República Federal de Alemania)
Se aplicaron por vía intratraqueal en hembras de rata
Wistar suspensiones de 15, 30 y 50 mg CdS. Este procedimiento provoco en el curso de 4 a 12 semanas la evolución
de una fibrosis pulmonar dependiente de la dosis de CdS y
de la duración del experimento« Se descubrió una estrecha
relación entre la ^dosis y todos ^los parámetros del efecto
fibrógeno (peso húmedo del pulmón, peso seco de los nodulos linfáticos, contenido en oxiprolina, fosfolípidos y lípidos en el pulmón).
462
I N D I C E
VI. I
S E S S I O N
VI
. Y.Hosoda., N.Salto., T.Kono., H.Ohteke and V.Chiba
Epidemiology of asbestos-induced pleural thickening
VI. II
m.L .Nenihouse
Asbestos-related diseases in relation to type of
ocouoatIon.
VI. III
Ruth Lilis., and J.Selikoff.
Asbestos disease In maintenance workers of the chemical
Industry.
VI. IV
S.r.mcCullagh
Biological effects of Asbestos - The unresolved matters
VI. V
VI. VJ
UJ.Weiler
Biological effects of Asbestos-Quartz dust-mixtures
L.m.Lacquet., L.van dar. Linden., J.Lepoutre
Prevalence of lung changes, and mortality In a belglan
Asbestos-Cement
VI. VII
factory.
A.Hirsch., L.Ol manza., HI.mangold., J.Blgnon
Ridldlte dlaphragmatlque et exposition a l'amiante:
Correlation radlologique et chirurgicale dans 47 thoracotomies.
VI. Vili
J.m.G.Davis., S.T.Beckett., R.E.Bolton.., Paula Collings.
The Pathological effects of asbestos clouds of different
fibre dimensions on the lungs of rats.
463
EPIDEMIOLOGY OF ASBESTOS-INDUCED PLEURAL THICKENING
Y. Hosoda, N. Salto, T. Kono,
H. Ohtake and Y. Chiba
JNR Central Health Institute
Yoyogl 2-1, Shibuya, Tokyo, Japan
Introduction
With the environmental Improvement of asbestos dust, the
cases with severe pulmonary flbrotic lesions will decrease in
number in the future. When people are exposed to low concentration of asbestos dust, pleural thickening is known as an
important sign. With regard to the X-ray reading of pleural
changes, however, no agreement is reached as to what is a lower
limit change in the pleura for an ILO U/C standard film.
Purpose
The purpose of this study, composed of 2 parts, is to investigate a lower limit of pleural thickening caused by asbestos
exposure.
Part 1• Reading Results bv Readers' Impression
Subject and method of study
As an epidemiological approach to these problems, a control
study was made of pleural thickening occurring in asbestosexposed and non-exposed workers.
The former comprised 130
railway factory workers exposed to a low concentration of asbestos dust during their jobs of cutting and grinding asbestos
slate or friction materials at present and repairing steam locomotives in the past.
As a sex and age matched control, the
same number of railway maintenance workers in a rural area was
465
used. We made a separate study on Tokyo clerks, but the prevalence of their pleural changes was higher that in the abovementioned control workers.
The pleural changes were observed according to age and the
duration of employment.
It is said that obese people tend to
present pleural thickening like shadows more often than slim
people. As for the physical constitution of the subjects of
the study, the workers generally had non-fatty muscular structure.
The body weight of asbestos workers was much lower than that of
the railway workers' average, while that of the controls was in
the workers' average.
X-ray films were taken in a PA direction and, when necessary,
in oblique positions at lOOkV using 12il movable grid.
As for the X-ray film reading, the PA films to be read
were serially numbered according to random numbers, and the
identity of the examinees was concealed for a blind reading.
The films with the closure of the cost-phrenic angles were
separately grouped in view of the possible tuberculous etiology and the recording was made according to localisations! in
the lateral chest wall, along the ribs, on the diaphragma and
over the lung field.
The rib companion shadows produced by
ribs themselves were excluded from the recording.
The reading
was based on the readers' comprehensive impression in combination with shape, width, density and localisations of the
pleural changes, referring to the ILO U/C standard films.
Results
1.
No apparent pulmonary parenchymal lesions due to asbes-
466
tosis were found in the
two groups«
No pleural changes were
seen on the diaphragma.
2.
The closure of the cost-phrenic angles was found in 7 of
130 in the asbestos group (5.4%) and in 5 in the control
group (3.8%).
3.
The prevalence of pleural thickening increased with the advance in age and the length of employment.
4.
The total number of cases presenting abnormal and suspected
abnormal changes in the lateral chest walls and along the
ribs was 19 in the asbestos group (14.6%) and 9 in the control
group (6.9%), the difference being
5.
significant (p¿0.05).
The number of cases with abnormal changes was 11 in the
asbestos group (8.3%) and 2 in the controls (1.5%), while
the number of those with suspected abnormal changes was 8
in the asbestos group (6.2%) and 7 in the controls (5.4%).
6.
Bilateral pleural changes were found in 11 of 19 asbestos
workers and in 4 of 9 controls. The shadows along the ribs
tended to appear more often on one side, while the costphrenic angle changes appeared on both sides in 11 of 12
cases.
7.
The pleural changes along the ribs were located In the 7th
and 8th ribs in almost all cases.
8.
After reading all films, the width of pleural changes was
measured by sliding callipers.
The width of pleural changes in an ILO U/C standard film
was 4mm.
In the films regarded as abnormal, 15 to 19 had
a width of 3mm or more, while in the films regarded as suspected abnormal, 3 of 11 had a width of 3mm or more.
467
The
Impression well corresponded to the measurement.
If one
should venture to set a safe cutting point between normal
and abnormal pleural changes only from the width viewpoint,
it would be necessary to minimise false positive and false
negative.
In this respect, 3mm or more in width would be a
tentatively acceptable lower limit.
Discussion
It should be remembered from the clinical point of view
that any asbestos-induced pleural thickening starts at nil,
reaching 3mm or more. The subjective reading of pleural
changes along the lateral chest walls and along, the ribs usually gives discrepant results due to inter-observers' error. However, when the
reading is repeated separately or jointly, there
was a tendency of reaching a point of agreement. As for the
cause of these pleural changes, further studies should be made
not only on asbestos but also on other materials.
Conclusion
As for the pleural changes, 3mm in width along the lateral
chest walls or along the ribs may be a'tentative criterion to
minimise false positive
and false negative.
Part II. Reading Results Based on the Width Measurement
Subject and method of study
In the foregoing part I, a 3mm width was proposed as a
lower limit for abnormal pleural changes based on the X-ray
reading by readers' impression.
The part II aimed to investi-
468
gate if the width measurement was useful in diagnosing pleural
thickenings
The subjects of the study were the same as in part I, and
the X-ray reading was made by measuring the width of pleural
changes by sliding callipers.
In this study, any shadows along
the lateral chest walls or ribs were recorded regardless of
the origin of the shadows, including normal soft tissues«
The
changes were grouped into 2 according to the localisation.
When the changes were situated along the lateral chest walls,
they were categorised as type I and when they were along the
ribs, they were placed in type II. The distinction of the two
types was not essential, because a type II shadow in a PA film
sometimes showed a type I shadow in an oblique radiograph.
In
this study, the distinction between the diffuse and localised
(plaque) pleural changes was not made, as the width was only
the parameter.
In this railway company, recruits were limited to new
graduates from schools, and
the employees usually remained in
the same jobs until retirement.
For this reason, the duration
of employment roughly corresponded to the age of the workers.
In consideration of a possible age factor relating to the
pleural changes, the observations were made according to age.
Those over 40 years old numbered 62, and those aged 39 or less
numbered 68. The prevalence rate was shown in the number of
sides.
Accordingly, the former group had 124 sides and the
latter 136 sides.
469
Results
1.
The prevalence of pleural changes was higher in the asbestos
group that in the control group in both types; 54/260 (20.8%)
in the asbestos group and
38/260 (14.6%) in the controls as
regards type I, and 9/260 (3.5%) in the asbestos group and 4/260
(1.5%) in the controls as regards type II.
If the changes with
3mm or more were consideredi the prevalence was 12/260 (4.6%)
in the asbestos group and 4/260 (1.5%) in the controls as regards type I and 8/260 (3.0%) in the asbestos group and nil in
the controls as regards type .II.
This nil figure should not be
generalised as the Tokyo clerks in our separate study had the
changes over 3mm in type II.
2.
When observations were made according to the two age groups,
40 years or more and 39 years or less, the older group had a
higher prevalence rate than the younger group. As regards type
I, the prevalence was 34/124 (27.4%) in the asbestos group and
22/124 (17.7%) in the controls in the older age group, while
it was 20/136 (14.7%) in the asbestos group and 16/136 (11.8%)
in the controls in the younger age group., With regard to type
II, the prevalence was 9/124 (7.3%) in the asbestos group and
1/124 (0.8%) in the controls in the older age group, while it
was nil in the asbestos group and 3/136 (2.2%) in the controls
in the younger age group. The last group showed an exceptional
result probably because the number observed
was too small.
When the distribution of the width was investigated between
the asbestos and control groups, the difference in prevalence
between the two groups became larger when the width exceeded
47o
3 or 4mm.
However, in the
95% confidence limit in digit analysis,
the difference was not significant.
3.
As for the side of changes in type I( the ratio of right«
left i both sides was 13t 9i16 in the asbestos group, while it was
8t6il3 in the controls.
In short, about a half of the changes
was found in both sides.
4.
As for type II, the shadows appeared along the inferior edge
of the posterior rib shadow with a rare exception and were most
frequently found in the 8th rib followed by the 7th and 9th.
Discussion
If the asbestos group had been a little more heavily exposed,
or if the asbestos group had had more number of cases with pleural
changes, the difference might have been significant.
At the same
time, it should be considered that the control group had no
evidence of freedom from asbestos dust exposure during their
lives.
At present, it would be no longer possible to find a
group completely free from asbestos exposure.
It should also
be remembered that this method of study included the
shadows
produced by the physiological elements in the asbestos and control
groups»
Conclusion
The asbestos-exposed group showed a higher prevalence of
pleural changes than the control group in terms of the width
of pleural changes.
When the width exceeded 3mm or more, the
471
prevalence showed a large difference between the two groups.
In the authors' opinion It may be safe to set a tentative
screening line for pleural changes In PA films at 3mm or more,
referring to the study in part I as well.
472
EPIDEMIOLOGIA DEL ESPESAMIENTO DE LA PLEURA
PROVOCADO POR EL AMIANTO
Informe Introductorio por
Y. Hosoda, N. Salto, H. Ohtake y Y. Chiba
(Japón)
El objeto del estudio es Investigar cual es el límite
inferior de espesamiento de la pleura en las radiografías.
Para hacer más claras las características de espesamiento se
excluyeron los casos con fibrosis pulmonar debida al amianto.
Así, los trabajadores que habían estado expuestos al amianto
en baja concentración fueron observados junto con trabajadores
casi exentos de amianto, emparejados por sexo y edad.
La incidencia de espesamiento de la pleura aumentó con
la edad y con la duración del servicio en el grupo expuesto, y
mostró una tendencia análoga en el grupo de control. Sin
embargo, la incidencia fue más elevada en el primer grupo.
Si se estiman en principio 3 mm como límite inferior de espesamiento de la pleura, la diferencia en la incidencia se
acentuó en ambos grupos.
Se intentó agrupar los tipos de espesamiento de la
pleura en ores« el de pared lateral, el de costilla y el difuso.
Es digna de mención la contracción de la caja torácica en el
lugar del espesamiento pleural.
473
ASBESTOS-RELATED DISEASES IN RELATION *
TO TYPE OF OCCUPATION
(Summary)
M. L. Newhouse
United Kingdom
The health risks of heavy and prolonged exposure to asbestos
are now well recognised.
There Is less knowledge of the degree
of risk In different sections of the asbestos Industry.
The literature In relation to asbestos-related diseases In
mining, the manufacture of different products and the usage of
asbestos-containing materials has been reviewed.
There are mark-
ed differences which will be demonstratedi but difficulties are
experienced In evaluating these differences due to lack of uniformity In methods of investigation and Insufficient Information
In many reports on method of dust control and levels of exposure.
It Is, however, clear that processes Involving the use of
crocldollté and amoslte asbestos carry a higher risk, particularly of mesotnellai tumours than that where only chrysotlle asbestos
Is used.
Crocldollte miners, textile workers amd Insulators or
laggers are at the greatest risk.
Asbestos cement workers, pro-
bably the largest section of workers In the asbestos Industry, are
believed to be at lower risk than Insulation or textile workers,
but marked differences In mortality In different sections of this
Industry have been demonstrated, probably dependent on the type
of fibre Incorporated In the product as well as the degree of
exposure.
A study of the mortality of workers who have been engaged In
production of friction materials Is now being undertaken, which Is
475
of particular interest as, apart from two short periods where
crocidolite was used, the only exposure has been to chrysotile
asbestos.
Epidemiological studies in the asbestos cement industry and
other sections of the industry such as those producing floor
tiles and asbestos/plastic products, are needed.
*
The paper "in extenso" to be asked to the author.
476
Enfermedades derivadas del amianto en
relación con el tipo de ocupación.
M. L. Newhouse (Reino Unido)
Actualmente se reconocen los riesgos que para la salud presenta una exposición importante y prolongada al
amianto. En cambio, todavía se sabe muy poco sobre el
grado de riesgos en los diferentes sectores de esa industria.
La literatura sobre las enfermedades producidas por
el amianto en las minas, la fabricación de diferentes productos y el uso de materiales que lo contienen ha sido
puesta al dfa. Existen notables diferencias, que serán
demostradas, pero también se tropieza con dificultades para evaluarlas, debido a la falta de uniformidad en los métodos de investigación y a la insuficiente información sobre métodos de control de polvos y niveles de exposición.
No obstante, es evidente que los procesos que involucran la utilización de crocldolita y amosita presentan un
mayor riesgo, en particular de tumores del mesotelio, que
cuando se utiliza solamente el crisotilo. Los mineros de
la crocidolita, los trabajadores textiles, los instaladores de material aislante o calorífigo son quienes corren
los mayores riesgos. Se piensa que los trabajadores del
cemento de amianto, probablemente los más numerosos en esta industria, corren menos riesgos que los trabajadores
textiles o instaladores de material aislante, pero se ha
demostrado que existen diferencias notables en la mortalidad en los diferentes sectores de esta industria, probablemente según el tipo de fibras incorporadas en el producto y
según el grado de exposición.
Se está haciendo ahora un estudio sobre la mortalidad
de los trabajadores de producción de materiales de fricción, de particular interés ya que, aparte de dos breves
períodos en que se utilizó la crocidolita, la única exposición es al crisotilo asbestiforme.
Es necesario emprender estudios epidemiológicos en la
industria del cemento de amianto y otros sectores, tales
como los de fabricación de baldosas y productos de amianto
y plástico.
477
ASBESTOS DISEASE IN MAINTENANCE WORKERS
OF THE CHEMICAL INDUSTRY
Ruth Lilis, and J.
Sellkoff
Environmental Sciences Laboratory, Department of Community
Medicine, Mount Sinai School of Medicine of the City University
of New York, USA
Introduction
Clinical field examinations of several large groups of
workers in various plants of the chemical industry, undertaken
by the Environmental Sciences Laboratory in the last years, have
called our attention to the frequency of chest x-ray abnormalities
(small irregular opacities and/or pleural changes) of the type
known to be induced by dust exposure«
Chest x-rays of workers
of three vinyl chloride polymerization plants (1,2), a styrene
polymerization plant (3), a titanium dioxide manufacturing (4)
and a dye manufacturing plant were read without knowledge of
age, past medical history, occupational history or findings
on physical examination.
Yet when parenchymal changes (irregular
or rounded opacities) and/or pleural changes (thickening or calcification) were found, possible exposure to asbestos, silica
or coal dust had usually occurred«
It had been our practice when examining workers from chemical
plants to make special efforts to include maintenance personnel,
since it is well known that such work may often include significant overexposure to toxic
substances, especially when repair
becomes urgently necessary.
In 1971 a report by Bittersohl and Ose had called attention
to asbestos hazards in the chemical industry (5,6).
479
26 cases
of mesothelioma had been observed over a period of 4 years (19671971)i this was in sharp contrast with the extreme rarity of this
type of malignancy in the preceding periodi
22 patients had
worked in a large chemical industry (Leuna), two in another
chemical plant (Buna), one in a foundry.
The only female patient,
while not having had any occupational exposure to asbestos, was
the wife of a worker at the Leuna plant. Only 16 patients had
had direct
occupational exposure to asbestos, while 9 had had
indirect exposure (working in areas where asbestos was occasionally handled by other workers); in one case there only was a history
of household exposure. Chest x-ray films preceding the development of mesothelioma were available in 23 cases i in 17 pleural
thickening and pleural plaques were present.
It was known that extensive insulation work had taken place
in several departments of the Leuna chemical plant in the early
1950's. Large amounts of asbestos had been used and evidence
for high concentrations of airborne fibers in the past was available.
In these production areas and in adjacent shops asbestos
exposure was subsequently a consideration for all workers, not
only for those installing new insulation or removing old material.
Maintenance work was thought to carry a special risk.
Other sources of asbestos exposure, identified in the second
chemical plant, were fire
resistant protective equipment used
by welders, and the manipulation of insulation with repair work
on pipes.
Population and Methods
To obtain information concerning the potential dimensions
48o
of asbestos hazards among workers of the chemical Industry, a
eross-sectional Investigation of maintenance workers of a large
chemical plant In New Jersey was undertaken.
All were volunteers, and represented about half the men In
maintenance categories In the plant (welders, carpenters, electricians, pipefitters, etc.).
as many of those with terms
We deliberately sought to Include
of employment of more than 10 years
as possible, and to examine only a sample of employees with shorter
durations of exposure. Age distribution and duration since onset
of exposure of the group are presented In Tables 1 and 2. 26%
of those examined had less than 10 years and 59% had more than 20
years from onset of exposure.
The examination protocol Included a lifetime occupational
history, past medical history, smoking history, MRC respiratory
questionnaire, complete physical examination, standard 14 by 17
Inch PA chest x-ray films and pulmonary function tests (spirometry and maximal expiratory flow volume curves).
Chest x-ray films were read in consensus readings by four
physicians experienced In occupational lung disease, without any
knowledge of the past medical history, occupational history, respiratory symptoms or finding on physical examination, and categorized according to the ILO U/C Classification of Radiographs
of Pneumoconioses.
Results of pulmonary function tests - measure-
ments of forced vital capacity (FVC), forced expiratory volume pen 1
second (FEV.) and forced expiratory flow over the mid FVC (FEF25-75^
were compared to the predicted values of Morris et al.(7), without knowledge of the occupational history, radiologic findings,
481
symptoms or findings on physical examination.
Results
Radiologic Findings
Small irregular opacities, mostly in the lower lung fields,
sometimes extending to the middle lung fields, of the type seen
with parenchymal interstitial fibrosis, were present in 24% of
those examined) in 11% this was the only abnormality (Table 3 ) .
Pleural thickening and calcification (with or without thicken'
ing) in 10% and 4% of cases respectively were found in the absence
of definite radiologically evident parenchymal abnormalities) a
total of 14% of those examined had pleural abnormalities only.
In another 14% both parenchymal and
pleural changes were seen.
The overall prevalence of parenchymal and/or pleural abnormalities
consistent with asbestos-induced changes was 33%.
As expectedf the prevalence of all chest x-ray abnormalities
was higher in workers with more than 20 years' exposure since
onset of work (Table 4)) pleural changes were a more frequent
abnormality in the group than were parenchymal.
Careful analyses of life-long occupational histories recorded for all the 185 maintenance workers revealed that in 140
there had been no previous specific, defined occupational or nonoccupational dust exposure.
In 45 workers, asbestos exposure
ranging from minimal to significant, had occurred in the past,
preceding employment in the chemical plant.
Among those considered to have had significant previous
exposure were workers who had been employed in an asbestos manu-
482
facturing plant, had been active as pipefitters or plpecoverers,
had worked In brake maintenance and repair, or had participated
in boiler repair work.
These considered to have had minor previous
exposure Included workers Involved In spackllng, shingle trimming,
brake repair (minimal, Intermittent), and In one case, residence
in the neighborhood (2 blocks) of an asbestos products manufacturing plant.
A separate analysis was made of workers without any (even
minimal) known
preexisting asbestos exposure. When comparing
the results with those obtained for the entire group of 185
workers, It was found that the prevalence of radiologic abnormalities, both parenchymal and pleural, was almost
Identical
(Table 5).
The relationship between radiologic abnormalities and duration
since onset of exposure (Table 6) was very similar In the group
of 140 maintenance workers without any previous known asbestos
exposure to that found In the total group of 185 examined workers
(Tables 4 and 6)j there was no statistically significant differences
in prevalence of parenchymal or pleural changes.
Clinical Findings - Symptoms and Signs
The only symptom reported with a higher frequency In workers
with radiologic abnormalities was dyspnea on exertion (In those
with both parenchymal and pleural changes) (Table 7).
Cough and
sputum production consistent with a diagnosis of chronic bronchitis
(Table 8) were found In 20% of those examined.
The differences
In prevalence between current smokers and Individuals who had never
smoked regularly was not significant (22% versus 14%).
483
(Exposure
to dust and irritant fumes and gases in an industrial environment is often an underestimated etiologtc factor in chronic
bronchitis) (Table 8 ) .
Abnormalities on physical examination were infrequent)
rales were present mostly in persons with pleural changes.
Clubbing and rales were detected in several cases with negative
chest x-rays, raising the question of parenchymal fibrosis not
yet radiologically detectable.
Results of Pulmonary Function Tests
Pulmonary function tests (Table 9) indicated a relative low
prevalence of restrictive disfunction (5% of cases), probably
related to the small number of cases with advanced parenchymal
fibrosis.
An obstructive pattern was more often found, and was, as
expected, more prevalent in current and ex-smokers. The finding
of a lower than normal FEV./FVC ratio in 17% of maintenance
workers with a negative smoking history again suggests that dust,
irritant fumes and gases in an industrial environment may have
an adverse effect on respiratory function.'
Discussion
While in this group of maintenance workers chest x-ray
abnormalities were relatively frequent, pleural changes being
more
prevalent than parenchymal
fibrosis, subjective symptoms
and pulmonary function abnormalities were much less prominent.
This constellation has been found to be rather characteristic
484
for relatively less Intense asbestos exposure. While progression
to severe disabling parenchymal asbestosls Is less probable under
such circumstancesf the risk for lung cancer and mesothelioma
remains•
The chemical plant maintenance workers examined had had
various degrees of asbestos exposurei while some of them had experienced direct and continuous asbestos exposure for periods of
time of more than 5 years, others had had direct, but intermittent,
exposure for shorter periods of time. More than half of those
examined had never been directly engaged In work with asbestosj
nevertheless they had been present In areas where such work was
performed by others (Table 11).
A list of some of the job
designations Included In this last category Is given In Table 12.
The prevalence of radiologic changes was higher In workers
with direct asbestos exposure. Nevertheless, It was considerable
(25%) even In those with Indirect asbestos exposure.
Comparative analysis of the entire group of 185 chemical plant
maintenance workers and of the 140 subject without any previous
asbestos exposure yielded interesting resultst prevalences of
radiologic abnormalities
(both parenchymal and pleural) were
almost Identical. The relationship between prevalence of radiologic abnormalities and duration since onset of exposure was
also very similar.
These findings strongly suggest that asbes-
tos exposure characteristic for maintenance work In chemical
plants, Including Indirect ("bystander") exposure results In
risks comparable to those
documented for other types of as-
bestos exposure, In other Industries and occupations.
485
The higher prevalences of radiologic pleural abnormalities
(pleural
fibrosis and/or calcification) than of parenchymal
small irregular
opacities (interstitial pulmonary fibrosis),
the relatively low prevalence of
restrictive ventilatory
functional impairment and the paucity of clinical
abnormalities
all indicate that the risk for disabling asbestosis is less
with this type of asbestos exposure. Nevertheless, the risk of
lung cancer
and mesothelioma is of concern, since accumulated
experience indicates that low level asbestos exposure (indirect
occupational, neighborhood or
household exposure) is sufficient
to result in a significant risk of developing mesothelioma
(8,9,10).
In the last several years, we have had occasion to
observe a number of cases of mesothelioma in workers employed in
chemical, oil refining, and petrochemical industries.
It is
possible that an increasing number of such cases may occur,
since spectacular growth of these industries has taken place
over the last 25 - 35 years, on the average, the critical latency
period (11).
486
References
1.
L i l i s , R., Anderson, H., e t a l . Prevalence of disease among v i n y l
chloride and polyvinyl chloride workers. Ann. N.Y. Acad. S c i .
246 (1975).
2.
L i l i s , R., Anderson, H., e t a l . Pulmonary changes among v i n y l c h l o ride polymerization workers. Chest 69(2):299-303 (1976).
3.
lorimer, W.V., L i l i s , R., e t a l . C l i n i c a l s t u d i e s of styrene workers:
i n i t i a l findings. Environ. Hlth. Perspectives 17:171-181 (1976).
4.
Daum, S . , Anderson, H., e t a l . ' Pulmonary changes among titanium work e r s . Royal Society of Medicine, Sec. on Occup. Medicine 7 0 ( 1 ) :
31-32 (1977, Abstract).
5.
B i t t e r s o h l , Von G. Epidemiologische Untersuchungen über Krebserkrankungen in der chemischen Industrie. Arch. Geschwulstforsch.
3 8 ( 3 - 4 ) ; 198-209 (1971).
6.
B i t t e r s o h l , Von G., Ose, H. Zur Epidemiologie des Pleuramesothe liorna.
Z. Gesamte Hyg. 17:861-864 (1971).
7.
Morris, J . F . , Kolski, A., e t a l . Spirometrie Standards for healthy
nonsmoking a d u l t s . Am. Rev. Respirât. D i s . 103:57-67 (1971).
8.
Wagner, J . C . , Sleggs, C , e t a l . Diffuse pleural mesothelioma and
a s b e s t o s exposure in the North Western Cape Province. B r i t . J.
Indus. Med. 17:260-271 (1960).
9.
Newhouse, M.L., and Thompson, H. Mesothelioma of pleura and peritoneum following exposure t o asbestos in the London area. B r i t .
J . Indus. Med. 22:261-269 (1965).
10.
Harries, P.G., Mackenzie, F . , e t a l . Radiological survey of men
exposed t o asbestos i n naval dockyards. B r i t . J . Indus. Med. 29:
274-279 (1972).
11.
S e l l k o f f , I . J . Cancer r i s k of asbestos exposure. In: Origins of
Human Cancer. Ed. H.H. Hlatt, J . D . Watson, and J.A. Wlnsten,
Cold Spring Harbor, N.Y., pp. 1765-1784, 1977.
487
Table 1
AGE DISTRIBUTION OF 185 MAINTENANCE WORKERS
Age
20-29.9
30-39.9
40-49.9
50-59.9
No.
*
No^
No^
No^
27
15%
IS
%
10%
34
%
lfl%
488
85
%
47%
60+
No^
21
%
11%
Table 2
DURATION SINCE ONSET OF FIRST
ASBESTOS EXPOSURE (YEARS)
< 10 y r s .
10-19.9
years ,
20-29.9
years
30+ y r s .
Ho.
%
No.
%
No.
%
No.
%
49
26%
27
15%
41
22%
68
37%
489
Table 3
Chest x-ray abnormalities consistent with asbestos-induced
changes (parenchymal and pleural) i n maintenance
workers - chemical plant
(N=18S)
Radiologic change
(IIO UVC)
None
0/0-0/1 .
Parenchymal changes, t o t a l
1/0-1/2
2/1-2/3
3/2-3/4
Parenchymal changes only
Pleural changes
Pleural thickening only
Pleural c a l c i f i c a t i o n (with
or without thickening)
A l l pleural changes
490
Number
Percent
115
62%
45
42
3
0
22.4%
1.6%
20
11%
18
10%
7
51
4%
28%
24%
-
Table 4
Duration since onset of asbestos exposure
and chest x-ray changes in maintenance workers
(N=185)
Radiologic
changes
Less than 20 years
More than 20 years
N = 77
N = 108
%
Mo.
%
66
86%
49
45%
Parenchymal
changes
(total)
9
12%
36
33%
1/0 - 1/2
2/1 - 2/3
3/2 - 3/4
8
1
0
10%
1%
34
2
0
31%
2%
Parenchymal
changes
only
8*
10%
11
10%
Pleural
thickening
only
1
1%
17
16%
1%
6
6%
4%
48
.44%
Ho.
Normal
(0/0-0/1)
Pleural
calcification
1
(with or without
thickening, without parenchymal
changes)
All pleural
changes
3
•See Table 6 .
491
Table 5
Chest x - r a y a b n o r m a l i t i e s c o n s i s t e n t with asbestos-induced
changes (parenchymal and p l e u r a l ) i n maintenance
workers - chemical plant - with no previous a s b e s t o s exposure
(N=140)
Radiologic change
(ILO U/C)
Number
None
0/0-0/1
Parenchymal changes, t o t a l
1/0-1/2
2/1-2/3
3/2-3/4
Parenchymal changes only
P l e u r a l changes
P l e u r a l t h i c k e n i n g only
P l e u r a l c a l c i f i c a t i o n (with
or without thickening)
A l l pleural changes
492
Percent
90
64%
34
31
3
0
24%
22%
2%
12
9%
14
10%
2
38
1%
27%
-
Table 6
Duration since onset of asbestos exposure
and chest x-ray changes In maintenance workers
with no previous asbestos exposure (N=140)
Radiologic
changes
Less than 20 years
More than 20 years
N = 61
N = 79
Wo.
Normal
(0/0-0/1)
54
%
Ho.
%
89%
36
46%
i
Parenchymal
changes
(total)
6
10%
28
39%
1/0 - 1/2
2/1 - 2/3
3/2 - 3/4
9
1
0
8%
2%
26
2
0
33%
3%
Parenchymal
changes
only
4*
7%
8
10%
Pleural
thickening
only
1
2%
13
16%
-
2
3%
5%
39
44%
Pleural
calcification
0
(with or without
thickening, without parenchymal
changes)
All pleural
changea
3
•Parenchymal changes (only) was the only
radiologic abnormality with significantly
higher prevalence In workers with previous
asbestos exposure (X =4.63; p<0.03).
*93
Table 7
Symptoms
.
Prevalence of respiratory symptoms
In maintenance workers
(N=185)
Abnormal chest x-ray
Parenchymal
Normal
Parenchymal
Pleural
and
chest x-ray
only
only
pleural
(«=118)
» (N=20)
(N=22)
(M=25)
ÏÏ2i
*
—
ïï£l
Ï
—
Ü2¿
%
—
No.
%
—
4
18%
11
44%
6
27%
7
28%
32%
6
24%
Shortness
of
breath
19
16%
2
10%
Wheezing
27
23%
S
25%
Chronic
bronchitis
20
17%
3
15%
7
494
Table 8
Prevalence of chronic bronchitis
In maintenance workers - chemical plant
Sknoklng
habits
Total number
examined
Chronic bronchitis
(MRC)
Ho.
%
67
IS
22%
Ex-smoker
75
15
20%
Never .
smoked
42
Total
184
Present
smoker
14%
36
495
20%
Table 9
Objective changes on physical examination
In 185 maintenance workers
Chest x-ray
Abnormalities
on physical
examination
Normal
chest x-ray
(N=118)
No.
X
Clubbing
7
6%
findings
Abnormal che St X -ray
Both
parenchymal
Parenchymal Pleural
changes
changes
and pleural
only
changes
only
(N=20)
(N=22)
(N=25)
No.
0
X
-
No.
No.
X
1
X
SX
1
4X
3
14X
3
12%
1
5X
1
4%
Rales
8
7X
0
Cyanosis
1
1%
0
-
Increased
AP diameter
4
3%
0
_
1
SX
5
20%
Decreased
breath
sounds
6
SX
1
5X
0
-
4
16%
Decreased
heart
sounds
3
3%
2
10X
2
9X
1
4%
Wheezing
and/or
rhonchl
7
6%
1
5%
2
9X
1
4%
5X
3
14%
P II > A II
5%
4%
8X
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ol
o
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ál
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00
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•» O)
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n U
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+> >>
e
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e
o >
«in
II
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s
o
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V «H
t«
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Svi
VI
3 S
.o
à. i
o
T
Il B
s a
h O
+» -H
n +»
J> u
O Q
3
•H VI
a n
S'
497
4» ( S
U i-l
fi
•» O
(9 • *
•S • *
o n
a
ST.
<H
•o
3
c
I
&
^ a
g
o o
> a
£1
<s a
Ì
a
SS
1 ? Îï
•»
u
s*
*«l
S
m
a
a a
o
a a
I!
o 9
*t o
Table
11
CHEST X-RAY ABNORMALITIES
IN CHEMICAL PLANT MAINTENANCE WORKERS
Abnormal c h e a t
x-ray
Number
Number
%
41
20
49%
Intermittent, l e s s than
S years)
36
17
47%
Never direct asbestos
exposure ("bystander")
108
27
25%
Direct asbestos .
e x p o s u r e (more t h a n
5 years)
Direct asbestos
exposure ("minor" -
498
Table 12
MAINTENANCE WORKERS - OCCUPATIONS
WITHOUT DIRECT HANDLING OF ASBESTOS
Laborer
Stock man
Area mechanic
Sheet metal mechanic
Mechanic helper
Maintenance helper
Millwright
Repair man
Pipefitter
Production worker
499"
BIOLOGICAL EFFECTS OF ASBESTOS - THE UNRESOLVED MATTERS
S. F. McCULLAGH
James Hardie & Coy. Pty. Limited,
Granville, N.S.W., Australia
We all recognise the serpentine asbestos chrysotlle and
the amphiboles crocldollte, amoslte, anthophylllte, tremollte
and actlnollte. However, the US National Institute for Occupational Safety and Health (NIOSH) In 1972 defined asbestos
as any substance which under phase contrast
microscopy at about
500 x, has a length greater than 3 times Its diameter, a length
>5jm and a width <3yum. This definition, now given the force
of law In the US by the Occupational Safety and Health Administration (OSHA) includes fibres which are not minerals and also
minerals which are not fibres»
Great semantic confusion will
result If we refer to these other substances as asbestos or even
as "asbestos" or as "asbestlform fibres"«
These other substances
may be most precisely referred to collectively as OSHAsbestos.
I am not trying to be funny.
I commend this term to youi for some
such term we must have If confusion Is to be avoided.
Hard rock gold miners in Lead, South Dakota, have been
exposed
to an amphibole OSHAsbestos and have been reported to
show an excess of lung cancer by Gillam et al. (1976), but
McDonald et al. (1978). In a much more extensive study and In
one much better designed to detect an excess If It Is there, found
none.
This OSHAsbestos Is harmless.
5o1
Barts (1978),. on the other hand, has described two small
foci of endemic mesothelioma in Turkey believed to be due to the
fibrous aluminium silicate erionite - this OSHAsbestos is dangerous.
Much work needs to be done to determine the biological
effects of the substances in the OSHAsbestos categoryi these
studies will have to be of immaculate design. The confusion,
misunderstanding and, sometimes, bitterness which has characterised the debate over the S substances that are asbestos has
been much contributed to by poor experimental design and unjustified inference! the consequences of permitting the same
thing to happen vis à vis the innumerable substances that are
OSHAsbestos are frankly too horrible to contemplate.
What Constitutes an Asbestos Exposure?
What constitutes an asbestos exposure?
It has long been
held that, generally, some 10 to 15% of mesotheltomata are not
attributable to asbestos exposure (Wagner et al., 1971), but
the most recent, and probably the most soundly based, estimate
puts the figure at 33% (McDonald & McDonald, 1977).
The figure
varies astonishingly widely from 5% in Scotland (McEwan et al.,
1970) to 80% in Italy (Rubino et al., 1972).
A comparison of the
case-control studies of McEwan et al., (1970) in Scotland and of
McDonald et al., (1971) in Canada shows that a history of asbestos exposure is likely to be elicited twice as commonly in
Scotland as in Canada, and this applies equally to cases and
controls.
It may be as McDonald (1977) argues that such
differences are reali "areas with high exposure rates in controls
are characterised both by the presence of dockyards and a high
5o2
high Incidence of mesothelioma! whereas areas with'low rates ....
have neither".
However, we will not know whether such differences are real
or whether they are due to differences In the definition of what
constitutes an asbestos exposure unless we reach agreement on
what, In fact, constitutes an asbestos exposure.
This will not
be easy but is needs to be done.
Morphology and Mesothelioma.
The relative potency of different types of asbestos as
causes of mesothelioma has been the subject of much debate, but
the data have recently been summarised by McDonald (1977) and
can leave us in little doubt that the great majority of cases
are due to the fine-fibred crocidolites, some to amosite, a few
to chrysotile and none to anthophyllite.
Studies of the morpho-
logy of these fibres have led to the conclusion that they are
most potent when they are durable in vivo, rod-like in shape
(not curly like chrysotile) and of diameter ¿-1.0pm and length
>10.^ura (Timbrell, 1973t Wagner et al., 1973| Stanton et al.,
1977).
It Is hypothesised that the curly fibres of chrysotile
are deposited proximally while amphibole deposition is preferentially peripheral as fibre diameter decreases, and thus it is
that the fine crocidolites predominantly reach the pleura and
cause mesothelioma - though how then are we to explain the
benign pleural lesions so commonly associated with anthophyllite?
The hypothesis Is further challenged by reports from France that
electron microscopy has revealed that it is amphibole asbestos
5o3
that is predominantly found in pulmonary tissue itself while in
the pleura it is chrysotile that one most commonly sees (Le
Bouffant, 1974| Desbordes et al., 1974| Le Bouffant et al.,
1976)i though one must observe that the number of cases that
have been studied and reported is small and, as Desbordes and
his colleagues have observed, the matter "mérite d'être confirmée
par de plus nombreauses observations."
Selikoff et al., (1973)
reported 7 cases of mesothelioma occurring between 1941 and 1971
among 877 men first employed in the manufacture of insulation
material containing only amosite asbestos between 1941 and 1945;
seven
is not a large number of cases, but the incidence
about 0.26/1000/year is higher than the South African
described by Webster (1973) would have led one to
observation is the main stumbling block to the
logical carcinogenesis, so largely based on
of
experience
expect. This
theory of morpho-
the work of Timbrell,
which I have already outlined.
Selikoffs 877 men worked in a factory in Paterson, New
Jersey, and there seems little doubt that their work there exposed them only to amosite asbestos. I Hovfever, a patient search
of the monthly trade journal Asbestos shows that crocidolite,
most of it South African, though also some Australian and some
Bolivian, was for some years commonly milled in the
New Jersey.
State of
Milling of crocidolite, and other types of asbestos,
appears to have commenced in 1921 at
Bound Brook, in NJ, to have
transferred to larger premises in Millington, NJ, in 1928 and
to have continued there until the end of 1946 when another
Company began similar operations in Jersey City, NJ.
5o4
How many
of the men employed in this Paterson Plant between 1941 and 1945,
who are subjects of Selikoff's study, had previously been exposed to crocidolite at Bound Brook or at Millington, we simply do
not know and whether the 7 mesothelioma were due to amosite or
crocidolite we cannot say.
The Company that operated the Paterson
Plant conducted similar operations at Cicero, 111., and at Blue
Island, 111.
In retrospect it seems likely that these two
Illinois workforces would have provided more satisfactory data.
Asbestosls and Lung Cancer
The International Labour Office, in 1972, stated that lung
cancer in asbestos workers "occur, so far as is known, only in
workers whose lungs show signs of pneumoconiosis"! the ILO, as
usual, felt sufficient in its own authority and
gave no indication
of the basis on which its statement was foundedt presumably it
rests upon the work of Doll (1955).
Martischnig et al., (1977) reported that of 201 men with
bronchogenic carcinoma, who were not regarded as "asbestos
workers", a history of asbestos exposure could be significantly
more
frequently elicited than from 201 controls. They stated
that none of their cases had asbestosis but unfortunately do
not set
forth the evidence on which this opinion was based)
we have, therefore, no more than their obiter dictum.
Were
Martischnig and his colleagues correct one would expect ferruginous bodies to be found more commonly in the lungs of people
with bronchogenic carcinoma than in controls i it has been re-
5o5
ported that this is so by Warnock and Chrug (1975), but
more
commonly reported that tt is not so by Elmes & Wade (1965), by
Doniach et al. (1975) and by Whitwell et al. (1977).
The limited
evidence of Fletcher (1972) remains the best we have - 16 of 408
shipyard workers died of bronchogenic carcinoma (cf. 6.74 expected)«
none had radiological evidence of pulmonary
who came to necropsy, only one had slight
asbestosis and, of 5
histological evidence
of this disease.
A study of this same group of workers suggests that
pleural
plaques are associated with an increased risk of bronchogenic
carcinoma but the findings are, as yet, inconclusive as Edge
reported in New York earlier this year (Edge, 1978).
On the
other hand, Kaski et al (1968), in Finland, in a case-control
study of 279 pairs reported no excess of
attributable to the presence of pleural
bronchogenic carcinoma
plaques, whether calci-
fied or not.
The Arc of Endemic Pleural Pathology
There is accumulating evidence of a great arc of pleural
pathology swinging through Central Europe' from Finland In the
north (Kiviluoto, 1965 and 1978), through the USSR (Ginzberg et
al., 1970), the GDR (Anspach, 1962), Czechoslovakia (Rous and
Studeny, 1970» Navratil, 1970), Bulgaria (Burilkov and Michailova,
1970), down to Turkey in the South (Yazicioglu, 19761 Yazicioglu,
et al., 1978, Baris et al., 1978» Baris, 1978).
These are a
most interesting series of endemics. We need further radiolo-
5o6
gical surveys to discover others i we need to determine the
airborne fibre thought responsible and Its
morphology and
concentration! and we need to determine whether or not there Is
associated morbidity or mortality.
In the case of Turkey It Is believed that the OSHAsbestos
erlonlte Is responsible for two small foci of endemic mesothelioma south of Ankara (Baris, 19781 Baris et al., 1978)j endemic
pleural calcification occurs at and about Dlyarblklr, south east
of Ankara, perhaps due to Chrysotile, the evidence of associated
disease Is somewhat confused (Yazlcloglu, 19761 Yazlcloglu et al.,
1978)i In another endemic to the north of Ankara pleural plaques
occur but mesothelioma has not been found (Baris, 1978).
On the other hand, at the north of this great arc, In
Finland, repeated studies have failed to find any excess of
bronchogenic carcinoma associated with the endemic pleural
disease (Ktvlluoto, 1965| Kaskl et al., 1968» Klvlluoto, 1978)
despite the fact that excessive exposure to the asbestos concerned, anthophylllte, has been shown to be associated with an
Increased risk of bronchogenic carcinoma (Meurman et al., 1974).
This Is a most Important observation since It strongly suggests
that there Is a level of exposure to this
which does not elicit the expected
known human carcinogen
carcinogenic response.
In
other words, there is a safe dose - we just need to know what
It Is.
5o7
References.
Anspach M. (1962), Int. Arch. Gewerbepath, 1£), 108.
Baris Y.I. (1978), Ann. NY Acad Sci, (in press).
Baris Y.I. et al., (1978), Thorax, 3¿, 181-192.
Burilkov, T. & Michailova L. (1970), Environm Res, ¿Î, 443-451.
Desbordes J. et al., (1974), Lyon Méditerranée Médical, X, 157-162.
Doll R. (1955), Brit. J. industr. Med, 1¿, 81-86.
Doniach I. et al., (1975), Brit. J. industr. Med, 3£, 16-30.
Edge J.R. (1978), Ann. NY Acad. Sci, (in press).
Elmes P.C. & Wade O.L. (1965), Ann NY Acad Sci, 13J2, 549-557.
Fletcher D.E. (1972), Brit. J. industr. Med, 29, 142-145.
Gillam J.D. et al., (1976), Ann. NY'Acad. Sci,, 271, 336-344.
Ginzberg E.A. et al., (1970), Kliniceskaya Med, lj2, 55-56.
International Labour Office (Report on the Meeting of Experts
on Control and Prevention of Occupational Cancar, Geneva,
10-17 Jan. 72, p. 6, para. 24.
Kaski P. et al., (1968), Proc. Internat. Konf. biolog.
Wirkungen des Asbestes, Dresden, pp. 274-275 (pubi. 1973).
Kiviluoto R. (1965), Ann. NY Acad. Sei, 132, 235-239.
Kiviluoto R. (1978), Ann. NY Acad. Sci, (in press).
Le Bouffant L. (1974), Environm. Hlth. Perspectives, 9, 149-153.
Le Bouffant L. et al., (1976), Revue Française des Maladies
Respiratoires, 4, (suppl. 2 ) , 121-140.
Martischnig K.M. et al., (1977), Brit. Med. J, i., 746-749.
McDonald J.C. (1977), Proc. Symp. Asbestos, Johannesburg, 67-78.
McDonald J.C. Û McDonald A.D. (1977), Prev. Med, 6, 426-446.
McDonald J.C. et al., (1971), Arch. Environm. Hlth, 22, 677-686.
McDonald J.C. et al., (1978), Amer. Rev. resp. Dis. (in press).
McEwan J. et al., (1970), Brit. Med. J, iv, 575-578.
Meurman L. et al., (1974), Brit. J. industr. Med, 31, 104-112.
Navratil M. (1970), Proc. Internat. Symp. Brit. Occup. Hyg.
S o c , London, Vol. 2, 695-703.
Rous V. & Studeny J. (1970), Thorax, 25, 270-284.
Rubino C F . et al., (1972), Brit. J. industr. Med, 29, 436-442.
Selkoff I.J. et al., (1973), Revue Française des Maladies Respiratoires,
4, (suppl. 2 ) , 121-140.
Stanton M.F. et al., (1977), J. Nat. Cancer Inst., 58, 587-603.
Timbrell V. (1973), Biologie Effects of Asbestos, IARC Scientific, Publication
No. 8, p.p. 295-303.
U.S. Occupational Safety and Health Administration, 1972, Fed. Reg., T7> (11a),
11318-113322.
Wagner
J.C. et al., (1971), 3ric . M.îd. lull. 27, 71-76.
Wagner J. C. et al., (1973), Brit. J. Cancer, 28, 173-185.
Warnock M.L. and Churg A.M. (1975), Cancer, 35, 1236-1242.
Webster I. (1973), Sth.Afr. Med. J., 47. 165-171.
Whitwell F. et al., (1977), Thorax, 3_2, 377-386.
Yazicioglu S. (1976), Chest, 70, 43-47.
Yazicioglu S. et al., (1978), Chest 73, 52-56.
5o9
Efectos biologicos del amianto:
problemas pendientes.
S. F. McCullagh (Australia)
¿Qué es el amianto? Es necesario definirlo, porque
la definición efectuada por la O.S.H.A., que tiene fuerza
de ley en Estados Unidos, incluye muchas substancias que
no son amianto en el sentido en que se entiende comúnmente la palabrai los efectos biológicos de estos otros materiales han sido poco estudiados, pese a que uno ha demostrado su nocividad y otro es mortal.
¿Que es la exposición al amianto? La proporción de
mesotelioma que puede ser atribuible a la exposición al
amianto va de 20 por ciento en Italia a 95 por ciento en
Escocia. Estas diferencias pueden ser reales, pero habría
que definir lo que se considera como exposición al amianto para resolver la cuestión.
¿Qué tipos de amianto y de qué morfología son los más
peligrosos? ¿Es posible escoger entre las opiniones de
Timbrell y sus colaboradores en el Reino Unido y las de
Bouffant y los suyos en Francia y las de Selikoff y los
suyos en Estados Unidos?
¿El carcinoma broncógeno atribuible a la exposición
al amianto se produce únicamente en presencia de asbestosis pulmonar o pleural o también puede presentarse en
ausencia de estas dolencias?
La incidencia de mesotelioma en trabajadores antes
ocupados en Patterson, Nueba Jersey, en la fabricación de
materiales aislantes que sólo contenían amosita ha sido
mayor de lo que se podía esperar en base a la experiencia
sudafricana. ¿Pero hasta qué punto han estado expuestos
anteriormente en Nueva Jersey a la crocidolita?
Parece existir un amplio arco de patología pleural
que a través de Europa Central pasa por Finlandia, República
Democrática Alemana, URSS, Checoslovaquia, Bulgaria y Turquía,
y que afecta a personas que no se encuentran expuestas por
razones profesionales, ni para-profesionales, ni de vecindad,
al amianto. Tenemos que determinar qué fibras son responsables,
cuáles son las concentraciones en el aire y si existe morbilidad o mortalidad asociada a las mismas.
51o
BIOLOGICAL EFFECTS OF ASBESTOS-QUARTZ DUST-MIXTURES
W. Weiler
Pneumoconiosis Research Institute, Bochum, Federal
Republic of Germany
Introduction
This experiment was carried out to study the combined effect
of chrysotile-quartz and crocidolite-quartz mixtures. The investigation of combined effects is also of great practical importance'.
For instance, asbestos cement as well as talc con-
tain asbestos and quartz. The intraperitoneal test applied is
a well examined method, not only for quartz dust injections, but also for asbestos dust administration (Pott et al., 1976; Weller,
1977).
On the whole this was a relative
long-term experiment
lasting 6 months. This period is certainly sufficient for the
recognition of fibrogenic properties, but generally insufficient
for the discovery of careinogenity.
On the other hand the method
applied in our tests permits the early recognition of modifications.
While evaluating the tests special attention was paid
to the determination of quantitative parameters.
Methodology
Tests were performed with a total of 197 female SPFSprague-Dawley rats.
Table 1 shows detailed data on test groups,
kind and quantity of the injected dust and also the number of
animals in each group. At the beginning of the tests animals
were 12 months old.
511
Name of
the qroup
Group
Treatment
Asbestos
Quartz
(mq)
(mq)
-
-
5
5
6
-
5
5
5
6
7
7
-
5
5
S
7
7
6
5
10
15
•*
5
5
5
7
5
7
15
10
5
15
10
5
-
5
5
5
7
7
7
5
5
5
7
7
6
Con crol
1
Chrysotile
ï a
b
c
3 a
b
c
5
10
15
-
5
10
15
-
Quartz
4 a
b
c
-
Chrysotile +
Quartz
S a
b
c
5
10
15
Crocidolite +
Quartz
6 a
b
c
5
10
15
Crocidolite
Number of examined anijials
o months 3 months 6 months
-
Table 1: Test scheine.
The applied asbestos dust was UICC standard dust crocidolite
and chrysotile B, the quartz dust was Dörentrup quartz No. 120.
The dust was suspended in physiological NaCl solution without
adjuvant.
1 ml.
Each animal received an intraperitoneal injection of
After test periods of 3 and 6 months a part of the animals
was etherised and sacrificed.
After body-weight determination
the following organs were removed and weighed! liver, lien, omentum, lung lymph nodes, cranial and caudal mesenteric lymph nodes.
According to the findings modifications outside the omentum, ovaries
and peritoneal liquid were removed.
From the removed material
histological sections and smears were taken.
Results
a) Animal and organ weights
The animal weights did not show any dependence on dust
type and dose.
exposure were
The organs that might show reactions on dust
omentum, liver and lien.
Because of the small
dust quantities and very high organ weights only slight modifications had been expected.
Only quartz groups showed a corre-
lation between organ weights and dust dose. We did not find
512
a direct dependence on dust type and dust dose tn the other groups.
Table 2 summarises the weights of different lymph node groups.
According to the manifold experience with quartz dust and coalquartz mixtures in intraperitoneal tests the lung lymph node
and cranial mesenteric lymph node' weights were added up to obtain the total lymph node weight.
Injection
Asbestos Quartz
Group
(ITO)
Control
1
Chrysotile
2a
2b
2c
5
10
15
Crocidolite
3a
3b
3c
5
10
15
Quartz
4a
4b
4c
Chrysotil«
• Quartz
Sa
5b
5c
6a
6b
6c
Crocidolite
+ Quartz
(TO)
Lung Lynch
notfes
3 Hon. 6 Hon.
21 i e 27 î 4
24 Ï 6
29 Î 11
26 * 6
5
10
15
5
10
15
15
10
5
5
10
15
15
10
5
28 | 7
n 19
Crani!
iresentfi]
lynph nrie
3 Man. jdes
6 Mon.
33 î 4
35 î 9
a
42 î 7
42 î 6
39-7
31-8
34-; 8
35 î 7 5 5 Î 1 7
S3 I 11 50 I 13 53 i e
53 - 22 54 - 11 6 2 - 8
78 - 15 1 0 8 - 2 6 63 - 13
129 î 24 134 ; 29 104 ï 20
164 - 24 186 - 42 131 - 30
66
52
48
164
144
101
;
Í
î
Ï
-
16
7
10
32
38
22
96 î 2S 68 J 11
69 ; 28 55 i 10
52 - 10
38-6
Total
lynph nodes
3 Mon.
6 Mon.
54 î 7
62 - 13
Cauda]
mesenteric
lynph nodes
3 Mon. 6 Mon.
28-8
34 t ,
26 î 5
27 î 5
34 î 8
32 i B
37 í 9
80 j 17 141 j 20 188 j 31 27 1 4
110. j 29 233 î 43 244 ; 57 48 I 15
155 - 45 295 - 52 341 - 81 37 í 5
97 Í 22 134 j 26 193 | 43 32 2 12
74 ï 13 107 î 14 143 j 35 3 0 Î 7
62 - 11 100 - 6 100 - 13 29 - 3
36 j 10 66 j 11
71 I 16
39 î 7
65 - 12
38 î 8
89 j 23
56 j 8
49 î 15 106 I 10
63 - 19 115 - 24
64
68
69
91
99
117
j
j
;
I
-
12
13
10
9
25
25
33 î 9
23 î 4
26 I U
26-6
35 2 16
32 í 8
30 î 7
36
37
33
42
40
36
î
j
i
î
2
î
9
12
6
10
14
7
166 Í 33 132 j 41 142 î 47 296 ; 48 308 j 43 43 j 13 41 I 11
126 j 31 113 - 21 121 J 37 257 I 57 247 j 53 46 2 9 53 j 12
108 - 38 93 - 25 110 - 17 194 - 34 218 - 48 32 î 7 47 î 10
Table 2: Organ weights of lymph nodes correlated to test period
(total lymph nodes = lung lymph nodes and cranial mesenteric lymph nodes). Mean values with single standard deviation. Rats, intraperitoneal test.
With the exception of the caudal mesenteric lymph nodes the
other lymph node weights show direct, dose-dependent relations.
The following graph, including a better survey on lymph node.
weights than the table, is based on results obtained after a three
months' test period (fig. 1).
513
Total lymph nodes
( mg )
-Quartz • Crocidolite
-Quartz
300 -,
200
o—Quartz« Chrysotile
—Crocidolite
100-
-Chrysotile
-Control
Dust types :
5
Dust mixtures: »15
Fig. 1:
10
>10
15
• 5
mg Quartz and Asbestos r e s p .
mg Asbestos
Total lymph node weight after a 3 months' test period
dependent on dust dose (total lymph node weight =
weight of lung lymph nodes and cranial mesenteric
lymph nodes).
Quartz shows the typical dose-dependent increase of the total
lymph node weight.
It is obvious that crocidolite has an essen-
tially greater quantitative effect than chrysotile. Asbestosquartz mixtures yielded surprising results. The quantitative
quartz effect is decreased, dependent on the dose, by addition
of chrysotile.
However, an addition of crocidolite causes, also
dependent on the dose, an increase of the quantitative quartz
effect.
514
This interesting reaction is investigated in more detail in table
3 by organ weight increases (= net weights, i.e. actual organ
weight minus organ weight of control group).
Increase of organ weights (üi mg)
Total
lymph nodes (lung lymph nodes + cranial mesenteric lymph nodes)
Dust
Chrysotile
3 Ntin. 6 Mon.
Crotitiolite
3 Mon. ó ton.
5 mg Asbestos
15 trq Quartz
12
241
2
279
35
241
29
279
Set v a l u e : Total of dust types
Actual v a l u e : Dust mixture {5 mq a s b e s t o s + 15 mq quartz)
253
80
281
131
276
242
308
246
% Actual value of s e t value
32%
474
88%
80%
10 mg a s b e s t o s
10 mq quartz
17
179
6
182
52
179
37
182
Set v a l u e : Total of dust types
Actual v a l u e : Dust mixture (10 mq a s b e s t o s + 10 mq quartz)
196
53
188
81
231
203
219
185
% Actual value of s e t value
27%
43%
15 mg a s b e s t o s
5 mq quartz
11
87
7
126
61
87
55
126
S e t v a l u e : Total of dust types
Actual v a l u e : Dust mixture (15 mq a s b e s t o s + 5 mq quartz)
98
46
133
38
147
140
181
156
% Actual value o f s e t value
47%
29»
88%
95%
84%
86%
Table 3: Presentation of organ weight modifications caused by
the particular dust types and dust mixtures.
The net weight determined after injection of the particular dust
type serves as reference value.
The actual value is the deter-
mined net weight of the identical dust mixture. When using
chrysotile all examined
mixture ratios show a substantial de-
crease of the quartz reaction both after 3 months and after a 6
months' test period.
After a 3 months' test period the determined
value of a dust mixture has on the average only 357. of the expected effect provided that the particular dust types have an
additional effect. After a 6 months' test period the value
515
months to 43% due to a progressive development after a pure
quartz Injection.
When using crocidolite, however, on an
average 90% of the expected quantitative
tained after a 3 months' test period.
reaction were ob-
Particularly mixtures
containing a high proportion of asbestos show an
almost addi-
tional reaction effect of both dust types. Regarding the quantitative progression of modifications the following observations
could be made; corresponding to the known typical reaction
the organ net weights increase after quartz injections from the
3r
to the 6
test month.
Thus, the maximum quantitative re-
actions might be obtained for the applied doses (Weiler, 1977).
The quantitative progression of asbestos is shown in figure 2.
Total lymph nodes
Increase of organ weights
rng
80 i
60-
o*
,.<r
40-
3 Mon.
6 Mon'— Crocidolite
-•or"'
20
0 i££
- 3 Mon.
•6 Mon."—I Chrysotile
-1—
10
15 mg Asbestos
Fig. 2: Presentation of the net weight increase of the total
lymph node weight due to asbestos dust dependent on
test period and dust dose.
516
These values indicate that in each dosage both chrysotile and
crocidolite do not react progressively, but regressively.
Besides, the different quantitative effect of the two asbestos
dust types is obvious again, showing in addition a relation
depending on the dose.
In summing up it can be said that the weight of the lung
lymph nodes and cranial mesenteric lymph nodes and especially
the total lymph node weight obtained by adding the two values
show unequivocal interpretable relations.
a substantially
Crocidolite provokes
greater reaction than chrysotile.
Mixed with
quartz, chrysotile has an inhibitory effect, whereas crocidolite
almost causes a synergism of the effect of the components
quartz and asbestos.
b) Macroscopic pathology
The macroscopically visible modifications on opening the
peritoneal cavity after a 3 months' test period, will be presented first.
After an injection of 5 mg chrysotile the omentum
only shows bright spots. With greater dosages there are, in
addition to the omentum small deposits on the peritoneum and on
the liver.
Similar grey-green deposits can be found in the cro-
cidolite group. These deposits are flat and streaky rather than
defined granulomes. With lower dosages conglutinations of
omentum, liver and diaphragm also occur.
Higher dosages result
in additional conglutinations of the lien.
The lymph nodes of
both groups do not present consistency modifications.
517
In the quartz group the typical solid white nodules can be
found on the omentum as well as outside the omentum.
the
The higher
quartz quantity the bigger and the more solid are the lymph
nodes•
The typical quartz effect is completely converted in the
chrysotile-quartz mixture group.
A mixture of 15 mg quartz and 5
mg chrysotile causes soft granulomas compared to the solid ones
obtained after an injection containing 15 mg pure quartz. The
appearance of the
of the typical
lymph nodes is almost normal; a great reduction
quartz effect can be observed.
There is a distinct quartz effect in the crocidolite-quartz
group.
The granulomas due to the crocidolite proportion show a
slight
grey-green colorationi besides, there are conglutinations
of omentum, liver, lien and diaphragm.
The lymph nodes are solid,
and their colour is white-grey.
After a test period of 6 months the macroscopic changes are
about the same. Compared to the findings after 3 months, the
granulomas and lymph nodes in the chrysotile-quartz mixture group
are of a more solid consistency, i.e. the quartz effect is a little
more distinct.
• c) Special pathological modifications
After a test period of 3 months as well as after 6 months the
appearance
of ascites, ovarian cysts and tumors was macroscopi-
cally observed.
Table 4 includes a summary of these findings.
518
Ndme of
the qroup
Control
Chrysotile
Crocidolite
Quarts
Chrysotils
+ quarts
crocldoUt»
+ quarts
Group
1
2 a
b
c
3a
b
c
4 a
b
c
Sa
b
c
6 a
b
c
N
5
5
5
5
5
5
5
5
5
5
5
S
5
5
5
5
3 months' test period
Ascites O/arian- Tutor
N
cvst
6
1
6
1
5
-
2
3
5
6 months' test period
Ascites Ovarian- Tumor
cvst
1
1
1
3
4
4
2
6
5
1
-
1
-
5
5
1
J
4
4
-
4
1
2
5
1
1
1
1
6
1
1
1
1
Table 4: Frequency of special pathological findings in the individual test groups.
Ascites only occur in the crocidolite group, the frequency of
which
increases with the test duration.
There seems to be a
certain dependence on the dose. Smears were taken and coloured
according to Papanicolau, and partly a HE-coloration was made.
Cytologic findings did not indicate tumor growth; crocidolite
fibres could
not be found either.
The animals of each group
showed ovarian cysts. However, compared to other test groups
their frequency is much higher in the crocidolite groups.
d.) Histology
The presentation of the results obtained by a histological
study mainly
comprises data after a test period of 6 months.
The chrysotile group, the group with the lowest dose, shows
a slight
cellular infiltration of single omentum ansea with a
fibrosis degree of I/II up to I1/II1 (King).
The group with the
highest dosage shows, in addition, to these infiltrations, single
and rather small granulomas with numerous cells and a fibrosis
degree of II/III.
are found.
Outside the omentum granuloma-shaped deposits
Liver, lien and the
519
different lymph nodes did not
show any particularities compared to the control group.
Even the smallest dosage in the crocidolite group causes granu=
lomas in and outside the omentum with fibrosis degree III. Especially the granulomas outside the omentum present outstanding
polynuclear giant cells (Langhans-type). Granulomas in the
group with the highest dosage are partly hyaline in the centre.
For the first time this group presents numerous asbestos fibres
at irregular distances, coated by oval deposits of different
sizes.
They are likely to be the so-called asbestos bodies or
"ferruginous
bodies". Liver and lien do not show modifications.
Regarding the lymph nodes, the most distinct modifications could
be seen in the lung lymph nodes. They are similar to typical
quartz-caused lymph nodes (foci with a diameter of almost lOÇum
containing a large number of fibres).
There is no evidence of
fucos-related fibrosis.
The group with pure quartz injections shows the usual, frequently discussed modifications (Weiler, 1977).
The test groups treated with chrysotile-quartz mixtures
present quartz-typical modifications in and outside the omentum.
Only in the group treated with a mixture of 15mg chrysotile the
cellular infiltrations of omentum ansae typical for this asbestos
type are present. However, the quartz-typical modifications in
liver and lien are scarcely found even in case of a high quartz
proportion.
The lymph nodes, too, show fewer quartz-typical
foci,, and frequently the absence of a confluence tendency can be
observed.
In the group treated by crocidolite-quartz injections the
52o
modifications in and outside the omentum were due to the quartz
proportion.
Large numbers of crocidolite fibres can be found.
The polynuclear giant cells typical for crocidolite asbestos
can be
found only in the modifications of the group with the
highest asbestos proportion.
quartz-typical
in the group
The number and extention of the
foci in liver and lien are more similar to those
with pure quartz injections.
In the lymph nodes
the reaction seems to be more distinct than in the corresponding
quartz groups.
Even if
the quartz proportion is small, confluent
quartz-typical
foci are present. The crocidolite fibres are
numerous! they exclusively occur in quartz-typical areas.
e) Discussion
The different reaction of chrysotile as compared to that of
crocidolite may
have the following causes: influence of fibre
length, higher natural quartz content in crocidolite and application
of a new evaluation
method.
According to Robock (1974) there are
no differences between the asbestos dust types used regarding
fibre length distribution
ranging from 0,2pjm up to 20Qum.
Therefore, it is more likely that a potentially present natural
quartz proportion and mainly, the evaluation method based on the
total lymph node weight, so far not used in asbestos studies, are
important factors.
Besides, there was a close relation between quantitative
evaluations and pathological findings in our tests.
The carcinogenic properties, not examined in this study, are
much more important that the fibrogenic effect of different asbestos types.
With great probability, the observed subcutaneous
tumors do not correlate to asbestos injections.
521
Histologically,
they are fibro-adenomas. Hemorrhagic ascites of experimental
animals after
asbestos injections were described only by Pott et
al., (1976).
It has not yet been defined whether they are due to
a mechanical effect only or whether they should be seen in connection with carcinogenic characteristics. The same can be said about
the numerous appearances of ovarian cysts that have not yet been
described.
It is interesting that both modifications can be ob-
served mainly after crocidolite
gated in future
injections.
It should be investi-
studies to which extent conclusions can be drawn
from the described different effects of chrysotile and crocidolite,
both isolated and in combination with quartz, regarding the different carcinogenic effects of the two asbestos types.
522
References
King, li..J . , <J.
Nage) uchmi ÜL
Die pathologische Wirkung verschiedener Minoici I üLüube im Tierversuch
In: Die Staublungenerkrankungen
'¿,
84-95, Darmstadt, 1954
l'ott, b". , K.ll. Friedrichs, F. Iluth
lirgebnisso aus Tierversuchen zur
kanzerogenen Wirkung faserförmiger Stäube und ihre Deutung im
Hinblick auf die Tumorentstehuni)
beim Menschen
Zbl. Bakt. Hyg. I., Abt. Orig.
13. lj>2, 467-505 (1976)
Koboek, K.
Die Wirkung mechanischer, thermischer und chemischer Behandlungen
von Siliciumdioxyd- und AsbestStäuben auf Zytotoxizität und
Elektronenstruktur
Beiti-, SiLikose-Forschung 26, , 1112f>> (1974)
Wullor, W.
Anthrakosilikose
Bergbau-Uerufsgenossenschaft,
Bochum, 1977
Address: Priv.-Doz. Dr. W. Weller
Silicosis Research Institute
Hunscheidtstrasse 12
D-4630 Boahum
Fed. Rep. Germany
523
Efectos biológicos de las mezclas de polvo
de amianto v cuarzo.
W. Weiler (República Federal de Alemania)
ha investigación de los efectos combinados de la exposición al amianto y al cuarzo es de gran Interés práctico,
por lo cual se estudiaron los efectos del crisolito B y de
la crocidolita, así como de las mezclas de polvo de cuarzo
y amianto, en pruebas intraperitoneales con ratas, de hasta
seis meses de duración.
Además, en este experimento de corta duración, se examinaron la eficacia de un nuevo parámetro cuantitativo y
los métodos de diagnostico de las alteraciones tumorígenas
precoces en la evaluación de los efectos del polvo.
Se obtuvieron los siguientes resultados i el peso de
los nodulos linfáticos del pulmón, de los nodulos linfáticos del mesenterio craneano y el peso de la mayoría de todos los nodulos linfáticos obtenido por adición de ambos
valores muestran una relación inequívoca con la inhalación
de polvo. La crocidolita provoca una reacción cuantitativa
considerablemente mayor que el crisotilo. Mezclado con
cuarzo, el crisotilo tiene un efecto inhibitorio, mientras
que puede observarse con la crocidolita casi una adición de
los efectos de los componentes cuarzo y amianto.
Después de una inyección de crisolito y crocidolita
las modificaciones del epiplón son más bien escasas i no se
producen en otros órganos. En cambio la crocidolita causa
adhesiones extensas del epiplón, el hígado, el espíenlo y
el diafragma. Los polvos de asbestos deben ser clasificados como fibrógenosi no se produce un progreso en las modificaciones. Los cuerpos ferruginosos se encontraron solamente después de un período de pruebas de seis meses en
el grupo sometido a las dosis más elevadas de crocidolita.
Como modificaciones patológicas particulares en todos los^
grupos con crocidolita se observaron ascitis y quistes ovárlcos. No se poseen Indicaciones sobre la patogénesis de
estas modificaciones.
524
PREVALENCE OF LUNG CHANGES, AND MORTALITY IN A BELGIAN
ASBESTOS-CEMENT FACTORY
L.M. Lacquet, L.van der Linden, J. Lepoutre
Department of Pathophysiology;
University of Leuven,
Academisch Ziekenhuis Pellenberg, Belgium¡
Eternit N.V., Kapelle o/d Bos, Belgium
The Eternit factory at Kapelle o/d Bos employs about 2000
workers and 400 clerks, and processes yearly about 35,000 tons
of chrysotile, 3,000 tons of crocidolite, and 1,000 tons of
amosite to manufacture a variety of asbestos-cement building
materials and pipes.
In the present study findings of yearly roentgenographic
examinations of the lung and the mortality of workers are related
to the age of the workers and to the duration and level of dust
exposure. We looked for possible effects of exposure to asbestos
in the way of pneumoconiosis, pleural changes, and malignancies.
The risks incurred by people engaged in mining, milling,
carding, and other manipulations of asbestos fibres are reasonable
well documented, but little epidemiological data have been published about the asbestos-cement industry.
In the factory studied,
asbestos fibres are manipulated only while unloading the
river
boats, while carrying asbestos in paper bags (jute bags until
1975), and while preparing the mixture consisting of sand, cement,
asbestos, and water.
Some asbestos may be set free during these
preparative stages and pollute other areas of the plant.
In
addition, dust of the asbestos-cement mixture, when dry, may become airborne.
: 525:
METHODS
DUST CONCENTRATION.
In 1969 the filter-membrane method for the
counting of fibres In the air was Introduced in the factory.
This
technique was described by Holmes (1965) and by the British Occupational Hygiene Society (1968).
The concentration of fibres was
measured twice a year at many different sites, distributed throughout the factory.
The sampling was done at mouth level, over a
period of 8 minutes, and during working hours.
We have considered the following five typical working areas,
in decreasing order of business i area 4. which involves the
handling of asbestos fibres, such as carrying asbestos bags,
milling asbestos, preparing the asbestos-cement mixture; area 3,
where asbestos-cement products are finished by the action of
sawing, drilling, chafing, and the likei area 2. which Is situated between the previous two and where the asbestos-cement
sheets and pipes are moulded, pressed, dried, and lifted off
the mould) area 1. where very little dust exposure is expected,
like the offices, area 0. which represents work outside the
asbestos industry, with negligible dust level.
Actual fibre counts obtained with the filter-membrane
method are available for 1970 through 1976 Table It dust concentrations have been much higher In previous periods, but the
actual values can be estimated approximately.
We reasoned as
follows i Since a roughly tenfold Increase in fibre concentration
can be measured during a break-down of exhaust ventilators, or
526
as a consequence of negligence, a dust level of that magnitude
probably reflects the
conditions which prevailed before 1940,
when little attention was being paid to dust control; no asbestos
was available from 1940 through 1944, so we- assigned a zero concentration to these years; in 1945 some of the equipment was renewed, and between 1955 and 1965 the factory was given a major
overhaul; minor
improvements have been added since.
In summary,
we believe that the dust concentrations have followed a more or
less logistic decay law, with an inflection point in 1960, which
can be expressed by the formula c
=
co/(l + 1.16 ^
), where
c is concentration in fibres/ml, y is a number (year) between
1928-1977, and c Q is 0.4, 16, 24, and 100 fibres/ml for areas 1,
2, 3, and 4 respectively (i.e. roughly 10 times present day
levels).
Although it is somewhat arbitrary to choose this parti-
cular function, it yields figures in compliance with the reasoning outlined above, and with the dust levels measured in recent
years (Fig. 1 ) .
FIBRE-YEARS.
The degree of individual exposure to asbestos was
expressed in fibres per ml multiplied by the duration in years,
or "fibre-years" in short.
Since employees may work consecutive-
ly in different areas, fibre-years for any individual were calculated as "Z. (fibres/ml).
, where i refers to the type of area
and y to the year.
The workers, and consenting clerks, were interviewed during
the year 1975 by a social nurse, who filled in a questionnaire
527
on past and present work with emphasis on any kind of dust exposure (also noted were any kind of lung disease and the smoking
habit).
From these data we calculated individual fibre-years
according to the above formula, and hence the fibre-years distribution of all intervieweesj extrapolating from this, the analogous
distribution was obtained for all workers in 1963 through 1977
(29,366 man-years), bringing into account the annual changes in
number enlisted and in dust concentration.
DIAGNOSIS OF ASBESTOSES. The name asbestosis is used in this
paper to designate a pneumoconiosis due to the inhalation of
asbestos, and consisting in
fibrosis of the lung interstitium
and/or if the visceral pleura, according with the definition
given by Becklake (1876)i the name does not cover other effects
of asbestos exposure, for instance the thickening of the parietal
pleura.
All cases of asbestosis
reported herein, were dis-
covered with the help of radiographs, and any employee
with
small opacities on his chest roentgenograph was subjected to
further investigation.
The requirements for making the diagnosis
of asbestosis were threefold« (a) the presence of irregular small
lung opacities with profusion of at least l/.Ot and (b) the presence of at least two of the following abnormalities! ill defined
outline of heart and/or diaphragm, clubbing of the fingertips,
crackling rales audible over the lung bases, carbon monoxide
transfer or vital capacity less than 76% of the predicted values.
A decrease of vital capacity was disregarded it if could be
attributed to some obvious restrictive lesions other than as-
528
bestosis, or to obstructive lung disease.
The mere presence oí
pleural plaques was not used as a criterion for asbestosis.
ASBESTOSIS AND MORTALITY STUDY.
The population studied consist
of all male workers who, within the 15 years period of 1963
through 1977, worked in the factory for at least 12 months.
Only for that group adequate medical and administrative records
were available.
The number of male workers for
each of these
years was obtained from the factory records; which yielded a
total of 29,366 man-years. The age distributions could be obtained from factory records for the years 1975 (Table 1), 1976,
and 1977; these were nearly identical, and the 1975 distributio
was assumed to be
representative for the whole period of
1963
tftmugh 1977. The female workers are not included in the mortal
study, as they suffered only 3 deaths during the given period,
which is not surprising as most female workers leave the factor
before reaching the age of 50.
ROENTGENOGRAPHIC STUDY.
In 1975, 2,650 employees were enlisted
of which 1,973 (74.5%) had both a history taken and a chest
roentgenograph made in that same year; they are distributed as
followst 1,963 male workers (85.5% of the enlisted), 214 female
workers (81.4%), 78 male clerks (25.1%), and 2 female clerks
(1.8%).
The distribution with respect to age and exposure is
given in Table 11. The yearly chest roentgenograph is compulsory for all workers, while clerks submit to this examination
on a voluntary basis.
529
The ro ent Reno graphs consist of an antero-posterior view of the
chest, on a full-size film (0.36 x 0.36m), taken at 60 to 80kV.
The films were read jointly by two of us, as part of a routine
industrial medicine program, and were always compared with the one
taken the year previously! all previous films were at hand to be
consulted in case of doubt.
The roentgenographic findings were coded according to the
extended system elaborated by the International Union Against
Cancer.
The irregular small opacities, were graded according to
the full 12 point scale of the UICC /Cincinnati Classification
(1970)i we considered the three normal subcategories! 0/-, 0/0,
0/11 and the three abnormal categories i 1, 2, and 3 (the subcategories were pooled because of the small numbers observed).
The pleural changes were interpreted ast (a) pleural adhesion«
(b) blurred contour of heart and/or diaphragm! (c) pleural plaquei
and (d) calcified pleural plaoue. Three grades (1= minimal, 2=
moderate, 3= marked) were noted and pooled for analysis because
of the small number observed.
Pleural adhesions are exudative
sequelae, e.g. obliteration of the costo-phrenic angle.
The
pleural plaques comprise "hyaline" plaques and probably a few
cases of post-exudative diffuse thickening, as it is not always
possible to distinguish these two on a routine chest roentgenogram.
Also noted were changes suggestive for cancer, tuberculosis, sarcoidosis, heart disease, active or inactive tuberculosis, and
trauma (e.g. rib fractures, thoracotomy).
53o
All causes of death were checked through the family doctor
and/or a social nurse who visited the relatives (Belgian authorities never release individual information from death certificates).
The one case of pleural mesothelioma was diagnosed by
one of the authors with the help of J. Lauweryns, head of the
department of pathology at the university of Leuven.
Expected mortalities by age group and by cause of death
were calculated from the yearly mortality rates for Belgium,
available in the tables of the World Health Organisation for
1965 through 1975¡ data for other years were extrapolated.
RESULTS
Table III gives the number of chest roentgenograms with
small lung opacities and pleural changes, by group of exposure.
We saw no small
opacities with profusion greater than 2.
We
pooled all grades of pleural changes because the numbers are
small; grade 3 was scored only by the calcified plaques.
We found 29 cases of asbestosis during the 15 years' period
of 1963 through 1977 (Table VII).
The total mortality, by age and by cause of death, is given
in Table VIII, and details concerning the malignant neoplasm
are given in Table IX.
Among the cases of respiratory cancer there were three
cancers of the upper airways, 17 cancers of the lung, and one
mesothelioma of the pleura.
531
DISCUSSION
FIBRE-YEARS
We realize our estimates of dust concentrations prevailing
in the past are good guesses as best. Nevertheless! it is unlikely that they would be off reality by more than an order of
magnitude andi more important, the figures proposed have at least
relative accuracy» the dust levels in areas where dry
asbestos
fibres are being handled is certainly higher than in other areas,
and the dust level certainly was higher during the first 30 years
than during the last 15 years of the factory's existence.
The concept of fibre-years is useful if indeed harmful
effects of asbestos are proportional both to the concentration
of fibres in the air breathed, and to the duration of exposure.
This appears to be a good approximation for the development of
asbestosis (Murphy et al, 1971), of benign pleural changes
(Rossiter et al., 1972), of lung cancer (McDonald et al., 1971),
and even of mesothelioma (McDonald, 1978), for which there also
is indirect evidence for a dose-response relationship from
autopsy studies (Whitwell et al., 1977).
Since workers may be
employed In different areas for different periods and even end
up as clerks, it was difficult to ignore the concept of fibre-years.
A limitation of the fibre-years concept is that It takes no account
of the level of first exposure. This should not invalidate our
analysis very much, as in most cases the relatively heavier exposure also came first for two reasons i initial employment at
the plant usually happened to be the dustier one, and for any
kind of employment the dust level has decreased with time (Fig.l).
532
ROENTGENOGRAPHIC CHANGES
We excluded 15 cases from the study, either because of a history of sarcoidosis or of exposure to silica dust, the roentgenographs changes of which would otherwise be interpreted due solely to asbestos exposure.
The profusion of small lung opacities
and of benign pleural changes correlate strongly with fibre-years
and with age. We therefore examined, by age group, the linear
trend in proportions (i.e. number with changes per number roentgenographed by fibre-years groups).
The trends are significant for
small lung opacities grades 1 and 2 (Table IV), and grade 0/1
(not shown, P = 0.001); the trend is also significant for pleural
adhesion (Table V ) , and for pleural plaque (Table VI)¡ the trend
is not significant for calcified plaque (not shown).
To rule out the effect on our analysis for post-inflammatory
pleural changes, unrelated to asbestos exposure, we reexamined
the given trends in proportion after eliminating 175 cases with
evidence of old or recent chest trauma (e.g. rib facture), tuberculosis (e.g. hilar calcification), or empyema. This did not alter
the conclusions given above (for pleural adhesion then P = 0.008;
for pleural plaque then P = 0.005).
We confirm the study on asbestos-cement workers by Weill et
al. (1977), who found dose-response relationship for small lung
opacities.
We now also find such a relationship for benign pleural
changes, which had already been described in the case of asbestos
miners (Weill et al., 1973, 75; Rossiter et al., 1972) and of
shipyard workers (Sheers and Templeton, 1968; Harries et al.,
1972).
The prevalence of calcified plaques in our study is not
533
related to fibre-years, although the number of cases in which
this lesion was seen may be too small to uncover the relationship.
ASBESTOSIS
The number of cases with diagnosed asbestosis increases
significantly with the degree of exposure expressed in fibre-years
(Table VII).
We observed no case of asbestosis for an exposure
below 100, and only one case in the range 100-200 fibre-years.
Only two workers who never had handled free asbestos fibres (area
4) developed asbestosis, but their degree of exposure (starting
around 1930) had nevertheless been high) 435 and 350 fibre-years,
respectively (on account of work in area 3). • The present study
thus indicates that the handling of asbestos-cement is less
dangerous than the handling of the free asbestos fibres. However,
less dust is generated in the former and therefore, from the present data, we cannot know whether asbestos-cement dust is less
fibrogenic in se than free asbestos.
MORTALITY
The total mortality is not significantly different from what
would be expected in a Belgian population of matched age and sex
(Table VIII).
There is, however, a significant excess mortality
due to external causes, probably because factory workers are at
higher risk of accident than the general population* indeed there
were 10 occupational accidents, of which two were actually traffic
accidents on the way to work.
There is also an excess mortality,
53*
not quite significant, due to non-malignant respiratory disease,
which probably must be attributed to the seven deaths due to
asbestosis (Table VIII).
The mortality due to all malignant neoplasm does not exceed
expectation
(Table VIII), but there is a significant excess of
deaths due to , and only to, digestive cancer (Table IX). A similar excess for digestive cancer, and not for respiratory cancer,
was found by Van de Voorde et al. (1967), for workers employed
in this same factory.
Either this excess is due to asbestos ex-
posure, or the workers studied differ from the general Belgian
population.
An argument
against the effect of asbestos expo-
sure is that we found no significant relationship between excess
of digestive cancer and fibre-years (Table X ) .
Since one might question the validity of comparing
the mor-
tality in a population of enlisted workers with the figures of
national statistics, we have also made comparisons with internal
case-controls.
The principles of the method were explained by
Liddell et al. (1977).
In the present analysis, for each male
worker who died of respiratory or digestive cancer, we selected
four controls, at random, out of the group of all male workers
alive at least one year after the date of expiration, and matched
for age ± 1 year and date of enlistment + 1 year.
We have compared
the distribution of the cases and the controls with respect to
dust exposure in fibre-years, which could differ only in the
fibres/ml and not in the years« there is no significant difference (Table XI).
This means that the dust exposure did not affect
the mortality due to respiratory cancer and digestive cancer in a
535
significant way (eventhough the one case of mesothelioma is almost certainly related to the heavy exposure, and is included
in the analysis).
Table XII shows that the incidence of asbestosis has markedly
decreased during the 15 years period of observation, which confirms the assumption of strongly decreasing dust concentrations
10 to 20 years earlier.
On the other hand, the incidence of
respiratory cancer, but not of digestive cancer, is increasing;
since the dust concentrations have been decreasing and, moreover,
we could not find a dose-response relationship, we believe this
finding merely
reflects the evolution in the Belgian population,
where the incidence of lung cancer has been increasing, and that
of digestive cancer is slightly decreasing.
CONCLUSIONS
The following is important with regard to the workers enlisted in the asbestos-cement factory we have investigated!
(1) there is a strong dose-response relationship for asbestosis,
and no case was observed for exposures less than 100 fibreyears ;
(2) there is a dose-response relationship for roentgenographic
small lung opacities, pleural adhesions, and pleural plaques;
(3) the general mortality is not in excess of the national expected figures, but there is an excess of accidental deaths i
(4)
the mortality due to malignant tumor is not in excess of
536
the national expected figures¡
(5) there is no excess mortality due to respiratory cancer¡
(6) there is an excess mortality due to digestive cancer, which
shows no dose-response relationship when compared with the
national expected figures or with internal case-controls•
537
fibres/ml
100 -
-
^
^
area U
90
80
70
60
-
50
1930
Fig. 1 .
1940
1950
year
1960
1970
1380
Evolution with time of dust concentrations in four types of area in
the plant as estimated according a logistic decay law ; points are mean values
actually measured in area 4 ( o ) , area 3 ( • ) ,
538
and area 2 ( + ) .
REFERENCES
Becklake , M . R . ( 1976 ) . Asbestos-related diseases of the lung and other
organs : their epidemiology and implications for clinical practice .
Amer.Rev. resp. Dis. , 114 , 187 - 2 2 7 .
British Occupational Hygiene Society ( 1 9 6 8 ) .
Hygiene standards for chrysoMIe
dust . A n n . occup. Hyg. , 11 , 47 - 69 .
Harries , P . G . , Mackenzie , F . A . F . , Sheers , G . , Kemp , J . H . , Oliver , T . P .
and Wright , D . S . ( 1972 ) .
Radiological survey of men exposed to asbestos
in naval dockyards . Brit.J.industr.Med. , 29 , 274 -
Holmes , S. ( 1965 ) . Developments in dust sampling and counting techniques in
the asbestos industry . A n n . N . Y . A c a d . S c i . , 132 , 288 - 297 .
Liddell, F . D . K . , McDonald , J . C . , and Tholas , D . C . ( 1 9 7 7 ) . Methods of
cohort analysis : appraisal by application to asbestos mining . J.roy.statist.
Soc.A. , 1 4 0 , Port 4 , 4 6 9 - 4 9 1
.
McDonald , J . C . , McDonald , A . D . , Gibbs , G . W . , Siemiatycki , J . , and
Rossiter , C . E . ( 1971 ) .
Mortality in the chrysotile asbestos mines and
mills of Quebec . A r c h , environm. H l t h . , 99 , 677 -
McDonald , J . C . ( 1978 ) . Exposure relationships and malignant mesothelioma .
Proceedings of Asbestos Symposium , 1977 , e d . H . W . G l e n , National
Institute for Metallurgy ,
Randburg 1978 , pp. 49 - 64 .
Murphy , R . L . H . , Ferris , B . G . , Burgess , W . A . , Worcester , P . H . J . , ond
Gaensler , E . A . ( 1971 ) . Effects of low concentrations of asbestos : C l i n i c a l ,
environmental , radiologic and epidemiologic observations in shipyard pipe
coverers and controls . New Engl . J . M e d . , 2 8 5 -
539
Rossiter , C E . , Bristol , L . J . , Carter , P . H . , Gilson , J ; C . , G r o i n g e r , T . R . ,
Sluis-Cremer , G . K . , and McDonald , J . C . ( 1972 ) . Radiographic changes
in chrysotile asbestos mine and mill workers of Ouebec . Arch.environm, H l t h . ,
24 , 388 -
Sheers , G . , and Temple.on , A . R . ( 1968 ) . Effects of asbestos in dockyard
workers .
B r i t . med. J . , 3 , 574 -
UlCC/Cincinnati
Classification of the Radiographic Appearances of Pneumoconioses
( 1 9 7 0 ) . Chest , 58 , 57 - 67 .
Van de Voorde , H . , Meulepas , E. , G / s e l e n , A . , en Koppen O . ( 1967 ) .
Doodsoorzaken b i j de bevolking woonachtig rond en b i j de arbeiders werkzaam
in een asbestverwerkende nijverheid in het noorden van Brabant . Acta rubere.
pneumol.beIg. , 58 , 924 - 942 .
W e i l l , H . , Zisktnd , M . M . , Waggenspack , C . , and Rossiter , C . E . ( 1975 ) .
Lung function consequences of dust exposure in asbestos cement manufacturing
plants . A r c h . environm.Hlth. , 3 0 , 88 -
Whitwell , F. , Scott , J . , and Grimshaw , M . ( 1977 ) .
occupations and asbestos- fibre
Relationship between
content of the lungs in patients with pleural
mesothelioma , lung cancer , and other diseases .
54o
Thorax , 32 , 377 - 386 .
Table I
DUST CONCENTRATIONS IN FIBRES/ml MEASURED IN FOUR TYPES OF WORK AREA
AREA 1
YEAR
mean
1973
-
1974
0.03
1970
1971
1972
1975
-
1976
0.05
x
SD ( n ) x
AREA 3
AREA 2
mean
SD (n)
mean
SD (n)
2.3
0.7(4)
-
2.1
0.4(4)
3.6
3.0 ( 8)
0.02(6)
0.02(6)
SD = Standard deviation ;
AREA 4
mean
SD
(n)
18.0
36.1 (33)
9.2
13.6 (39)
1.6
1.7(37)
2.4
2.3 (20)
10.8
22.-1 (115)
2.0
2.2(14)
2.2
1.7(15)
9.8
16.1 (85)
1.5
1.8(31)
2.6
5.8(23)
13.9
23.0 (47)
1.1
0.9 (31 )
2.1
3.3(52)
11.2
22.2 (152)
1.3
1.4(27)
1.8
1.5(19)
10.7
25.0 (85)
n = number of measurements .
541
Table II
DISTRIBUTION BY AGE AND BY EXPOSURE OF WORKERS AND CLERKS
EXAMINED anno 1975
FIBRE-YEARS
AGE-GROUP
TOTAL
15-34
35-44
45-54
186
180
94
1062
259
0-
49
602
50-
55-65
99
34
96
94
35
1 0 0 - 199
1
121
162
67
351
2 0 0 - 399
0
22
137
82
241
4 0 0 - 799
0
1
17
13
31
800-1599
1
1
3
9
14
638
427
593
300
1958
total analyzed :
total roentgenographs
1973
cases of silicosis and sarco idosis eliminated :
5^2
15
Table III
NUMBER OF ROENTGENOGRAPHS LUNG CHANGES FOUND IN 1 958 EMFLOY'ES
EXAMINED
anno 1975
SMALL OPACITIES
PLEURAL CHANGES
FIBRE-YEARS
0/-
0/0
0/1
1
2
., .
adhesion
1,2
0-49
50-
128
886
46
2
0
36
contour
plasue
celo': - '':
piar,-.;'.?
0
15
4
blurred-
1,2
1,2
1 , 2. :
99
3
225
29
2
0
15
0
7
7
1 0 0 - 199
5
302
35
9
0
34
3
23
6
200 - 399
5
184
40
11
1
30
2
16
6
4 0 0 - 799
0
22
6
5
8 0 0 - 1599
1
11
142
1630
total changes
2
1
157
1
27
1
7
1
0
3
0
2
125
6
5*3
0
1
67
0
23
Table IV
PREVALENCE IN % OF
FIBRE-YEARS
s - t - u LUNG OPACITIES GRADES 1 AND 2
anno 1975
x
AGE - G R O U P
15-34
35-44
45-54
TOTAL
55-65
0-
49
0
1.1
0
0
0.2
50-
99
0
0
1.1
2.9
0.8
1 0 0 - 199
0
0
2.5
7.5
2.6
2 0 0 - 399
0
4.5
2.2
9.8
5.0
4 0 0 - 799
0
0
5.9
15.4
9.7
800-1599
0
0
33.3
0
7.1
total %
0
0.7
1.7
5.3
1.5
linear trend with pooledregressioncoefficients : P = 0.001
x
median taken as the score
544
Table V
PREVALENCE IN % OF PLEURAL ADHESIONS , anno 1975
FIBRE -YEARS"
0 - 4 9
TOTAL
AGE-GROUP
15-34
35-44
1.2
3.2
45-54
55-65
6.7
11.7
3.4
5.8
99
0
4.2
6.4
14.3
100- 199
0
3.3
12.3
14.9
9.7
2 0 0 - 399
0
4.5
11.7
15.9
12.4
4 0 0 - 799
0
0
17.6
30.8
22.6
800 - 1599
0
0
33.3
22.2
21.4
1.1
3.5
9.8
15.0
6.4
50-
total %
linear trend with pooled regression coefficients : P = 0.002
x
median taken as the score
545
Table VI
PREVALENCE IN % OF PLEURAL THICKENING , onno 1975
FIBRE-YEARS
x
AGE - GROUP
15-34
35-44
45-54
TOTAL
55-65
0-
49
0
0.5
3.3
8.5
1.4
50-
99
0
0
6.4
2.9
2.7
1 0 0 - 199
0
2.5
8.0
10.4
6.6
2 0 0 - 399
0
0
9.5
3.7
6.6
4 0 0 - 799
0
0
17.6
15.4
16,1
8 0 0 - 1599
0
0
33.3
11.1
7.1
total %
0
0.9
7.1
7.3
3.4
linear trend with pooled regression coefficient»: P =0.01
x
median token as the score
546
Table VII
INCIDENCE OF ASBESTOSIS anno 1963 THROUGH 1977
FIBRE-YEARS X
0-49
50-
number
%
11 340
0
0
99
4 094
0
0
100- 199
5 791
1
0.02
2 0 0 - 399
6 629
7
0.11
4 0 0 - 799
1 179
8
0.68
8 0 0 - 1599
307
10
3.26
1600-3200
26
3
11.54
total
29
29 366
Inear trend in proportions
x
NEW CASES
MAN-YEARS
:
P < 10
median taken as the score
547
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o
o
oo
co
CM
OS
S 2 5
M
h- Q
M
¿
z>S
O v> U
3
CM
O-'
3
<
(-
O
<o
8,
Z
«o
<
z
o
C- 0* MJ
—
z
o
z
O
—
-<>•<*
Ji-S
H-E a
o«t5
m
oo
4
«
N
v o o
vi
S fc* Z
li
z
<
z
,—
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co
— </>
—
=
S
«
2
-JI3
<
iiü
20
co
r<» oo
o
CM
« S 5
^
CO
•O
CM
•*
-*
—
CO
<0
—
M}
CM
M)
O
^
O
MJ
53
co
—
CK
>0
co
o>
CN
CN
o.
.5
S S 5 S 53
0°=
<o
io <o >o vt <o
IM n
^ «i
UJO
1!
"8
ir
5^P
O
8
I
e e ç
Table IX
DEATHS DUE TO MALIGNANT NEOPLASM OBSERVED IN MALE WORKERS
BY
AGE AND SYSTEM AFFECTED ( 2 9 366 man-years)
AGEGROUPS
respiratory
digestive
nervous
lymphoid
& hematopoietic
other
not
specified
TOTAL
15-24
1
25-34
35-44
2
45-54
6
3
14(1)
55-65
1
2
1
14
4
2
17
4
2
2
total :
22
expected!
22.3
11.8
2.1
3.9
2.4
P (2)
N.S.
0.04
0.10
N.S.
N.S.
(1)
(2)
.
1
includes one case of pleural mesothelioma
in a Poisson-distribution with the expected number as the mean .
5^9
11
34
1
12.9
48
55.4
Table X
DEATHS OF MALE WORKERS DUE TO RESPIRATORY AND DIGESTIVE CANCER
BY EXPOSURE GROUP
FIBRE - YEARS '
MAN-YEARS
1963-77
.
RESPIRATORY CA.
2
expected
observed
DIGESTIVE
CA.
observed
expected
2.76
0-49
11340
6
5.16
4
50-99
4 094
3
2.43
1
1.32
1 0 0 - 199
5 791
5
4.60
1
2.46
2 0 0 - 399
6 629
4
7.47
7
3.93
400-799
1 179
1
1.95
2
1.00
800-1599
307
2
0.57
2
0.29
1600 - 3200
26
l3
0.17
0
0.04
22.35
17
total
29 366
linear trend In proportions :
1
22
P =0.22
median taken as the score
2 adjusted for age distribution within fibre-years groups
3 pleural mesothelioma
55o
11.80
P=0.16
2
Toble XI
DISTRIBUTION BY EXPOSURE GROUP OF CANCER CASES AND OF
MATCHED INTERNAL CONTROLS ( 4 per cose )
FIBRE-YEARS"
0-49
RESPIRATORY CANCER
cases
controls
6
3
DIGESTIVE CANCER
cases/total
cases
controls
cases/total
20
a23
4
16
0.20
17
0.15
1
5
0.17
a42
1
14
0.07
50-
99
100-
199
5
7
200-
399
4
32
ail
7
20
0.26
400-
799
i
8
an
2
8
0.20
800 - 1599
2
4
0.33
2
5
0.29
l*x
0
1.00
17
68
1600-3200
total :
22
88
linear trend
in proportions :
x
xx
p = aii
median taken as the score
pleural mesothelioma
551
P = 0.23
Table XII
NEW CASES OF
PERIOD
ASBESTOSIS,AND DEATHS BY CANCER
MAN-YEAR S
ASBESTOSIS
MALIGNANT NEOPLASM
respiratory
digestive
%
%
other
%
%
1963-1967
9 805
13
0.13
5
a05
6
0.06
2
0.02
1968-1972
10 423
ii
an
8X
a08
6
a06
4
0.04
1973-1977
9 138
5
0.05
9
aiO
5
0.05
3
0.03
29 366
29
0.10
22
0.07
17
a06
9
0.03
to fai
x
includes one case of pleural mesothelioma
552
Cambios rontp.enop.rá fieos del rjnlmón
relacionados con la exposición al
polvo de los empleados de una
fabrica de fibrocemento.
L. M. Lacquet y J.Lepoutre, M.D.
(Bélgica)
En una fábrica de fibrocemento que funciona desde
1905 y emplea 2.400 obreros y 400 empleados se ha examinado a codo el personal a partir del I o . de mayo de 1963.
til estudio muestra que para el período 1963 a 1976 se
produjeron 23 casos de asbestosis, 1 caso de mesotelioma
pleural, 7 casos de cáncer de pulmón, 2 casos de cáncer
gastrointestinal y 12 casos de tuberculosis evolutiva.
El diagnóstico de la asbestosis se basó no sólo en
el rontgenograma de pulmón sino también en la espirometría, en la prueba de difusión del óxido de carbono y en
exámenes clínicos y de laboratorio relacionados con la
cantidad de oolvo en la fábrica.
El promedio de tiempo de exposición de los 23 obreros con asbestosis era de 24 años, y la intensidad de la
exposición era de 1.077 fibras-año.
Es interesante señalar que no se encontró ningún
caso de asbestosis con menos de 100 fibras-año. La asbestosis se encontró únicamente en los obreros que trabajaban con amianto puro. La prevalencia de asbestosis en
ìa fábrica no se ha modificado en los últimos 13 años.
En los últimos tiempos han ido disminuyendo claramente
los nuevos casos.
Se han encontrado menos casos de lo previsto de tumores malignos de pulmón, durante este período de trece
años y medio, esto es, se detectaron sólo ocho casos de
los 14,6 esperados. También el número de cánceres gastrointestinales es ligeramente inferior al esperado.
553
vi/7
RIGIDITE
OTAPHRAnniTinilF
CPRRFLATTPM R A n i P I . P n i ^ M F
A.
HIRSCH,
L.ni
FT FXPPTTTTPM
A L'O^TA^TF
FT rHTRHrinT , "AI F HAMS 47
HEflZA,
CI. HANnnLO,
3.
:
T'lPRAPnTPHIFS
RTGMCM.
S e r v i c e de Pnaumolooie, H o o i t a l Intercommunal,
Créteil
France.
L'atteinte pleurale radioloqiciue (énaiRsissement pleural,
nlanue pleurale hyaline, calcification pleurale) est classiquement considérée comme un bon indice d'exposition a l'amiante (1,2,3).
Au cours des examens radiolooiques effectués
chez des sujets exposés ou ayant été exposés a l'amiante, nous
avions constaté un sinne fréquent et non encore décrit : une
ou plusieurs rectitudes seqmentaires
d'une coupole, inter-
rompant ou remplaçant la courbure normale du diaphranme, et
non associées a un épaississement ou a une hyperdensification
(fiqure. 1 ) . L'objet du présent travail est de vérifier que
ce signe rediologique correspond a une modification anatomique du diaphragme, d'établir sa relation avec une exposition
professionnelle a l'amiante, et d'étudier sa sensibilité, en
précisant l'intensité et la durée de l'exposition
profession-
nelle, la longueur de la période de latence, et sa fréquence
par rapport aux autres anomalies pleurales et/ou parenchymateuses observées lors de l'exposition a l'amiante.
Matériel et méthodes:
Ce travail porte sur 47 observations (43 hommes et 4 femmes, âgés de 20 a 75 ans, age moyen : 57,6 - 4) de thoracotomies consécutives. Les patients opérés pour mesothelioma ont
été exclus, la majorité des malades ayant été opérés pour
cancer bronchique (37
cancers bronchiques et 10 autres causes).
555
Avant 1'intervention, l'un de nous (FI.PI.) a procédé a une
enquêta a l'aide d'un questionnaire standardisé, constitua
de questions a réponses fermées, portant sur le curriculum
laboris ot l'existence d'une exoosition professionnelle a
l'amiante (résultats tableau 1). Il a ainsi été possible
de déterminer la durée de l'exposition et celle de la période
de latervte s'écoulant entre le début de l'exposition et la
date de la thoracotomie. L'existence d'une exposition professionnelle était indépendante du motif de la thoracotomie.
D'autre part, il a été impossible, lors de l'étude des relations entre exposition et manifestations pleurales radiolooinues et chirurnicales, de distinnuer entrB expositions
définies et suspectes, du fait de la faiblesse des effectifs
et du caractère subjectif de cette distinction qui ne reposait que sur la connaissance par le sujet d'une exposition
professionnelle a l'amiante. Des radiooraphies thoraciques
frontale et latérale de routine ont été effectuées dans tou3
les cas. Elles ont été analysée par deux lecteurs (A.H et
L«.n.) selon la Classification internationale BIT U/C 1971 avec
arbitrane anres discussion. Les lecteurs précisaient en cutre l'aspect radiolonique des diaphrapmes, en mentionnant
l'existence d'une rioidité, son siane, sa taille, snn aspect
calcifié nu non. Lors rie la thoracotomie, le chirurpien inspectait soinneusement la olevre pariétale, dans la rénion costale et diaphraomati que, et notait sur un shéma les anomalies
observées. Smiles les rinidités diaphraomatiques observées
du enté ooéré et sur les deux incidences frontale et latérale
ont été retenues nnur l'étude des corrélations anatnmn radiolorini.ier!, F?n nutre, una biopsie pulmonaire et une étude minéralooinun sur la nlevr'o et le narenchyme ont été effectuées,
dont les résultats seront publiés ultérieurement.
556
Résultats :
Nous av/ons noté dans 30 ?•> des cas (14 cas) des rioidités
diaphragmatiques visibles sur les deux indidences radioloqiques, des ôpaississements pleuraux uni ou bilatéraux dans
13 % des cas (6 cas), des calcifications pleurales, de sieoe
diaphraqmatique ou costal, uni ou bilatérales dans 14 % des
cas (7 cas, dont 4 siépeant du coté de 1'intervention), et
3 aspects de fibrose parenchymateuse. Sur le cliché frontal,
les rigidités diaphraqmatigues étaient de siBqe moyen 19 fois,
externe 7 fois, interne 4 foi9, enfin sur toute la coupole
dans 1 cas.
Sur le cliché latéral, le siane était moyen 20
fois, postérieur 11 fois, antérieur 2 fois, sur toute la coupole dans 2 cas.
Les dimensions de la zone raide dépassaient
5 cm dans 18 cas sur l'incidence latérale, dans 16 cas sur
l'incidenca frontale.
Lors de la thoracotomie, dans 38 % des cas (18 cas) il
existait des plaquea de la plèvre pariétale, de localisation
diaphraqmatique
at costale dans 9 cas, diaphraqmatique dans
I cas, costale dans 8 cas.
Le tableau 2 montre 80 % de concordance entre rigidité .
diaphraqmatique sur les incidences frontale et latérale et
plaque diaphraqmatique a la thoracotomie (6 cas) et absence
riqidité radioloqique et de plaque a l'intervention
(32 cas).
II existait 5 faux positifs (rigidité radioloqique aans plaque
a l'intervention) et 4 faux négatifs (plaque chirurgicale
sans rigidité radiologique).
Les tableaux 3 et 4 indiquent 1 B 9 relations de9 rigidités
diaphragmatiques radiologiquea et des plaques diaphraomatiques
chirurgicales avec l'exposition • l'amiante.
Le tableau 3
montre la fréquence des anomalies radiolooiques dans les deux
groupes, normalité du cliché et riqidité diaphraqmatique
557
étant
si"nifinativement différentes dans les deux oroupes.
Le tableau 4 montre la fréquence relative des plaques chiruroicales dans 1 B 3 deux nroupes, 46 % des sujets exposés
ayant des plaques visibles a l'intervention, de siene diaohranmatique et costal dans 9 cas sur 17.
La durée d'exposition chez les sujets porteurs de
plaques chiruroicales était en moyenne de 19,6 ans - 12,6,
contre 16,9 ans - 7,56 chez les sujets exposés indemnes
de plaquen chiruroicales, cette différence n'étant pas siqnificative.
La période de latente chez les sujets exposés a l'amiante indemnes de plaque pleurale a la thoracotomie était
de 25,9 ans - 13,9, contre 39,3 ans - 5,9 chez les sujets
exoosês porteurs de plaque pleurale chiruroicale, la différence étant sinnificative a 0.001. La période de latente
était sensiblement identique pour les sujets Bxposés présentant une ridioité diaphraomatique radioloqique (37,6 an3 5,2), une calcification pleurale radioloqique (37,2 - 6,3),
ou un énaissement pleural radioloqique (35 ans - 5,5). Par
contre, elle était nettement moindre chez les sujets a radionraphie normale (27,6 ans - 10,1) sans qu'il soit possible
d'effectuer un test statistique.
Discussion:
Les calcifications pleurales sont observées dans 0,15
a 0,20 r'> des radiooraphies thoraciques de routine dans la population étudiée (l).
Elle sont actuellement considérées
comme le témoin d'une exposition pasaée a l'amiante ou au
talc, rsi l'on a éliminé un antécédent pleural infectieux ou
traumatique (2,3).
Elles sont plus fréquentes que les anoma-
lies onrenchymateuses, représentant le seul sinne radiolonique
dans la moitié des cas (4,5 , 6, 7 ) . Des plaques pleurales ont
558
pu etra observées a l'état endémique dans une rénion bulnare
dont le sol était riche en matériaux fibreux (8).
Leur va-
leur morbide repose sur la olus orande fréquence chez les ouvriers exposés a l'amiante et porteurs de plaques pleurales,
de l'asbestose (1), du cancer bronchique (9), et du mésothéliome (1,9). On a rapporté un cas de mesothelioma développé
au contact d'une plaque (10).
La fréquence des plaques pleurales au cours des thoracotomies consécutives effectuées dans un service rie chirurnie thoracique a antérieurement été ««tintée a 10 % (11).Dans
des Séries autopsiques consécutives de sujets adultes, les
plaques ont été constatées avec ries fréquences variables,
allant de 2,7 & dans une série de 1B29 autopsies faites chez
des vétérans (12) a 32 % chez les ruraux et 52 % chez les citadins dans une série de 438 autopsies effectuées dans 3 hôpitaux (13).
La fréquence constatée dans la présente étude
se rapproche de cas derniers pourcentages.
Il était indispensable de vérifier les relations entre rigidité diaphragmatique et aspect anatomique du diaphragme. En
effet, l'intérêt de cette confrontation eat illustrée par un
travail récent dans lequel 10 % des asbestoses histoloçiquement
démontrées s'accompagnaient
ment normal (14),
d'un cliché thoracique riqoureuse-
L'étude comparative de la riqiditô diaphra-
matique Bt de l'aspect macroscopique du diaphragme lors des
thoracotomies consécutives a montré une concordance satifal*»
sante.
Cependant, 4 plaques chirurnicales sur 10 n'ont pas
été vues sur les films, et 5 rigidités diaphraqmatiques sur 11
ne correspondaient pes a des plaques chirurnicales. Ces discordances font discuter les limites das môthories radiolonique et
chirurgicale.
De même que les épaissements pleuraux sont dif-
ficiles a distinguer du tissu oraisseux snus pleural (15,16),
B5 % ries plaques pleurales'hyalInes sont invisibles sur les
films (2).
Dans une série d'asbestoses autopsiées, l'examen
55?
histnlnnj.nua rlu diaphraonte a permis rie constater des microcalcifinations chez 86 '.•' des sujets, la frequence des calcifiontinns radiolnninues ne déoassant pas 9 75 (13). L'utilisation d'incidence nbliaue (17) ou des ultrasons (18) a été
prnpnséee nour améliorer la détection des plaques. L'asnect
macroscopique normal d'une coupleriiaphranmatiquene présume
pas non plus de son intéorité histolonique.
Los nlaquos pleurales pariétales sont habituellement
de siepe costal et diaphranmatique (19). Pour ces dernières,
elles sont localisées au niveau du centre tendineux du diaphranme, ce qui est a rapprocher du siepe habituellement moyen des rinidités diaphranmatiques rapportées dans cette
étude.
Le mécanisme de production des plaque9 reste obscur
et doit tenir compte de leur situation sous-pleurale, de
l'intégrité* fréquente du mesothélium qui les recouvre, de
l'abscence de symphyse pleurale ainsi que de leur sieqe, au
nivBau du centre tendineux ppur les plaques diaphranmatiques,
A
en renard des cotes pour les plaques de la paroi (20). Les
fibres d'amiante pourraient soit minrer au travers du poumon
(21), soit miprer a contre-courant par les lymphatiques thoraciques et intercostaux (22).
Nous nous sommes heurtés aux difficultés habituellement
siqnalées Dar les utilisateurs de questionnaire pour préciser
la ou les professions exppsées a l'amiante, l'intensité de
l'exposition, sa durée exacte ainsi que celle de la période
de latence (23). En définitif, nous n'avons ou distinquer
que 2 nroupes, exposés et non-exposés, l'exposition étant
toujours de niveau faible au moyen. Entre ces 2 nroupes, les
différences sont sionificatives pour la normalité du cliché
56o
et l'existence, chez les sujets exposés d'uno rinidité diaphraomatique nues sur les incidences frontale et latérale.
Par contre, elles sont peu sionificativ/es pour 1ns planues
costale et/oudiaphragmatiqueconstatées par le chirurnien.
Des réserves s'imposent toutefois, compte tenu notamment
de l'abscenca d'une population témoin, les sujets non eapssés
étant dans l'ensemble plus jeunes (aqe moyen : 51 an3 - 13)
que les sujets exposés (ane moyen : 59 ans - 12,5). Il est
d'autre part nécessaire, pour étudier la spécificité de ce
sinne, de préciser sa fréquence d'une part chez des témoins
appariés pour l'aae, le sexe, la consommation de tabac,l'état
respiratoire, et d'autre part dans diverses conditions dans
lesquelles l'exposition aux fibres n'intervient pas.
fl l'exposition de la période de latence chez les sujnts
exnnsés porteurs de plaques chirurgicales, nous n'avons pas
mis. en évidence de différence entre durée d'exposition et période de latence pour lea anomalies pleurales radioloniques
et chirurgicales. On sait que la durée d'exnosition neut être
tres breve, quelques mois (2à) ou même quelques semaines pour
les calcifications pleurales. La période minimale de latence
pour les plaques calcifiées, observées en renie générale chez
les sujets de plus de 50 ans (24), serait de 18 a 20 ans (4),
peut être beaucoup plus courte, inférieure a 8 ans (7). Le
fait qu'il n'a pas été possible de mettre en evidence une
différence entre nos deux groupes de sujets peut s'expliquer
par notre recrutement, la majorité des maladen étant onérép
pour un cancer bronchique, et présentant donc une période de
latence tras supérieure a la période de latence minimale des
calcifications pleurales. La lecture de clichés séquentiels
permettra de préciser la durée s'ôcoulant entre exposition et
anomalies radiologique pleurales. Il est vraisemblable que
l'aspect de rigidité précède la calcification dianhraqmatique
(24).
561
La si^nif icat.i on rip la ri ni dite dianhranmatique comme
indice nréc.ncn at/ou sensible ri'exoosition a 1 * amiante nécessite d'uno part uno annrnchn technique permettant, sa recnnnaiasancfi simplp, d'autre part dos études complémentaires précisant la snéfificité, la sensibili tí et la fidélité de ce sirne.
On nourra alors eovisaper de l'inclurn dans la classi-
fication radiolooique internationale des pneumnnonioses, dont
on a soni inni In caractère inadapté Pour les mapifnstatinps
pleuralnn liées a .1 'exnnsiti on a 1'amiante (75).
Remerciements:
Les conseils du flncteur PERDRIZET (Groupe Maladies
Respiratoires - Institutut natinnal de la santa et de la Recherche médicale) nnus ont Até tres utiles lnrs de la rédaction du manuscrit.
flous remercions les Docteurs RTSSC1N, CHAPANEIX, GUILLE
et LflfinE nui ont opéré les malades, et ont décrit soigneusement les modifications de la plèvre.
562
nTRLinnaAPmc
KLETNFELu, PI. (1966) Pleural ralniflcat.ion a.i sinn nf
silicatosis. Ann. 3. Fl. S c , ?51 : 215-224.
HOMRIHANF:, D. n»R; I.ESSOF, L.; RICHARDSON, P.C. (.1966)
Hyaline and calcified pleural plagues as an index of
exnosure to asbestos. A study nf rartinloniral and
pathnlonical features nf 100 cases uith a consideration
of epidemiolony. Rrit. med. 3., 1 : 1069-1074.
MiWRATIL, Fl., TRIPPE, F. (1972) Prev/alence nf nleural
clacificatinn in persons exposed to asbestos dust, and
in the aeneral population in the same district. Environ.
Res. 5 : 210-216.
SELIKOFF, 1.3. (1965) Occurrence of pleural calcification
amonn asbestos insulation workers. Ann. Neu York Acad. Sc.
132 : 351-367.
FREUNDLICH, I.n., GREENING,. R.R. (1967) Asbestosis and
associated medical problems. Radiology, 89 : 224-229.
KIVILU0T0, R. (1970) Asbestosis : aspects of its radiological features. Pneumoconiosis Proceedings of the
International Conference, 3ohannesbouro 1969, 1 vol.,
Cape Toun Oxford University Press 253-255.
FLETCHER, D.E. (1911) Asbestos-related chest disease in
Joiner9. Proc. Roy. Soc. ned., 64 : 837-838.
RURILKOV, T., FIICHAILOVA, L. (197Ö) Asbestos content of
the soil and endemic pleural asbestosis. Environ. Res.
3 : 443-451.
FLETCHER, O.E. (1972) A mortality study of shipyard worker
uith pleural plaques. Brit. 3. Industr. fled. 29: 142-145.
LEWINSOHN, H.C. (1974) Early malionant changes in pleural
plaques due to asbestos exposure : a case report. Brit.
3. Ois. Chest 68 : 121-127,
HERTZOG, P., TOTY, L., PERSONNE, Cl (1972) Plaques pleurales .pariétales fibrohyalines. 3. Franc, ned. Chir.
Thorac. XXVI : 59-70.
ROBINSON, 3.3. (1972) Pleural plaques and splenic capsular
sclerosis in adult male autopsies. Arch. Pathol. 93 :
118-122.
563
HFiiRpiAtl, L. (1966) Asbestos bodies and oleural plaques in
a finnish series of autonsy casus. Acta Path. Microbiol .
Scand. Suppl. 101 : 1-107.
E P L m , G.R.; rie LOUD, T.C.; GAENSLER, E.A. (1978) Normal
chest roentnenonrams in chronic diffusa infiltrative luno
disease. N. Enn. 3. («led. 298 : 934-939.
CLOCK, M.C., TUTGC, H a . , BALL, M.F. et coll (1972) SHB00US
borderinn the luno on radiooraphs of normal and obese
persons. Thorax 27 : 232-238.
«IX, U.A. (1974) Extrapleural costal fat. Radiology 112:
563-565.
riAKENZIE, F.A.F., HARRIES, P.G. (1970) Chanoino attitude
to the diannosis of asbestos disease. 3. Roy. flav. Fled.
Serv. 56 : 116-123.
Symposium nn the radio.l.oov of onaumoconiosis, Pneumoconiosis
Prnceedinnr. of the International Conference, 3ohanne5bourn
.196°, 1 un].. , Gape Toun Oxford University Press, 197Ô. 279.
RORERTS, U.C., FERRANS, V.3. (1972) Pure collaoen plaques
nn the dinohranm and pleural Ghost 61 : 357-360.
THQflSONv
3. G. (197P) The pathogenesis of pleural plaques.
Proceedings of the International Conference, Johannesbourn
1969,
lvol., Caoe Toun Oxford University Press, 138-1¿1.
KIVILUOT0, R. (1960) Pleural calcification as a roentnenolonic
sion of nonoccupational endemic anthoohyllite asbestosis.
Acta Radio, Suppl. 194.
TA SKI NEH, E., AHLFIAN, K., UIIKERI, PI. (1973) A current
hypothesis of the lymphatic transport of inspired dust
to the parietal pleura. Chest 64 : 193-196.
SAMFT, 3.n.: SPETZER, F.F.: GAENSLER, E.A. (1978) Questionnaire reliability and validity in asbestos exposed uorkers.
Oull. Euron. Phvsiopath. Resp. 14: 177-1B8.
SARGENT, U.E.; 3RC0RS0N, G.: WILKINSON, E.É. (1974) Oianhranmatic pleural calcification fnlloui.nn short occupational
nxnosuro to asbestos.
The Am. 3.of Rnentnenol., 115:
A73-47".
npHLIG, I'. (1970) The problem of ashestosls in relation to
thn International Classif icnt.i nn nf Radinnraohs in
564
pn«?umncnni nsirs, Pnnnniornni.ORÌs PrncRnd.innr> o f
International
thn
H n n f e r n n r n , Hnhsnnprïhmirn 19fi9, 1 v n l . ,
Caon Tnun P x f n r r i U n i v e r s i t y
565
Prrr.s,
?Af)-?ri?.
TABLEAU 1 - PROFESSIONS RETENUES EN RELATION AVEC L'EXPOSITION A L'AMIANTE
CHEZ 47 PATIENTS THORACOTOMISÉS
EXPOSITION A L'AMIANTE
PROFESSIONS RETENUES
DÉFINIE
+
SUSPECTE*
N = J0
N = 27
MAGASINIER
PLOMBIER
MANOEUVRE
CHAUDRONNIER
CARRELEUR
INDUSTRIEL DU BOIS
FRAISEUR/ TOURNEUR
CHANTIER NAVAL
SERRURIER
REPASSEUSE
GARAGISTE
BONNETIER
PCMPIER
SOUDEUR
CHARPENTIER
PROTHÉSISTE DENTAIRE
INGÉNIEUR EN FONDERIE
N-JCT
3
3
3
1
1
0
0
0
H
2
CALORIFUGEUR-CHAUFFAGISTE
MAÇON
ELECTRICIEN
NON EXPOSÉS*
0
0
0
0
0
0
0
0
0
0
0
0
10
+
DÉFINIE
: EXPOSITION A L'AMIANTE CONNUE PAR LE MALADE
+
SUSPECTE
: EXPOSITION A L'AMIANTE POSSIBLE, IGNORÉE PAR LE MALADE
+
NON EXPOSÉS
: AUCUNE EXPOSITION PROFESSIONNELLE A L'AMIANTE
i-|+ : 9 CAS :;nr." EXPOSES : DOCUMENTES ET I CAS OU L» INTERROGATC1IRC « ETE
IMPASSIBLE
566
TABLEALL2 - ELfiQUE.DLAPHRAfflfiriQUL CHlRURGlCALLi E I B J G l ü l t í .DlâPHFWïWIQlJE
RAMOLOGIQUE. HCMPLATERALE VUE SUI LES INCIDENCES FRONTALE .ET LATERALE CHEZ 4 7
PATIENTS JTORACOTQMJSES
\
RIGIDITÉ
\
+
DIAPHRAGMATIQUE
-
+
P-
\RADIOLOGIQUE
PLAQUE
\
DIAPHRAGMATIQUEX
CHIRURGICALE
\
+
6
H
0,01
-
5
+
2
567
32
TABLEAU 3 - ANOBLIES RADIDLOGJQUES UNI OU.BILATEBALES E I
EXPQSJTJON PROFESSJONNELLE CHEZ 1 7 PATIENTS THORACDTQMISÉS
^ s .
EXPOSITION À
NON-EXPOSÉS
EXPOSÉS
N-37
+
p=
N-10
^NJ/AMIANTE
N
(Z)
N
CD
16
W3)
9
(90)
0,05
M
(38)
0
(0)
0.06
7
a®
0
(0)
4+
EPAISSISSEMHNT PLEURAL
5
(13)
1
(10)
t++
FIBROSE PARENOWE
3
(8)
0
(0)
4+
RADIOLOGIE
^ X .
I.T.N.
RIGIDITÉ DIAPHRAGMATIQUE
HOMO ET/OU CONTROLATÉRALE
À LA THORACOTCMIE
CALCIFICATION PLEURALE
+
-H-
^2C
EFFECTIF CALCULE INSUFISANT POUR EFFECTUER LES TESTS
STATISTinUES
568
TABLEAU 4 - PLAQUE PLEURALE CHIRURGICALE ET
EXPOSITION PROFESSIONNELLE CHEZ 17 PATIENTS THORACOTCMISES
. +
\
EXPOSITION A
^SL'AMIANTE
THORACOTDMIE
ABSENCE DE PLAQUE
^ V
EXPOSES
N = 37
N
20
NON-EXPOSES
p =
N = JD
ÖD
N
(X)
(90
9
GO)
0.09
PLAQUES PLEURALES
+
17
^.2c
569
<«)
l
(10)
Uigidez del diafrapjna entre las personas
expuestas al asbesto i correlación entre
los exámenes radiológicos v el aspecto
real en 47 toracotomias.
A. Hirsch, L. di Menza, M. Mangold, P. Sebastian
y J. Bignon (Francia)
Se ha observado rigidez del diafragma entre personas
sujetas a una exposición baja o media al asbesto. A fin
de estudiar la relación entre la rigidez del diafragma y
la exposición al asbesto, hemos comparado la incidencia de
esta manifestación radiológica con el aspecto real del diafragma en las intervenciones quirúrgicas (35 carcinomas
pulmonares y en diez casos otras causas, con exclusión de
la mesotelioma). Se observó una rigidez del diafragma en
23 por ciento de los exámenes por rayos X y se hallaron
placas pleurales del diafragma en 21 por ciento de las toracotomías. Los resultados de los exámenes por rayos X
concordaron con la realidad en 80 por ciento de los casos
(6 casos positivos y 32 negativos). Se estudia la relación
entre la manifestación radiológica y la existencia de esta
anormalidad habida cuenta de la exposición al asbesto, procediéndose a la correspondiente evaluación sobre la base de
los antecedentes profesionales y el número de cuerpos ferruginosos presentes en los pulmones o en los esputos.
57o
THE PATHOLOGICAL EFFECTS OF ASBESTOS CLOUDS OF DIFFERENT
FIBRE DIMENSIONS ON THE LUNGS OF RATS
J. M. G. Davts, S. T. Beckett, R. E. Bolton, Paula Collings
United Kingdom
For some years now it has been suggested that the levels of
pulmonary fibrosis and neoplasia resulting from asbestos inhalaion depend on a number of different dust parameters.
Fibre length
and the number of fibres per unit mass of dust have been both
suggested as important and so has the duration of inhalation.
It is also thought possible that short periods of exposure to
very high levels
of dust may be more dangerous than continuous
exposure to low levelSf although the same dust mass is inhaled
in both instances.
The first studies indicating the importance of fibre length
were reported by King et al., in 1946. These workers administered
chrysotile fibres, cut on a special microtome at lengths of 15^
and 2.5^ to rabbits by intratracheal Injection.
They reported a
greater tissue reaction from those animals that had received the
long-fibre sample.
Similarly in 1951 Vorwald et al reported
that animals which had inhaled chrysotile fibres in the 20 - 50/J
range had more pulmonary fibrosis than those breathing only
fibres below 3ju in length.
studies using both the
In 1968 Klosterkötter extended these
intraperitoneal and intratracheal in-
jection of crocidolite and chrysotile.
Some dust samples had a
very high average fibre length while other had been grounded to
an average length of less than 5/J. The short-fibre samples
produced little fibrosis in either site while the long-fibre
571
specimens resulted in considerable fibrosis in both regions.
The importance of long fibres was further emphasised by Timbrell
and Skidmore in 1968 and Webster in 1969 using inhalation techniques.
In 1972 Davis reported a series of experiments in which
several type of mineral fibre were administered to mice by intrapleural injection.
This series of dusts included standard UICC
chrysotile and chrysotile fragmented by ultrasonic treatment
until all fibres were below 1/J in length. While long-fibre
samples produced massive fibrosis, the short-fibre specimens
produced almost no reaction.
Very similar results were obtained
by Wright and Kuschner in 1975. These authors injected a number
of types of mineral fibre intratracheally into guinea pigs.
Each
of the minerals was prepared in both long and short-fibre forms
and crocidolite asbestos was included.
In all cases the long-
fibre samples resulted in marked fibrosis while the short-fibre
specimens produced only a macrophage reaction.
There is considerable evidence that the neoplastic as well
as the fibrogenic potential of asbestos and other mineral fibres
is also dependent on fibre length with long-fibre dust samples
producing more tumours than short.
reported that the
In 1972 Stanton and Wrench
partial pulverisation of crocidolite to reduce
the average fibre length resulted in a reduced carcinogenic potential following intrapleural implantation.
Also in 1972 Smith
et al. obtained similar results using chrysotile.
In 1977
Stanton et al. published some new results which confirmed the importance of fibre length, and this report suggested that only
572
fibres over IQ/u in length and less than ^u in diameter were
carcinogenic.
Recently we have undertaken a series of inhalation studies
using rats in order to gain further information on the importance
of the various dust parameters.
In the first study the importance
of fibre mass and fibre number was examined using the UICC standard
reference
samples of asbestos.
Five groups of rats were treated
with dust for one year following which small groups were killed
at intervals to establish the levels of pulmonary fibrosis and
the remainder were allowed to survive for their full lifespan,
to study the development of pulmonary neoplasia.
were treated with clouds of equal mass (10 mg/m
crocidolite, or amosite) and since the
Three groups
of chrysotile,
amosite fibres were found
to be the largest, the chrysotile and
crocidolite experiments
3
3
were duplicated at lower levels (2 mg/m and 5 mg/m respectively),
at which concentrations it was estimated that the number of
fibres greater than 5/i in length would be equal to that in the
3
10 mg/m amosite cloud.
The lung dust content and the levels of pulmonary interstitial fibrosis and neoplasia found in these groups are shown
in Table 1.
Both chrysotile clouds have caused the development
of more fibrosis than
any of the amphibole clouds, and all the
malignant pulmonary neoplasms occurred in chrysotile-treated
animals.
It is evident that the dust
important parameter.
mass is not the most
These findings could be
taken to indicate
that chrysotile per se is the most dangerous form of asbestos,
but the most likely reason for these results was found when the
fibre length distribution of the dust clouds was examined in the
573
scanning electron microscope.
It was found that the dust gene-
ration methods used had produced clouds in which about 7% of
the chrysotile fibres were over 2Qu in length but only about
0.5% of the crocidolite and amosite fibres. These results,
therefore, give strong support to the suggestion that it is the
long asbestos fibres that are the dangerous ones.
In studies aimed at examining the importance of exposure
to high levels of asbestos for short periods, the effects of
this "peak" dosing were compared to those obtained for amosite
and chrysotile in the previous studies, in which the dust had
been administered for. 7 hours a day and 5 days each week.
"peak" studies clouds of amosite at 50 mg/m
10 mg/m
In
and chrysotile at
were administered for one day each week for comparison
with the results obtained from even dosing with amosite at 10 mg/m"
and chrysotile at 2 mg/m
respectively.
The use of the 2 mg
cloud as a chrysotile base-line was necessary since it proved
physically impossible to produce a chrysotile cloud of 50 mg/m
of respirable dust owing to flocculation of the fibres. The
levels of dust deposition and retention in the lungs following
the different inhalation techniques are shown in Table 2 along
with the levels of fibrosis and the number of pulmonary tumours
found in the different groups of animals.
It had been suggested
that short periods of high intensity dust exposure might swamp
the pulmonary clearance mechanism
dust retention in the lung.
and lead to greatly increased
These
figures show, however, that
dust deposition during the 12 months' inhalation period and dust
retention after a further six months are remarkably close. There
is a slight indication of greater deposition and retention with
574
the "peak" doses but since the estimations are made on small
groups of rats the differences are within the limits of experimental error. When the levels of lung pathology were examinedi
however, it was found that the "peak" dusting groups showed more
interstitial fibrosis in the later stages of the study than the
evenly dusted animals (Fig. 1). The number of pulmonary tumours
found in the two groups were close with the peak amosite animals
having slightly more pulmonary adenomas than the evenly dusted
amosite group and the
peak chrysotile animals having slightly
less than their evenly dusted counterparts. Of possibly greater
importance was the fact that two
malignant lung tumours were
found in the peak amosite group when none had developed in the
evenly dosed amosite group. No mesotheliomas were
found in
any animals from the "peak" dosing experiment.
From these results it would appear that while"peak" dosing
did
not produce large changes in the resulting levels of lung
pathology compared to the same dose administered over a five-day
period, there were some indications of increased lung damage
which were more marked with amosite than with chrysotile.
The
reasons for this are difficult to explain since the amount of
dust found in the rat lungs at the end of the dusting period
were very similar in both experiments.
It is possible, however,
that more of the dust from the "peak" doses had penetrated to the
alveolar regions rather than being retained near to the bronchial
tubes.
This would be likely to result in increased levels of
interstitial fibrosis.
575
In another experiment, the effects of Inhalation of heated
chrysotile were examined because of worries concerning the possible
hazards of the inhalation of automobile brake-lining dust.
In
what will probably be the first of a series of studies the chrysotile was heated to 850°C for
24 hours.
Following this treatment
rats were exposed for one year to a dust cloud containing 10 mg/m
of this material.
The length distribution of the fibres in the dust
cloud was similar to that for UICC chrysotile. However, the heated
chrysotile was a fragile material and the dust generation process
had produced many non-fibrojs particles, so the actual fibre
numbers were low (150/cm ). This study is now complete and histological examination has shown that levels of pulmonary fibrosis were
too low to estimate even in the oldest animals and no pulmonary
neoplasms developed in any of the group.
The only indication of
dust inhalation in the lungs of animals treated with heated chrysotile was clusters of dust-containing macrophages which filled a
few alveoli (Fig. 2 ) .
Another inhalation study on the pathological effects of different
asbestos types that is in progress at the present time, involves
the use of samples of chrysotile and amosite collected from the
atmosphere of
asbestos factories. These have been administered
to groups of rats at a dose level of 10 mg/m
since both samples contain
ral were somewhat below this
for one year although,
impurities, the levels of asbestos minefigure.
tion of the factory chrysotile dust
The fibre length
distribu-
was similar to the UICC samples
but the factory fibres tended to be thicker so that fibre numbers
3
per cm were lower. The factory amosite dust, however, contained
more long fibres than its UICC counterpart and fibre numbers were
576
also rather higher.
Only preliminary results are available
from this study but while the mass of dust found in the lungs
of animals at
the end of the dusting period was very similar
to the figures for
experiments using UICC asbestos, the levels
of pulmonary fibrosis were
different.
The factory chrysotile
samples produce less early fibrosis that UICC chrysotile, but
the factory amosite produced more than UICC amosite. This is
further evidence that the mass of inhaled asbestos is relatively
unimportant in determining levels of lung damage and the
most
important factors are fibre numbers and especially fibre length.
577
REFERENCES
DAVIS, J.M.G. (1972) The fibrogenic effects of mineral dusts injected
into the pleural cavity of mice.
Brit. J. Exp. Path. ¿3, 190 - 201*.
KING, E.J., CLEGG, J.W., RAE, V.M. (^6)
Effect of asbestos, and of
asbestos and aluminium, on the lungs of rabbits. Thorax 1, I88 - 197.
KLOSTERKÖTTER, W. (1968)
Experimentelle Untersuchungen über die
Bedeutung der Faserlänge für die Asbest-Fibrose sowie Untersuchungen
über die Beeinflussung der Fibrose durch Polyvinylpyridin-n-oxid.
In:Biologische Wirkungen des Asbestos.
Internationale Konferenz,
Dresden.
Deutsches Zentralinstitut für Arbeitsmedizin, Berlin, ¿»7 - 52.
SMTTH, V.r.., mmKRT, n,n,, RAnoLLET, M , S . (1972)
Biological differences
in resDonse to long and short asbestos fibres. Ann. Ind. Hyg. Assoc. J.
j£, A162.
STANTON, H.F., LAZARD, M. < TEGjERIS, A., MILLER, E., HAY, H. and KENT, E.
(1977) Carcinogenicity of fibrous glass. J. Nat. Can. Inst. ¿8,
587 - 603.
STANTON, M.F., WRENCH, C. (1972)
Asbestos and Fibrous Glass.
Mechanisms of Mesothelioma Induction with
J. Nat. Can. Inst. Jt8_, 797 - 822.
TIMBRELL, V., SKIDMORE, J.W. (I968)
Significance of fibre length in
experimental asbestosis.
Iw Biologische Wirkungen des Asbestos Internationale Konferenz, Dresden.
Deutsches Zentralinstitut für
Arbeitsmedizin« 52 - 56.
VORWALD, A.J., DURKAN, T.M., PRATT, P.C. (1951)
Experimental studies of
asbestosis.
A.M.A. Arch. Ind. Hyg. Occ. Med. ¿, 1 - '»J.
WEBSTER, I. (1970) The pathogenesis of asbestosis.
lie Pneumoconiosis,
Proceedings of the International Conference, Johannesburg, 1969.
Ed.
H. Shapiro, Pubi. Oxford University Press, 117 - 119.
WRIGHT, G.W. and KUSCHNER, M. (1975)
The influence of varying fibre lengths
of glass and asbestos fibres on tissue response in guinea pigs.
In:
Inhaled Particles IV (ed. W.H. Walton), Pergamon Press, London, Vol. Zy
455-472.
578
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Levels of interstitial
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FIGURE CAPTIONS
FIG. 1
An area of interstitial fibrosis from the lungs of a rat
in the "peak" amosite experiment.
The animal was killed
29 months after the start of dusting.
The alveolar
septa are greatly thickened and within most alveolar spaces
are large numbers of macrophages containing asbestos fibres.
Hagr.ificatien X 250
FIO. 2
An area of lung tissue from the lungs of a rat which had
Inhaled heated Chrysotil« dust for twelve months.
The
animal was killed 29 months after the start of dusting.
The alveolar septa are normal and the only indication of dust
inhalation is a cluster of macrophages containing dust which
fills an alveolus which is connected to a respiratory
bronchiole.
Magnification X 500
581
Efectos patológicos de las nubes de amianto
con fibras de distinta dimension sobre los
pulmones de las ratas«
J. M. G. Davis y R. E. Bolton (Reino Unido)
Se trataron a grupos de ratas por inhalación de nubes
de polvos procedentes de diferentes muestras de asbestos,
inclusive muestras de crisotilo y de amosita de la UICC.
Fueron administradas a distintas dosis, cinco días por semana durante un año y también con dosis de "punta" a muy
alto nivel un día pori semana. Otros tipos de asbestos estudiados eran muestras de crisotilo y amosita recogidas
directamente en las fábricas de amianto y una muestra de
crisotilo recalentado durante 24 horas a las temperaturas
a que están sometidas las zapatas de los frenos de automóvil.
Se dispone de datos no sólo sobre los niveles de fibrosis pulmonar producida por las diferentes nubes de polvo,
sino también sobre las cantidades de asbestos presentes en
los pulmones de las ratas al término del perfodo de inhalación. Se dispone también de la gama completa de longitudes
de las fibras para todas las nubes de polvos, calculadas
tanto al microscopio óptico como al electrónico.
En estudios con muestras de asbestos de la UICC se encontró que el crisotilo produce mucho más daño en los pulmones que la crocidolita o la amosita. No obstante, las
cifras de longitud de las fibras muestran que las nubes de
crisotilo tienen fibras mucho más largas que las de los anfiboles.
Se descubrió que las dosis de "punta" causan un aumento del nivel de fibrosis intersticial en los animales más
viejos, comparativamente a los otros grupos que habían recibido la misma dosis de inhalación administrada a un nivel
uniforme durante toda la semana. No obstante, los niveles
de polvo encontrados en los pulmones después de la aplicación de ambos métodos de aplicación de polvo eran casi idénticos. La inhalación de crisotilo recalentada producía muy
582
poca fibrosis en Codos los animales. Cuando se comprobó en
las ratas una muestra de crisotilo recogida del medio ambiente de una fábrica, se descubrió que en una primera fase
habCa menos fibrosis pulmonar que con el crisotilo de la
UICC. Pero una muestra similar de amosita de fábrica produjo más fibrosis que la muestra correspondiente de la UICC.
Estas diferencias podrían explicarse por la distribución de
la longitud de las fibras en las diferentes muestras de
polvo.
583
¡3N_g_i_ç.|._5=£-§,5»I.C-|v.,\/II
VII. I
P.Sadoul., D.Teculescu
Epreuves Fonctlonnelles dens le diagnostic orecnce et la
réadaptation des Pneumoconioses
VII. II
L.baldonado., W.Martha Méndez., J.A.Leqapsl. , A.ronzai e«.
The value of studying pulmonary function with a view to
the early diagnosis of silicosis.
VII. Ill
K.Wilson., R.Richie., P.Stevens.,
Cfect of chronic amorphous silica exposure on sequential
pulmonary function.
VII. IV
P.Garcia Herreros., G.Scano., L.Stendardi., S.Degré.,
R.Sergysels * A.De Coster.
L'Adaptation eardiopulmanalra a L'effort chez les mineurs de charbon
VII. V
J.t.Diem., R.N.Jones., J.C.Gilson., H.nilndmeyer. , H.Weill
The Influence of asbestos exposure on radiographic progression and functional decline a preliminary report
585
ni/i
FPRFUVFS FONCTIONNELLES HAMS LE DIAHNnsTir PRECOCE
ET LA READAPTATION OES PNEUMOCONIOSES
P. SADOUL, D. TECIILESCU
Université de Mnncv, France.
A l'heure actuelle, le diannostic des pneumoconioses
renose sur deux bases essentielles: les modifications radiolonioues pulmonaires et la nature des risques courus.
Quelle que soit la v/aleur de la radiolonie, celle-ci
ne peut être considérée comme suffisante.
En effet, certai-
nes pneumoconioses donnent des opacités radioloniques tres
discretes, alors que l'incapacité fonctionnelle est évidente
et qu'a l'examen anatomo-patholopique les lésions apparaissent
non nôqliqeablBs. Il en est ainsi de l'asbestosa ou de la sidérose.
Chez les mineurs de charbon les lésions ne sont pas
en corrélation étroite avec les modifications radioloniques.
Enfin, durant ces dernières années, il est apparu que certaines
lésions parenchymateuses d'orioine professionnelle ne s'accompaqnaient pas d'anomalies radioloniques mais donnaient des
troubles fonctionnels. Il en est ainsi des pneumopathies des
i90cyanates (5,15).
Il apparaît donc loqique de chercher des éléments de
diannostic autres que radioloqiquas. Les tentatives faites
pour trouver des moyens surs d'identification
biologiques
n'ont jusqu'ici donné aucun résultat concluant.
Pour évaluer la nlace des éoreuves fonctionnelles
dans le diannostic précoce dB9 pneumoconioses, il apparaît
587
utils de rapneler tout d'abord les nrandes lianes des ex-'
plpratinns fonctionnelles les plus courantes puis de rechercher
s'il existe un profil fonctionnel des stades infra-radioloniques dans quelques-unes des pneumoconioses les mieux étudiées jusqu'ici,
nien entendu, il faudra discuter les cau-
ses d'erreurs qui pourraient conduire a un diaqnostic précoce
erroné. La conclusion du rappel de ces travaux sera d'évaluer
ce qu'il est possible de réaliser en 1978 et de discuter les
les recherches a entreprendre.
0an3 une dernière partie nous
envisanerons la place des épreuves fonctionnelles dans la
réadaption des pnleumdconioses.
La multiplicité des examens fonctionnels proposés par
les physiolooistes pousse parfois le non-spécialiste a se
cantonner dans des' examens classiques qui ne sont pas hélas
les plus riches d'information.
On peut distinguer parmi les
examens fonctionnels la mesure des volumes pulmonaires, celle
des résistances et des débits, l'étude de la distribution
intra-pulmonaire et enfin celle des échanges respiratoires.
Ceci laisse de coté les études hômodynamiques par cathétérisme cardiaque droit ou les tests d'exercice dont la valeur
pour
l'évaluation de l'invalidité ou pour la réadaption n'est
plus a démontrer.
La frénuence des amputations de la Capacité Vitale
dans les nneumoconioses débutantes est tres diversement appréciée.
Pour la majorité des auteurs, la diminution n'est pas
sionificative (13,16,18,19) tandis pue pour d'autres (1,8,9)
un svndrnme restrictif est souvent observé.
Ces discordances
sont secondaires a la diversité des valeurs théoriques retenues et souvent a la mauvaise coopération des sujets examinés.
La dispersion tres importante des valeurs
normales comme les
discordances relevées dans la littérature empêchent de retenir
la seule capacité vitale comme test de depistane.
588
In ni ansi nun VE l'i S (Wnlumn rfr.ni ratoi rn max imn1/innondp)
a éti lamamant nti lisi.
pnrsés ( 1-"O •
Tei nncort! les résultats snnt din-
Cependant Rnnan ct. m i l . (17), dan? uns des pre-
miaras enquêtes britanniques, notaient qua la VTFIS s'abaissait
ninnifinativemBnt chnz las mineurs soumis a un important entooussiérane mais exempt de nanumoconinsa radioloniquRment décelable.
Tenant compte des valeurs mnvennes observées chez
plusieurs centaines de sujets comparées a celles d'un oroupe
témoins, SNIDT et coll. (19) concluent qu'il existe une diminution du l/EFIS chez les mineurs exempts d'anomalies radioloniques et exposés depuis 8 ans, et plus ancore, chez les pneumoconiotiques.
DECHOIIX et PIVOTEAU (5) suivant durant plusieu
années un petit nroupe de mineurs avant toute modification radiolooique jusqu'à l'apparition d'imanes micronodulaires 1 observent une chute du VEI"1S de 44ml/an, valeur nettement supérie
a celle tirée des normes CECA qui est dB 21 ml. Flalnré l'intérêt de ces résultats, il ne parait pas possible de retenir
comme test diaqnostique le VENS car il n'est ni assez sensible
ni assez spécifique.
Le dispersion autour des valeurs prédi-
tes n'est pas nénliqeable.
La fréquence des diminutions du
VENS chez les tabagiques et les bronchitiques est tres élevée.
Enfin, 11 a été largement souligné que le VEMS était peu sensible a l'obstruction périphérique.
Dans les pneumoconioses,
la conséquence la plus précoce de l'inhalation et de la rétention des poussières est leur dépôt au niveau de la bronchiole
terminale.
Cet empoussiérane entraîne des lésions élémentaire
bien connues : infiltration cellulaire, prolifération fibreuse
et modification de calibra. Ces anomalies anatomiques peuvent
retenir sur les fonctions respiratoires.
La mesure des débits maximaux a différents niveaux de
la capacité vitale permettrait de mieux connaître l'état des
petites voies aériennes (2). LAPP et SEATON ont trouvé une diminution du débit maximal a 50% de la capacité vitale chez des
mineurs sans perturbation spironraphique (11).
589
I.'aiinmentati.on Hu Volume Résiduel, observée par MORGAN
p.t cnll. 'l?) cho7 lp.n mineurs avec ou sans nneumnconiose simple, n'avant ni abaissement du VEfS/CW, ni antécédent tabaniA
nun, p-.h nnut. PA.TR imputable a cos lisions distales.
Cette
hvnothfîpR est confirmée par 1 R S mesures de compliance dynami—
nue effectuées en ventilation spontanée ou a différentes fréquences, ou encore oar des mesures plus complexes (il). Les
examens mettent en évidence les altérations da la distensibilité pulmonaire et 1'inhnmonénéité du poumon empoussiéré
secondaire a l'obstruction des petites unies aérienne. Toutefois les mesures de compliances ne sont pas aisément praticables en mutina pt les aunmentations du volume résiduel
sinnificatives, pour un oroune do sujets, ne sont pas asse7
marquées au stade radinlonique
de détectinn précoce.
pour être retenues comme test
L'élévation du volume résiduel n'est
d'ailleurs pas retrouvée avec les techniques de dilution(l9).
L'étude des troubles de distribution aérienne ou mixique peut être faite au cours d'une ventilation calme ou sur
un seul cycle ventilatoire. Les techniques en ranime stable
montrent fréquemment de3 anomalies alors qu'il n'existe pas
ennorB de pneumnconiosB radioloqiquement décelable (19 ,2P).
Cependant, la variabilité de3 résultats avec le réqime ventilatoire comme la multiplicité des indices choisis les ont fait
abandonner pour les tests d'inspiration unique qui, propqsés
il y a 3D ans par CDPIROE et FOULLER, ont joui d'une grande faveur durant ces dernières années. La mesure du volume de fermeture a été larnement utilisée pour détecter précocement
l'obstruction des bronches distales.
Le transfert du CO étudié en réoime stable décelé souvent
les anomalies. PH/OTEAII et OECHOUX le trouvent perturbé dans
plus d' un cas sur deux chez des mineurs porteurs d'opacités
59o
micronodulaires, alors nue le test en aonée ne l'est que
rarement (14*).
Les résultats do la mesure en ranime
sta-
ble dépendent larnement des troubler, de distribution aérienne (16).
Le transfert du Hfl en apnée neut être perturbé précocement dans l'asbestose mais cette anomalie, souvent retrouvée dans les formes avancées (l) t ne peut constituer
un sinne prénoce (8). TRANS et coll. montrent (7) nu'entre
oenumnconiotiques débutants et témoins, seul le volume sannuin capillaire pulmonaire est sionificativement différent,
Uns des perturbations 1 B 9 plus fréquentes, révélées
par 1 R S investioations détaillées, est l'auomentation du
nradient alvôolo-artériel d'oxypène (19) et 2 2 ) .
Malheu-
reusement, sa mesure exioe un prélèvement de sano et mesures
rinoureuses;de plus, la reproductibilité de ce oradient
n'est pas excellente.
EXAHENT UTILISABLES DANS LE DEPISTAGE PRECOCE
Au total, parmi les tres nombreuses techniques d'études des fonctions respiratoires pulmonaires,il convient de
sélectionner celles qui sont utilisées pour le diaqnostic
précoce des pneumoconioses.
Les conditions que doivent rem-
plir les tests retenus pour les enauetes épiriémiolooiques,
ont été précisées par de nombreuses réunions, en particulier
celles organisée en 1973 par le National Heart and Luno
Institute (21) :
IB) Validité î le test ôvalue-t-il les perturbations
susceptibles d'apparaître dans la maladie considérée?
591
2 9 ' Sensibili t_é: Huells est la prooortion de sujets
attnints riécelée nar le test?
39) qpijcifité: n uelle est la proportion rie sujets
sains identifiers oar l'examen?'
4S
) Precision : Le test donne-t-il le mame résultat
quand il e3t appliqué de façon répétée dans des conditions
nnrnparah.1es,
59) Acceptabilité : L'absence de caractère traumatisant le rend acceptable oar la population a examinar.
65) Faisabilité : Est-il applicable sans difficulté
majeure a un nombre élevé de sujets (technique simple et rapide)?.
70) Coût; Fst-il proportionné au bénéfice obtenu?
Quoique la mesure dB la capacité vitale et du VEPIS
soit considérée par beaucoup d'auteurs comme répondant a
toutes ces conditions, les recherches faites sous l'éoide
de la Communauté européenne du Charbon et de l'Acier, les
résultats publiés dans la littérature montrent que la préoisinn des mesures diffère larnement suivant l'habileté du
technicien et la coopération du sujet.
L'examen attentif
du soirooramme est indispensable pour vérifier la validité
des mesures.
Les mêmes remarques peuvent être formulées
pour tnutes les épreuves utilisant une mesure des volumes
et des débits maximaux en particulier les boucles débitvolume.
L'intérêt des débits maximaux a 5055 et à 2à% de la
caoacité vitale est indiscutable, toutefois pour la dernière
mesure il existe une disoersion non néqlineable des résultats.
592
l.es risili tats' rt' autres mesures sont ranina dépendantes H B la coopération du sujet; il en est ainsi ries techniques étudiant la mixinue.
La pente d'azote nu partie
3 do la cnurbe est maintenant préférée, a juste titre, a
la détermination précise du volume de fermeture. Le test
do transfert du CD en ranime stable a l'avantaoe de constituer un index global puisqu'il reflète non seulement la
qualité des échanqes respiratoires, mais
aussi la mixioue.
Si 1'nn nrend la précaution ri'enrenistrer le spirorramme
pendant la mesure et d'étalonner l'appareil sur l'air expiré par le sujet, on obtient facilement des mesures reproductibles.
Puisque de discrets troubles des échannes
snnt l'une des premieres manifestations des penumoconioses,
cet examen devrait être plus snuvent utilisé.
Compte tenu du fait que les valeurs prédites restent
toujours quelque peu imprécises, la détection précoce sera
plus fiable si des mesures fonctionnelles respiratoires
ont été pratiquées avant l'exposition aux risques pneumoconiotiques. Il est souhaitable que le sujet soit en quoique
sorte son propre témoin.
En l'abscence de ces mesures d'em-
bauché, les premieres anomalies risquent de passer inaperpues.
RECHERCHES A ENTREPRENDRE
Pour préciser les anomalies les plus précoces, secondaires aux pneumoconioses, il apparait indispensable de multiplier les enquêtes épidémiolooiques longitudinales. Certes
plusieurs équipes en ont pratiqué, mais mis a part les mineurs de charbon, le nombre de sujets soumis a ces enquêtes
reste modeste et le recul ne dépasse pas quelques années.
Il serait souhaitable que certaines de ces enquêtes lnnoitudinalB3 soient effectuées an utilisant des tests multiples
593
explorant différentes fonctions élémentaires pulmonaires.
Oe telles recherches permettraient de préciser quels sont
les examens les plus sensibles.
De telles enquêtes prospectives sont indispensables
dans les industries utilisant de nouveaux procédés de fabrication.
Files devraient être entreprises des qu'une aug-
mentation de la fréquence des infections pulmonaires ou de
phénomènesdyspnôiquea a été notée par le médecin du travail.
Si des procédés de fabrication nocifs ou des substances toxiques sont utilisés, de tallas anquetas épidémiolooiques
devraient être systématiques afin d'identifier des bronchopneumonathies professionnelles encore inconnues.
Une enquê-
te faite dans une usine utilisant les isocyanates, ou les
ouvriers n'avaient aucune doléance, montre bien la nécessité
de telles investiaations (15).
EXPLORATION FONCTIONNELLES RESPIRATOIRES ET READAPTATION
DES JJNE. U.^£0_NJ£TJU]JJEJ3
Si la place exacte des épreuves fonctionnelles dans
le diapnostic précoce des pneumoconioses dépend encore du
résultat des recherches a entreprendre, il n'en est pas de
même en ce qui concerne la réadaptation. Qu'il s'aqisse de
réentrainement a l'exercice ou d'affection dVinpneumoconiotique handicapé a un nouveau poste, le bilan préalable fait
nécessairement appBl aux éoreuves fonctionnelles.
S'il n r en
est nas ainsi, de nraves mécomptes seront rencontrés en metieres de réadaptation.
Pour évaluer l'aptitude
d'un ouvrier a un nouveau
noste de travail, il est indispensable d'évaluer son déficit
fonctionnel respiratoire.
Los éprmivss de repos ne nnnt pas
alors suffinant.es, il faut recourir A dna tests d'exercice.
I.'énreuve triannulairn nronosée par la Communauté européenne
59*
du Charbon et de l'Acier il « a tifi ja 1? ans, avec nunmentatinn rie la charno rie 30-U nhanue 3 minutes, est narticul i T 9 nnnt satisfaisante (23).
Elle rinnne dos résultats nratinue-
mont aussi fidèles que les énrauves rraotannulaires répétées
qui permettent le calcul rie la Puissance Maximale Supportée
(fi).
Par contre, les déterminations baseras uniquement sur
la fréquence cardiaque donnent rie nraves mécomptes che? les
pneumnconiotiques et ne sauraient être retenues. De memn les
exercices sous maximaux risquent de conduire a des conclusions
trop optimistes.
Le recours au cathétërisme cardiaque droit
ne nnut nuere être envisaqé comme épreuves de routine.
Il
donne des informations extrêmement satisfaisantes si les
nrnssions mesurées dans la petite circulation sont confrontées avec le débit cardiaque et les naz riu sang, au repos
comme au coui9 d'un exercice.
La rééducation respiratoire et le réentrainement au
travail donneront dBS résultats d'autant plus satisfaisants
qu'il existe un élément réversible, c'est-a-dire des manifestations bronchitiques.
En effet, on ne peut espérer améliorer
l'état du parenchyme ou réduire les lésions vasculaires
par une physiothérapie aussi bien conduite soit-elle. Cependant, a un stade avancé de la maladie, la rééducation et le
réentrainement au travail donnent un confort aux pneumoooniotiques qui leur permet d'utiliser leurs réserves respiratoires diminuées.
Les résultats obtenus par la rééducation
respiratoire
ne sont certes pas nénlineables, mais ils ne doivent pas faire
oublier que les x premieres mesures à prendre dans les pneumoconioses sont une prévention efficace et celle-ci ne peut être
595
e n t r e n r i rçn nun >Îi n<">us s a i n i s s n n s de façon t r e n nrilcnce
n r n n i i n r n s m a n i f e s t a t i o n s des nneumnoonioses.
C'est
pourquoi
1R9 i n r n t i v e s f n n r t i n n n G l l e s comme moyen de d i a g n o s t i c
coco de eos m a l a d i e s d o i v e n t f a i r e
ri'investioatinns
s " s t i m a t i ni l e s .
596
les
oré-
l ' o b j e t de r e c h e r c h e s
et
Pruebas funcionales en el dlagnótlco precoz v la
readaptacíón de las neumocontosis
Informe Introductorio por
P. Sadoul, D. Teculescu
(Francia)
El diagnóstico de las neumoconlosls se basa actualmente
en la radiografía y la naturaleza de los riesgos sufridos i las
pruebas funcionales respiratorias se utilizan normalmente para
la evaluación de la Invalidez. La utilización de pruebas funcionales para el diagnóstico precoz de las neumoconiosls no ha
sido objeto de Investigaciones sistemáticas ni de confrontaciones análogas a las que han tenido lugar para la radiografía.
Numerosos factores entorpecen las tentativas en esta esferai la
frecuencia de las afecciones broncopulmonares extraprofeslonales,
particularmente las vinculadas al tabaquismo, la escasez de
estudios longitudinales en obreros sometidos a riesgos neumoconlótlcos, la falta de especificidad de las perturbaciones funcionales, las lncertldumbres Inherentes a los valores de referencia, etc. Las encuestas epidemiológicas efectuadas con trabajadores expuestos han demostrado que los Individuos sin anomalía
radiológica presaltaban perturbaciones de que carecían los pacientes de muestra. De todos modos, estas anomalías no quedan
siempre puestas en evidencia por las pruebas esplrográflcas
clásicas, sino que son reveladas a menudo por la exploración
de los Intercambios.
Las diversas neumoconlosls no crean perturbaciones funcionales de Igual tipo. En la neumoconlosls de los mineros del
carbón es bastante frecuente un síndrome obstructivo, Imposible
de disociar del de la bronquitis banal. En las silicosis puras
la hipertensión arterial pulmonar puede ser relativamente precoz.
En la asbestosls, las perturbaciones de los Intercambios pueden
597
preceder a cualquier otra anomalía. Además» un mismo riesgo
puede acarrear modificaciones funcionales muy diferentes de
un individuo a otro.
En la medicina del trabajo no es posible recurrir a
pruebas traumatizantes o caras. Es preciso respetar los criterios de selección adoptados por los epidemiólogos. Las pruebas
funcionales sólo constituyen actualmente un elemento de apoyo
para la obtención de un diagnóstico. Sólo investigaciones sistemáticas de tipo prospectivo permitirán concluir si aquéllas
desempeñarán en el futuro un papel tan importante como el de
la radiología.
La readaptación de los neumoconióticos es una tarea
dificil. Las pruebas funcionales respiratorias desempeñan un
papel esencial en la selección de los obreros enfermos. La
gravedad de ciertas perturbaciones vinculadas a lesiones anatómicas irreversibles impide un reentrenamiento físico. La
evolutividad, siempre difiel de prever, puede hacer inútiles
los esfuerzos realizados. Por el contrario, la readaptación está
muy indicada en determinados obreros que padecen bronquitis
de acompañamiento o bien una neuraoconiosis no evolutiva.
598
EL VALOR DE LAS PRUEBAS DE FUNCIONAMIENTO
PULMONAR EN EL DIAGNOSTICO OPORTUNO DE LA
SILICOSIS.
... It 1s argued that... disabling
silicosis can only exist where
"nodulation" is present 1n the x-ray
picture, then 1t 1s possible, and even
likely, that workers may unjustly be
denied compensation 1 . Greenburg.L. ,1972
*
*
*
**
Dr. L. Maldonado T.,
Dra. M. M. Méndez V. ,
Dr. J. A. Legaspl V. y
Dra. A. González Z.
I N T R O D U C C I Ó N
En México, los padecimientos broncopulmonares ocupan el
primer lugar dentro de las enfermedades consideradas como de 2 4
trabajo, puesto que constituyen casi el 80% ' . Dentro de es^
tos padecimientos broncopulmonares, los más frecuentes son las
neumocon1os1s, ocupan el 90S 3 * 4 y de estas neumocon1os1s alre_
dedor del 60 al 65%, *•* son producidas por mezclas de sílice
y silicatos, a excepción del asbesto.
Cuando en 1973, propusimos * en el Instituto Mexicano del Seguro S o d a i , que: "para establecer el diagnostico de neu^
moconiosls es Indispensable que coexistan el antecedente de ex.
posición a ambiente polvoso (o con humos y algunas nieblas) y
las alteraciones radiográficas compatibles con el p a d e c i m i e n to, pudlendo o nó encontrar datos clínicos"; consideramos como
* Jefatura de Medicina del Trabajo.
** Hospital de Cardiología y Neumologfa.
Centro Médico Nacional, Instituto Mexicano del Seguro Social
México, D. F., MEXICO.
599
compatibles únicamente las opacidades redondeadas característl
cas y se recomendó clasificarlas siguiendo las pautas de la -Clasificación Internacional de Radiografías de Neumoconlosls (Revisada, 1968), Corta, de la O.I.T., con un criterio conservador estricto; aunque algunos de los Integrantes del Grupo de
Estudio de Enfermedades Broncopulmonares de Trabajo, que establecimos los requisitos, en la Institución mencionada, o p i n a mos, desde entonces, que se deberían considerar también las -opacidades irregulares, usando la Ampliada, con un criterio -más abierto; solo que predominó el anterior. S1n embargo, para aprovechar que nos eran enviados desde esa época, trabajado,
res expuestos sobre todo a la Inhalación de partículas de mezclas de polvos de sílice y silicatos, en quienes se tenía la sospecha o se hacía la reclamación, por el mismo trabajador, el sindicato o el patrón, de que padecían silicosis y solicita.
ban la compensación y de que muchos de ellos presentaban única,
mente opacidades Irregulares, en su radiografía de tórax, é s tos se estudiaron de la misma manera que los que tenían opacidades redondeadas. Es decir, todo trabajador expuesto a m e z clas de polvos de sílice y silicatos, con opacidades redondeadas o Irregulares, en su radiografía del tórax, se estudió de
manera similar y se clasificaron las opacidades de acuerdo a la Clasificación Internacional de Radiografías de Neumoconlo—
sis U/C, 1971, Corta, de la O.I.T.; en la que se anota que ad£
más de en la asbestosls, se observan radiografías con opacidades Irregulares pequeñas también en la silicosis, la neumoconlosls por polvos mixtos, etc..
En cada uno de ellos, se hizo Interrogatorio y exploración
física, se midieron la estatura y el peso, la hemoglobina, el
hematocrito, los leucocitos y la fórmula diferencial; se hiele,
ron reacción de Mantoux, baclloscopías y cultivos, en serle de
tres días, si el trabajador presentaba expectoración así como
telerradiografías de tórax en póstero anterior, en Inspiración
y espiración forzadas, oblicuas anteriores, derecha a Izquier-
600
da, estudio electrocardiografía y pruebas de funcionamiento pulmonar. Aparte, para completar el estudio, en algunos ca- sos, otros exámenes de laboratorio, según se requiriera.
MATERIAL Y METODO
Para este estudio, se seleccionaron los expedientes en -los cuales las radiografías de tórax mostraran opacidades 1rre_
guiares pequeñas, en el orden en que estaban archivados y se desecharon los demás, hasta reunir 500 expedientes.
De estos se obtuvieron datos tales como número secuenclal, datos para identificar al trabajador, sexo, edad, lugar
de nacimiento, empresa, puesto, antigüedad, tabaquismo, patolo_
gfa pulmonar previa, síntomas, estatura, peso, frecuencias re£
plratorla y cardiaca, signos, síndromes, cifras de: hemoglobina, h e m a t o c H t o , leucocitos y formula diferencial, resultados
de la prueba de Mantoux, de las baclloscopías y de los c u l t i vos, las radiografías se clasificaron de acuerdo con el código
de la Clasificación Internacional de Radiografías de Neumoco-niosls, 1971, UIC/UC, Corta, de la O.I.T., las alteraciones -electrocardiografías y los resultados en cifras de la capacidad vital, de la velocidad de flujo máximo espiratorio, de la
velocidad de flujo medio espiratorio, de la presión alveolar de oxígeno, de la presión alveolar de dióxido de carbono, del
pH, de la relación e s p a d o muerto/aire corriente y de la existencia de cortos circuitos, correspondientes a las pruebas de
funcionamiento pulmonar y su correlación con respecto al estado de la mecánica respiratoria, ventilación e Intercambio g a seoso.
R E S U L T A D O S
La mayoría de los trabajadores seleccionados fueron
bres, 470 (94«) y 30,(6Ï) mujeres.
hom-
La edad varió entre 16 y 80 años; la gran mayoría se en--
6o1
contro entre 26 y 60 años (463; 92.6%); entre 16 y 25 (11; 2.2«)
y entre 61 y 80 (26; 5.2%).
El lugar de nacimiento permitió verificar que ninguno fue_
ra originarlo de una zona minera.
Las empresas y los puestos en que trabajaron, correspon-den en la casi totalidad (388; 77.6%) a fábricas en que se eia,
bora porcelana, semlporcelana y loza; (93; 18.6%) a una fábrica de tabiques refractarlos y el resto (19; 3.8%), a diferen-tes empresas generadoras de polvo de mezclas de sílice y silicatos.
La antigüedad de la exposición fue en la mayoría de 10 a
30 años (439; 87.5%), pard algunos de 31 a 45 años (44; 8.8%)
y para la minoría de 3 a 5 años (16; 3.2%).
El tabaquismo se encontró negativo en 159 (31.8%); de 1 a
5 cigarrillos, en 227 (45.4%), de 6 a 10 cigarrillos, en 73 -(14.6%) y de 11 a 20 cigarrillos, en 27 (5.4%) y de más de 20
cigarrillos en 14 (2.8%), en 24 horas. La duración fue de 1 a
55 años.
Sólo en 3 casos se encontró patología pulmonar previa - (0.6%), provocada por tuberculosis pulmonar.
En 182 (36.4%), no se encontró sintomatologia del aparato
respiratorio, 41 (8.2%) presentaron disnea de esfuerzo y 277 (55.4%) síntomas de bronquitis. De estos 85 nunca habían fuiM
do (17%) y 192 (38.4%) SÍ.
En (377; 75.4%) se encontraron dentro del peso normal y (133; 24.6Ï) fueron obesos. Grado 1-103 (20.6%). Grado II- 28 (5.6%) y Grado III-2 (0.4%).
La exploración de tórax fue en casi todos negativa, pero
en 5 (1%) se encontró síndrome de condensación.
La hemoglobina y el hematocrito fueron normales en 450 -(90%), se encontraron disminuidos en 3 (0.6%) y hemoconcentra-
6o2
clon en 42 (8.4%).
Tanto los leucocitos como la fórmula diferencial se encoja
traron normales en 200 (40%), hubo Hnfoc1tos1s en 237 (47.4%),
eosinofilia en 26 (5.2%) y Hnfoc1tos1s y eosinofilia en 15 -(3%).
El Mantoux fue positivo en 285 (57%) y negativo en 153 -(30.6%).
Las badloscopfas para BAAR fueron negativas en 200 (40%).
Las opacidades Irregulares en las radiografías de tórax fueron finas 1, en 4 (0.2%); finas 2, en 11 (2.2%); finas 3 en
210 (42%); en total finas en 225 (45%); medianas 1, en 9 (1.8%); medianas 2, en 22 (4.4%); medianas 3, en 196 (39.2%);
en total medianas en 227 (45.4%); gruesas 1, en 0 (0%); g r u e sas 2, en 3 (0.6%) y gruesas 3, en 45 (9%); en total gruesas en 48 (9.6%).
No se tomo electrocardiograma en 397 (79.4%). En 49 - (9.8%) se encontró dentro de limites normales y en 29 (5.8%) se observó crecimiento de cavidades Izquierdas en 16 (3.2%), de cavidades derechas en 16 (3.2%) y crecimiento de cavidades
derechas e Izquierdas en 9 (1.8%).
Los resultados de las pruebas de funcionamiento pulmonar
se encontraron normales en 109 (21.8%) y, en el resto, se e n contró: restricción en 28 (5.6%), obstrucción bronquial cen- trai en 4 (0.8%), obstrucción bronquial periférica en 78 (15.6%); hlpoxemla en 56 (11.2%) y combinaciones de las a n t e riores en 225 (45%). Cuadro I .
C O M E N T A R I O
Trabajan más hombres que mujeres en la Industria, por lo
que los datos encontrados de mayor nomerò de hombres, nó son de
extrañar.
6o3
La edad concuerda con la de la época productiva (25 a 60
años); algunos segufan trabajando despues de la edad de jubila^
ción, aparentemente en buenas condiciones.
No encontramos en ninguno el antecedente de haber sido mj_
nero. Esto es Importante puesto que generalmente lo niegan en
el Interrogatorio, debido a que atribuyen su patología a la -contaminación del medio ambiente de la ocupación actual y buscan nueva compensación.
El que la mayoría hayan trabajado en fábricas de cerámica
se debe a que estudiamos principalmente trabajadores de las 1r^
dustrlas de transformación y muy pocos de la de extracción, -ya que el aseguramiento de mineros se Inició a partir de 1972.
La gran mayoría de los casos estudiados, estuvieron ex- puestos por tiempo suficiente a las partículas del polvo dañino.
En general, no se observó patología pulmonar previa que hubiera dejado secuelas que se reflejaran en el estudio func1o_
nal, excepto en un caso de toracotomía.
Es de esperarse que en algunos no exista cuadro clínico,
que otros presenten disnea y que algunos refieran síntomas de
bronquitis, Incluyendo los nó fumadores, con el antecedente de
hasta 20 años de exposición al polvo.
En los obesos las alteraciones en los resultados de las pruebas de función respiratoria son atribulóles parcialmente al sobrepeso.
En los que se encontró patología pulmonar previa y ésta obviamente contribuye a la alteración funcional.
En los casos de hemoconcentraclón, esta es significativa,
en ausencia de opacidades redondeadas. La llnfodtosls y la eosinofilia, solas o combinadas, no es f S d l su explicación, sin embargo, son un hallazgo frecuente en las neumoconlosls.
6o4
El Mantoux positivo, como Indicio de la pr1mo1nfecc1ön tu_
berculosa, es significante, porque sus secuelas, aún las nó vi
slbles radiográficamente pueden dar lugar a alteración funcional .
No encontramos correlación entre opacidades Irregulares de
tipos finas, medias y gruesas, n1 de profusión 1, 2 y 3 con el
grado de alteración funcional.
C O N C L U S I O N E S
En la práctica vemos que por lo menos en algunos casos -las opacidades Irregulares pequeñas coinciden con opacidades redondeadas o evolucionan a ellas.
Es por tanto importante que se estudien de la misma manera los trabajadores que presenten radiografías con opacidades
Irregulares pequeñas que los que presenten opacidades redondea,
das pequeñas.
Se considera que por lo menos en los nó fumadores, las ai
t e r a d o n e s funcionales deben atribuirse a las opacidades irregulares pequeñas. Además, es muy probable que estas o p a c i d a des representen el estadio Inicial de este tipo de neumoconlos1s.
R E F E R E N C I A S
1.-
Greenburg, L.: The classification of dusts which cause
pulmonary disability. Journal of Occupational Medicine
14: 146-148, 1972.
2.-
González, Z., A., Maldonado T., L., Sepûlveda L., D. y Rodriguez R., D.: Neumopatfa laborales no traumáticas. Valoración del grado de Incapacidad. Criterios clínico,
6o5
radiologico y funcional. Patología Laboral, Fascículo -13, Volumen V, Anuario de Actualización en Medicina. I.M.S.S., 1973, Págs. 37-43.
3.-
Maldonado T., L.: Las enfermedades de trabajo mas frecuen.
tes en México. Condiciones de Trabajo. Vol. 2. No. 2. -Mayo-Agosto, 1977. Págs. 103-104.
4.-
Maldonado T., L.: Estadística sobre enfermedades de traba,
jo en México, en 1977; aún no publicada.
5.-
González Z., A., García P., E., González Q., E., Landini
C , R., Maldonado T. , L. y Montoya C , M. A.: Normas para
el diagnostico, tratamiento y profilaxis del trabajador expuesto a Inhalación de polvos Inorgánicos. Edición en
fotocopia. Departamento de Riesgos de Trabajo y Hospital
de Enfermedades del Tórax, en el Centro Médico Nacional,
de la Subdlrecdön General Médica, del Instituto Mexicano
del Seguro Social, Noviembre de 1973.
6.-
González Z., A., García P., E., González Q., E., Landini
C , R., Maldonado T., L. y Montoya C , M. A.: Diagnóstico,
tratamiento y profilaxis de las enfermedades provocadas por la Inhalación de polvos Inorgánicos. Boletín Médico,
I.M.S.S. Vol. 16. Nûm. 7. Julio, 1974. Págs. 258-267.
7.-
ILO U/C International Classification of radiographs of -pneumoconioses 1971. Occupational Safety and Health Series
22 (rev.), International Labour Office, Geneva,
Switzerland, 1972, Pág. 22.
606
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The value of studying pulmonary
function with a view to the early
dla^noslB of alíjeosle
li. Maldonado T.. M. Martha Mènde a 7., J.A. Legaspi V,.
A. González Z. (Mexico)
As a general rule, sllioosis develop« asymptomatically,
at least in ite initial stages, so that in studying it one
cannot expeot X-rays to show the oharaoteristio epeokled
pattern formed by small round opacities in X-ray photographs
taken of workers who have been exposed for a sufficiently
long time to particles of silica and silicate dust, but the
examination has to he undertaken when small irregular opacities are already to be observed, in the same manner as in
the previous oase. by means of olinloal study, laboratory
tests, radiographic and eleotro-oardiographlo examination and
pulmonary funotioni teats.
This manner of prooeeding has «any advantages in day-today praotioe as it enables a high percentage of early alterations to be deteoted. In the majority of cassa there are
signs of pulmonary restriction, medical or peripheral bronchial
obstruction, hypoxemia or hyperoapnia, alón« or in combination. Only in a small percentage of oases are the results
of the pulmonary function tests nonni, despite initial radiographic evidenoe of lung disease*
Although unfortunately the majority of workers in our
oountry oontlnue to work in the saae unsatisfactory condition«, this s'mdy may serve as a basis for their protection.
And, in the oase of the luokier ones, it may save them from
exposure.
608
EFFECT OF CHRONIC AMORPHOUS SILICA EXPOSURE ON SEQUENTIAL
PULMONARY FUNCTION
K. Wilson, R. Richie, P. Stevens
Braes Valley,
Houston, Texas, United States
Although the flbrogenlc effect of crystalline silica on the
lungs is well known, amorphous silica is reported to be relatively
harmless in both animal and human studies. However, previous workers have reported pulmonary fibrosis in workers exposed to calcined
diatomite known
to contain crystalline silica, and Vitums has re-
cently reported pulmonary fibrosis in 11 of 40 workers exposed to
fumed amorphous silica.
Because there are several different pro-
duction methods of amorphous silica, the potential toxic effects
may vary.
We have studied retrospectively the chest radiographs,
serial spirograms, and screening respiratory questionnaires of a
group of workers exposed to precipitated amorphous silica.
Precipitated amorphous silica Is produced by subjecting a
sand and alkali solution to heat to form sodium silicate in solutioni
Amorphous
silica is then precipitated from solution by
adding CO2 or CaCl2<
The resulting product has no crystalline silica detectable
by x-ray crystallography.
Particle size varies depending on the
production method from submicron to micron size, all within the
respirable range.
The study population consisted of 165 male workers with a
mean age of 42 years. The only requirement for inclusion in the
6o9
study was that the workers have at least one year of precipitated
amorphous silica (PAS) exposure so that serial radiographs and
spirograms would be available.
Chest radiographs and spirograms
using variably a Collins Water seal. Donti electronic, or Vitalor
spirometer have
been obtained on all PAS workers on beginning
employment and yearly thereafter for the last 10 years. Respiratory screening questionnaires modified from the British Medical
Research Council format were completed by all workers during the
last year.
Chest radiographe wetre reviewed independently by two experienced chest physicians and a radiologist, and classified for
pneumoconiosis using the UlCC/Cincinnati criteria.
Spirographic data obtained from each tracing included forced
vital capacity, forced expired volume in one second, and maximum
mid-flow or FEF25-75. Each tracing was reduced by an experienced
pulmonary function technician.
Change in pulmonary function
variable per year was obtained by subtracting final from initial
value and dividing by years between the tests.
The extent of each worker's exposure to PAS was expressed
so as to reflect both the quantity and duration of exposure. The
cumulative exposure index, reflecting total PAS exposure, was calculated for each worker by multiplying months of exposure times
relative concentration of atmospheric dust in his work area. Dust
concentration was measured by personal airspace gravimetric monitoring and graded on a scale of 1 (minimal) to 4 (extensive).
61o
The
mean exposure Index Indicates average monthly exposure for workers
with variable exposure, and was calculated by dividing the cumulative exposure index by total months of exposure.
The relationship between yearly change In forced vital capacity and cumulative exposure index was evaluated by linear regression analysis.
As seen here, with an R value of 0.1, there was no
correlation between these variables.
Using similar analysis, no correlation was found between
yearly change In FEV1 and cumulative exposure or yearly change of
FEF25-75 and cumulative exposure.
To avoid possible masking of an effect of increasing exposure,
the overall group was divided into four subgroups with Increasing
exposure.
There was no statistical difference between yearly
change in any pulmonary function variable and Increasing exposure.
To evaluate possible latency of PAS effect, the relationship
between yearly change of FVC and total years of exposure was examined with linear regression analysis. With an R value of 0.13,
there was no correlation between total years of exposure and
decrement In FVC.
Similarly, there was no correlation between
yearly change in FEV1, and total years of exposure or between
yearly change of FEF25-75 and total years of exposure.
611
Further to evaluate the effects of total time of exposure on
pulmonary function, a group of 44 workers exposed for 11-35 years
with a mean exposure time of 18 years was compared to workers with
less than 10 years exposuret
Again, there was no difference in
yearly change of FVC or FEV1 between
the two groups«
There was no relationship between mean exposure index and
clinical symtoms of coughi sputum production, wheezing or dyspnea.
However, there was an interesting inverse relationship between cumulative exposure index and both sputum production and dyspnea. Workers with these symptoms had statistically less exposure than those
without symptoms, raising the interesting but unproven hypothesis
that symptomatic workers may drop out of this type work.
Symptoms
of cough,and dyspnea, but not sputum production, were statistically
more common in heavier smokers. Additionally, and not surprisingly,
all symptoms but dyspnea were more common among smokers than among
non-smokers.
Of the 143 workers with chest radiographs prior to PAS exposure
and during the past year for comparison, 11 (7.5%) had radiographic
change consistent with 1/1 or 1/0 small rounded p or small irregular
t-type opacities.
All 11 workers had a previous history of working
in a local limestone mine or in a soda ash plant using crushed limestone.
No workers with up to 35 years exposure and a work history of
exposure only to PAS had any evidence of pneumoconiosis.
CONCLUSIONI No relationship was found between yearly change in
612
pulmonary function parameters and either quantity of or duration
of exposure to PAS. There was no radiographic evidence of pneumoconiosis In workers exposed only to PAS. Symptoms had no relationship to or correlated Inversely with PAS exposure, but symptoms
were directly related to cigarette smoking.
613
VII/4
L'ADAPTATION
CARDIOPIILdOMATRe
CHEZ I F S
A L'EFFORT
NTNFJ.mS OF CHARRON
P. GARCIA-HERREROS, C. SCANO, L. STENDARDI, S. DEGRE,
R. SERGYSELS 4 A. DE COSTER.
Hospital Universitaire Saint-Pierre,
Bruxelles, Bitloique.
L'évaluation fonctionnelle au repos et pendant
l'exercice ds3 patients atteints d'anthracosilicose
(AS)
est souvent difficile car cette patholooie est souvent
associée a une bronchopneumopathie chronique obstructive
ispeo) qui ne permet pas de faire clairement la distinction entre
lea altérations dues a la pneumoconiose pure
et les maladies surajoutées.
Pour ce travail, nous avons' étudié la fonction
i
pulmonaire et l'adaptation cardio-pulmonaire a l'effort
chez 26 mineurs sans siqnes évidents cliniques et/ou fonctionnels de BPCO associée.
615
PATIEMTS ET METHODES
l e r e diapositive
Les 26 mineurs ont été répartis en 3 groupes d'après les critères radioloqiques du B.I.T. (classification,
1971). Le premier qroupe (c) ou groupé controle se compose
de 8 mineurs sans signes radioloqiques de pneumoconiose.
Le deuxième aroupe (Si) comporte 10 patients dont
l'image radiolooique varie entre P3 et q(m)3.
Le troisième groupe (S2) se compose de 8 mineurs au
stade pseudotumors! : A, 8 et C.
Il n'y a paa de différence nette d'âge moyen pour
les trois groupes.
Tous les patients ont subi un bilan fonctionnel respiratoire au repos comportant la mesure dea volumes pulmonaires et la capacità de diffusion au CO en apnée inspiratole. Ils ont également effectua une épreuve d'effort par
paliers en position assise 9ur cycloergometre. Les paliers
maintenus environ 6 minutes ont été réalisés aux charqes de
250 et 400 Kqm.min* '. les paramètres suivants ont été mesurés:
la ventilation (VE), la consommation d'02 (V02), les gaz
du sann artériel (Pa02, PaC02, pP, acide lactique), la pression artérielle pulmonaire (PAP, par microcathéter de SuanGanz), le débit cardiaque (0, technique de dilution du colorant-cardionreen), La FC, la TA, l'ECG et le volume svstolique ( n s). L'ERP? a été calculé en divisant 1/E/V02; et les RPT
en divisant Pp/fl.
RESULTATS
Les résultats de la fonction pulmonaire 9ont exprimés
en "íringvaleurs normales (CECA); dans l'nnsemble des trois
nrnunnn la fonction est PRU altérée, montrant toutefois une
tßndance a 1'aunmentation du VR notamment dans les groupes
61f
SI et 52. On note aussi une réduction pronrfissive de la
CV dans les t.rnis oroupes mais s.tnnif inative seulement
dans le proline S2.
Malore 1'aunmentatlon du VR le rapport VEFIS/CU reste
dans les limites physioloniques. Les résultats observas
au repos et a la chame de 400 Knm.pour ce. nroupe C (le
nroupe de sujets a Rx normale et fonction normale) ont été"
pris comme référence pour les autres nroupes (SI et S2).
L'évolution de la VE et de la U02 n'est pas différente pour trois groupes. Pour les trois oroupes la Pa02
de repos est normale. A l'effort C et SI améliorent nettement la Pa02; par contre dans le groupe S2, 3 sujets sur
8 abaissent leur Pa02.
La PaC02 est normale au repos dans les trois groupes.
La chute de celle-ci par hyperventilation relative a l'effort est moins marquée dans le proupe S2 pour une même
ventilation d'effort. La chute du p'H est quasi identique
dans les trois groupes et est a correlar avec l'augmentation
de l'acide lactique.
La PAP au repos est normale pour les trois qroupes;
toutefois a l'effort,.le niveau atteint de PAP est le plus
élevé dans le groupe S2; 4 sujets ayant une PAP 30 mm Ho.
L'évolution du 0 et du Os est normale pour les trois groupes.
Les RPT au repos sont anormalement élevées dans les
groupes SI et S2; a l'effort les RPT s'abaissent dans les
trois groupes mais la chute est moins nette pour le groupe
S2.
617
*
*
\
I. ' ¿voluti on tins naramotres analyses par rapport a
la VD? peuvent être résumé brièvement ainsi: par rapoort
au oroupn de référence (c), la PAP ainsi que
les RPT se
montrent dss le dénart plus élevées dans les nroupes SI et
S2; toutefois l'évolution a l'effort reste assez parallèle
dans les trois rroupes.
Par contre D et Qs ont un compor-
tement similaire dans les trois nroupes.
En résuma les anomalies hémodvnamiques et des naz
du sano observées dans les nroupes SI et S2 sont caractérisées par une aqumentation de PAP et de RPT. au repos et
a l'effort par rappprt ,au nroupe controle. Nous avons essayé d'établir des corrélations entre les paramètres hémodvnamiques et la fonction pulmonaire de repos et la Pa02 a
l'exercice. Pour l'ensemble des sujets étudiés les RPT
d'effort ont été córreles sinnificativement avec la CV exprimée en % de la' valeur prédite et la Pa02 a 400 Kqm.min"" ;
La PflP est éqalement sinnificativement corrélée avec la C\l%
mais pas avec la Pa02. Ni les RPT ni la PAP ne sont córreles avec la DLCO.
(Cn conclusion rie l'évaluation fonctionnelle des patients atteints d'AS a divers stades et indemmes de BPCO
évidente on peut déoaqer les points suivants:
au repos, une élévation de VR plus marquée pour SI et S2 mais
un rapoort l/EHS/CV conservé.
Un déficit restrictif sionifi-
catif n'apparaît nue nour le oroune S2.
Les naz du sano sont
normaux. Les PAP ßt RPT auomentent pnur les nroupes SI et S2,
1 'f-xercicf!, las paramètres ventilatnires, la V02, les débits
carriianuf! et systolique restent dans les limites physioloniques.
618
Une chute do la PnD? et unn hypertensinn pulmonaire a été
notée che7 Ì
SP ^ ries sujets du nroune S?.
Les PPT élevées au renos s'abaissent neu a l'effort.
t'auomentation de RPT semble bien rorrélée avec la réduction du parenchyme nulmonaire et la chute de la PaCO? qui
semble secondaire aux altérations V/0. D I U S au'a un trouble de
diffusion.
En effet la 0LCC1 est tres faiblement abaissée me-
mo dans le nroupe S?, de nlus aucune corrélation n'a oa nu
être établie entre DLCO et RPT ou PAP ou Pa02.
619
C O R R E L A T I O N S
TPR Ex
PpEx
THP Ex
VC %
r = 0.48
p < 0 ..01
V C JÉ
r = 0.43
p <o..05
Pa02
r = 0.45
Ï<.
r » 0.17
NS
r =
US
Ex
PP
TPR
Pp
E
Pa0o
Ex
T1C0
*
TICO JÉ
°* 2 8
r = 0.30
62o
RS
o..01
CONCLUSION
AT REST
AS
without BPCO
^ RV 71 with quasi normal FEV.,/VC
VC \¿ significantly for S2
blood gases in normal range
Pp /» PVH
DURING EXERCISE
*
VE
Q
(S1 - S2)
V0 2
Qs
Pa02 Vg in +, 50 # of S2
Pp v 30
RP1
mm Hg
in 50 5É of S2
elevated at rest remain high
HEMODYNAMIC IMPAIRMENT ARE WELL CORRELATED WITH RESTRICTIVE
LUNG IMPAIRMENT AND PaOg DURING EXERCISE.
621
Adántacion cardiopulmonar en el curso
del ejercicio de mineros del carbon.
P. García-Herreros, G. Scano, L. Stendardi,
S. Degré, R. Sergysels y A. De Coster (Belgica)
La evaluación funcional en reposo y durante el ejercicio de pacientes de antrasilicosis (AS) suele ser difícil porque los sujetos asocian con frecuencia una neumopatía obstructiva crónica (COLD). Por lo tanto, hemos estudiado la función pulmonar en reposo y la adaptación cardiopulmonar en el curso del ejercicio en 26 mineros del carbón, con exclusión de los sujetos con una COLD asociada
evidente, clínica y/o funcional.
Se clasificaron los sujetos en tres grupos según los
resultados radiográficos i un grupo testigo (C)i 8 sujetos
que. habían estado expuestos al polvo pero cuya radiografía
era normal; un gruño SI : 10 sujetos con AS micronodular
en la fase PI M3; un grupo S2i 8 sujetos con AS pseudotumoral en la fase AC.
La función pulmonar en reposo muestra una insuficiencia pulmonar significativa pero ligera únicamente en el
grupo S2 (VC 75 por ciento). Todos los sujetos cumplieron un ejercicio progresivo en posición sentada, en una
bicicleta, con los siguientes parámetros controlados en
reposo, 250 y 400 kgi ventilación (VE), consumo de oxígeno (V02), gases y lactatos en la sangre arterial (Pa02,
PaC02, pH), presión pulmonar (Pp, catéter de Swan-Ganz),
rendimiento cardíaco (Q, técnica de dilución cardíaca del
verde brillante) y volumen de expulsión (Qs). Los valores en descanso a 400 kg no mostraron ninguna diferencia
significativa entre los tres grupos en cuanto al $E, Í02«
622
ER02, pH, laccato, PaC02, Q y Qs. El Ta02 en reposo se encontró en valor normal, y en aumento durante el ejercicio
en los grupos C y SI, pero sólo ligeramente en cuatro de
los ocho sujetos del grupo S2.
Se halló que el Pp era normal en reposo en tres grupos, pero ligeramente superior en los grupos SI y S2Í durante el ejercicio, el Pp era superior en el grupo S2, seguido por los grupos SI y C.
Se observó hipertensión pulmonar durante el ejercicio
(Pp ^ 30 nun Hg) en dos de diez pacientes (grupo SI) y en
cuatro de ocho pacientes del grupo S2. La resistencia vascular pulmonar total (T.P.R. = Q/Pp) en reposo y a 400 kg
iba en aumento del grupo C al grupo S2.
En todo lo que antecede, llegamos a la conclusión de que
en ausencia de una COLD asociada evidente, en una fase micronodular, pese a cierto aumento del T.P.R.. la AS es relativamente bien tolerada en cuanto a los parámetros funcionales
estudiados. En una fase pseudoturooral, si bien la insuficiencia pulmonar en reposo es típicamente restrictiva, la
mayoría de los pacientes desarrollaron hipertensión pulmonar
y anormalidades tf/Q que afectaban al Pa02 durante el ejercicio.
El aumento de T.P.R. parece vinculado a la reducción
del parénqulma pulmonar y al nivel del Pa02 durante el
ejercicio. En realidad podría establecer una relación linear negativa entre T.P.R. y VC por ciento (r = -0.48) y
el Pa02 en ejercicio (r = -0.46).
625
THE INFLUENCE OF ASBESTOS EXPOSURE ON
RADIOGRAPHIC PROGRESSION AND FUNCTIONAL DECLINE
A PRELIMINARY REPORT
J. E. Diem, R. N. Jones, J. C. Gilson, M. Glindmeyer, II. Weill
Tulane Medical Center,
New Orleans, Louisiana, USA
In a three-phase study of the health effects of asbestos
exposure in the asbestos-cement manufacturing industry, workers in
two New Orleans area plants have been studied.
The first phase, a
cross-sectional study of approximately 900 workers employed at the
two plants on November 3, 1969, related radiographic and physiologic evidence of asbestosis to level of exposure (1,2,3).
A
mortality study of 6500 current and ex-employees formed the second phase and demonstrated a dose-response relationship between
excess lung cancer mortality and level of exposure (4,5).
Final-
ly, a cohort of the 244 male workers, aged 45 to 59 at the beginning of the cross-sectional study, is being followed longitudinally with regard to both radiographic and physiologic change.
The
cohort was selected with this age range in order to obtain participants who had both sufficient time to exhibit effects of exposure and high probability of continued participation in the study.
The subject of this report is a preliminary analysis of the longitudinal data.
Intensity of exposure between 1952 and 1969 was assessed
from midget itnpinger sampling data collected by job title. Pre1952 estimates of dust levels were made by interviewing employees
of long service in an effort to compare more recent dust levels
with earlier conditions. This information, when combined with
individual job histories, produced a profile over time of the
dust concentration expressed as million particles per cubic
625
feet (mppcf) to which an individual was exposed.
This profile
was integrated over time to produce cumulative dust exposure
(mppcf-years) which, when devided by years of exposure, yields
average exposure.
PA chest radiographs of each subject, taken in 1969-1970
and 1976-77, were read (side-by-side with order known) for progression of rounded small opacities, irregular small opacities,
pleural thickening and pleural calcification by two readers (JCG
and RNJ) using the ILO U/C 1971 Classification for definition of
these features.
scale«
Each reader assessed progression on a 6-point
real regression, apparent regression, no change, possi-
ble progression, probable progression, and definite progression.
Progression was then assumed to have occurred in those indi-.
viduals for whom at least one reader read probable progression
or higher.
Otherwise no change was assumed.
If one reader
thought the films to be unreadable, progression was not determined.
This occurred in 9 of the 204 individuals in the origi-
nal cohort with two films. Of the 195 individuals with 2 readable
films, 3 showed progression of small rounded opacities, 17 pro- "
gression of irregular small opacities, 40 progression of pleural
thickening, and 12 progression of pleural calcification.
Table I presents descriptive statistics on the 204 individuals with 2 radiographs. These statistics are calculated
as of the time of the 1969-1970 cross-sectional study.
With the exception of chronic bronchitis there were no
statistically significant differences between this group and the
40 without the two necessary films. 12.8% of those lost to
626
follow-up had chronic bronchitis at the time of the cross-sectional
study.
Eleven of the 40 had died.
Thus there are indicators that
there is a selection bias in favor of healthy individuals (the survivor effect noted in longitudinal cohort studies).
In the 195 individuals on whom it was possible to assess
progression, associations between progression and cigarette smoking
(ever versus never), average exposure, length of exposure (years),
cumulative exposure, and age at the time of cross-sectional study
were sought.
Time since initial exposure and length of exposure
v*ere too highly correlated (r = .98) in this cohort to permit separation of their effects.
First-order relationships, as determined by logistic regression, between possible influencing variables and progression
of irregular small opacities, pleural thickening, and pleural
calcification are summarized in Table II. Progression of irregular small opacities shows a significant dependence on average
and cumulative exposure. This is in contrast to progression of
pleural thickening and calcification which both depend only
on length of exposure.
Conclusions based on associations with length of exposure
should be viewed with caution since length of exposure and time
since initial exposure are synonymous in this group (r = .98)
and length of exposure is heavily concentrated in the narrow
range 20 to 25 years (63% of the 195 individuals lie in this
range even though length of exposure varies from 3 months to
38 years).
Additionally, with regard to progression of irregular
627
small opacities, the percentage progressing in the categories ^
20 years, >20 to < 25 years, and >25 years was 0, 12.3, and
6.5 respectively, indicating a non-linear relationship between
probability of progression and length of exposure.
If linear
relationships are sought in situations where the relationship
has no linear components, then a conclusion of no association
results.
Because of the observed non-linear relationship between
probability of progression of irregular small opacities and length
of exposure, it is not surprising that the analysis performed here
(where the logit was linearly regressed on length of exposure)
did not produce statistical significance.
Subsequent analyses
will search for good fitting non-linear models incorporating
lag time.
In order to determine if the dependences observed in
Table II were effects beyond other influencing variables, logistic regression was performed on the progression of each radiographic abnormality using age, the dichotomized smoking variable,
length of exposure, and average exposure as independent variables.
Table III displays for each four-variable logistic regression
equation the four coefficients, standardized coefficients
(coefficient/standard error), and the likelihood ratio statistics (distributed as chi-square with 1 degree of freedom) for inclusion of each influencing variable after the other three are
in the equation.
The results of this calculation confirm the
"each variable separately" analysis given above, with the added
628
Information that smoking and progression of pleural thickening
almost obtains a statistical^ significant (p = .08) relationship.
The difference in the way exposure seems to relate to
progression of parenchymal and pleural disease adds validity
to the separate recording of these two kinds of abnormality in
the ILO U/C 1971 Classification.
The findings of this study also add to the evidence for
differences in the natural history of the effects of asbestos on
the parenchyma and pleura.
In pleural thickening, progression
was first detected at about 12.5 years, after which the proportions of subjects with progression increased with time up to the
longest observed period of 38 years.
For pleural calcification,
progression started rather later, at about 20 years, then increased with time. Progression of parenchymal disease (irregular small opacities) showed a different patterni
first cases
of progression occurred at about 20 years, but nearly all instances of progression fell within the period 20 to 27 years,
with very few beyond this period.
Thus a lag period was follow-
ed by progression of asbestosis» but the probability of progression increased with Increasing average and cumulative dust exposure, rather than with increasing time.
These data accord with epidemiologic and clinical observations that asbestosis correlates better than does pleural
disease with dust dosage.
In a population with a wide range of
average dust exposure and a long follow-up time, the time-dependence of pleural progression and dose-dependence of parenchymal
progression should operate to produce a number of persons with
629
extensive pleural disease but no parenchymal disease.
This
also accords with clinical and epidemiologic experience.
Ventilatory function, lung volumes, and diffusing capacity measurements are available from each of two occasions for
subsets (n = 151 for ventilatory function and n = 178 for lung
volume and diffusing capacity) of the original cohort.
The
first measurements were taken during late 1973 and early 1974,
and the second approximately three years later.
Mean time
between visits for the 198 not lost to follow-up was 3.15 years
(standard deviation = .18).
Non-participation or inability of
the participant to produce Acceptable spirometrie tracings or,
in the case of diffusing capacity, to produce repeatable results, account for the reduction of the cohort.
Multiple regression of annual change on the dichotomized
smoking and cumulative exposure variables showed a significant
association with cumulative exposure beyond the smoking effect
only for FVC and FEVi.
Table IV presents the results of these
regressions together with the marginally significant exposure
association for total lung capacity.
Of the 155 participants with complete ventilatory function
measurements and the two necessary x-rays, twelve showed progression of irregular small opacities.
Table V summarizes the
relationship between ventilatory function change and progression
of irregular small opacities and shows that AFVC, 4FEVj, and
â FEF2c TIT declined significantly more in the progressors.
The association between total lung capacity and progression of
irregular small opacities was of marginal statistical significance (p = .07).
No significant association was found for pul-
monary diffusing capacity.
63o
TABLE I
DESCRIPTIVE STATISTICS FOR THE 204 WITH 2 PA RADIOGRAPHS
L. X Current or ex-cigarette smokers
75.5
2. X White
37.3
3. X Chronic bronchitis (MRC Questionnaire definition)
Mean
2.5
Standard
Deviation
4. Age'
50.9 years
4.2
5. Time since first exposure
21.9 years
6.7
6. Length of exposure
21.4 years
6.4
7. Average exposure
12.64 mmpcf
8.6
8. Cumulative exposure
288.75 nmpcf-years
631
215.75
TABLE II
p-VALUES FOR RELATIONSHIPS BETWEEN RADIOGRAPHIC
PROGRESSION AND POSSIBLE INFLUENCING VARIABLES*
Progression of:
Influencing
Variables
Small Irregular
Opacities
Pleural
Thickening
Calcification
Age
.14
.39
.41
Smoking
.57
.16
.57
Length of Exposure
.13
.02
.03
Average Exposure
.0001
.22
.34
Cumulative Exposure
.0002
.11
.19
* Based on the likelihood ratio test using a logistic regression model. Each
variable treated separately.
632
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O
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V)
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H
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14
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o
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en
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•ri
t)
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ïfl -H
C <M
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o 3
s mg
>-l
-H
h
633
4J
B
Ol
f-l
ü
-HO
O -H
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•HS
i-l i-l
^
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a TÍ
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•Ö <M
(3 >M
C T4
iH
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M-I
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u
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Cî **-»
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C TÍ
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(0
tt)
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i IM
TABLE IV
PHYSIOLOGIC ANNUAL CHANGE REGRESSIONS
FVC
Intercept
Sraokinx
.052
-.034
Cumulative*
Exposure
(n - 151)
Coefficient
p-value for
partial t-test
FEVj^
-.00061
.014
.030
.027
.000044
.010
.030
.016
.00086
.500
.064
(n - 151)
Coefficient
.032
p-value for
partial t-test
(n - 178)
TLC
Coefficient
.080
p-value for
partial t-test
* Cumulative exposure means for those participants available
for use in the three regression equations are 284.6, 284.6
and 284.8 mppcf - years respectively.
634
TABLE V
RELATIONSHIP BETWEEN PROGRESSION OF IRREGULAR
SMALL OPACITIES AND CHANGE IN VENTILATORY FUNCTION
Irregular Small Opacities
Non-progressors
(n=133)
Progressors
(n=12)
Function Test
X
p-value
S
X
S
A FVC (ml)
-.060
.069
.005
.050
.0002
A FEV (ml)
-.061
.107
.017
.064.
.0001
A FEF25_75 (ml/sec)
-.149
.111
-.068
.129
.038
A FEF 2 5 (ml/sec)
-.101
.169
-.083
.104
.59
A FEF50 (ml/sec)
-.175
.136
-.224
.228
.45
Other Variables
Years since
initial exposure
23.3
3.17
21.5
7.24
.38
Age
52.8
4.22
50.7
4.33
.11
Average Exposure
mppcf
22.0
12.4
11.6
7.67
.001
Length of Exposure
(years)
23.1
3.3
21.0
6.9
.31
495.3
246.8
263.0
199.4
Cumulative Exposure
mppcf-years
Z Smokers
83.3
635
75.2
.0002
.53
REFERENCES
1. Weill, H., Waggenspack, C , Bailey, W., Zlsklnd, M., and Rossiter, C. :
Radiographic and Physiologic Patterns Among Workers Engaged in
Manufacture of Asbestos Cement. Products, 1973, Journal of Occupational
Medicine, L5, pp. 248-252.
2.
Weill, H., Ziskind, M., Waggenspack, C , and Rossiter, C : Lung
Function Consequences of Dust Exposure in Asbestos Cement Manufacturing
Plants, 1975, Archives of Environmental Health, 30, pp. 88-97.
3. Weill, H., Rossiter, C , Waggenspack, C , Jones, R., and Ziskind, M. :
Differences in Lung Effects Resulting from Chrysotile and Crocidollte
Exposure, Inhaled Particles IV, W. H. Walton, ed., 1977, Pergamon
Press, New York.
4.
Hughes, J., Waggenspack, C , Weill, H. : Mortality Study of Workers
Engaged in Manufacture of Asbestos Cement Products, 1978, American
Review of Respiratory Diseases, 117, p.292.
5. Weill, H., Hughes, J., and Waggenspack, C : Influence of Dose and
Fiber Type on Respiratory Malignancy Risk in Asbestos-Cement Manufacturing, 1978, Submitted for publication.
636
Influencia de la exposición al amianto en la
progresión radiográfica y el empeoramiento
funcional
J. E. Diem, R. N. Jones, J. C. Gilson, H. Glindmeyer y H. Weill
Estados Unidos
Estudios anteriores efectuados en esta unidad han demostrado que la presencia radiográfica y fisiológica de asbestosis y
el exceso de mortalidad del cáncer del pulmón tienen una relación de.dosis en los trabajadores de las fábricas de fibrocemento.
En una muestra de esta población seguida longitudi-
nalmente (6 años), la duración media de exposición fue de 22
años y la dosis de exposición individual se reconstruyó utilizando la duración y el nivel medio de exposición al polvo.
La exposición media en el momento de la anotación coincidía
significativamente con la progresión de pequeñas opacidades
irregulares (p<0,001), pero no con el fumar.
El decaimiento
anual de la capacidad vital forzada y del volumen de expiración forzado por segundo concordaba significativamente con la
exposición pasada ( p<^0,04) más allá de un efecto de fumar
significativo (p = 0,01).
La progresión radiográfica estaba
firmemente asociada al mayor decaimiento anual de la función
pulmonar ( p<.0,001).
La progresión de pequeñas opacidades
irregulares parece estar más específicamente relacionada con
el efecto del polvo del amianto que no el decaimiento de la
función pulmonar.
637
I- l\! D_! C_Ç__S_E: 5_|
VITI. I
I P •'
VIII
. 'il.T.Ulmer
•HologlcBl and Functional t*>9ts In early diagnosis oF
Pneumoconiosis and rehabilitation
VIII. II
CI.Adrianz8. , C.Frnould., v.Sanchez
Pulmonary Function oF Smoking workers exoosed to Inorganic Duat.
Villi. Ill Richard R.martin., Jean-Jacque9 Gauthier et Charles Bernai
Exploration Fonctionnelle dans le diagnostique
pmcooe
de l'Asbeatose.
VIII. IV
K.Nobutomo
Air pollution and cytological changes in sputum
VIII. V
VIII. VI
m.L.H.Fllndt.
IdentiFicetion oF illness From allergenic dusts by
T.raattaaon. , P.L.KalliomSki. , O.Korhonen., and V.Vaaranen
magnetic measurements and radiographic Findings
VIII. VII
T.lflattsson., N.S.Huuskomen., and A.ZIttlng
Correlation Between Radiographic and Physiological Findinc
In asbestosis
VIII.VIII
T.L.Guidotti
Arc Weldera'Pneumoconiosis: Studies nith advanced techniques oF scanning electron microscopy and microprobe
ana-
lysis,
VIII. IX
H.SIlbg., K.Chlyotani., V.Saito.
Application oF the Four-Fold maqnlFled selective 8lveolohronchography to Pneumonloses.
659
BIOLOGICAL AND FUNCTIONAL TESTS IN EARLY DIAGNOSIS
OF PNEUMOCONIOSIS AND REHABILITATION
by
W. T. Ulmer
Pneumoconiosis Research Institute, Bochum, Federal
Republic of Germany
Introduction
There are no real biological tests available for early
diagnosis of pneumoconiosis.
There are two types of functional
impairment in patients with pneumoconiosis.
The one is the as-
bestos type = restrictive pulmonary function impairment.
The
best way to measure this is to measure the lung compliance.
The
other is the coal workers* pneumoconiosis type = obstructive
pulmonary function impairment.
The best way to measure this
is to measure the airway resistance.
Inhalation of broncho-
constrictive substances can show the onset of an airway obstruction at a relatively early stage. The measurement of the airway
resistance breaking volume or airway resistance breaking capacity
is not appropriate for detecting early signs of airway obstruction.
The recognition of the early signs of obstructive airway disease
is very important for the prognosis of these workerst because there
are excellent possibilities for treatment with good long-term
results.
There is a general agreement between our experience gained
with man and our animal experiments showing that some Individuals
develop, following the same
quality and quantity of dust exposure,
a serious pneumoconiosis (according to the X-ray or the anatomopathological findings ) and others do not.
641
In the field of
pneumoconiosis due to inorganic dust, it has been suggested for
many years that there might be an individual factor responsible
for the fast progression and the development of pneumoconiosis.
Various research teams discussed these possibilities, and at this
time there are some comprehensive research projects in progress in
Great Britain and in the Federal Republic of Germany to understand
more about this individual factor (or factors).
But till now
there is to my knowledge, no biological test available for the
early diagnosis of inorganic-dust pneumoconiosis.
However, in the field of organic dusts which cause allergic
disease by antigen-antibody reactions following dust inhalation,
there are some tests available, which are either purely biological
or combined biological and functional tests. The biological tests,
such as the skin test or the radioallergosorbent test, are of some
help and interest, but only one test can be decisive for the
existence of a disease of the bronchopulmonary system due to dust
inhalation, i.e. the inhalation test, which is again a combined
biological and functional test.
But these allergic diseases of
the broncho-pulmonary system I have in mind, such as bakers'
asthma or wood-dust asthma, also recognised as occupational diseases and caused by dust, are not pneumoconioses by definition.
So the border line between these two types of dust-induced
diseases are not always distinct (Ulmer and Berges, 1976).
Among the pneumoconioses caused by inorganic.dust, coal
workers• pneumoconiosis and asbestosis play the most important
role.
So far, however, there is no biological test available
642
for their diagnosis«
Even the pulmonary function tests, which can
serve as diagnostic tools, are more or less non-specific.
Other
non-occupational diseases also produce similar or identical changes
in pulmonary function. As regards the radiographs and pulmonary
function in man, however, special types of functional impairment
are known, which can be very different according to the types of
pneumoconiosis•
For this reason it is useful to discuss coal workers' pneumoconiosis and asbestosis, because each of them is a typical example
of a very particular picture of functional impairment of the lung.
A large number of pulmonary function tests are available for
clinicians.
The better we understand the disease the less tests
are necessary to become sure about the typical picture and the
amount of functional disturbances.
Many tests are relatively un-
specific. They only show us that something is wrong, like vital
capacity or the arterial blood gases. Others
need a certain
amount of co-operation of the persons tested, which cannot always
be assumed as on forced expiratory volume manoeuvres. The best
solution seems to be a small number of tests which are well-defined
for special areas of the lung function and therefore are relatively specific for a particular
disease. Also, the test results
should be as far as possible Independent of the co-operation of
the persons tested and of the motivation of the technicians.
The typical functional Impairment In asbestosis Is of the
restrictive pattern (Becklake et al., 1972i Becklake, 1976¡
Woltowitz and Valentín, 1977| Woitowltz et al., 1978).
643
Figure 1 shows test results of a typical case. The vital
capacity Is decreased but this Is unspeclflc.
The decreased com-
pliance of the lung is very specific, so is the decrease In arterial
oxygen pressure.
Fig. 11 Typical lung function tests in a case of
asbestosis with severe X-ray opacities.
The airway resistance in the early stage of asbestosis is always normal, and so is the forced expiratory volume/second in percent of vital capacity (FEV).
The decrease in vital capacity and
the decrease In compliance are relatively early signs of the
disease, and they sometimes show deviations earlier than the X-ray.
But are these tests positive early enough?
Coal workers' pneumoconiosis, i.e. pneumoconiosis in which
silica plays an important role, gives a completely different
pic-
ture of the lung function disturbances. Apart from silica mostly
present in the dust mixtures, which these workers inhale, there
are also other components in high concentrations than silica.
These other components too, influence more or less the picture of
the disease (Weiler, 1977» Relchel, 1976).
As we were able to show, the typical disturbances of the lung
function In this kind of pneumoconiosis is the obstructive airway
disease.
There are for a long time no typical changes of lung.
function; though there may be very severe X-ray changes, the arterial
blood gases and the ventilation behaviour of the lungs are almost
normal.
As regards the mechanical properties of the lung, some of
the cases present small restrictive functional abnormalities.
the whole, however, these changes are without any important in-
644
On
fluence on the well-being and working capacity of these persons
(Ulmer, 1976i Ulmer and Reichel, 1972).
On the other hand, some of the miners develop a serious
dyspnoea.
This dyspnoea is always caused by obstructive airway
disease.
Obstructive airway disease is a very common disease in
the non-dust-exposed (general) population.
Comparative studies have shown that this kind of obstructive
airway disease is more often encountered in coal miners with coal
workers* pneumoconiosis than in the general non-dust-exposed
population showing type B and C opacities (according to the ILO
classification of radiographs of 1971-72) (fig. 2 ) .
Fig.21 Percentage of persons which show increased
airway resistance (Rt> 3,5 cm HjO against
ï sTï
non-dust-exposed men. Coal workers with CWP
category PQR and A and CWP category B, C of
different age groups.
Increased values of airway resistance were seen about twice
as often in categories B and C than in the other groups.
In
the categories with earlier X-ray changes, however, there is no
sign of a higher percentage of chronic obstructive airway disease
in these miners as compared to non-dust-exposed men.
Increased
airway resistance is a relatively late sign of airway obstruction, especially, when the obstruction starts in the peripheral
airways.
Sometimes, one of the earliest signs is the hyper-
sensitivity of the bronchial system to bronchoconstrictive substances (De Vries, et al., 1964| Ulmer et al., 1976).
645
An increase in airway resistance greater than R
= 6 cm H^O/l's"
following acetylcholine exposure under our experimental conditions is
indicative of a
hypersensitive bronchial system (fig. 3 ) . In a
comparative study we were unable to show a more frequent hypersensitivity of the bronchial system in coal miners than in non-dustexposed men.
Fig.3: Airway resistance (Rt) following acetylcholine
inhalation in persons with normal reactivity
and in persons with a hypersensitive bronchial
system.
There was some hope to find earlier signs of obstructive airway disease by measuring the closing volume or the closing capacity
of the lung (Macklem, 1972).
We developed a method for direct
measurement of airway closure (Islam and Ulmer, 1976, 1977) by
plotting airway resistance against lung volume. However, in coal
miners with and without X-ray changes, the age dependency of the
airway resistance breaking point, measured as closing volume or
closing capacity, is comparable with the closing volume and the
closing capacity of non-dust-exposed men (fig. 4 ) .
Fig.41 Airway resistance breaking volume in percent
of vital capacity (StaV % VC) and airway
resistance breaking capacity in % of total
lung capacity (StaC % TLC) in non-dust-exposed
men (left) and in coal workers with and without
X-ray changes in different age groups.
A few words about rehabilitation.
There are some excellent
possibilities to control the most dangerous complication of this
pneumoconiosis, i.e. the control of airway obstruction.
646
Many of
the patients start too late with the important long-term treatment.
In most cases we can maintain the situation of the patients at
this stage by applying our treatment.
In the other paper which
I will present on this meeting, I will go into more detail on
this point.
But the results obtained during many years of sur-
veillance of these coal miners show the importance of controlling
any dangerous exacerbation of chronic obstructive airway disease
and also the importance of a continuous adequate long-term treatment.
647
Ci., Fr. born 6. 8. 1920
• '<88
H29) IGV 3090 ml
( Ts "' '
( 2990 ml Soil )
Compliance
VC
=
Asbestosis
14. 3. 73
0,055 ( ¿j^pj-5)
- 65 V.
( 0,3 - 0,12 = Norm )
F E V Ì / °/o VC = 75
P02a
54 mmHg ( rest ) 47mmHg (60 Watt )
PCO 2 a
38 mm Hg ( rest ) 39 mm H g (60 Watt )
Fig. 1j Typical ldng function t e s t s in a case of
asbestosis with severe X-ray opacities.
Frequency
R t > 3.5
V.
70 -1
60
504030 -
coal miner» without CWP
20
10 -
-I
«0
1
I
1
I
45
50
55
60
1
65 age
years
Fig.21 Percentage of persons which show increased
airway resistance (R > 3,5 cm H^O against
Í s^l
non-dust-exposed men. Coal workers with CWP
category PQR and A and CWP category B, C of
different age groups.
648
Inhalation 3°/o Acetylcholine 1min
Fig.31 Airway resistance (R ) following acetylcholine
inhalation in persons with normal reactivity
and in persons with a hypersensitive bronchial
system.
to -
'It
non dust exposed men
80
70
70 «0 -
Coal workers with and without
changes on the X-ray
5UC
|„."|
y
,LC
•"•
St»C V. TLC
Í0
S
SO 40 JO 20 -
a<ie (years)
age (years)
Fir.4: Airway resistance breaking volume in percent
C
of vital capacity (Stav 7. VC) and airway
resistance breaking capacity in /< of total
íung capacity (StaC 7. TLC) in non-dust-exposed
men (left) and in coal workers with and without
X-ray changes in different age groups.
649
R e f e r e n c e s
Becklake, M.R.
State of the art - asbestos-related diseases of the
lung and other organs: Their epidemiology and implications for clinical practice
Amer. Rev. Resp. Dis. 114, 187 (1976)
Becklake, M.R., G.G. Fournier-Massey, C R . Rossiter, J.C. McDonald:
Lung function in chrysotile asbestos mine and mill
workers of Quebec
Arch. Environm. Hlth 2±, 401 (1972)
Islam, M.S., W.T. Ulmer: Die Strömungswiderstands-Volumenbeziehung als
Maß des Closing Volumen
Pneumonologie 153, 289 (1976)
Islam, M.S., W.T. Ulmer: Der Strömungswiderstand in den Atemwegen
und das Lungenvolumen
Dtsch. med. Wschr. 102, 1187 (1977)
Macklem, P.T.:
Obstruction in small airways, a challenge to medicine
Amer. J. med. 52, 721 (1972)
Die Silikose (Anthrakosilikose)
In: Pneumokoniosen. Handbuch der inneren Medizin,
5. Auflage, Bd. 4, Atmungsorgane 1. Teil, p. 159
Hrsg.: W.T. Ulmer u. G. Reichel
Springer, Berlin Heidelberg New York, 1976
Ulmer, W.T.:
Pneumokoniosen und Lungenfunktion
In: Pneumokoniosen. Handbuch der inneren Medizin,
5. Auflage, Bd. 4, Atmungsorgane 1. Teil, p. 599
Hrsg: W.T. Ulmer u. G. Reichel
Springer, Berlin Heidelberg New York, 1976
Ulmer, W.T., G. Reichel: Functional Impairment in Coal Workers'
Pneumoconiosis
In :.Coal Workers' Pneumoconiosis
N.Y. Acad. Sci., p. 405, 1972
Reichel, G.:
Ulmer, W.T., G. Berges: Untersuchungen zur Reaktionsbereitschaft
des Bronchialsystems bei Gefährdung durch Inhalation
von Allergenen und chemisch irritativen Stoffen
Verh. dtsch. Ges. Arbeitsmed. 16, 329 (1976)
Ulmer, W.T., G. Reichel, D. Nolte: Die Lungenfunktion.
Physiologie und Pathophysiologie, Methodik.
2. Überarbeitete und erweiterte Auflage.
Stuttgart, Thieme, 1976
65o
De Vries, K., H. Booij-Noord, J.T. Goei, H.J. Grobler, H.J. Sluiter,
G.J. Tammeling, N.G.M. Orie: Hyperreactivity of the
bronchial tree to drugs, chemical and physiological agents
In: Bronchitis II
Assen, Royal Vangorcum, 1964, p. 167
Weiler, W.: Anthrakosilikose. Tierexperimentelle Forschung
Bergbau-Berufsgenossenschaft,Bochum, 1977
Woitowitz, H.-J., H. Valentin: Zur arbeits- und sozialmedizinischen
Begutachtung von Asbestinhalationsfolgen
Prax. Pneumol. 31, 153 (1977)
Woitowitz, H.-J., G. Krieger, R.H. Woitowitz: Berufliche
Asbeststaubexposition und obstruktive bronchopulmonale
Erkrankungen
Arbeitsmedizin, Sozialmedizin, Präventivmedizin
(1978 i. Druck).
651
INFLUENCIA DEL HABITO DE FUMAR EN LA MORBILIDAD RESPIRATORIA DE LA POBLACIÓN LABORAL VENEZOLANA EXPUESTA A LOS RIESGOS DE INHALACIONES PULVIGENAC. HUMOS, GASES Y VAPORES DEL MICRO CLIMA
INDUSTRIAL MANUFACTURADO, ,-v?
INTRODUCCIÓN:
Hoy día la relación del pulmón y la vida, no solamente está medida por la función respiratoria, sino que debido a los a.
POBLACIÓN LABORAL EXPUESTA A RIESGO PULVIGENO
DE ORIGEN INORGANICO
h f l u t a d i étel hAbko dt fkuev Matta fai *4ba1
Grupo Boad
Parador
P
21
22
N
1)
24
15 • J4
Total
50
/110
<0
P
n
41
N
51
10
P
«6
42
24
»
/1«1
53
• P .
51
22
TI
N
1»
20
P
If
9
n
•
/40
12
2Sa34
15*44
45 a 54
55rnáa
4
N
TOTAL
Na Fumador
2M
/3«
131
P = PATOLOGICO.
120
/2II
91
.
»
010101
033»
IM
/1I2
J9
ÌMO
4J4I4
tma
14]
nei
614
Slaat
1192
124
N = NORMALES.
Manuel Adrlanza H. ministerio da Sanidad y Asistencia Social («ISAS)
Amllker Torrsalba, ministerio dal Trabajo (HIT)
Erich Semldt.
Ministerio da Sanidad y Asistencia Social (PISAS)
Catherine Crnould. Conlclt
Francisco Fuenmayor.Instituto Venezolano da los Seguros Soclales(IVSSj
Maximiliano Acosta, ministerio del Trabajo (WT)
653
ces de la Inmunología y las técnicas de ultraestructura celular le
confieren una función de defensa frente a los agentes irritantes,
tóxicos vivientes o inertes respirables.
El macròfago alveolar, célula ésta que puede medir hasta 12 mieras en su diámetro mayor, llamada libre porque no está fi
ja a la pared y se le puede encontrar tanto en los alvéolos y lavji
do bronquial, hace una defensa primaria tanto frente a los microorganismos como a las partículas inertes. Igualmente el aparato mu
cociliar traqueobronqulal originado en las células celíadas las
cuales dan origen a más de 270 cilios por célula con propiedades pulsátiles de 20 veces por segundo sincronizadas con las células vecinas. Se estima que alrededor del 90% del material extraño dep¿
sitado en las mucosas bronquial es limpiado en una hora.
El Dióxido de Silicon, el Asbesto, el Dióxido de Nitrógeno, Ozono y buen número de componentes del cigarrillo no absorb¿
dos por la membrana tráqueo bronquial dañan el macròfago y en consecuencia la función de esta célula.
El humo del cigarrillo ha sido reportado por afectar el
macrofago alveolar inhibiendo la actividad metabòlica y la fagocitosis. (Kennedy,J.R. and Elliot S.M. Science 168: 1097-1970 y Green,G.M. and Carolin, D: N.Engl. J. Med. 276: 421-1967) y se ha de¿
crito a la inhibición de la dehidrogenasa glyceraldeica y a la glv_
colisis anaeróbica (Green G. M. Med, Clin. North. Am. 57: 547-1973).
El numero de macrófagos desciende con la exposición aguda y eumene
ta con la exposición prolongada al humo del cigarrillo. (Am. Rev.
Resp. Diseasm 107: 596-1973) macrófagos obtenidos del lavado bronquial mostró diferencias entre fumadores y no fumadores: 30 al 95Í
de los macrófagos de los fumadores presentan material autoflorecen
te de inclusiones citoplasmátlcas, refráctiles y cristaloides y mje
nos del 5% en los macrófagos de los no fumadores. También las célu
las polinucleares gigantes se encontraron en los lavados de 3 de once fumadores y ninguno de 13 fumadores.
El daño del humo del cigarrillo al aparato mucociliar está desde hace tiempo establecido en relación con la duración a -
65*
C— 2
POBLACIÓN LABORAL EXPUESTA A RIESGO PULVIGENO
DE ORIGEN ORGANICO
Influencia del hábito de f amar según la edad
Grupo Edad
Fumador
No Fumador
Total
Xa
17
/27
10
0.0032
P
10
7
N
6
4
P
22
26
48
N
11
11
/77
29
52
13 • 24
23 • 34
P
27
25
N
4
9
33 • 44
P
23
21
N
3
7
P
«2
79
N
31
31
113
ito
45 • 54
/65
13
1.9154
1.1655
44
/M
10
1.6106
55 y mí»
TOTAL
P = PATOLOGICO.
N
=
NORMALES.
655
223
JC5.39
NoSígnif.
P > 0.05
la exposición tabáquica, Así pues, jugando el humo del cigarrillo
un papel perjudicial tan importante, la hipótesis de buscar mayores enfermedades respiratorias en los fumadores de acuerdo con los
años de exposición a contaminantes del humo y ambientes profesionales es materia que justifica esta observación que hoy presentamos como nuestra población, igual que muchos otros comienzan a fju
mar antes de los 20 años la agrupación por grupos de 9 años nos pa
rece muy apropiada para el estudio de los efectos del factor ciga
rillo.
MATERIAL Y METODO;
La población laboral venezolana para el año de 1978 fue
de 3.890.312 y de esta clflra la población expuesta a riesgos respi
ratorios fue de 309.382, (7,95?): 84.738 correspondientes a las áreas de polvos orgánicos y 154.293 al ¿rea inorgánica. Estas últimas cifras hacen un total de 239.738 trabajadores mayormente expues_
tos a riesgos de exposición específicos.
La actividad de muestreo de la Encuesta Nacional de Neu_
moconiosis durante el primer semestre del año de 1978, tocó a H actividades económicas con 73.296 trabajadores,(30,5$ del universo)
Se estudiaron además dos muestras de la población general en calidad de grupos testigos en las ciudades de Coro y Caucagua; centros poblados sin contaminación ambiental extra o intramural.
Los trabajadores encuestados fueron inquiridos en relación con el Hábito de Fumar para calificarlos en grados de acuerdo
a la intensidad, siguiendo las pautas del Departamento de Emplea-dos y Productividad de Londres. Sin embargo las comparaciones de =
este trabajo solamente toma en cuenta la condición de ser o no ser
fumador.
Se establecieron los años de exposición profesional a
los riesgos respiratorios y en general se cuantificó la intensidad
de la contaminación pulvígena la cual se encontró muy alta en to-das las industrias y en todos los puestos de trabajo.
656
C —J
TRABAJADORES NO FUMADORES CON EXPOSICIÓN AL rOLVO
ORGANICO COMPARADO AL GRUPO TESTIGO
ENFERMO
NORMAL
TOTAL
EXPUESTOS
79
31
110
TESTIGO
20
38
58
TOTAL
99
69
168
X« = 2I,«7
P < 0,03
C — 6
TRABAJADORES NO FUMADORES CON EXPOSICIÓN A POLVO
INORGANICO COMPARADO AL GRUPO TESTIGO
EXPUESTOS
TESTIGO
TOTAL
X« =6,91
ENFERMO
NORMAL
TOTAL
143
124
267
20
38
58
162
325
163
P < 0.03
657
Con los datos anteriores se hicieron las tablas que a
continuación copiamos con los resultados expresados en porcentajes con el objeto de conocer:
a)
b)
c)
Los daños atribuíales al cigarrillo;
Los daños atribuibles a la exposición profesional y;
Los daños atribuibles a la combinación de ambos efectos: humo
de cigarrillo más exposición profesional.
Estas variables se estudiaron en el área de polvos àngánicos y en área de polvos inorgánicos dividiendo a los trabajadores entre fumadores y no fumadores y comparándola con la población testigo.
Debido a los efectos conocidos del cigarrillo de mayor
o menor importancia sobre la patología respiratoria específica e
inespecífica investigada en la encuesta, se consideró unir todos
los casos patológicos para conocer su porcentaje en cada grupo de
edad en relación con los normales.
El diagnóstico integrado final se hizo bien estable
ciendo el hallazgo de Silicosis en los obreros expuestos a polvos
de Sílice, bien a la Bisinosis o Bagazosis en aquellos sometidos
a las exposiciones orgánicas específicas o bien se establecieron
los diagnósticos de Bronquitis Crónica y Asma y, finalmente, a un
grupo de síndromes respiratorios no completos pero con evidentes
alteraciones funcionales, clínicas o radiológicas, se agruparon como OTROS diagnósticos.
CONCLUSIONES:
1) (CUADRO 1.-): El aumento del tiempo de exposición al cigarri
lio asimilado a través del aumento de la edad del grupo de trabajadores (N===634) expuestos a inhalaciones pulvígenas inorgánicas
mostró una relación directa de efectos significantes a nivel de P 0.05.
658
C — 3
GRUPO D E FUMADORES EXPUESTOS A POLVOS
ORGÁNICOS Y FUMADORES TESTIGO
EXPUESTOS
ENFERMO
NORMAL
TOTAL
236
131
367
29
48
77
265
179
444
TESTIGO
TOTAL
X» = 1Í.7B
P < OJ»
C —4
TRABAJADORES FUMADORES CON EXPOSICIÓN A L POLVO
ORGANICO COMPARADO AL GRUPO TESTIGO
EXPUESTOS
TESTIGO
TOTAL
X« = ÎJ.96
P < 0.05
659
ENFERMO
NORMAL
TOTAL
82
31
113
29
38
77
111
79
190
2) (CUADRO 2.-): El Cuadro C-2 agrupa a 223 trabajadores expues
tos a polvos orgánicos (Textileros, Tabacaleros, Azucareros, etc.),
este cuadro no muestra diferencias estadísticas significativas entre Normales y Enfermos en relación a los grupos de edades. Ya habiendo hecho la observación al comprobar en la Tabla 3s-3 la inexi_s
tencia de diferencias significativas entre los subgrupos de fumad¿
res y no fumadores de la exposición orgánica manufacturera. Igualmente en relación con el tiempo de exposición estudiado én la T a bla 3-4- habíamos comentado la ausencia de diferencias significativas entre los grupos menores y mayores de 10 años de exposición, lo cual parece demostrar oue en el caso de la respuesta orgánica el tiempo de exposición no juega un papel tan importante como en la exposición a polvos inorgánicos.
3) (CUADRO 3.-)i La exposición combinada del humo del cigarrillo
más inhalaciones pulvígenas inorgánicas tienen efectos de significación estadística en el trabajador.
i)
(CUADRO ¿.-): El mismo efecto le produce la combinación humo
de cigarrillo + exposición pulvígena orgánica.
5) (CUADRO 5.-): En el grupo de no fumadores los efectos de la exposición orgánica aumentan con el tiempo de exposición.
6) (CUADRO 6.-): El mismo efecto se observó en el grupo de no fu
madores expuestos a polvos inorgánicos.
Para terminar debemos decir que el Hábito de Fumar incre
menta la patología respiratoria de manera evidente con la exposición pulvígena profesional y los factores inherentes al micro-clima
laboral.
Las campañas preventivas contra él "Hábito de Fumar" deben hacer énfasis en los sectores laborales en general y más especialmente allí donde los riesgos respiratorios están incrementados
por la naturaleza de los procesos industriales.
66o
vin/3
EXPLORATION FOHCTIONNEUF DAMS LF OT.nnNOSTiniiF
PRECOCE OF L'ASBESTOSE
Richard R. Nartin, Dean-Jacnues Gauthier et Charlea Bernard.
Université de Montréal - Canada.
"Récemment, un comité canadien charoé d'étudier les
critères d'évaluation de la fonction pulmonaire dans les maladies industrielle,concluait que 1'«obeat03e risulte en une
Pneumopathie restrictive classique, dont les siones fonctionnels précèdent souvent les anomalies radioloaiques".
Ceci rejoint les données de Jodoin et Becklake, qui
démontrèrent en 1971, chez 23 travailleurs de l'amiante avec
imaqe radioloqique normale, une diminution de la compliance
statique et une tendance a l'augmentation de la pression de
recul élastique maximal.
Par ailleurs, vu le tabaqisme important que l'on retrouve dans ce oroupe de travailleurs entre autres, (85% des
sujets de cette étude) on reconnaît que la symptomatolonie
aussi bien que les épreuves de fonction respiratoire conventionnelles, (capacité vitale, capacité pulmonaire totale,
diffusion du monoxyde de carbone ou aradient alvéolo-artériel
capillaire pour l'oxyqene) reflètent mal l'exposition antérieur.
En effet, parfois nous nous trouvons dans une situation
paradoxale, ou une composante tabaaisme peut conduire a un syndrome obstructif qui, comme on peut le voir au niveau des volumes pulmonaires, se manifeste par une augmentation du volume
résiduel et de la capacité résiduelle fonctionnelle, alors que
661
la capacité vitale est normale ou léqerement diminuas. D'un
autre coté, le syndrome interstitiel se caractérise par une
diminution de tous ces paramètres.
En ce qui a trait aux débits expiratoires forcés«
ceux-ci sont diminiés dan9 le syndrome obstructif et normalement augmentés dans un syndrome interstitiel. Enfin, si
nous étudions la diffusion du monoxyde de carbone, que ce
soit au repos ou encore suite a un effort, on voit que les
deux patholoqies résultent en une diminution de celle-ci.
Le qradient alvéolo-artériel pour l'oxyqene sera aussi aunmenté, aussi bien dans'le isyndrome obstructif que dans le
syndrome interstitiel.
Ainsi, une exploration fonctionnelle respitatoire
aura-t-elle deux zones d'achoppement dans l'investigation
de l'abestose.
D'abord, a cause des effets contraires des deux syndromes sur les volumes pulmonaires et les débits expiratoires
forcés, des valeurs dans les limites de la normale en seront
souvent les résultantes. En ce sens, nous pouvons dire que ces
épreuves manquent de sensibilité dans la détection de la maladie.
Par ailleurs, l'étude de la diffusion du monoxyde de
carbone, aussi bien que celle des échanqes nazsux, sera perturbée par l'un ou l'autre des syndromes, et bien que noua puissions alors reconneître un état anormal, l'ôtioloqie est impossible a définir. Dans ce sens on doit les considérer comme
peu spécifique.
Les trois exemples suivants représentent bien le dilemme posé par les épreuves conventionnelles.
662
Nous avons examiné le cas d'un travailleur de 53 ans,
avec une exposition totale de 18 ans dans l'industriB secondaire, dont 14 furent, de façon intensive, qui présentait un
tabagisme de 35 paquets/année. Il se plainnait d'une dyspnée
de orade I/IV, et a l'examen nous notions des raies secs,
mais l'abscence d'hippocratisme dipital. La radioaraphie
pulmonaire montrait une catégorie Sl/l - Tl/l. Le3 études de
fonction respiratoire montrèrent un bilan classique d'osbestose
pulmonaire: on a noté une restriction importante des volumes
oulmonaires, un rapport UEHS/CU auqmenté, une capacité de diffusion du monoxyde de carbone abaissée au repos aussi bien
qu'a l'effort, et le oradient alvéolo-artériel B3t élevé au
repos, et augmente encore plus a l'effort.
En examinant l'enregistrement d'une courbe pressionvolume, c'est-à-dire la représentation qraphique de l'élasticité parenchymateuse., I'image est clsssique. La courbe est
déviée vers le bas et vers la droite, avec augmentation tres
importante de la pression de recul élastique au niveau de la
capacité pulmonaire totale, c'est-a-dire la pression élastique
maximale.
On peut citer un autre cas représentatif d'un sujet
porteur d'association d'un syndrome obstructif-abestose. Agé
de 65 ans, il a travaillé 37 ans dans l'industrie primaire avec
une exposition intense durant 13 ans. Il avait un tabagisme
de 40 paguets/année, et l'anamnese dévoile une dyspnée 1/lV alors
qu'il n'y a ni raie sec ni hippocratisme dioital a l'examen. Sur
le plan radioloaique, il est classifié Sl/l.
Le bilan respiratoire est celui d'une bronchite tabagique,
avec capacité vitale normale et volume résiduel augnante»Les débit:
663
exniratoires sont lénsrement diminués, la diffusion du monoxvde de carbone est normale au repos et léoèrement abaissée
a l'effort.
Le nradient alvôolo-artériel pour l'oxygène est
auomenté au repos et ne change pas de fapon siqnificative a
l'effort. Par ailleurs, l'étude des propriétés élastiques du
ppumpn donne une toute autre perspective.
La courbe est dé-
viée vers le haut et vers la qauche, comme dans toute hyperinflamation, cependant sa pente est aplatie et il y a une
forte aunmentation de la force de recul au niveau de la capacité pulmonaire totale, sinnes pathoonnmnniques d'une composante interstitielle significative.
Le dernier exemple se rapporte plus spécifiquement
au theme d'aujourd'hui c'est-à-dire au dépistaqe précoce
d'un syndrome interstitiel.
Un sujet de 51 ans, avec 14 ans d'exposition intense
dans l'industrie primaire, présente un tabaqisme léger pour
l'âqe à 10 paquets/année.
Nous retenons une dyspnée l/lV,la
présence de raies secs et l'abscence d'hippocratisme diqital.
La radioqraphie pulmonaire est interprétée comme normale,
alors que l'exploration fonctionnelle respiratoire est essentiellement normale dans toutes ses composantes.
Cependant, l'étude de l'élasticité parenchymatous.
et
met en évidence un syndrome interstitiel frane, avec aug-
mentation importante du recul élastique et déviation vers la
droite de l'ensemble de le courbe.
En se basant sur le fait
qu'une auamentation de la rigidité parenchymateuse doit signer
une atteinte interstitielle, ce qui est diamétralement opposé
a ce que l'on retrouve dans le syndrome obstructif, il est looinue et raisonnable de croire que le sujet avant eu une exoo<sition suffisante a l'amiante, et chez qui on retrouve de la
664
rinidité parenchvmateuse, est porteur d'une asbestose.que
sa radiographie pulmonaire soit nórmala ou non.
Par ailleurs, une épreuve ou un groupe d'âoreuv/es
simples qui offriraient une bonne corrélation avec la pression de recul élastique maximale pourraient être employées
dans le dépistaqe précoce de l'asbestose.
Un petit nombre de faux positifs et de faux néaatifs
témoignerait de la sensibilité et de la spécificité de cette
épreuve.
C'e9t ce que nous avons voulu évaluer chez 105 travailleurs de l'amiante qui se sont présentés a notre comité
de compensation dans les derniers 12 mois.
Aucun critère de sélection autre que la visite a notre
comité n'est entré en ligne de compte. Chez tous ces sujets,
nous avons procédé a une étuda complete de la fonction respiratoire selon lea critères déjà établis c'est-à-dire capacité pulmonaire totale et set subdivisions, débits expiratoires
forcés avant et après bronchodilatateurs, diffusion du monoxyde de carbone par la méthode en état stable au repos, aussi
bien que lors d* un effort de 40U, de même que l'étude des
échanges gazeux au repos et lors d'un effort de 40U. Par la
suite, après installation d'un ballonnet au tiers inférieur
de l'oesophage, le sujet étant assis dans un Plethysmographe
volumétrique, nous avons mesuré les résistances pulmonaires
totales de même que la relation volume-pression transpulmonaire
par blocaqe itératif de l'expiration de la capacité pulmonaire
totale à la capacité résiduelle fonctionnelle. Ainsi, nous
avons pu reproduire la courbe prassion-volume pour chacun de
ces sujets.
665
Une étude complémentaire a été effectués sur notre
population. Sur 105 sujets préalablement sélectionnés, 83
présentent un dossier complet et techniquement faible. Le
manque de coopération, la claustrophobie, les contractions
oesophaqiennes intempestives, le manque de compréhension des
épreuves, ou encore des tracés techniquement inacceptables,
nous ont obline de renoncer a un nombre de 22 cas.
L'objectif de cette étude était d'évaluer la prévalence d'hyper-ripiditô parenchymateuse dans une population
de travailleurs exposés a l'amiante, et d'isoler des épreuves simples offrant Uns 'bonne corrélation avec celle-ci.
Ainsi, un certain dente d'erreur dans le calcul de l'exposition ne devrait pas nous affecter de faoon importante.
Nous avons donc évalué l'exposition de chacun en faible, moyenne et qrande, la faible ayant la valeur 1 et la
qrande la valeur 3, et multiplié ce facteur par le nombre
d'années d'exposition.
Nous obtenons ainsi une distribution relativement symétrique et il n'apparait pas de groupe tranchant de facon
évidente sur la masse.
Enfin, l'examen des résultats témoiqne de l'atteinte
radioloqique de notre population; 30 sujets ont une imane 0/0,
c'est-a-dire essentiellement normale, alors que celle-ci est
franchement positive S l/l ou plus orande chez 39 autres.
13 sujets se retrouvent dans le proupe douteux O/l et pour
cette raison, ils seront éliminés de toutes comparaisons ultérieures.
Ici, nous avons évalué donc deux populations bien isolées quant aux critères radioloniques, une normale et l'autre
avec sinnes classiques d'asbestose.
666
Nous avons estimé qu'il serait important d'attirer
l'attention sur la différence qui existe quant au nombre de
sujets dans chacune des populations.
Il est a noter que la
population a radiographies pulmonaires positives représente
38 sujets, alors que celle avec radioqraphies pulmonaires
normales ne représente que 28 sujets.
Comme on a pu constater, la dyspnée demeure un sione
extrêmement suqqestif, et la majorité des sujets avec imaoes
pulmonaires normales ou pathologiques, se plaint d'un certein
denré de dyspnée.
Il n'en est pas de même cependant pour
l'hippocratisme diqital et les raies secs.
En effet, un seul
sujet a radiographie normale présentait de l'hippocratisme digital, alors que nous n'entendions des raies secs que chez 4
sujets avec une radiographie pulmonaire normale.
Cependant,
ces deux signes étaient beaucoup plus fréquents chez les sujets présentant une radiographie pulmonaire positive.
Les sujets a radioqraphies normales sont olus jeunes
de 6 ans, et cette différence est d'ailleurs sionificativa.
Par ailleurs, leur tabagisme est a toute fin pratigue
identique.
Tout au plus, vu la différence d'aoe, pourrions-
nous croire que la population a images normales eut un tabanisme un peu plus important.
En ce qui concerne la durée et l'intensité de l'exposition de nos deux populations.
Nous avons trouvé une différence
significative entre nos deux oroupes.
Cependant, alors gu'll
est probable que la différence d'âge par elle seule peut l'expliquer, pour ce qui a trait aux années d'exposition, il semble bien que, vu l'écart entre les deux moyennes (60 contre 4 3 ) ,
l'intensité d'exposition soit plus importante chez les sujets
radioloniquement anormaux.
667
Les résultats de l'exploration fonctionnelle montrent que
bien qu'il n'existe pas de différence sionificative entre les
nroupes pour la capacité vitale et le volume résiduel, il est
intéressant de noter une tendance a de plus petits volumes
chez les sujets avec asbestose reconnue. En fait, 13 sujets
avec des imanes radioloqiques d'asbestose ont une capacité
vitale inférieure a 80$ de la valeur prédite, alors que nous
n'en retrouvons que 5 dans l'autre oroupe.
Une étude de la' diffusion au repos aussi bien qu'a
l'effort d'un exercice de 40U, a été éoalement effectuée.
Comme nous l'avons dit précédemmment, un syndrome obstructif
tout autant qu'une atteinte interstitielle se manifeste par
une réduction de ce facteur: aussi, nous nous attendrons a
trouver un plus fort pourcantane d'anomalies dans ces épreuves sans pouvoir toutefois isoler l'agent causal. De fait,
%
i
en ce qui a trait a la diffusion au repos, environ 40% des
sujets dans chaque oroupe présentent des valeurs Inférieures
a 80$ de la valeur prédite.
Certains sujets offrant des suspicions de pathologie
coronarienne, seule une partie de la population a pu bénéficié
des épreuves a l'effort. Les résultats ne s'avèrent pas tres
satisfaisants en ce qui a trait a la detection d'un individu,
cependant la population a radiographies pulmonaires anormales
montra en moyenne des valeurs plus basses.
Compte tenu du tabagisme moyen avoué, une incidence de
2St des sujets présentant un VEPIS/CV inférieur a 70% est tres
certainement sionificatlve, nema en acceptant une erreur de
ÎOCK dans l'estimé da la dose, cette incidence est nettement
plus importante que celle que l'on pourrait prédire pour une
population du même age et du même tabaaisme, mais non exposée
668
a l'amiante.
Malheureusement, notre type d'étude ne nous
permet pas de nréciser davantane un phénomène d'addition
ou de synernisme.
Notons enfin qu'il n'y avait pas de dif-
férence entre nos deux populations.
Toute infiltration interstitielle entraînant une aunmentation de la riniditô parenchymateuse, on ne doit pas
s'étonner que 75% de la populatipn avec imaaes radioloqiques
présente un recul élastique parenchymateux supérieur a 1201?,
de la valeur prédite a capacité pulmonaire totale.
De même, ne doit-on pas s'étonner de ce qu'il v ait
une différence sionificative entre les deux croupes de sujets.
Cependant, une pression élastique maximale moyenne de
123% ppur les sujets a radionraphies pulmonaires normales
est beaucoup plus sionificative.
Déjà en 1971, Dodoin et
collaborateurs avaient noté une telle tendance a l'élévation
de la pression élastique maximale dans leur étude.
14 des
28 sujets présentant une radionraphie pulmonaire normale,
offrent aussi des valeurs individuelles supérieures a 120%,
certains allant Jusqu'à 2003. .
L'abscence d'adénopathie hilaire ou d'autres sinnes de
sarcoidose, de même que la faible incidence de fibrose interstitielle diffuse idiopathique dans notre milieu, nous laissent
en droit de suspecter fortement la présence d'une asbestose a
son début chez ces sujets.
Enfin une hyper-riqidité parenchymateuse, témoionant
tres certainement d'une asbestose e un stade précoce, peut
être mise en évidence avant l'apparition da siqne radinloqique.
En effet, lorsque nous évaluons la pression élastique maximale
en fonction de notre index d'exppsition, nous obtenons une corrélation sionificative. La même corrélation se retrouve Bntre
669
la compliance statique, et notre index d'exposition, et ceci
avait d'ailleurs deja été noté par Jodoin et collaborateurs,
employant un index d'exposition beaucoup plus fiable.
Cependant, si l'étude des propriétés élastiques parenchymatöses neut devenir une étude quasi routiniere dans
un centre spécialisé, il serait irréaliste de croire pouvoir
appliouer ceci a des études de dépistape en masse.
*
Parmi les paramètres conventionnels, d'exécution simple, nous avons évalué ceux qui seuls ou en association pouvaient offrir a la fois une corrélation significative avec
la pression élastique maximale, tout en conservant un degré
de spécificité satisfaisant.
D'autre part dans un syndrome obstructif pur, nous
pouvons prédire une chute du l/EPIS associée a une augmentation
du volume résiduel liée au trapping gazeux. Ainai, le rapport
de ces deux paramètres, avec le volume résiduel exprimé en
pourcentage de la valeur prédite sera diminué. Compte tenu de
l'aoe moyen de notre population, la rapport VEMS/CV prédit est
d'environ 70$ chez une population normale de non-fumeurs. Pour
le volume résiduel, comme il est exprimé en pourcentage de la
valeur prédite, il serait de 100$ ou 1 dans une population normale,
Ainsi, la valeur moyenne prédite pour ce rapport serait.
de 70$; toute valeur inférieure a ce niveau signera donc soit
une chute du rapport UEfIS/CU ou encore une augmentation du volume résiduel, ou encore l'association de ces deux signes,
c'est-a-dire un syndrome obstructif typique.
670
a l'amiante.
Malheureusement, notre tvpe d'étude ne nous
permet pas de préciser dauantane un phénomène d'addition
ou de synernisme.
Notons enfin qu'il n'y avait pas de dif-
férence entre nos deux populations.
Toute infiltration interstitielle entraînant une aunmentation de la riniditô parenchymateuse, on ne doit pas
s'étonner que 75% de la population avec imaaes radioloqiques
présente un recul élastique parenchymateux supérieur a 120%
de la valeur prédite a capacité pulmonaire totale.
De même, ne doit-on pas s'étonner de ce qu'il v ait
une différence sionificative entre les deux oroupes de sujets.
Cependant, une pression élastique maximale moyenne de
123% pour le9 sujets a radiooraphies pulmonaires normales
est beaucoup Dlus sionificative.
Oé.ja en 1971, Jodoin et
collaborateurs avaient noté une telle tendance a l'élévation
de la Dression élastique maximale dans leur étude.
14 de3
28 sujets présentant une radionraphie pulmonaire normale,
offrent aussi des valeurs individuelles supérieures a 120%,
certains allant jusqu'à 200%.
L'abscence d'adénopathie hilaire ou d'autres sinnes de
sarcoidose, de même que la faible incidence de fibrose interstitielle diffuse idiopathique dans notre milieu, nous laissent
en droit de suspecter fortement la présence d'une asbestose a
son début chez ces sujets.
Enfin une hyper-riqiditô parenchymateuse, tômoionant
tres certainement d'une asbestose a un stade précoce, peut
être mise en évidence avant l'apparition de siqne radinloqique.
En effet, lorsque nous évaluons la pression élastique maximale
en fonction de notre index d'exposition, nous obtenons une corrélation sionificative. La même corrélation se retrouve entre
669
la compliance statique, et notre index d'exposition, et ceci
avait d'ailleurs dsja été nota par Oodoin et collaborateurs,
employant un index d'exposition beaucoup plus fiable.
Cependant, si l'étude des propriétés élastiques parenchymateuses peut devenir une étude quasi routiniere dans
un centre spécialisé, il serait irréaliste de croire pouvoir
appliquer ceci a des études de dépistaqe en masse.
Parmi les paramètres conventionnels, d'exécution simple, nous avons évalué ceux qui seuls ou en association pouvaient offrir a la fola (JOB corrélation significative avec
la pression élastique maximale, tout an conservant un degré
de spécificité satisfaisant.
D'autre part dans un syndrome obstructif pur, nous
pouvons prédire une chute du VERS associée a une augmentation
du volume résiduel liée au trapping gazeux.
Ainsi, 1 B rapport
de ces deux paramètres, avec le volume résiduel exprimé en
pourcentage de la valeur prédite sera diminué. Compte tenu de
l'aoe moyen de notre population, le rapport VEPIS/CV prédit est
d'environ 70$ chez une population normale de non-fumeura. Pour
le volume résiduel, comme il est exprimé en pourcentage de la
valeur prédite, il serait de 100% ou 1 dans une population normale.
Ainsi, la valeur moyenne prédite pour ce rBPPort serait.
de 705?; toute valeur inférieure a ce niveau signera donc soit
une chute du rapport V£flS/CV ou encore une augmentation du volume résiduel, ou encore l'association de ces deux signes,
c'est-a-dire un syndrome ob9tructif typique.
670
Fnfi.n, comme la presninn f*lnstinut; maximalR 15t aus'îi
nxorim^r. en nourcentane rie la valeur nrflrtjf-.R, la linne dn normal i té sarà aussi de IPO1"'.
Toute valeur inférieure a lnn^ siqne done une norte
rie recul élastique, celle supérieure a lPPr'. sinne une aunmentation de la rinldité du parenchyme.
Par ailleurs, dans l'éventualité d'une atteinte interstitielle, le contraire peut se présenter: les débits cxniratoires tendent a être supernormaux, et le volume résiduel demeure inchangé ou chute lénerement. Le rapport débits expiratoires/volume résiduel sera donc supérieur a 0,70 et la pression élastique maximale doit auomenter, et ainsi se situer a
la droite de la aone de normalité.
En Baissant ainsi, nous pouvons donc définir 4 catégories di répartition possible d'une population. La premiere
caténorie, ou le recul élastique est diminué et ou le rapport
débits expirés/volume résiduel est bas, est la définition même du syndrome obstructif pur. Le deorê d'emphysème sera fonction de la chute de la pression élastique maximale.
La deuxième catégorie représente exactement l'opposé;
forte pression de recul élastique et rapport débits expirés/volume résiduel augmenté: c'est la définition d'un état d'hyperrinidité parenchymateuse et c'est la zone ou une amiantose pure
devrait être trouvée. Enfin il demeure deux cadrans: La troisième représente une caténorie intermédiaire ou le syndrome
obstructif contre-balancerait l'effet recul élastique auomenté,
et résulterait en un rapport débits/volume résiduel diminué
malgré une pression de recul élastique augmentée. Un trop nrand
671
nombre de sujets existant dans cette catégorie diminuerait
la specificità du rapport comme moyen de dépistage.
La dernière catégorie est une impossibilité physiolooique: on ne peut avoir des débits supernormaux avec une perte du recul élastique parenchymateux.
Nous avons examiné individuellement les sujets avec
radioqraphies pulmonaires normales. (Rapport l/EPIS/Ct/ volume
résiduel en pourcentage de la valeur prédite, pression élastique maximale en pourcentage de la valeur prédite). Les catégories décrites 'sonf représentées, on a ainsi constaté que,
de tous les sujets présentant un rapport débits/volume résiduel inférieur a 60%, un seul a une pression de recul élastique augmentée. Ainsi, nous pouvons dire et affirmer de
fapon quasi certaine que ceux-ci sont des obstructifs purs.
Par ailleurs, pour les sujets présentant une pression
élastique maximale supérieure a 120% de la valeur prédite, 9
sur 14 présentaient un rapport définitivement supérieur a T0%,
les 4 autres se situant entre 60 et 70%.
Ainsi, si nous gardons la limite a 0,70 comme limite
patholooique, 9 sujets pourraient par un test simple être détectés précocement.
Par ailleurs, tous les sujets moins 1, ayant un rapport inférieur a 0,60 présentaient une pression élastique
maximale normale ou franchement abaissée, signant un syndrome
obstructif franc sans évidence d'altération interstitielle.
Reste la région intermédiaire, 8 des 9 sujets se situaient entre 60 et 70%, et de ceux-ci 5 présentaient une
pression élastique maximale franchement auamentôe.
672
Cnmntr! tenu de lRur tahanisme, eh den rinnníes récentes He Fletcher et collaborateurs et Raten et collaborateurs,
qui ont 3ionalé_u/n taux de diminution annuelle du rapport
VFCIS/CU deux fois plus oranri chez les fumeurs nue chez les
nnn-fumeurs, (6Dml oar an Dlutot nue 30ml) il est probable
que le tabaqisma devrait être pria en considération dans l'établissement de cette limite et ainsi, tnut travailleur rie
l'amiante avec tabaqisma supérieur a 20 oanuets/année, avant
uno valeur entre 60 et 70, riBvrait être consideró comme tres
susoect de présenter une hyper-rinidité parenchymateuse.
En conclusion, nous avons démontfe que dans une population de travailleurs de l'amiante, l'association
fréquente
d'un sydrome obstructif lié au tabaoisme rend tres difficile
vnir impossible le dépistaqe précoce d'individus avec hyperriqidité parenchymateuse en utilisant le3 critères fonctionnels usuels.
Chez ceux avec radioqraphies pulmonaires normales,
l'étude directe des propriétés élastiques parenchymateuses
a révélé que 50$ de la Dolulation présentait une hyperrioiditô.
L'association de deux tests simples, le rapport VEPIS/CV
et le volume résiduel, nou9 a Dermis d'obtenir une tres bonne
corrélation avec le deqré d'élasticité, et de déceler précocement 9 des 14 sujets avec hyper-rigidité définitive. La zone
intermédiaire déterminée avec ce test est faible, ce qui est
du probablement a un choix trop ripide de la limite inférieure.
675
R
X Pulm
(+)
Observé
CU
UR
VENS/CV
Deo R
Normal
2.08
1.42
8B<
3,.52
1,.95
9.82
14..7
15.16
22
22,.01
\
E
(A-a)0,_iR
N
29
67*
R X Pulm
Observa
(+)
Normal
CV
3.69
3.27
VR
3.42
2.1
VEMS/CV
62'S
Deo— R
9.94
E
14.66
(fl-a) 0 2 — R
27
N
E
24
675
12.0
R X Pultn (N)
™
»R
VEHS/CU
Observa
Normal
. 3.64
4,.05
1.83
2..01
80%
Dco_R.
E
(A-a)02-R
E:
13.3
16.,5
23
19. 1
7
13
676
1
IO
in
O
111
n= 28
RADIOGRAPHIE PIJLMONAIRE NORMALE
1
o
IO
ro
O
to
X
E
(M
-i
Q.
O
CM
. m
. o
-
i
O
O
CM
O
O
o
CD
UJ
z 8 1s l-sí •
z>
o-J 3 Eps
>
677
i \ .
O
^*"*-0 •
o
io
s.
co
co
ce
3.-=*-
S
aiiapud un3TVA\n 3 Q % | N 3
"SBälVNOIMIhd saiflfTTOA !
678
o
co
£2
CD
ce
allanad
LDäfS unaiVÁ VI i a % N3
3UIVNÜWTñdSÍMVT0A
SIUÏN
679
to
>.
co
co
o.
Œ
UJ
CD
CE
aiiaaud »naivA v i 30 % N3
sauíVÑüwnnd sai/vmoA "
680
X
E
o
-I
û-
UJ
S
lili
>
3S0.
P
5 o
¿ o^
"II?
o.
681
e
OD
—
01
f\>
-t»
Ol
m
H
o
O
z
m
Oí
o
e
m
P
3J 3)
x x
Z +
3
II
ro oí
œ oo
682
Rx + : 59-7
Rx N : 53-3
AGE
IO
I
8
6
i
4
2
O
4
40
I
5
45
t = 3-98
•
6
50
7
55
;UJETS
8
60
•
9
10
65
70
AGE -ANNEES
TABAGISME
^
I2h
Rx + : 25
Rx N : 28
t = 0-88
I
10
8
6
4
2
0
I
I
I
10
I
2
20
f£
3
30
!
4
40
5
50
683
M
6
60
70
PAQUETS-ANNEE
ANNEES
I6r
D'EXPOSITION
14-
1
12 -
Rx + : 31
Rx N •- 27
t = 2-22
108 6-
"S5Î
4 2-
_££
0 I
13
2
17
3
22
iï
4
26
SUJETS
INDEX
i u
• I
É
5
31
6
35
7
40
9
10
ANNEES
8
45
D'EXPOSITION
Ü Rx + : 60
Rx N : 43
IO
t = 4-65
8
6
4
2
O
I
13
I
2
26
1
i
3
39
4
52
6
78
5
65
68"
I
7
9!
¿J
8
104
_!_
9
IC
117 INDE)
DIFFUSION REPOS
lOh
Rx + : 85
Rx N : 9 I
Li
8
6
t= 1 0 6
1
4
2
1
54
•
2
69
ii ì
1
3
84
4
99
5
114
•
6
129
JO.
7
144
8
9
159
174
% VALEUR PREDITE
SUJETS
Rx + : 96 t = 2-5
Rx N : 112
DIFFUSION EXERCICE
«Or
8
eh
•I
I
69
2
79
M
3
89.
•• j i
•
4
99
5
6
109
685
7
119
129
8
9
10
139
149
159
% VALEUR PREDITE
Rx + : 75 t = 1-25
Rx N : 72
VEMS/CV
IO 8
s
i
6
4 -
1
2
O
I
44
2
49
M3
54
4
59
I
5
64
I
6
69
I
^
^
1
7
74
i
ss
«
8
79
9
84
P
^
10
89
SUJETS
Pel
max
Rx + : 163 t= 3 34
Rx N : 123
lOr
8
lí-s?
6
1
4
2
«
1
84
1
Ï i
È
i
2
3
4
5
109
134
159
184
i
6
209
686
1
7
234
8
9
10
259
284
309
% VALEUR PREDITE
O
(0
evi
O
CM
o
CM
CM
X
ço JJ
<
o
>
oc
o
° i5
X
O
«a-
co
z
co
CL
o
><
oc
aiipajd
L_
O
(O
o
_E
jnajDA
o
o
O
o
co
oc
>
co
UJ
>
>
o
687
X
<
OC
o
<
z
o
><
oc
688
1.20
--
1.10
-Rinidité oarenchynateu
l.nn -VEWS/CV
.90
--
.80
--
Vol. Res.?
Préd.
.70
.60
--
,5n
--
.40
--
.30
--
.20
--
Intermédiaire
Obstruction
I
40
I I I 1
50
60
70
BO
190
100
Pel max
% valeur prédite
Syndroms Obstructif!
VCflS/CV
: 4r
UR<ÍP
: >f
Pel max
.'.Rapport V
^ Valeur prédite
Atteinte I n te r 3 tit i el le :
VENS/CV
"RAP
Pel max
: f
/.Rapport
: noul
^ V a l e u r prédite
689
Contaminación atmosférica v cambios
citologicos en los esputos.
K. Nobutomo
(Japón)
Se comparó el aumento de la celularidad en los esputos (con células epiteliales inflamatorias y bronquiales)
en dos grupos de 308 y 399 sujetos provenientes de poblaciones expuestas a niveles de contaminación atmosférica
corrientes en los pafses industrializados. Se examinaron
muestras únicas de esputos matutinos, y se evaluó la diferencia de aumento en la celularidad de los esputos entre
los dos grupos, clasificados por edad, sexo y consumo de
tabaco, aplicando el test sumario x de Mantel-Haenszel.
En el grupo expuesto a una mayor contaminación atmosférica
eran más numerosos los casos de aumento de los fagocitos
alveolares, neutrófilos y linfocitos, pero no de los eosinófilos ni de las células epiteliales bronquiales. También
se pidió a los sujetos estudiados que llenaran un cuestionario sobre los síntomas de la bronquitis crónica i el estudio mostró que la reacción inflamatoria precedía la aparición de los síntomas. Por consiguiente, los cambios citológicos en los esputos probablemente sean el indicador
más sensible de los efectos de la exposición a una atmósfera contaminada.
691
IDENTIFICATION OF ILLNESS FROM ALLERGENIC DUSTS
by
M. L. H. Flindt,
United Kingdom
I have found that it is common for users of material which
may give rise to allergenic dust to be, either unaware of the
health danger, or to be aware of the danger but to have taken
inadequate preventive precautions.
Consequently, the first
warning of a hazardous situation will come from identification
of illness, or subclinical effects, in those exposed to the material.
Unfortunately, it cannot be assumed that this identifi-
cation will be made, and, if it is made, it will not always be
made promptly, so I thought it would be helpful to discuss this
problem.
There are two main ways in which illness caused by allergenic dusts differs from those relating to the longer-established
pneumoconioses. The first relates to the dusts themselves and,
the second to the diagnostic criteria.
In respect of the dusts themselves, the difference is a
quantitative one relating to the amount of dust required to
cause illness. One has only to compare the suggested threshold
limit value for quartz, which in 1976 was set by the ACGIH at
3
0.1 mg/m , with that for an allergenic material, subtilisins,
the enzymes derived from Bacillus subtilis, for which the
suggested TLV was 0.00006 mg/m , more than a thousand times
less.
Theoretically, the ideal airborne level of a sensitising
693
dust Is nil, so even such a low TLV figure represents a compromise.
It can be difficult enough, when, say, handling silica flour,
to achieve the TLV levels for quartz, so it is clear that allergenic dusts present
tal control.
a major challenge in respect of environmen-
This underlines the importance of identification of
illness due to such dusts because, with threshold limit value
bordering on the limit of detectability, the occurrence of illness
may be a major factor in demonstrating a need for improved measures
of prevention, apart from its role in drawing attention to the
existence of a hazard ir. che first place.
There are two main categories of substance which, if inhaled,
may be capable of sensitising and causing allergic disease. They
are substances of large molecular weight, such as proteins and
certain polysaccharides, and a few substances of smaller molecular weight,
which are usually highly reactive chemically.
These simpler chemicals do not in themselves act as antigens.
They have to be combined with a larger molecule, such as a body
protein, to become a "complete antigen".
The substances them-
selves, the incomplete antigens, are known as haptens, but they
need to be handled
with the same care as other allergens. How-
ever, the fact that they are haptens is not entirely academic, as
their allergenicity may not be so easily anticipated or confirmed.
Another consideration is that many sensitising materials are also
primary irritants, capable of causing
can complicate diagnosis.
"direct" effects, and this
However, in general, it is likely that
69A
sensitlsatton effects from a given material will still occur
with airborne levels well below the lowest level at which primary irritant effects occur, and, thus, measures to prevent
sensitisation effects should also suffice to prevent direct
effects.
The other main difference between illness caused by allergenic dusts and
the older established pneumoconioses relates
to identification.
Most of the other pneumoconioses are iden-
tified and assessed by radiological changes, but, with the exception that I will describe later, a feature of the commoner
occupational illnesses due to allergenic dusts is that they may
cause severe functional disturbances, and even death, with no
radiological changes. Hence the whole emphasis of diagnosis
and assessment is different» and the role of radiology is secondary, perhaps mainly to exclude other conditions.
In respect of diagnosis, it is unlikely that a relationship
between the use of an allergenic material at work and allergic
illness in a patient will be considered if the doctor has
failed to realize that the presenting illness is indeed due to
allergy.
So the necessary factors are, first, that a diagnosis
of allergic illness is made and, secondly, that it is deduced
that the illness is, or could be, derived from a dust inhaled
at work.
Concerning both these factors, I think that the most important diagnostic component is the taking of an adequate history, and it will be necessary to take the history of the
695
presenting illness and the occupational history in some detail,
It may be even necessary to approach the employer for further
details, as not all workers are aware of the nature of the materials handled by them, or by adjacent workers. Also, as the history often includes episodes of illness that may have occurred
over quite a long period, the employer's records may be more
reliable than the patient's memory in respect of substances
handled on given dates.
In most cases where there is a type I reagin-mediated response the presenting symptoms are similar to those of hay fever
or pollen asthma i Typically, a person will give a history of
developing mild symptoms after he has started work on a Monday,
following a week-end away from work, and he may then develop
worse symptoms on the following day, perhaps persisting into the
night or awakening him at night, the symptoms recurring each day
with increased severity and duration until, often before the end
of the week, he may be unable to continue at work.
With each day
away from work symptoms are likely to improve steadily.
As an
adjunct to the history, it is always worth enquiring whether the
patient's fellow-employees have experienced similar illness.
•Naturally, a degree of acumen is required not to be misled by
the answer, because a pattern of respiratory illness might develop
in a given group of workers which was due to transmitted infection.
In respect of the history, both patient and doctor may be
misled for several reasons. The first is that the patient may
have been exposed to a large amount of the dust on earlier
occasions without developing symptoms and then, once sensitised,
696
develop marked symptoms following a much lesser exposure.
He
is thus inclined to exclude a possible association between the
material in question and his symptoms. This period of latency,
before allergic symptoms develop, is in contrast to direct
"irritant" effects which usually develop immediately after exposure, or when delayed, tend
to bear a direct relationship
to the amount of exposure. Additionally, direct effects tend
to be most marked on first exposure, and to be less marked on
subsequent exposures, with the development of tolerance or
"hardening".
Another cause for failure to identify the occupa-
tional allergic source is that quite often the respiratory
symptoms in a sensitised individual do not develop until several
hours after the exposure responsible for them.
A further source
of difficulty is that allergic chest disease may mimic infections
and other non-occupational conditions.
The following symptoms
and signs in various combinations may occur in patients' with
type III precipitin-mediated allergic chest diseasei malaise,
cough with or without sputum, tachycardia, fever, loss of weight,
physical signs on chest auscultation, radiographic opacities,
and leucocytosis. In consequence, a diagnosis of an infection,
such as bronchopneumonia, is an understandable error, and, even
in the case of more straightforward allergic asthmatic illness,
I have commonly seen patients who have first been treated with
antibiotics".
In cases of precipitin-mediated disease, crepitations may
be heard during an attack of acute alveolitis and its late
697
fibrostng stages, but these
manifestations are relatively un-
common.
However, the commoner manifestation of asthma may be confirmed
by auscultation during an attack, and in making a diagnosis of
.asthma it is
then important for the doctor to consider possible
extrinic causes, which will include occupational ones«
Even in
the case of atopic asthmatics of long standing he should always
bear in mind the possibility that a new extrinsic allergen has
started to cause trouble.
The first case of allergic asthma due to the detergent enzymes
that I was able to confirm by prick-tests was an atopic who regularly suffered from pollen asthma in the summer. The attacks
of asthma due to the detergent enzyme occurred in the winter, and
the link between his work and his asthma was not identified by
his doctor.
But, even if his doctor had asked him about his
occupation, he might have been misled, for the patient was an
office worker who had never handled enzymes. However, his office
was within a larger factory room and, a few metres away from his
office door, was the tipping-in point for high-potency enzyme
powder.
This serves to underline the importance of probing deep-
ly into the occupational history and, if necessary, visiting the
workplace.
As regards further investigations, if a doctor can make a
diagnosis of, say, asthma and rhinitis, and the patient has been
working with a recognised allergen and has given a consistent
698
history concerning Incidence of symptoms In relation to his work,
there may be no useful purpose to be served by elaborate diagnostic
measures, because removal of the patient to an uncontaminated workplace will normally prevent further attacks of occupational illness.
As by far the commonest reaction to airborne industrial
allergens, other than skin ones, is rhinitis or an asthmatic
response, chest X-rays play a relatively small part in their identification.
An X-ray will exclude other chest abnormalities and
will serve as a base-line for future comparison, but, except
in the acute, or the late fibrosing, phases of a type III precipitin
mediated disease, such as farmer's lung, radiological abnormalities
are not likely to be found.
If the material is one for which a skin prick-testing
solution is suitable and available, confirmation of a state of
sensitisation may usually be obtained.
However, prick tests are
not always applicable and may be misleading.
A negative prick-
test does not conclusively exclude the suspect material as having
caused the symptoms, as it is possible to cause symptoms and
signs by bronchial challenge test in patients who have given
negative skin prick-tests. Some substances are not suitable for
prick-tests.
This can be because they are highly irritant, or
are such potent allergens that the normally negligible risk of
sensitising the patient by doing the tests is present. Alternatively, it may not be easy to get the material into solution,
or, in the case of haptens, the material will not elicit a
699
response unless coupled to the material which makes it a complete
antigen.
Care is needed over prick-tests.
It is important that the
solution is weak enough not to cause irritant or other reactions
in non-exposed control patients.
It is also essential to do a
control prick-test on the patient with the solvent alone, to exclude dermographism, or to reveal its extent if the dermographic
reaction is to serve as a control to be compared with reactions
to suspect materials.
The findings of sputum or blood cosinophilis is a pointer
in support
of allergy, but is not specific.
It may be of little
help in the case of an atopic patient who may also be sensitised
to non-occupational allergens". The same applies to non-specific
IgE.
Eosinophilia, and a raised serum IgE, would be of more signi-
ficance in a non-atopic worker, as I have found that both these
manifestations will cease after the patient has been removed from
exposure to the suspect allergen.
Neither eosinophilia, nor a raised level of non-specific IgE,
will contribute more in terms of practical management than an
appropriate history and skin prick-tests to the suspect material.
Indeed, a specific IgE test, as by RAST, will seldom provide any
moire helpful information than can be obtained by a skin pricktest i They both indicate a reagin-mediated reaction, involving
IgE.
Simple
spirometrie
lung
function
7oo
tests will confirm
obstructive changes during an acute attack of asthma, and
are
particularly useful in that they will also detect such changes
when they are insufficiently marked to be noticed by the patient.
Under ideal circumstances, a pre-exposure lung function test on the
same individual will provide a more precise interpretation of
changes than by comparing them with a table of "normal" values«
It is also helpful, when a obstructive pattern is observed or
expected , to test for reversibility - by use of a bronchodilator.
This will show the degree to which the patient's airways obstruction is derived from muscle constriction, and therefore potentially of asthmatic origin.
More sophisticated tests may be required
if alveolar or small airway changes are to be detected.
A further use of lung function tests is at the workplace
to compare pre- and
postworkshift values. The finding of signi-
ficant changes between these tests may obviate the need for formal
challenge tests.
A formal provocation challenge test under hospital conditions
is seldom necessary, as a good history and clearance of symptoms
after removal to another workplace usually fulfills the practical
needs of the situation, particularly when á known sensitiser is
involved.
Bronchial challenge tests should be reserved for cases
of genuine doubt, perhaps when the consequences of removal to
other work would be particularly disadvantageous to a patient.
From the clinical aspect, I have dealt mostly with the
diagnosis in individual cases, which is the way
first come to light.
these problems
In concluding, I should like to stress again
7o1
that an epidemiological approach can also be invaluable, either
in drawing attention to a problem or when following up a suspicion . One reason why the occurrence of occupational respiratory illness is not always apparent is that not all people who
leave their jobs
on account of chest symptoms notify their em-
ployers accordingly.
Indeed, the chest symptoms may be a second-
ary reason for leaving.
Sometimes, when I have been told by a
firm that they have not had any problems with a given powder,
I find that they have failed to take account of those who have
left the firm on their own accord, and those who have been transferred to other departments.
Consequently, although there are a
few firms who deliberately try to conceal their problems, in
most cases the ignorance is genuine. There is little doubt that
problems of this sort can readily be missed unless they are
specifically looked for.
7o2
Identificación de enfermedades producidas
por polvos alergenicos.
M. L. II. Flindt
(Reino Unido)
En dos circunstancias principales es menester identificar una enfermedad causada por polvo alergénico. En
primer lugar, cuando podrían producirse efectos patológicos de índole conocida a causa de un alérgeno profesional
conocidoi en segundo lugar, cuando el estado patológico
se ha presentado ya y es causado por un alérgeno hasta
ahora desconocido, o un alérgeno conocido que afecta a alguien de quien no se pensaba que podía ser afectado. Para
distinguir una enfermedad profesional de una no profesional, es de fundamental importancia conocer la historia médica y profesional del paciente, así como para distinguir
una enfermedad debida a efectos directos de la substancia
sospechosa. La investigación no específica incluye el examen físico, los tests de función pulmonar, la radiografía
torácica, la numeración sanguínea, la serologia y los tests
de esputos. Cuando se conoce el alérgeno potencial, pueden
completarse las mencionadas pruebas con pruebas específicas
como la puntura cutánea, los tests serológicos de la precipltina y de la inmunoglobulina específica. En algunos de
los exámenes mencionados es más útil conocer los valores
individuales previos a la exposición que la gama de valores
"normales".
7o3
CORRELATION BETWEEN RADIOGRAPHIC AND PHYSIOLOGICAL
FINDINGS IN ASBESTOSIS
Tor Mattsson, Matti S. Huuskonen, and
Anders Zlttlng
Department of Occupational
Medicine,
Institute of Occupational Health,
Helsinki, Finland
The correlations between radiographic findings and tests
of the lung function of asbestos workers have varied (2,11,13).
According to Bader et al. (1) the most sensitive Index of the
progression of the disease Is the change In vital capacity,
which correlates well with the radiographic changes.
Different
opinions have been presented concerning the value of the transfer factor In the diagnosis of asbestosls (11, 13).
Asbestosls Is regarded as a disease difficult to diagnose.
The problem Is to Identify early changes, which are barely outside the normal limits, and to distinguish cases, even when
ad-
vanced, from the many other conditions that can cause similar
radiographic changes (5, 8, 12).
The aim of the present study was to analyse the radiographic
and physiological findings of 133 subject with asbestosls, to compare the results i and to determine the radiographic
progression
of asbestosls.
SUBJECTS AND METHODS
In 1976 the 140 living asbestosls patients of the 202 diagnosed at the Institute of Occupational Health In Helsinki between
1964 and 1976 were asked to attend a reexamination.
7o5
Of these,
133 (95%) participated.
In accordance with the usual practice in Finland, we used
the following diagnostic criteria for asbestosis«
(a) a confirmed history of occupational exposure to asbestos
dust, and
(b) a positive radiographic finding of lung fibrosis.
Additional supporting features includedi
dyspnea on physi-
cal effort, persistent basal crepitations, clubbing of fingers,
reduction in vital capacity, reduction in forced expiratory
volume in one second, and the single-breath carbon-monoxide
transfer factor.
These were not, however, used as essential
diagnostic criteria.
Detailed information concerning work conditions in regard
to asbestos exposure and other data were available (Table I ) .
The reexamination consisted of a radiographic examination,
physiological respiratory measurements and a clinical examination.
The radiographic examination included two full-size posteroanterior chest films and one lateral film.
One of the postero-
anterior films was taken with a kilovoltage of 125 and the other
with 70-80 kV.
125.
The kilovoltage used for the lateral film was
The mAs value was adjusted to obtain films of a suitable
shade.
All the chest films (i.e. those taken at the time of
diagnosis and those taken at the reexamination) were analysed
according to the ILO U/C International Classification of Radio-
7o6
graphs of Pneumoconioses 1971 (9). They were all examined by
the same three persons, two of them radiologists in the Section
of Radiology at the Institute of Occupational Health and the third
a specialist In occupational medicine.
Vital capacity (VC) and forced expiratory volume in one second (FEV. 0 ) were analysed from flow-volume curves registered
with a pneumotachograph.
FEV% was calculated as (FEV. Q/VC) X 100.
The single-breath carbon-monoxide transfer factor (TT
L
measured according to the usual procedure.
) was
co
Three subjects re-
fused to participate in lung function tests.
All the clinical examinations were performed by the same
physician (M.H.).
Each patient was placed In one of the follow-
ing three categories i (a) smokers, who habitually carried cigarettes or cigarette tobacco for their own use, (b) ex-smokers,
who had stopped smoking one year earlier or more, (c) nonsmokers, who did not and had never smoked cigarettes regularly
(Table II).
The statistical analyses were primarily made with the chisquare test, but in some comparisons of low frequencies Fisher's
exact probability test was used.
Students t-test was also used.
RESULTS
Radiographic findings
Radiographs taken at the time of diagnosis were available
for 116 of the Í33 asbestosis patients. Sixty-six of these
7o7
patients had been exposed to asbestos after the date of diagnosis.
Table III shows the profusion of small opacities In the
different occupational groups at the time of diagnosis and at the
reexamination.
The types of small opacities seen at the re-
examination were as follows i s 98 (74%), t 11 (8%), u 1 (1%),
p 11 (8%), q 3 (2%), r 1 (1%), and combined 8 (6%).
opacities were found.
No large
The opacities (small Irregular or small
rounded) were generally of the same type in both sets of radiographs.
In the radiographs taken at the reexamination, the small
opacities were more pròfuste than at the time of diagnosis. At
the time of diagnosis opacities were found in the lower zones
in all subjects, in the middle zones In 78%, and in the upper
zones in 16%. At the reexamination the respective figures were
100%, 94% and 34% for the lower, middle and upper zones.
The profusion of fibrosis and the length of exposure to asbestos varied greatly among the patients (Table IV).
There was no
significant difference in the type, profusion or extent of the
opacities between workers in different occupations. Poor delineation of the diaphragm and/or cardiac outline was as frequent at
the time of diagnosis as at the reexamination.
Pleural thickening was present in 66 of the 116 radiographs
available from the time of diagnosis (57%) and in 88 of the
133 taken at the reexamination (66%).
In regard to the site ,
width and extent of the pleural thickenings, no significant
differences were found between the two sets of radiographs or
between workers in different occupations.
7o8
Pleural calcifications were seen in 41% of the radiographs
taken at the time of diagnosis and in 59% of those taken at the reexamination.
Insulators had relatively fewer calcifications than
workers in other occupations ( X
=
7.43ip <0.01).
There was no significant difference in the occurrence of
other diseases (additional symbols of the ILO U/C classification)
at the time of diagnosis and at the reexamination nor between
the different occupations. Of the 133 patients who were reexamined, 19 (14%) showed radiographic signs of emphysema and
22 (17%) of honeycombing.
Pulmonary function
Among the 130 patients reexamined, VC was normal (= 80%) in
47 (36%) and decreased (<80%) in 83 (64%).
F E V 1 0 was normal
in 44 subjects (34%) and decreased (<80%) in 86 (66%).
T.
was
L
co
decreased (<80%) In 46 subject (35%).
The patients were grouped according to smoking habits, profusion of radiographic small opacities, VC, FEV.
Q
and FEV%.
In
addition to opacities the presence of pleural thickening was
evaluated, and the various groups were compared with respect
to pleural changes and respiratory function.
The more severe the fibrosis, the greater, as a rule, the
decrease in VC and FEV, Q. T L , on the contrary, was generally
co
impaired only in advanced cases (fibrosis 2/3 or more).
Obstruction was rarely observed among the patients (10%).
7o9
Smoking habits showed no correlation with VC, while FEV, Q
correlated with smoking habits among the patients with the mildest
lung fibrosis (less than 1/2)i ex-smokers had somewhat higher values
than smokers (t= 1.86, p<0.07).
The transfer factor, as the other lung function tests, did
not differ significantly according to the smoking habits of the
patients with severe fibrosis.
In the groups with moderate and
mild fibrosis, there was a correlation between T.
habits.
and smoking
co
In the group with moderate fibrosis, smokers showed
signs of impaired diffusion when compared with ex-smokers
(t= 2.42, pi.0.05) and non-smokers (t= 1.91, p<.0.07).
In the
group with mild fibrosis the Tt
values were lower for smokers
co
than for non-smokers (t= 2.26, p<.0.05)f and lower for ex-smokers
L
than for non-smokers (t= 2.11, p<0.05).
In the group with mild fibrosis, VC and FEV.
n
were signifi-
cantly lower in the patients with pleural thickening than in those
without (p<0.01i t for VC = 3.02, for FEV,
Q
= 2.72).
No association could be shown between pleural calcifications
and functional impairment.
DISCUSSION
The diagnostic criteria for asbestosis have been much debated
(11).
Some authors (7) have advocated more rigorous criteria.
In the present study widely accepted diagnostic criteria were
71 o
used (4).
However, a person with an occupational history of ex-
posure to asbestos dust and interstitial lung fibrosis does not
necessarily have asbestosis.
Doubt can particularly be cast
on cases with a relatively slight exposure and fibrosis classified as 0/1.
Furthermore, additional diagnostic criteria do not
afford an absolutely certain diagnosis but
only
increase its
probability.
Of the 54 patients in whom lung fibrosis was classed as
grade 0/1 at the time of diagnosis. 37 had moved to a higher
grade in the follow-up.
The clear progression of the condition
supports the diagnosis.
For the remaining 17 patients, the appa-
rent quiescence of fibrosis could in many cases have been due to
the short interval between the time of diagnosis and the followup.
If a person has been exposed to asbestos dust and has interstitial lung fibrosis (and other signs of disease), there is
no test that will rule out asbestosis, even if there is evidence
for some other disease that produces similar signs.
Fibrosing
alveolitis, although a rare condition, should be borne in mind,
since it produces similar picture (12).
In the radiographic analyses the sole criterion for such
qualities as "irregular" or "rounded", as well as for profusion,
was the similarity to the reference films of the ILO U/C classification (9,10).
Vital capacity has generally been considered to be a good
711
measure of asbestosis.
Evidence has been published suggesting
that it may even be affected before the disease appears radiographically. (3)t
Different opinions have been presented concerning the value
of the gas transfer factor in the diagnosis of asbestosis (6,13).
In the present study it was generally impaired only in advanced
cases.
Pulmonary fibrosis is thought to be accompanied by a greater
degree of functional abnormality than any of the pleural changes.
The hypothesis was supported by the present study.
712
niJKKNKNCES
Bader,M.E., Bader,R.A. and Sclikoff,I. (3.961) : Pulmonary function
in nube?, tos i s of tho lung, an alveolar capillary block syndrome.
Am.J.Med. 3J), 235-242.
Badcr,M.E., Bader,R.A., Tierstc.in,A.S., Miller,A. and Selikof f,I..
(1970): Pulmonary function and radiographic changes in 598 worker;
with varying duration of exposure to asbestos.
Mt Sinai J.Med. N.Y. 3_7, 492-500.
Becklakc,M. (1973): Lung function. Biological effects of asbestos
IARC, Lyon. pp.31-39.
Becklake,M. (1976): Asbestos-related diseases of the lung and oth>
organs: Their epidemiology and implications for clinical practice
Am.Rev.Resp.Dis. 114, 187-227.
Bohlig,H. and Gilson.J.C. (1973): Radiology. Biological effects o.
asbestos. IARC, Lyon, pp. 25-30.
Britton, M.G., Hughes,D.T.D. and Weaver,A.M.J. (1977): Serial pulmonary function tests in patients with asbestosis. Thorax 32:1,
45-52.
Evans,C.C., Lewinsohn,H.C. and Evans,June M. (1977): Frequency of
HLA antigens in asbestos workers with and without pulmonary
fibrosis. Br.Med.J. 1, 603-605.
Fletcher,D.E. and Edge,J.R. (1970): The early radiological change
in pulmonary and pleural asbestosis. Clin.Radiol. 2_1, 355-365.
International Labour Office (1972): ILO U/C international classification of pneumoconioses. Occupational Safety and Health series ¿2 (rev.), Geneva, pp. 1-32.
Liddel,F.D.K. (1977): Radiological assessment of small pneumoconiotic opacities. Br .J. Ind.Med. 3_4:2, 85-94.
Parkes,W.R. (1973): Asbestos-related disorders. Br.J.Dis.Chest,
67, 261-300.
Turner-Warwick,M. (1974): A perspective view on v/idespread pulmón
fibrosis. Br.Med.J. 2, 371-376.
Woitowitz,H.-J. (1976): Pulmonary function in workers exposed to
asbestos. Results of epidemiological studies in Federal Republic
Germany. Hefte zur Unfallheilkunde, Heft _12j6, 598-603.
713
Table I
Occupation
and number
Insulators
Occupation, number, age and length of exposure
at the time of reexamination
Age at the reexamination,yrs.
Exposure, years
< 40
40-49 50-59
^60
¿10
10-19 20-29
1
N= 55
15
19
20
3
mean 55.6
Asbestos
sprayers
N= 8
5
Asbestos
cement factory workers
N= 32
0
Asbestos
quarry
workers
N= 29
1
Others
N= 9
0
Total
N= 133
7
1
2
7
0
1
13
23
6
29
43
6
1
0
4
15
7
mean 22.3
6
3
8
12
6
mean 21.8
mean 52.9
2
2
mean 57.3
16
mean 12.8
mean 64.0
9
22
mean 24.6
mean 41.0
2
14
^30
5
4
54
17
714
3
1
mean 14.8
35
51
1
30
Table II
Smoking habits
Occupation
and number
Smoking habits
Nonemokcrs
N
Exsmokors
N
Smokers
N
Insulators
N= 55
8 (15%)
26 (47%)
21 (38%)
Asbestos
sprayers
N= 8
2 (25%)
3 (38%)
3 (38%)
Asbestos
cement
factory
workers
N= 32
15 (47%)
10 (31%)
7 (22%)
Asbestos
quarry
workers
N= 29
8
Others
N=-- 9
1 (11%)
6 (67%)
34 (25%)
53 (40%)
Total
(28%)
N- 133
715
8
(28%)
13 (45%)
2
(22%)
46 (35%)
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717
LUNG CONTAMINATION AMONG WORKERS EXPOSED TO DUST WITH AN IRON
COMPONENT
Magnetic measurements and radiographic findings
T. Mattsson, P. L. Kalllomäkl, O. Korhonen, and V. Vaaranen
Department of Occupational Medicine,
Institute of Occupational Health, Helsinki, Finland
The diagnosis of slderosls has so far been based on radiographic findings and a careful penetration of the history of exposure.
Iron Is an Inert dust which does not Induce flbrotlc
changes In the lungs«
benign pneumoconioses«
Slderosls Is thus Included among the
However, other more active dusts and
gaseous pollutants are often Inhaled simultaneously and may
give rise to flbrotlc lung lesions«
Since the classical report
by Dolg and McLaughlin In 1936 (5) several extensive reports have
dealt with probiens related to Inhaled dusts with an Iron component (1,2.6,7,9,16,18,19,20).
The radiographic changes that occur In slderosls have been
described In different ways (8,13,15).
The fact that siderotic
changes have generally not been considered to cause disability
accounts, at least In part, for the fact that less attention
has
been paid to slderosls than to, for Instance, asbestosls and
silicosis.
With a recently developed method, It Is possible to determine
several lung contaminants quantitatively In vivo In persons exposed to dust with a magnetic component (3,4,11,12,17).
719
The aim
of this study was (a) to evaluate the clinical
suitability of applying the magnetic measuring method to mildsteel and stainless-steel welders and foundry workers» (b) to
determine the amount of dust retained in the lungs of these
workers, and (c) to evaluate the radiographic findings of the
different groups.
SUBJECTS
A.
Mild-steel welders
Fifty-one mild-steel arc welders from two shipyards and
10 referents were examined.
They had homogeneous exposure but
different lengths of exposure time.
Details of the exposure
are presented in Table I.
B.
Stainless-steel welders
Stainless-steel welders from eight workplaces were studied.
They had used both manual metal-arc (MMA) and tungsten inert
gas (TIG) welding techniques.
C.
Foundry workers
Ten workers from an iron foundry were examined.
Their
occupations represented typical foundry jobs, e.g. molding,
coremaking, fettling, melting and casting.
Most of the workers
had had a mixed exposure to sand dust and metal fumes, which,
for three, included metal dust from grinding operations.
The age and exposure time of the subjects in the different
groups are presented in Table II. About 45% of the subjects
In each group were smokers.
72o
METHODS
A clinical examination, including a detailed occupational
history, was performed by the same physician in all cases-
Res-
piratory symptoms were evaluated according to the MRC standardized questionnaire (14).
Lung function tests includedi spirometry, flow volume curves,
transfer factor (carbon-monoxide single-breath method), closing
volume (helium method), and the histamine provocation test (for
stainless-steel welders only).
The radiographic examinations Included two full-size posteroanterior chest films and one lateral film.
One of the postero-
anterior films was taken with a kilovoltage of 125 and the
with 70-80 kV.
The lateral film was taken with 125 kV.
value was adjusted to obtain films of a suitable shade.
other
The mAs
The
radiographs were all examined and graded by two radiologists as
follows i 0= normal, 1= small discrete opacities, 2= more distinct
opacities, 3= numerous opacities involving both the central and
lateral parts of both lungs.
The method used for measuring ferromagnetic pulmonary contamination has been described in detail by Kalliomakl (10). It
is based on the permanent field of magnetized particles.
First
the thoracic area of the subject is magnetized in a low external
magnetic field.
Thereafter the permanent field caused by conta-
minants is measured with a sensitive magnetometer on five transsectional planes of the thoracic region, both on the anterior and
posterior sides, because the spatial resolution of the magnetometer is only about 100 mm (Figure 1).
721
Thus the distribution of contaminants could be evaluated
from the measured permanent magnetic field (PMF) curves. As
a first approximation the half widths of the PMF curves, both
in the transverse and longitudinal directions, represent the
distribution.
The half width is the distance between the two
lateral points of the PMF curve where its height has reached
half of the maximum value.
The results have been expressed as
the average magnetic field (AMF), and converted to the estimated
amount of contaminants in the lungs.
RESULTS
A. Mild-steel welders
For studies investigating lung retention and clearance under
continuous exposure, the shipyard welders served as suitable
subjects because their exposure was homogeneous.
According
to these studies, retention and clearance seem to be balanced
after five years of continuous exposure.
The average of the measured magnetic fields (B), the geometric standard deviation (J ), and the approximate equivalent
o
amount of welding dust are shown in Table III.
Figure 2 shows the estimated amount of lung contaminants in
welders from the same shipyard.
A good correlation between the radiographic findings and
the magnetic measurements has been shown before (10).
B. Stainless-steel welders
The estimated amount of retained dust averaged about 20 mg
for TIG welders and 600 mg for MMA welders.
722
The radiographic changes were In all cases discrete, but it
was possible to grade them into the three categories. The interpretation of the radiographs was performed critically, and nonspecific changes such as old Inflammatory changes were taken Into
consideration.
Such changes were found In 377. of the subjects
when even slight abnormalities were noted.
Changes that could be attributed to Inhaled dust were encountered In 17 (25%) of the subject (grade 2-3 changes).
In
addition, 30 subjects (45%) showed very discrete changes (grade 1
changes).
These results are preliminary and further evaluations
will be made in connection with the planned follow-up studies.
C. foundry wo»*?"
The mean value of the measured average magnetic field was
0.8 nT (range 0.1 - 8 nT), and the typical amount of retained
contaminants was 200 mg (range 30 - 600 mg).
An attempt was made to differentiate the radiographic changes
caused by quartz and metal particles. The changes encountered
seemed to be primarily caused by metal dust.
Thus "siderotic" lesions were noted In all of the subjects»
whereas "silicotic" changes occurred In only half of the subjects.
The radiographic findings correlated with the measured
average magnetic field.
In this study there was no blurring of the heart outline, nor
any confluent opacities. The hilar shadows appeared prominent In
some cases, but the hilar nodes were not enlarged.
In these
series possible regression of the lesions has not yet been eva-
723
luated.
DISCUSSION
In this study, three groups were examined which represented
exposure to metal aerosols in different occupations.
Shipyard
welders were chosen because of their homogeneous exposure, which
aided the study of lung retention and clearance rates under continuous exposure.
Stainless-steel welders formed an heteroge-
neous exposure group In that welders use several welding techniques.
The last group,; thqt of foundry workers, was selected to
represent all typical occupations, because the properties of
foundry dust differ from one foundry occupation to another.
In addition to determining the average amount of retained
lung contaminants for each group, we gained a conception of lung
contaminant distribution.
The estimated amount of lung contami-
nants in the groups differed by more than one decade. The content
of lung dust was the highest In shipyard welders.
This variation
was due to the differences In exposure, and perhaps also to
different deposition and clearance rates.
Determining the cor-
relation between retained lung content and the concentration
of Inhaled pollutants will require systematic follow-up studies.
A correlation between the radiographic findings and the amount
of contaminants was found for the mild-steel arc welders and
foundry workers.
Conclusions regarding pathogenesis, the health
hazards caused by Inhaled aerosols In each group and the doseeffect relationship would require more extensive data than were
provided by this study, as well as follow-up studies.
12H
REFERENCES
Barhad,B., Teculescu,D. and Craciun,0.(1975): Respiratory
symptoms, chronic bronchitis and ventilatory function in shipys
welders. Int.Arch Occup.Environ.Hlth, 3j5, 137-150.
Charr,R. (1953): Respiratory disorders among welders.
J. Amer.Med.Ass. 152,1520-1522.
Cohen, D. (1973): Ferromagnetic contamination in the lungs and
other organs of the human body. Science 180,745-748.
Cohen, D. (1975) : Measurements of the magnetic fields produced
by the human heart, brain and lungs. IEEE Trans.Mag. 11,694-700
Doig, A.T. and McLaughlin, A.I.G. (1936) X-ray appearances of
the lungs of electric arc welders. Lancet 1, 771-775.
Einbrodt, H.J., Maass, W., Josten, H-G. and Stecher, W. (1971):
Untersuchungen Über die Lungenveränderungen bei Elektroschweiss
öffentliche Gesundheitswesen, 3_3, 286-299.
Enzer, N. and Sander, O.A. (1938): Chronic lung changes in
electric arc welders. J.Ind.Hygiene and Toxicology, 2Q_:S, 333-3
Haglind, 0. (1972): Occupational health in the shipbuilding
industry. Safety and health in shipbuilding and ship repairing
Occupational safety and health series 27. International Labour
Office, Geneva, pp. 5-12.
Harding, H.E., McLaughlin,A.I.G. and Doig, A.T. (1958):
Clinical, radiographic and pathological studies of the lungs
of electric-arc and oxyacetylene welders. Lancet, 2_, 394-398.
Kalliomäki, P-L. (1977): Measurement of Magnetic Lung Contaminain Vivo: Evaluation of the Method and its Application to Arc
Welders. Doctoral dissertation, Helsinki, 64 p.
Kalliomäki, P-L., Alanko,K., Korhonen, 0., Mattsson, T., Vaaranen, V. and Koponen, M. (1978): Amount and distribution of
welding fume lung contaminants among arc welders. Scand.J.Work
Environ.» Health, £, 122-130.
Kalliomäki, P-L., Korhonen, 0., Vaaranen, V., Kalliomäki, K. anc
Koponen, M. (1978): Lung retention and clearance among shipyard
arc welders. Int.Arch.Occup.Environ.Health, (in press).
Kleinfeld, M., Messite, J., Kooyman, 0. and Shapiro, J. (1969):
Welders' siderosis: A clinical, roentgenographic and physiologic
study. Arch. Environ.Health, 19., 70-73.
Medical Research Council's Committee on the Aetiology of Chronic
Bronchitis: Standardized Questionnaire on Respiratory Symptoms.
(1960). Brit.Med.J. 2_, 1665.
Parkes, W.R. (1974): Occupational lung disorders. Butterworth s.
Ltd. London.
725
2
16. Piscator, M. (1976): Health hazards from inhalation ®f metal fumes.
Environmental Research. Ll:2f 268-270.
17. Robinson, S.E., Freedman, A.P. and Johnston, R.F., (1977):
Non-invasive Magnetometric Determination of Lung Dust Loads in
Active and Retired Coal Workers. The Hahnemann Medical College
and Hospital Philadelphia, Pennsylvania 19102, 103 p.
18. Schüler, P., Maturana, V., Cruz, E., Guijon, C., Vasquez, A.,
Valenzuela, A. and Silva, R. (1962): Arc welders' pulmonary
siderosis. J.occup. Med. £, 353-358.
19. Slepicka, J., Kadlec, K., Tesar, Z., Skoda, V.. and Mirejovsk?, P.
(1970): Beitrag zur Problematik der Elektroschweisserpneumokoniose.
Int. Arch.Arbeitsmed. 2J, 257-280.
20. Spac'ilova, M. and Koval, Z. (1975): Pulmonary X-ray and functional
findings in electric-arc welders. Int. Arch.Arbeitsmed. 34:3,
231-236.
726
TABLE I
GROUP
MILD STEEL WELDERS
N EXPOSURE
. MEAN
TIME/Y. LENGTH OF RETIREMENT,Y.
MEAN
SD
SD
o
REFERENTS
10
0
SHIPYARD A
- GROUP 1
- GROUP 2
- GROUP 3
- RETIRED
9
8
17
7
1.8
10
18
26
6
7
SHIPYARD B
- GROUP 1
- RETIRED
5
5
18 •
H
30
3
0.1
t\
727
0
0
0
1.6
1.1
0
7
l\
TABLE II
OCCUPATIONAL GROUP
AGE AND EXPOSURE TIME
N
AGE
MEAN SD
EXPOSURE (YRS)
MEAN
SD
A. MILD STEEL
ARC WELDERS
51
39
10
14
7
B. STAINLESS STEEL
WELDERS
68
36
10
13
.8
C. FOUNDRY
WORKERS
10
58
6
33
7
728
TABLE III
RESULTS OF MAGNETIC MEASUREMENTS IN
MILD STEEL WELDERS
GROUP
B, NT
¿
G
REFERENTS
AMOUNT OF DUST, MG
MEAN
RANGE
<1
0.003
SHIPYARD A
- GROUP 3
0.2
1.1
1.5
•3.5
- RETIRED
0.83
1.7
27
190
200
110
1.9
1.5
3.0
2.3
700
200
- GROUP 1
- GROUP 2
2.0
3.6
13
25
30
10
- 53
- 1500
- 1500
- 250
SHIPYARD B
- GROUP 1
- RETIRED
729
150 - 2000
60 - 500
LU
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731
4J
ARC WELDERS' PNEUMOCONIOSIS!
STUDIES WITH ADVANCED TECHNIQUES OF
SCANNING ELECTRON MICROSCOPY
AND MICROPROBE ANALYSIS
Tee L. Guidottl
Dept. of Environmental Health Sciences,
The Johns Hopkins School of Hygiene and Public Health,
Baltimore, Maryland, U.S.A.
Jerrold L. Abraham
Dept. of Pathology,
University of California at San Diego School of Medicine,
La Jolla, California, U.S.A.
Phillips B. DeNee
Appalachian Center for Occupational Safety and Health, NIOSH,
Morgantown, West Virginia, U.S.A.
(Present address i Lovelace Foundation, Alburquerque, New Mexico
Josef R. Smith
Dept. of Pulmonary Medicine
Youngstown Hospital Association,
Youngstown, Ohio, U.S.A.
Arc welders' pneumoconiosis is compatible with a long and
vigorous life. Patients with the disease seldom come to necropsy
during their working years so that the pathologic findings of
the condition are not fully characterized.
A recent case pro-
vided the opportunity to study the condition using newly developed, sophisticated analytical techniques. A previous report summarized the case and salient features of histology and
elemental analysis.
This discussion will examine additional
instructive findings and will use the case to demonstrate and
to validate the recently developed techniques.
733
Case History
The patient was a 58 year old white male who had been a
welder for 39 years with no other occupation or knowidust
exposure.
He smoked two packs of cigarettes daily.
For 15
years before his death, he had a gradually increasing, bilateral
micronodular and interstitial pattern on serial chest films
(Figure 1).
rous, with
Despite this, he was in excellent health and vigono respiratory complaints or limits to exertion.
His hematocrit was 45% before his death.
For two weeks prior
to his death, he experienced a febrile, influenza-like illness
that ran a fulminant course progressing to pneumonia, respiratory failure, congestive heart failure, and finally cardiopulmonary arrest.
Sputum cultures, viral antibody titers, and cold
agglutinins all failed to implicate an organism.
He was treated
with oxygen, antibiotics, assisted ventilation, and diuretics.
At autopsy, the lungs were brick red and honeycombed with fibrosis.
There were extensive subpleural and deep plaques of
black pigment.
Methods
Lung tissue from the necropsy in Youngstown, Ohio, was
fixed in buffered 10% formalin solution and blocks were embedded
in paraffin.
Sections were stained with hematoxylin and eosin,
Van Gieson's stain for elastin, and Prussian blue stain for iron
and were examined by light microscopy.
734
The tissue was prepared for scanning electron microscopy
following standard methods used at the Appalachian Center for
i .i-
Occupational Safety and Health.
Two paraffin sections were
deparaffinized and critical point dried with liquid CC^.
An
evaporated carbon coating was applied to enhance electrical
(R)
conductivity.
The sections were then scanned with an Etec1--^
scanning electron microscope (SEM) using both secondary electron
(SE) and backscattered electron (BSE) imaging.
The principles
and differences in these techniques will be described below.
The SEM system was interfaced with an Ortec^
solid-state
detector with a Northen Scientific V* 880 multichannel analyzer.
The accelerating voltage was 20 keV and the specimen tilt angle
was 45°. The detector was a modified solid-state backscattered
2
electron detector available commercially.
The principle of microprobe analysis is the detection by
spectrophotometry of electromagnetic energy in the X-ray wavelength which is generated by bombardment of the target with
electrons.
When an atom in the target is excited by capture of
an electron it becomes energetically unstable and ejects an electron to return to a stable energy state.
The energies with
which these so-called "secondary electrons" are ejected reflect
the binding energies i photons of X-ray energy are also given
off and balance the energy equation.
These X-rays are of a
set of wavelengths characteristic of the atomic number of the
atoms in the target.
identified.
In this way, elemental composition can be
The secondary electrons ejected from the excited
atoms are the signal generating the secondary electron image.
735
Backscattered electrons are electrons which are reflected back
from the target when the target Is bombarded by the cathode ray
(electrons).
The technical details of these phenomeona have
been well summarized and the state of the art has progressed
further since this study was performed.
' '
Results
A typical high-power view is shown in Figure 3 with an
alveolar macrophage in the center field.
The BSE image in
Figure 4 clearly identifiés a large particle of approximately
14 yüm diameter within the cell. The particle is not visible
in the SE image in Figure 3 because it is obscured by the overlying plasma membrane and cytoplasm.
The BSE signal derives
from the reflection of electrons that have penetrated a fewyum
into the cell and are then reflected from the surface of the
particle.
Microprobe analysis yields the spectrum seen in
Figure 5.
The two spectral lines, termed K«. and Kg, are unique
to element 26 which is iron.
Thus the system is capable of
locating particles contained in the cells and of Identifying
their elemental composition.
A peribronchial alveolus is selected in Figure 6, arrow.
The cathode-ray (primary electron) beam is very narrow (0.1 yum
diameter), permitting exceedingly fine resolution of elemental
distribution.
Thus, iron was demonstrated in the macrophage
in the alveolus (Figure 7, labelled a), but was present only
in trace amounts in the lnterstitlum.
736
This fine resolution
maps the elemental distribution over the morphological Image
with great precision.
An unexpected finding was a flbrotlc plaque with the characteristic whorled morphology of silicosis (Figure 8).
Within
the Interstices of the loose fibrous stroma of the plaque are a
number of cells, Including the macrophage In the center of Figure
9.
This macrophage bore a large extrusion, seen In the fore-
ground of Figure 10.
Examination by three-dimensional SE Imaging
was performed by changing the specimen tilt angle slightly and
then viewing both
Images through a stereoscope.
appears to be in continuity with
certainly a pseudopod.
The extrusion
the cell body and Is almost
BSE Imaging demonstrated a particle In
the distal part of the pseudopod, which microprobe analysis revaled to contain Iron.
and within the
In other macrophages In this plaque,
fibrous stroma In lesser amounts, traces of
silicon were Identified.
Discussion
Scanning electron microscopy
In this case the diagnosis of arc welders' pneumoconiosis
had already been made.
The SEM studies were primarily intended
to demonstrate the utility of
pneumoconioses.
the techniques In studying the
It thus came as a surprise when evidence for
an unsuspected second process appeared.
The case shows how
versatile and precise these methods are when applied to heterogenous chemical
systems such as a pneumoconlotlc lung.
The various SEM methods used In this study are complementary!
737
(1) SE Imaging yields data on surface features and morphology.
The image is psychologically familiar and relatively easy to interpret.
It is easy to construct three-dimensional views.
(2) BSE imaging penetrates several hundred A below the surface and
identifies objects, such as intracellular particles, that cannot
be seen by SE imaging.
Thus BSE images are similar in some res-
pects to transmission electron microscopy because they both reveal
some degree of internal structure.
The BSE signal is strongest
with reflection from an object of high atomic number, so that some
information can be gained regarding chemical composition.
This is
particularly useful in the case of metal pneumoconioses because
the contrast is strong and makes location of the particles obvious.
(3) A BSE imaging technique that was not used in this study is
hlstochemical staining using metal ions.
It is possible to stain
tissue with metal stains such that surface features stand out in
BSE as clearly as in the SE image with appropriate hlstochemical
methods.
Localization techniques can show the distribution of
2 7
enzyme activities or a variety of chemical characteristics.
This feature is not very useful in metal pneumoconioses because
the elemental composition of the dust is obscured by the content
of the hlstochemical stain.
(4) Microbeam analysis is a convenient and non-destructive method
of elemental analysis, which allows the elemental distribution to
be mapped over the visual image.
With its narrow beam and high
resolution, this mapping can be quite precise down to the cellular
and sometimes even subcellular localization.
738
Microprobe analysis
can detect elements with atomic numbers from sodium (11) through
uranium (92).
Although it is not particularly sensitive for low
concentrations, requiring 0.1 to 1.0% content by weight before
an element is detectable, it is capable of detecting 10
g of
the heavier elements with sufficient concentration in the field
of the beam.
Unfortunately, it cannot be used to identify specifi
compounds, nor can it detect light elements such as oxygen or
hydrogen.
Other techniques, such as secondary ion mass spectro-
metry or Raman laser microprobe analysis, must be used for these
purposes. 4' 7
o
Since the earliest demonstrations,
techniques of scann-
ing electron microscopy have proven their utility In the study
1-3 6
of pneumoconioses.
'
They have an Important role In
o
basic studies of particle handling and distribution in the lung.
These methods may be useful diagnostlcally If the
cause of the
lung disease Is unknown, or If the exposure source is not obvious. '
In most cases, precise Identification of the metal
would not have Important Implications for therapy.
The role In
diagnosis Is further limited by the expense of the SEM equipment
and the need for highly trained technicians and pathologists.
In a national research center such as the Appalachian Center for
Occupational Safety and Health, cases can be studied on referral.
Finally, a major Intrinsic limitation of the
field of electron
microscopy In general applies to these techniques.
The amount
of tissue sampled is exceedingly small compared to the total mass
of the organ, and it Is seldom practical to correct the sampling
739
error merely by examining more sections at random.
One must there-
fore take great care in selecting representative tissue blocks
and must be cautious in extrapolating findings beyond the limits
of the data.
Arc welders' pneumoconiosis
Arc welders' pneumoconiosis has been recognized since 1936,
when it was first described by Doig and McLaughlin.
The pre-
valence of the X-ray findings of this condition varies with age
12
and duration of employment as an arc welder.
Pulmonary function
abnormalities appear to be associated with a history of chronic
bronchitis among welders
, and probably also with smoking history
The correlation between X-ray changes and pulmonary function abnormalities is much less clear.
In one extensive study on several worker groups In a Polish
shipyard, Dobrzynski, Kisielewicz, and Koclecka studied 50 arc
welders with a mean age of 38 years and an average duration of employment of 12.4 years. They found an overall prevalence of chest
film abnormalities of 92X in their unselected population.
Arc
welders who smoked (68%) had the same prevalence of X-ray abnormalities (67.ST. of all abnormalities, as reported in the paper) as
non-smokers, but gave a history of chronic bronchitis more often
(77.5% of total positive histories for chronic bronchitis), and
were more likely to show obstructive patterns on pulmonary function
testing (.807. of such abnormal tests).
Thus, holding the X-ray
categories constant, the prevalences of pulmonary symptoms and
74o
functional abnormalities appear to vary with smokingi there does
not seem to be much association between these findings and radiological abnormalities'. The lack of a sufficiently large subgroup of arc welders without X-ray changes makes this conclusion
tentative.
Further data on this high-risk population would be
welcome.
A similar group of Polish arc welders studied by Marek and
his colleagues demonstrated surprisingly low exercise capacity
and pulmonary function during exercise despite their relative
youth.
These were 30 young shipyard welders with micronodular
patterns on chest film whose physiological performance with
exercise compared unfavorably with 30 young coal miners matched
for age (35 to 45), duration of employment (about 10 years),
weight, height, and gradation of X-ray abnormality.
Such
comparisons between worker groups may prove very useful in assessing the differences in the pathophysiology of the pneumoconioses.
These two studies suggest that there is more than meets the
eye in reading
the chest film when it comes to arc welders'
pneumoconiosis. The simplistic concept of the condition as an
accumulation of ferric oxide (Fe^Oo) in the lung is inadequate
to explain the Striking differences In prevalence between populations and the lack of a close association between chest film
abnormalities and Impairment of pulmonary function.
'
The
simplest explanation for these observations is that other Inhaled
agents besides Fe 2 0 3 play a major role In modifying the response
to the Inhaled dust and contribute their own pathological
741
features.
Nitrogen dioxide is one such agent known to exist
as a hazard in welding and may serve as a model for study.
Silica is another and was an additional feature in the patient
we have described.
Arc welders' penumoconiosis is more complicated than we
thought it was.
742
References
1.
Guidottl TL, Abraham JL, DeNee PB, Smith JR. 1978. Arc welders' pneumoconiosis:
Application of advanced scanning electron microscopy. Arch Environ Health
33:117-124
2.
Abraham JL, DeNee PB. 1974. Biomedical applications of backscattered electron
imaging-One year's experience with SEM histochemistry. Scanning Electron
Microscopy 1974 (Proceedings of the 7th Annual Scanning Electron Microscope
Symposium). Chicago, ITT Research Institute, pp. 251-258
3.
DeNee PB, Abraham JL, Gelderman AH. 1973. Methods for a SEM study of coal
workers' pneumoconiosis. Scanning Electron Microscopy 1973 (Proceedings
of the 6th Annual Scanning Electron Microscope Symposium). Chicago, ITT
Research Institute, pp. 411-418
4.
Woldseth R. 1973.
Kevex Corp.
5.
Maugh TH II. 1977. Electron probe microanalysis: New uses in physiology.
Science 197:356-358
6.
Abraham JL. 1978. Diagnostic applications of microanalysis. Presentation to
the Annual NIH Instrumentation Symposium, Bethesda, Maryland, 7-9 August 1978.
7.
Abraham JL, DeNee PB. 1973. Scanning electron microscope histochemistry
using backscattered electrons and metal stains (letter). Lancet 1:1125
8.
HoIman B. 1969. Scanning electron microscopic observation of particles
deposited In the lung. 18:330-339
9.
Sorokln SP, Brain JD. 1975. Pathways of clearance in mouse lungs
exposed to iron oxide aerosols. Anat Record 181:581-626
X-ray Energy Spectrophotometry.
Burlingame, California,
10.
Siegesmund KA, Funahashl A., Pintar K. 1974. Identification of metals from
a patient with interstitial pneumonia. Arch Environ Health 28:345-346
11.
Dolg AT, McLaughlin AIG. 1936. X-ray appearances of the lungs of electric
welders. Lancet 1:771-775
12.
Attfleld MD, Ross DS. 1978. Radiological abnormalities In electric arc
welders. Brit J Indust Med 35:117-122
13.
Spacilova M. Koval Z. 1975. Pulmonary x-ray and functional findings in
electric-arc welders. Int Arch Arbeitsmed 34:231-236
14.
Peters JM, et al. 1973. Pulmonary function in shipyard welders- An
epidemiologic study. Arch Environ Health 26:28-31
15.
Dobrzyfiski, Kisielevicz J, Kociecka I. 1970. (Clinical and statistical analysis
of chronic bronchitis in port and shipyard workers.) Medycyna Pracy 21:294-306
(Polish, summaries in English and Russian)
743
16.
Marek K, et al. 1970 (Effort capacity In patients with initial
pneumoconiotic changes.) Polski Tygodnik Lekarski 25:1015-1018
(Polish, abstracts in English and Russian)
17.
Guidotti TL. 1978. The higher oxides of nitrogen: A role in altering
pulmonary response to injury? Presentation to the 5th International
Conference on the Pneumoconiosis, Caracas, Venezuela, 30 October 1978.
744
Neumoçonlosis de los soldadores con arcoi estudios
con técnicas avanzadas do microscopía electrónica
de exploración y análisis por microsondeo.
T. L. Guidotti (Estados Unidos)
Rara vez se consigue material de necropsia de pacientes
con neumoconiosis de soldador con arco, ya que esta enfermedad rara vez es mortal« El caso actual era un hombre de
58 años de edad que llevó hasta el fin de sus días el diagnóstico basado en la historia clínica y en la radiología torácica. Se encontró la pigmentación característica mediante
un examen somero de los pulmones y con la microscopía luminosa con azul de Prusia. La microscopia electrónica de exploración demostró claramente una importante infiltración
celular entre los espacios alveolares, en el tejido intersticial y en los intersticios de los nodulos fibróticos areolares verticilados. Las imágenes electrónicas retrorreflejadas, que aportan información sobre los rasgos por debajo
de la superficie y sobre el número atómico elemental, demostraron numerosas partículas intracelulares con numero atómico elevado. El análisis por microsondeo identificó concretamente el hierro como elemento predominante en las partículas, pero también reveló una tnexperada presencia de silicon
asociada con los nodulos. Las imágenes electrónicas retrorreflejadas resultaron muy útiles para identificar ciertas
características para el análisis elemental por microsondeo.
Estas técnicas adelantadas confirman lo ya descubierto por
métodos tradicionales y contribuyen a obtener nueva Información. Son muy adecuadas para estudiar los sistemas químicos
heterogéneos y los tejidos complejos como el del pulmón.
745
APPLICATION OF THE FOUR-FOLD MAGNIFIED SELECTIVE ALVEOLOBRONCHOGRAPHY TO PNEUMOCONIOSES
Hlsao Shlda, Kelzo Chlyotanl, Yoshlakl Salto
Department of Radiology and Internal Medicine, Rosal
Hospital for Silicosis, 632 Takatoku, Fujlwara, Tochtgl
Prefec, Japan.
Plain chest films have been one of the primary aids In the
diagnosis of pneumoconiosis and have been useful In the assessment of pulmonary Impairment.
However, they may not always
exactly show the features of respiratory disease, for example,
pulmonary fibrosis, emphysema and
focal emphysema or duct
ectasia.
The histological aspect of pulmonary Impairment has been
dealt with by many authors, but there are several discrepancies
between radlographlcal and histological findings of pulmonary
function test results.
The four-fold magnified selective alveolo-bronchography
(S.A.B.) Is a useful procedure which can clearly represent the
anatomy at the levels of the air-conducting systems.
With the aid of slides the authors demonstrate that the
manifestation of pathological air space is difficult to be
detected by conventional bronchography, but that four-fold
magnified S.A.B. enables typical centrllobular emphysema to be
made visible, whereas the chest radiograph taken In a case of
silicosis reveals no significant small opacities and no evidence
of pulmonary emphysema.
In another case of silicosis, the S.A.B. demonstrates
typical panaclnar emphysema, features of which are marked
747
destruction of alveolar architecture.
In a case of a foundry worker's lung, the chest radiograph
shows disseminated mlcronodular opacities In the upper lung fields
and a hyperlucent area In the lower lung fields.
The S.A.B.
demonstrates typical centrllobular emphysema In the upper lung,
which area Is not hyperlucent In the plain film.
In the lower
lung the S.A.B. demonstrates panlobular emphysema, a progression
from centrllobular emphysema.
In a case of slderosls with Increased abnormal pulmonary
markings and bullous emphysema, the S.A.B. demonstrates a typical
centrllobular emphysema and focal emphysema, associated with
bullous emphysema In the right middle posterior segment.
The
S.A.B. of the lower lung demonstrates bronchiectasis and bullous
emphysema, associated with irregular emphysema.
trees show severe chronic bronchitis.
All bronchial
In spite of the presence
of dyspnea and cough, pulmonary function tests are within normal
limits, except for a decreased percentage of DLCO.
In a case of carbon pneumoconiosis, the chest radiograph
reveals gland glass appearance.
The S.A.B. demonstrates focal
emphysema or ectasia of the small air ways, suggesting the process
of centrllobular emphysema.
Furthermore, poor definition of
alveolar pattern may be Indicative of bronchiolitis obllterance.
In a case of asbestosls, the chest radiograph shows characteristic pleural thickening with
abnormal pulmonary markings.
calcified plaque and Increased
The S.A.B. demonstrates typical
bronchiolitis obllterance with no filling of alveoli, and with
the presence of ectasia of the small air waysi these findings
748
are Indicltlve of pulmonary fibrosis.
In a case of glass wool pneumoconiosis, the chest radiograph
Is quite similar to that of asbestosis.
The patient had been
engaged on glass wool cutting for only two years.
The S.A.B.
demonstrates typical bronchiolitis obliterance and ectasia of
the small air ways, findings which are more advanced than in
asbestosis. According to the A.C.C.P. Committee's report, there
Is no evidence of pulmonary reaction to fibre glass. The authors
experience Is limited to only two cases, but structural alterations of the air conducting system in glass wool pneumoconiosis
is remarkable, and this can only be shown by S.A.B. and
biopsy.
It is concluded that there are several methods for morphological analysis, but that the S.A.B. procedure is suitable to
demonstrate the anatomy and pathology of the air-conducting
systems without lung biopsy and accompanied risk.
749
Aplicación de la alveolo-broncorradiografía
selectiva con ampliación 4il a la neumoconlosis.
H. Snida. K. Chiyotani e Y. Saito
(Japón)
La alveolo-broncorradiograffa selectiva (ABS) con
ampliación 4il obtenida con un tubo de rayos X equipado
con un reflector focal de 50>jm de diámetro y pantalla de
lantánidos constituye un procedimiento útil para demostrar los cambios radiomorfológicos en la patología de las
vfas respiratorias.
Los autores ,ap(lic§ron este procedimiento a 218 casos
de neumoconiosis, silicosis, neumoconlosis del carbón
activado, neumoconiosis de los fundidores, neumoconiosis
de los soldadores, siderosis, asbestosis y neumoconiosis
producida por la
de vidrio.
La ABS se realizó previa Inyección de 1 a 3 mi de
sustancia de contraste (de ácido 3 acetllaraino-2-4-6triiodo benzoico) administrada mediante un catéter de
angiografía (KIFA núm. 7). El catéter se introdujo fácilmente en el decimocuarto bronquio.
La ABS demostró i a) en sistemas centrilobular o
panacinar, en los casos de silicosis y de neumoconiosis
de los fundidores; b) enfisema focal o estasis de los
conductos en la neumoconiosis del carbón activado y en
la neumoconiosis de los soldadores i y c) también estasis
de los conductos con obstrucción de los bronquiolos en
la neumoconiosis provocada por la
de vidrio. Las
comprobaciones no contradijeron las clasificaciones
histológicas (Gough, Heard, Heppeleston, Wyatt y Sano).
La broncorradiograffa convencional era insuficiente
para demostrar con exactitud los cambios morfológicos en
75o
las vías respiratorias. El enfisema pulmonar o estasis
que no se observa en la radiografía habitual de tórax se
visualiza claramente con este sistema, que muestra el
desorden estructural sin necesidad de efectuar una biopsia
pulmonar y sin riesgo.
751
I f ~¡ I r r
I
K.Ronock and
"i : '
r
, I r- t, f
[v
U.Teichprt
Tpchniques, Strategies and results of" dust «onsurompnts
In the asbestos industries.
II
P.H.Conner., J.C.Day., C.A.Kennedy. , H.C.Lewinsohn
Dust control in a conventional asbestos textile factory
III Progress In the control oF asbestos dust in the u/ork place
Alex A. Cross.
IV
Graham W.Gibbs
Thp envioonmentel data basa Tor prevention studies in
Quebec
V
A.SchOtz
Protection against quartz and asbestos dust exposures at
workplaces
VI
9.Carton., E.Kauffer., J.C.Vigneron et m.Villi
Efficacité des masques antipoussleres Vis-A-Vts de liAmiante
comparaisons des différentes techniques de de comptage des
fibres d'amiante.
TT
A.Dogoumols
Cas d'application de le convention de 1 ' oit(NM39)sur le
Cancer professionnel, 1.974, en relation avec le flocage
a l'amiante dos structures métalliques et des tuyauteries
d'un immeuble en construction a Geneve.
753
Vth INTERNATIONAL CONFERENCE ON PNEUMOCONIOSIS ILO
Caracas / Venezuela
29.10 - 3.11.1978
Techniques. Strategies and Results of Dust Measurements In
the Asbestos Industries
K. Ronock and U. Telchert.
Oust Measurement Advisory Panel,
Asbestos International Association
(AIA)
Asbestos fibre concentrations In the working environment
are generally determined by the membrane filter method, developed and Introduced by the Asbestosls Research Council (U.K.),
but experience has shown that the technique does not always
produce comparable results.
Differences can arise due to va-
riations in sampling, preparation of slides, optical counting,
and the calculation of the results.
International comparison
and epidemiological studies are meaningful and feasible only If
agreement can be reached concerning all details of the method.
Furthermore, differences due to specific conditions and
therefore different risk factors have to be associated with the
various fields of the asbestos producing and asbestos processing Industries. These are not to be generalized for Instance for
the spray Insulation Industry, textile Industry, asbestos mines
and mills, the asbestos cement Industry and the users of asbestos
containing products.
Values of past dust situations without any
dust control In these various branches, reported by different
authors and measured by ourselves, are presented In Figure 1,
using a logarithmic scale for the fibre concentrations per ml.
The 2 fibres per ml value Is marked by a dotted line.
755
The maximum concentration In the general environment Is also
included In this flguret
The variation scope for average fibre
concentrations Is marked by crossed lines, short-term peak concentrations are marked by darts.
By controlled handling of
asbestos and application of the most recent technical dust suppression methods we have now achieved dust concentrations equal
to or below 2 fibres per ml.
This means concentrations up to 3
orders of magnitude less than we had in the past or, in other
words, from several hundreds up to more than thousand fibres per
ml In the past down to 2 fibres per ml and below.
The maximum
concentration of the general environment, however, Is by 2 orders
of magnitude (factor 100), below this 2 fibres per ml value with
a maximum of 0.05 fibre per ml. The use of gravimetric units
(nanogram per m ) with concentrations of 1 up to 1000 nanogram
3
per m sounds very high for the general environment, but Is regardless of the biologically important fibre dimensions. For
a rough estimâtIoni 0.05 fibre per ml are equal to 2500 ng per
3
3
m or In the other way, 100 ng per m are equal to 0.002 fibre
per ml.
Additional physical and physico-chemical investigations
(fibre dimensions, elastic properties, surface adsorption properties, foreign substances
in the raw asbestos) are necessary
to detect those properties representing a health risk on its
own or in connection with other factors (smoking habits).
Only
when these results are available and found to be In accordance
with extensive medical findings, will re-conslderation of the
threshold limit value via dose-response or concentrâtIon-
756
response-relationship be possible and objectively and well founded.
Till then asbestos dust exposure at workplaces has to be kept as
low as feasible through effective technical measures.
Dr. R. Murray (U.K.), a former officer to ILO, created last
week a new definition!
That we all are archaelogists in this
field of industrial hygiene when we try to explain the medical
findings to-day by past dust situations.
On Initiative of the Executive Committee of the Asbestos
International Association (AIA) It is intended to follow up the
"Counting Trial" (on behalf of the International Agency for Research on Cancer of the WHO, Lyon 1972) which took place 4 years
ago under H. Walton (Edinburgh) and G. Glbbs (Montreal) and with
the participation of 9 countries.
The aim at that time was to find
out the differences which may occur at light-microscopic counting
of membrane filter samples of asbestos dust.
At a first Inter-
national Colloquium on Dust Measuring Technique and Strategy in
Warmensteinach (Germany), August 1977, with 39 participants from
government, academies and industries of 15 countries, organized by
the Wirtschaftsverband Asbestzement (Germany),on behalf of the AIA,
we discussed for the first time the whole set of problems connected with the way of sampling and evaluation.
Final aim of this and
a following meeting should be to achieve International standardization of technique, strategy and evaluation of measurements at the
workplaces and thus to come to an overall uniformity for determination of person-related dust exposure.
At a second International
Colloquium 3 weeks ago (October, 1978) In Washington, organized
757.
by the Asbestos Information Association of North America on
behalf of the AIA, the established "Dust Measurement Advisory
Panel", of the AIA under the chairmanship of myself presented a
"Reference Membrane Filter Method for the Determination of Fibre
Concentration at Workplaces in the Asbestos Industry".
This
"reference method" set out in a detailed way in 45 pages is an
attempt by the asbestos industry to reach an international
accord.
It is not Intended to affect national regulations but
to permit international comparison of data. After presentation,
introduction and discussion the 39 participants of 13 countries
were asked to give their comments, suggested changes and additional remarks until 15 December this year.
Additional im-
provements may be included until middle of February 1979, the
final Draft Proposal should be mailed end of February 1979 to
all participants of the Washington Colloquium.
The AIA will
publish and distribute the agreed Reference Method within 4
weeks (end of March 1979) and will also hand it over to ILO
and WHO as a responsible contribution of the industry In this
matter.
In the course of this year many measurements have been
taken in the laboratories of the 7 members of the Dust Measurement Advisory Panel (from 6 countries) to approve the details
of the Reference Method.
a special paper.
We will publish all the results in
I would like to inform you about some Inter-
esting facts i
For the estimates of a workman's exposure, samples must be
758
taken In the operator's breathing zones, that means a hemisphere
of 300 mm radius extending In front of the face, and measured
from a line bisecting the ears.
Exposure can be assessed by
long-term sampling or by short-term sampling (describing fluctuations in the work process).
Static sampling can be useful it it
is shown that the dust is uniformly distributed over large areas.
In view of individual working practices it Is not possible in gene
ral to assume that data from one operator can be used to judge the
exposure of another, even if the persons concerned are engaged in
similar or even identical jobs. Any transfer of data must therefore be validated by appropriate relative measurements.
The flow rate of the pump has to be determined with an
Installed or external flowmeter and has to be checked at least
before and after sampling (Figure 2).
In case of long-term
sampling the flow rate must also be checked during the sampling
period.
The average flow rate is used for evaluation.
The
sampling has to be repeated if the initial and final flow rates
differ by more than + 10 %.
During short-term sampling (10 - 30 minutes) the filter
can be held by a technician in the breathing zone of the worker
or worn by the worker (Figure 3).
Static samples, i.e. samples at fixed locations, may be
suitable for some control purposes but are not recommended for the
measurement of workmen's exposure to asbestos dust (Figures 4 7).
For continuously recording the dust concentration at a work-
place at certain distances from the dust source, taking Into accou
a special air flow direction the Tyndallometer (measuring scatter»
759
light, Leltz, Wetzlar) was used.
Point sources cause considerable
concentration gradients thus causing the results of static samples
to vary considerably over short distances«
However, static sampling
can be useful It It is shown that the dust Is uniformly distributed
over large areas.
At a typical workplace of the asbestos cement Industry (punching of sheets) comparative measurements at various distances from the
dust source have been made with the Tyndallometer of Leltz and the
Personal Dust Sampler of Casella.
With constant dust composition
and distribution of fibre dimensions a good correlation was obtained (Figure 8) which is, however, not transferable to other
workplaces.
Here, diverging distribution of fibre diameter and
fibre length may occur and thus lead to another correlation between
both methods.
Investigations have been conducted to test the permeability
of membrane filters of 0.8 >um pore size for fibres perceptible under
a light microscope (length 7-5 ;um, diameter<3yum). Three filters
(SM 11304) of 140/jm thickness were placed one after the other and
sampled at a flow rate of 24 1 per minute. The results (Figure 9)
show that the share of fibres perceptible under the light microscope (down to a diameter of 0.3/an) penetrating the first filter
Is too low to have any influence on the measuring result.
Mounting the Samplet
For mounting use the acetone-triacetine
method only (Figure 10). All other mounting procedures will give
a lower counting rate (20% and more).
is the better background of the filter.
76o
But the main reason for this
Figure 11 shows a slide
mounted with acetone vapour and trlacetlne which can be compared
with Figure 12 which has been mounted with trlacetlne only.
Regarding the Influence of the filter loading with fibres
on the counting result, the following may be statedt
Generally,
during longer sampling times, loading on the filter Increases,
This will Influence the measuring result.
The higher the filter
loading, the more difficult It Is to detect all fibres or to
decide whether a fibre should be counted or not, specifically If
additionally to the fibres non-fibrous particles are present.
The results may be taken from Figure 13, With high filter loading
(more than 5 fibres per field) the determined fibre concentration
3
per cm declines on behalf of visually lnterferring factors.
This should be considered for long-term sampling.
It Is Im-
portant to assure always the same filter loading.
There are problems arising from utilization of different
graticules.
pare
It Is much harder and more tiring for the eye to com-
the fibre with a reference size (British Standard 3625 /
Figure 14) than to have an Immediate scale available (Figure 15).
The latter Is a grid of 5 jum mesh length.
Even so we aim to de-
velop a better type of graticule for International acceptance.
Last not least, graticules with mesh length of 5>um, but
different total counting areas have been examined (Figure 16).
For comparison we used 3 "5jum grids" with 250 jum, 175jum and
125/urn edge length and accordingly with counting areas of 0.08,
0.03 and 0.016 mm .
10 preparations with different filter
761
loading have been counted (0.1 fibre per field up to about 3
fibres per field).
and triacetlne.
Mounting was performed with acetone vapour
On average evaluation of the grid with only 125
>um edge length was about 7OX higher than by application of the big
grid of 250 um.
However, the difference declines with decreasing
filter loading.
Apart from these examples there are additional factors
(absorption of phase rings> etc.).
You will have seen how essen-
tial it is to standardize the membrane filter method in detail.
In this respect,
lacking accord may already lead to differences
up to 300%. Moreover, there is the problem of how to perform
sampling itself (location and sampling time) which nay lead to
even greater differences up to 800Z in total«
This means that
the accuracy of measurements may be between 0.25 fibre per ml and
4 fibres per ml when a concentration of 1 fibre per ml is evaluated.
This embraces the whole range of the present TLV of 2
fibres per ml and a proposed TLV of 0.5 fibres per ml.
It also
highlights the irrelevance of discussion about a TLV of 2, 1 or
0.5 fibres per ml by extrapolating from past dust situations with
respect to our present technical knowledge.
Of more significance
is that there has been a reduction in the workplace from hundreds
of fibres per ml down to few fibres per ml.
Data on dust concentrations hitherto available which has
been taken for epidemiological investigations may therefore only
be considered as estimates.
Only by close cooperation between
physicians, epidemiologists and physicists and bringing together
762
of medical findings with the data of dust measurements may clarification of causal connections be achieved.
Furthermore, close
cooperation Is essential between all Institutions Involved In the
asbestos question In order to protect workmen from health hazards.
The Industry Is willing to contribute their experience on the
situation at workplaces.
For protection of the general environ-
ment AIA Is also prepared to monitor the environmental asbestos
concentration since In future the Dust Measurement Advisory Panel
will be dealing with questions not only of emission from asbestos
plants, but also the presence of asbestos dust In the ambient air
Including electron microscopy anyway, exchange of samples and
slides, training of measuring technicians, advise by establishment
of measurement laboratories and organizing colloquia concerning
this matter.
Last not least, let me finalize by citing the Interpretation
of an average or mean value, mainly used by statisticians and
epidemiologists, published last week In a German Journal! When
a man stands with one leg on a hot plate and with the other In
ley-water than his average temperature Is very pleasant I We
have to step Into a detailed description of the real personal
exposure and not only to use average values.
763
Figure 11
Asbestos dust concentration (fibres/ml) In different
branches of the asbestos Industry and of the general
environment (dotted linei 2 fibres/ml) - logarithmic
scale
Fleure 2i
Flow rate of 3 Personal Dust Samplers as a function
of operating time
Fleure 3i
Fibre concentrations measured by Personal Dust Sampler
worn by the worker in comparison to a Personal Dust
Sampler carried by a technician
Fleure 4i
Disposition of 2 Tyndallometers on both sides of a
dust source, taking into account the air flow direction.
Fleure 5t
Dust concentration recorded by Tyndallometers 1 and
2 disposition of which is depicted in Figure 4
Fleure 6>
Tyndallometers 1 and 2 at different distances from
a dust source, taking into account the air flow
direction
Figure 71
Dust concentration recorded by Tyndallometers 1 and
2 the disposition of which is depicted in Figure 6
Figure 8»
Correlation between results of Tyndallometer and
Personal Dust Sampler at a typical workplace of the
asbestos cement Industry (punching of sheets)
7fia
Figure 9i
Permeability of membrane filter with 0.8 urn pore
size for fibres
Fleure lOi Counted fibres by application of different mounting
substances
Fleure 111 Slide mounted with acetone vapour and trlacetlne
Fleure 121 Slide mounted with trlacetlne only
Fleure 131 Influence of filter loading on the counting results
Fleure 14i Gratlculei
British Standard 3625
Fleure 15» Gratlculei
Grid of 5 urn mesh length
Fleure 161 Influence of the size of the graticule area on the
counting result
765
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767
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16
DUST CONTROL IN A CONVENTIONAL ASBESTOS TEXTILE
FACTORY
P. H. Cooper, J. E. Day,
C. A. Kennedy, H. C. Lewinsohn
Raybestos-Manhattan Industrial Products Company, North Charleston,
South Carolina 29406, U.S.A.
INTRODUCTION
The first recommended threshold limit value (TLV) for asbestos
exposure was that of Dreesen et al. of the U.S. Public Health
Services.
In 1938 following a survey of 5A1 employees of four
North Carolina asbestos textile mills, they proposed a standard
of 5 million partlcles/cublc feet (mppcf) for the prevention of
asbestosls. This standard was Included In the American Conference of Governmental Industrial Hyglenlsts (ACGIH) list of
maximum allowable concentration (MAC) values In 1946 and, In
1948 was placed on the ACGIH listing of TLVs. ACGIH TLVs became
legally enforceable standards In 1968 for those Industries to which
2
the Walsh-Healy Act applied.
The standard proposed by the British Occupational Hygiene
Society In 1968
and adopted In Britain In 1970
was based upon
the concept of a cumulative dose and the risk of less than 1%
of exposed persons developing the earliest signs of asbestosls.
This standard of 100 fiber years per cm
was interpreted as mean-
ing that a similar risk applied for an exposure of 2 fibers/cm3
for 50 years, 4 fibers/cm
for 25 years, etc.
In the United States, a federal standard of 12 fibers/cm3
775
greater than 5yu In length, 2 mppcf, was promulgated on May 20,
1969, under the provisions of the Walah-Healy Public Controls
Act*
This also was proposed as an Interim standard under the
Occupational Safety & Health Act (1970) on May 29, 1971, but was
soon replaced by an Emergency Temporary Standard of 5 f/cm
on
December 7, 1971.
As required by the Occupational Safety & Health Act, a permanent standard for asbestos exposure was promulgated six months
later in June 1972 . This standard permitted exposure to airborne concentrations of asbestos fibers, longer than 5 micrometers, provided that the 8-hour time-weighted average (TWA)
concentrations to which any employee may be exposed "shall not
exceed 5 fiber per cubic centimeter of air". The standard also
stipulated that, effective July 1, 1976, "the 8-hour TWA airborne concentrations of asbestos fiber to which any employee may
be exposed shall not exceed two fibers, longer than 5 micrometers,
per cubic centimeter of air".
Thus, industry knew that it had a target to obtain by July,
1976 and decisions had to be taken as to how the task of complying would be achieved.
We decided that, Irrespective of the
standard demanded, we would use the most effective and practicable
means of reducing dust to the lowest possible level and would continue to manufacture asbestos textiles by conventional methods.
In this paper we will describe the engineering methods which
enabled us to achieve our target and still maintain the continuity
776
of the operation.
The project was completed in July 1977.
HISTORICAL DETAILS
The plant, acquired by us in November 1969, was run down in
the preparation-carding and weaving areas. Much work was needed
to make it productive and a profitable venture.
The employee
union demanded certain commitments before signing over its negotiated contract to us and one of those, the development of a
"safe workplace" for its membership, we readily agreed to.
In 1969 approximately 87,000 cubic feet per minute (CFM) of
exhaust air was collected in a baghouse and could be recycled to
the workplace.
Approximately 9,000 CFM of exhaust air was collect-
ed in a cyclone collector exhausting to the atmosphere.
The baghouse air was collected from preparation and carding.
The cyclone air was collected from weaving and filling winding.
There were no other areas in the plant with exhaust ventilation.
Waste fiber was removed from the baghouse in open-top boxes and
from the cyclone periodically by shovels.
The Chrysotile asbestos fiber was brought into the plant in
compressed bales. The asbestos and carrier fiber storage areas
were orderly with little or no noticeable dust emission.
Old-fashioned methods were used for fiber preparation, including blending, opening and mixing.
The opened fiber was stored
in stock-holding bins of about 3,000-4,000 pounds capacity.
The
pneumatic line that fed fiber to the bins did so by means of a
777
ceiling condenser mounted over a crossing conveyor belt that was
located on top of the bins some 25 feet above floor level. The
fiber had to be removed from the bins by hand, using a pitchfork
to transfer it to a loose cart from whence it was taken to the front
of the card-feed hopper and hand-fed to the carding machines.
The cards were built in the late 1930's and early 1940*s.
The roving from these cards• wound on wooden spools, was very
weak and broke constantly.
Breaks of this type contributed to
the dust problem in the later spinning operation.
The cards had
enclosed and exhausted cylinders but were dusty due to poor
design, poor upkeep and inadequacy of the extraction system.
Under-card wastes were removed by a mechanical rake, delivered
pneumatically to the baghouse and removed by shakedown.
A portion
of the waste was re-used and the rest bagged off and sold.
Spinning was dusty mainly due to yarn breaks. As the end
broke, it hit the adjacent ends and created dust.
Twisting suffered from the same problem but to a lesser degree.
Winding was done dry without exhaust ventilation and this created
dust.
Weaving was done dry with air extraction on some looms.
Attempts at exhausting automatic looms had been unsuccessful and
those fitted with wet pans were not effective because only a portion
of the yarns in each type was wetted.
The yarns for weaving were
wound dry and the warp yarns were supplied from creels in a dry
state.
No dust controls had been attempted on these processes.
778
Inspection and shipping was probably the cleanest operation
In the plant due to the nature of the job and there were no dust
controls. The cloth and tape was wrapped In kraft paper and shipped«
At the time of the plant's acquisition, dust counts were
q
barely below 12 f/cm
(the maximum allowable concentration re-
commended by the ACGIH), and the
productive process was Inade-
quate for a profitable venture.
We recognized that the plant had
potential and needed a textile facility for our friction materials
plant In Pennsylvania.
It was decided to convert the product line from typical
asbestos textiles Into yarn and cloth for use In friction materials manufacture and to reduce dust generation where possible.
The strategies to be used werei
1.
Increase carding production by upgrading and reclothlng
the cards, convert the tape condenser cards to ring
condensers and produce a quality roving of a coarser
count from all cards wound on cheeses Instead of jackspools.
2.
Upgrade the raw material by using Casslar fiber In
Grades A and AA and Bells 3-T, by using good long
staple cotton combined with rayon and by the Introduction
of a core yarn (for carrier) at the card to allow for
good roving strength for spinning.
3.
Change the method of spinning and twisting from ring
spindles to flyer spindles.
779
4.
Start a program to reduce dust generation In weaving by
dampening the yarns at the loom and winding for weaving»
The action plan'necessary to accomplish the above took nearly
four years from 1969 - 1973.
CORPORATE POLICY
In 1974 we formulated a comprehensive corporate policy which
included the elimination of asbestos from products where a viable
substitute for it could be found»
All other asbestos-containing
products would be manufactured by a "clean system".
Control
measures were to be developed to cover the entire process from
the introduction of the raw asbestos through the disposal of waste,
scrap and rejected material.
An intensive study was made of all asbestos and asbestoscontaining products.
Products were Identified for elimination
from manufacture and others were identified as candidates for manufacture under the "clean system" concept.
Restructuring of the
manufacturing system and capacities was then planned.
In June 1975 a comprehensive "clean system" plan for asbestos
textiles> requiring the expenditure of $12.3 million, was approved.
It provided $2.6 million for the redesign and conversion of the
conventional textile operation to a "clean system" process.
The
remaining $9.7 million was for a wet extrusion process plant and
for the close out of yarn manufacturing at the Pennsylvania plant.
STRATEGIES DEVELOPED FOR THE "CLEAN SYSTEM"
PLAN
In order to accomplish the objectives for the conventional
78o
textile pianti the following strategies were developedi
1.
Elimination of all man-handling of raw asbestos fiber
by use of a closed system where possible«
2.
Reduction of dust generation by effective exhausting
or wetting where possible.
3.
Utilization of as much of the existing equipment as
possible from the Pennsylvania plant and the textile
plant by relocating, rebuilding and modifying as required»
4.
Upgrading an expansion of existing buildings and simplification of vacuum cleaning by having smooth walls
and avoiding ledges and surfaces that catch and retain
dust.
5.
Provision of a maximum volume of fresh clean air to the
workplace by use of heated or humidified make-up air
units.
6.
By design« provide for a safe, clean method of waste
collection and reuse and/or removal.
The action plan required nearly two years for completion, reducing fiber counts to less than 1 f/cm
and increasing the plant
capacity considerably,
ACTION PROGRAM
Plant Facility
A new addition of 50,000 square feet of floor space was built
781
utilizing the "smooth surface" approach.
This new floor space was
designated for spinning, twisting equipment, an office and a maintenance shop/boiler room.
Fresh make-up air with added heat and humidity was provided
for by installing three 50,000 CFM, and one 65,000 CFM roofmounted units.
These required that an additional 500 horsepower
boiler be Installed giving a total boiler horsepower of 750.
Additional exhaust air was provided by Installing a 110,000
CFM baghouse of the pull-through type having two 125 horsepower
backward Incllded blade fans. There are ten bag-cell modules,
five on each fan. Shakedown and waste removal Is accomplished
by screw conveyors dumping through rotary air locks into plastic
bags.
air.
This allows for a total of nearly 200,000 CFM of exhaust
The building Is thus under a slight positive pressure.
The
starting and stopping of the make-up and exhaust air have to be
tied together electronically to prevent damage to the building.
Blending/Opening
A "fiber control" blending line Is used to blend the asbestos,
carrier and waste.
Each feed hopper Is enclosed and under a
negative pressure, opened at the feed end only so as to allow the
bags of asbestos to be opened In an area draughted away from the
operator and Into the hopper.
The under-card waste Is returned pneumatically to Its respective feed hopper of the blend line, where the long fibers are
separated from the shorts and sand, by passing through the screen
of a celling condenser directly Into the hopper.
782
The hopper Is
completely enclosed and exhausted.
This eliminates the job of
under-card fly removal once done manually.
The blended stock is conveyed pneumatically to a "reserve
hopper" kept under negative pressure where up to 5,000 pounds can
be stored for work in process inventory, allowing blendline changes
for versatility in mixes.
The stock or mix is transferred pneumatically to card feeds.
It has been found that air velocity of 2,000 fpm minimum will carry
the mix through a ten inch diameter duct up to three hundred feet
away to a card feed provided that there is no increase in duct
elevation and a minimum number of turns.
4300 fpm is used to main-
tain the efficiency of the system.
These processes eliminated the job of "stock hauling".
Carding
An acceptable, high-quality roving can be produced from a
single cylinder card provided the card is fed with a mix having an
intimate blend, uniformly opened and made into a web having uniform
density and weight.
This conserves exhaust air in carding, allows
for higher card loads per operator and reduces card maintenance.
The feed decided upon is the CMC "EVETJFEED".
cept of the feed is an air-laid web.
The design con-
Level control in the hopper
is controlled by two photo-electric cells, a high level, and a lowlevel control.
The ceiling condenser runs constantly.
An air-
operated damper valve is controlled by the indications of the photo
cells.
Low-level indication will open the damper located on the
783
clean-air side of the celling condenser, allowing fiber-laden air
to pass through the condenser, and thus depositing fiber into the
feed hopper of the "EVENFEED".
High-level indication will close
the damper, stopping the flow of fiber to that unit.
It has been determined that no more than six "EVENFEEDS" can
be serviced at a time due to the production capability of the fiber
opening mechanisms (FOM) and amount of fiber that can be kept moving
through an air duct.
Thus, there are six cards to a line.
Controlling the total system (six cards, six EVENFEEDS, one
FOM, one reserve hopper) for one line of cards demands sophisticated electronic controls.
An electronic scanning system that can
scan the photo cell indications in any predetermined sequence is
employed on each card line.
Depending on roving count desired
and production rate of the cards, the system Is scanned once every
15 to 45 seconds for hopper-level control.
This allows a uniform
feed to the cards.
Controlling dust emission at the cards has been accomplished
by double enclosing the cards and exhausting the enclosures into
a baghouse, and at the same time forcing fresh make-up air from
overhead ducts downward through the
work alley, passing by the
operator and into the enclosure opening.
The function of the double enclosure is to minimize and contain dust generated by the card.
The secondary enclosure surrounds
the immediate card area, opening only at the front for roving
removal.
There are service panels that may be opened or removed
for card maintenance.
784
Spinning and Twisting
The spinning room has been designed to create a cross draft
in the room.
Fresh make-up air is brought Into the room through
the celling on one side and distributed by means of a header and
duct system accross the room.
This allows approximately 5 air
exchanges per hour with no air extraction from machinery.
The spinning and twisting is done on flyer type frames, although they have had their speed reduced to minimize noise and dust
(approximately 900 RPM spindle speed).
and carrier core yams are used.
Roving is wound on cheeses
Work practices are the main
contributing factor in reducing dust in this area.
Winding for Sales
We use mainly Foster 77 winders. The winders are enclosed
and exhausted effectively, having the backs, sides and top covered, leaving a portion of the front open for operator access.
Suspension of heavy, clear, plastic strips vertically in the face
opening of the enclosure allows good operator access and visibility while maintaining a high-air-velocity low-volume system.
Work practices In this area are also major contributing
factors in achieving low dust counts.
Weaving
All weaving is now performed with wetted yarns.
The wetting
of the warp yarns is done by padding-rolls immersed in water
troughs located behind the harness section of the looms.
yarns are wetted in the same manner during winding.
again immersed in water just prior to weaving.
Filling
They are
A resin treat-
ment is also applied at the loom in the same manner as wetting.
785
This serves to "lock In" the fibers in the woven fabric, minimizing
dust generation from the fabric in later use. The weaving area
has narrow fabric and heavy hand looms.
Yarns manufactured by
the wet dispersion process elsewhere are now being introduced in
weaving in this plant and this will further insure low dust counts.
Inspection and Shipping
Due to the nature of the job and resin treatment applied to
the cloth in weaving, dust has nearly been eliminated in inspection.
The yarns are now packaged in stretch-wrapped plastic on
pallets.
The cloth is packaged in plastic bags and tapes are
packaged in shrink-wrapped plastic.
Dust has virtually been eli-
minated in this area.
OPERATING PRACTICES
Before the implementation of engineering design and methods at
the plant, it was recognized that engineering alone would not maintain a "clean system".
During the construction phase, development
of work practices and administrative procedures was given a high
priority.
When the construction phase was completed, these new
practices and procedures were ready for implementation.
Work Practices
All employees, including supervisors and management, are
expected to maintain constant attention to performance of stipulated work practices.
Examples of work practices to assure the efficient operation
786
of the "clean system" arei
a.
Maintenance - All processes except spinning, twisting
and weaving are enclosed and ventilated.
Special pro-
visions, such as lock-out procedures, protective clothing
and equipment, and supervisory monitoring procedures have
been instituted to protect personnel from excessive
dust exposure during periodic and emergency maintenance
situations in the enclosed operations.
b.
Waste Handling - These operations can easily get out of
control without good work practices.
Wetting methods
and bagging procedures have been given priority consideration.
Waste is handled by classification, such as
baghouse waste, loom waste, roving waste, etc. with
specific responsibility for proper handling being
assigned to designated personnel.
c.
Baghouse Operations - These areas offer the greatest
probability for spills or malfunctions to occur.
At-
tending personnel are required to wear protective cloth-ing and respirators when entering the hopper areas of the
interior baghouses. These areas are posted, requiring
authorized entry only with protective equipment.
d.
Clean-up Methods - Routine clean-up operations at Marshville require the use of industrial utility vacuum
cleaners on a continuous basis.
Special clean-ups of
building overhead areas, pipes, etc. are performed by
personnel wearing protective clothing and respirators.
787
e.
Equipment Removal - From time to time It Is necessary to
move machinery and equipment«
The work practice used
requires a thorough cleaning of the equipment to eliminate loose asbestos and then oiling to suppress any dust
that may have escaped the cleaning process«
f.
Warehouse Surveillance - In the storage and moving of
bagged raw asbestos fiber or packaged finished goods•
tears and holes are sometimes created by handling equipment which allows the escape of airborne asbestos dust.
The work practice requires the Immediate patching of all
bags or containers at the time of rupture, or when discovered! and before further moving«
Administrative Procedures
Administrative procedures are used to supplement the engineering controls« methods and work practices and to further assure
effective use of the "clean system".
These procedures range from
mandatory measures to optional additional personal protection for
employees.
The following are examples of the administrative pro-
cedures used at Marshvllle.
a.
Protective Equipment - During any emergency situation, protective clothing Including a respirator must be worn. This
Includes, for example, emergency maintenance of enclosed
equipment or rupture of a pressurized fiber-carrying duct.
Special clean-up crews must also use this equipment.
These
procedures are necessary as airborne levels of asbestos
788
dust during clean-up or emergency maintenance operations
are unpredictableRespirators and dual lockers are made available to all
employees regardless of how little asbestos dust exposure
may occur«
b.
Disciplinary Enforcement - Employees are required to adhere
to the work practices and procedures developed to operate
the "clean system".
To enforce the program graduated dis-
ciplinary measures are used up to and including dismissal
to emphasize and support the importance attached to carrying out the work practices.
c.
Clean-UP Personnel - Clean-up personnel , working continuously on each shift have been added to compliment the
engineering achievements.
These employees are in addition
to those who performed this function prior to the engineering changes and represent more than a doubling of this
effort.
d.
Employee Information - Achievement of a "clean system" procès
stimulated a renewed effort in the employee educational
program.
Audiovisual instruction materials, pamphlet
handouts and verbal instructions by first-line supervision
are all used to re-emphasize the importance of limiting
asbestos dust exposure to the lowest achievable level.
e.
Dust Monitoring -
Monitoring of asbestos dust exposure
to individuals and work area dust levels Is performed
at a frequency considerably greater than Is now required
789
by che OSHA asbestos standard in view of the fact that
dust levels in all areas are controlled to levels well
below the permissible limits.
Each month a selected
number of dust samples are taken. Additionally a complete and extensive survey is accomplished annually to
assure that the baseline exposure level is known.
CONCLUSION
The plant has approximately 150,000 square feet of floor
space and employs slightly over 200 people.
It has capacity for
making in excess of 8,000,000 pounds of asbestos textile products
and friction yarns annually.
The clean-up and expansion program
was completed under the forecasted budget monies and slightly over
in time.
Despite increased energy costs, the manufacturing cost
has not increased per pound of product made.
Increased produc-
tivity has helped offset inflation and energy costs.
The improvements in dust control can be quantified by studying
the mean asbestos fiber counts in various manufacturing areas.
All levels are maintained below 1 fiber/ml, 8 hour TWA.
The
dustiest operations have been totally enclosed or eliminated.
The importance of work practices cannot be over-emphasized,
Poor work practices, or carelessness in adherence to good work
practices at any single operation within the plant, can result in
widespread contamination and possible dust exposure.
It is recognized and accepted that, although the engineering
designs embarked unon have been completed, experience will determine what additional improvements can be made or need to be made.
It is also roco/;,nized that operational procedures may have to be
79o
modified from Cime co Cime,
le is our incencion co reduce employee
dusc exposure Co Che lowesc possible level achievable by reasonably oracCicable means wich che goal of providing a safe and
healchy workplace.
Ic is also our incencion Co concinue Co pro-
duce convencional asbesCos cexciles in che knowledge chac che plane
described is probably Che eleanese of ics kind.
This paper also serves Co illuscrace Che difficulcies which
mighc be encouncered when conduccing epidemiological studies in
industry to determine dose-response
relationships when Cechnical
achievemencs in environmental sampling, raw material production
and engineering controls undergo changes over a period of time
while the process and final product remain essentially unaltered.
791
REFERENCES
DREESEN, W. C , J. H. DALLAVALLE, T. I. EDWARDS, J. W. MILLER AND
R. R. SAYERS.
1938, U.S. PUBLIC HEALTH BULLETIN NO. 241.
2
NICHOLSON, W. J., 1976, in Occupational Carcinogenesis.
and Joseph X. Wagoner, Edsi
Umberto Saffiotti
Ann. N. Ï. Acad. Sci., 271, 152-169.
BRITISH OCCUPATIONAL HYGIENE SOCIETY - SUBCOMMITTEE ON ASBESTOS HYGIENE
STANDARDS FOR CHRYSOTILS ASBESTOS DUST.
1968.
Ann. Occ. Hyg. 11: 47-69.
4
HYGIENE STANDARDS FOR AIRBORNE ASBESTOS DUST CONCENTRATIONS FOR USE WITH
THE ASBESTOS REGULATIONS 1969.
TECHNICAL DATA NOTE 13, DEPARTMENT OF EMPLOYMENT,
H. M. FACTORY INSPECTORATE.
5
OCCUPATIONAL SAFETY AKD HEALTH ADMINISTRATION, DEPARTMENT OF LABOR, 1972.
PART 1910 - OCCUPATIONAL SAFETY AND HEALTH STANDARDS.
TO ASBESTOS DUST.
Fed. Reg. 37: 11318.
792
STANDARD FOR EXPOSURE
PROGRESS IN THE CONTROL OF ASBESTOS DUST IN THE WORK PLACE
Alex A. Cross, United Kington
Beginning of Control
Although there had been Isolated reports of lung disease
among asbestos workers In the early part of the century, there
was little general awareness of an occupational hazard until
the 1920s. This Is clear from the Merewether and Price report
to the U.K. Factory Inspectorate In 1930 referring to the
dis-
covery In 1928 of "a case of non-tubercular fibrosis of the
lungs in an asbestos worker of sufficient severity to necessitate
treatment in hospital".
Dr. Merewether's Investigations on the medical side (during
the years 1928 and 1929) were considered to be of great scientific value and were said to establish that asbestosis "was the result of Inhalation of asbestos dust over a period of years and
that the development of the disease varied in direct proportion
to the length of the exposure".
In this paper,' we are considering the development of controls
for the protection of those who work with asbestos.
Important
though the conclusions of the medical expert are, I am referring
to this report mainly to provide a starting point In our review
of the extent to which progress has been made In the development
of dust control for the protection of people from the risk of
asbestosis.
The conclusion of the report by the Chief Inspector
of Factories is worth quoting in this connection.
793
"The remedy
as in the case of so many industrial diseases, is in the suppression
of dust".
He goes on to add "In the non-textile section of the in-
dustry no serious difficulties arise as regards the application
of exhaust ventilation.
For the textile section, it is evident
that a good deal of experimental work will have to be carried out".
Following this report, the U.K. Asbestos Industry Regulations
were enacted in 1931, to be implemented by 1933. These were the
first governmental regulations to be introduced specifically
applied to work with asbestos.
They reflected the primary concern
with the textile side of the industry, and it was in this sector
where the main efforts at the
centrated.
development of controls were con-
A committee was set up consisting of technical experts
from the leading asbestos textile manufacturers and from the govern2
ment. Their report, published in 1931 , Includes detailed designs
for dust extraction equipment, and their application to all stages
of asbestos manufacture, from the emptying of sacks of asbestos
fibre to the weaving of asbestos cloth.
on
It also includes sections
mattress making, recommends the preparation of a "precautionary
leaflet for the guidance of workers" by the government department
concerned, and even a brief reference to a method for the gravimetric determination of dust.
Effectiveness of Control
One has heard many stories of the obvious improvement in the
atmosphere of the work place from old-timers from the industry who
remembered the pre-control days.
In
794
one factory it was said that
for every kilowatt of power used for production machinery another
kilowatt was used for dust extraction equipment.
Certainly great
efforts were made, but at that time and for many more years such
efforts lacked any guidance as to the level of concentration of
asbestos dust which could be regarded as a target.
Neither at
that time was there any Indication that certain specific size
ranges of asbestos dust might be harmful. The U.K. Asbestos
3
Industry Regulations
simply referred to "asbestos dust" and
failed to define dust.
In the absence of any proper definition,
this was interpreted by factory inspectors, industry and employees as "no visible dust" ("visible" meaning visible to the
human eye under normal working conditions).
It was not until the early sixties that the experts began
to suggest that health risks from asbestos arose from a certain
size range of asbestos fibre Invisible to the human eye under
normal lighting.
Clearly the apparent elimination of visible
dust was no guarantee that all harmful exposure had been avoided,
though conversely observation of visible dust might be taken to
indicate the
presence of an invisible component. Nevertheless,
the improvement in controlling the dust In the textile industry
from 1933, in spite of some relaxation during the war years, was
seen to be having its effect in reducing the Incidence of asbestosis to that sector by the early fifties.
The progress achieved in a major asbestos textile plant can•
be judged from the data included as Appendix (i) of the British
Occupational Hygiene Society's publication "Hygiene Standard for
Chrysotile Asbestos Dust". 4
This shows the progress achieved
between 1952 and 1966 when routine dust sampling results became
795
available.
There can be no doubt that dust levels tn earlier
years were considerably higher, though no measurements are available.
Control to a Standard
The occurrence of asbestosis in the textile industry was
beginning to show the benefit of improved control, but after fifteen or more years of new applications, such as sprayed insulation
and the growing popularity of preformed thermal insulation, especially in war-time ship construction, it was observed that other
areas of manufacture and use were in even greater need of control.
As the ILO report of 1973 stated, control measures effectively
applied in the factory situations were more difficult in the case
of such work as lagging and insulation, in which sector, as a report by McVittie in 1965 showed
, the greatest number of cases
were being observed.
As data accumulated and as sufficient time elapsed for evidence of a beneficial effect of sustained control to become available, as in the textile industry, it became apparent that risk
was related to a combination of duration and level of exposure.
Tentatively, levels of exposure were suggested which it was believed would lead to minimal risk.
The passage of time provided
increasing evidence of the long term effect of past measured exposure, on the basis of which threshold limit values were calculated that would provide a practical and effective standard of
control.
796
Ac last management and its engineers could monitor the effect
of their control measures and select the priority target for their
efforts.
Control engineering became a much less hit-or-miss affair
and could be organised and checked in a scientific manner.
Modern Aids to Effective Control
Sophisticated techniques of sampling the atmosphere In the
work place have been developed which helped Identify areas where
concentrations of dust were greatest.
A further development -
the use of quartz-iodine lamps (the Tlndall Beam) - helped to
pinpoint sources of dust emission responsible for or contributing
to the concentrations.
Thanks to the co-operation of the British
Factory Inspectorate and the Asbestosls Research Council, we are
able to see examples of such dust emission location using the
Tlndall Beam technique. Photographs taken using the same technique
also show the effect of dust control by comparing machines operating
with and without dust exhaust.
It must be pointed out that dust seen under the beam does not
indicate the level of concentration of resplrable asbestos dusti
this must be measured by one of the approved sampling techniques.
The Approach to Control
In seeking the most effective means of reducing risks to
health by control all the available methods should be considered.
These will be well known to most delegates, but recapitulation may
be worthwhile. They arei
797
1.
Modification of the product so that it is less
likely to emit dust.
2.
Elimination of the duet producing operation or
process.
3 . Suppression of dust - for example, by damping.
4.
Avoidance of personnel exposure by mechanisation.
5.
Enclosure, usually in combination with exhaust
ventilation.
6.
Exhaust ventilation
7.
Good factory hygiene.
8.
Personal protection.
(dust extraction).
Personal protection is deliberately placed last.
It should
be regarded as the line of last resort where all other measures
are impractical or insufficiently effective, such as during breakdown, emergency or maintenance operations.
It must not be regard-
ed as an alternative to other practical forms of control.
Work Procedures
Coupled with these approaches, and essential to them, is the
establishment and careful observance of work practices which will
contribute to the control of risk.
There are many substances
in common use which could be highly dangerous if not used properly, i.e. by the scrupulous observance of
certain rules.
In the
prevention of occupational risk in the use of many asbestoscontaining products, correct work practices have been established
which, conscientiously applied, prevent the possibility of harm-
798
ful dust emission.
The essential requirements here are not only
well thought-out methods and equipment, but sound training and
effective supervision.
This particularly applies to work away
from static workshop conditions and facilities.
Record of Progress
Those who have conscientiously applied themselves to the
prevention of asbestosis - and any other asbestos related disease have some reason to be proud of the extent to which their dedication has achieved such greatly improved control, especially during
the last decade.
It should be emphasized that until little more
than ten years ago, plant engineers and managers had only the
most general direction of their efforts from medical and scientific
experts.
With the introduction of the sampling and spotting
technique referred to earlier, for the first time they were able
to focus their efforts on the vital part of a machine or operation
and check on the results obtained by measurement.
Some idea of the progress made possible by systematic attentic
to first-priority problems and by regular and consistent monitoring
- "control accounting" - can be gained by the following comparisons
Table anf figure 1 covers six factory locations in different
parts of the U.K. and relates to three different types of product
containing asbestos.
The Improvement between 1971 and 1978 speaks
for itself.
Table 1
The second figure shows progress made in one factory in
799
Denmark between 1971 and 1975, indicated by the decrease in the
number of persons whose occupation fell within the higher of
the concentration groups.
Conclusion
Regrettably it has to be recognised that this standard of
control is not universal.
In most industrial countries there
are now laws which require measures to be taken similar to those
recommended by ILO in 1974.
The responsible firms in the asbestos
industry in those countries have already developed control techniques to an advanced stage and are giving a lead in many other
Q
states where statutory requirements have not yet been introduced.
But, as with many other occupational hazards, the process of
education of managers and workers to recognise and observe safe
work practices is one requiring skill, experience and enormous
patience and dedication.
It will require the combined and co-
operative efforts of government, workers and managements, and
it is a prime objective of the international asbestos industry
to take a responsible lead in ensuring a consistent and effective
level of control for the prevention of health risks in the use
of asbestos.
The ILO Booklet "Asbestos Health Risks and Their Prevention"
(No. 30 in ILO Occupational Safety and Health Series) first published in 1974, provides practical guidelines for the control
of risk bases on a very thorough and unprejudiced review of the
evidence available.
Although this review is now four years old,
the advice of the experts from government, trades unions and
8oo
industry contained in the report is just as valid today.
Indeed
if all the member states of ILO had followed this advice, perhaps
we should have heard less of the often emotional demands for unnecessarily extreme measures which have so confused the issue
in recent years.
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REFERENCES
1.
Report on Effects of Asbestos Dust on the Lungs and Dust Suppression
in the Asbestos Industry.
Merewether and Price, HMSO, 1930.
2.
Report on Conferences between Employers and Inspectors concerning
Methods for Suppressing Dust in Asbestos Textile Factories, HMSO, 1931••
3.
Asbestos Industry Regulations 1931.
4.
Hygiene Standards for Chrysotile Asbestos Dust.
Hygiene Society, Pergamon Press, 1968.
5.
Asbestosis in Great Britain.
McVittie.
Conference on Biological Effects of Asbestos.1964.
6.
Control of Asbestos Dust - Technical Data Note 35.
Inspectorate,1972.
7.
Asbestos: Health Risks and Their Prevention.
Occupational Safety and
Health Series No. 30.
International Labour Office, 1973.
8.
The Control of Asbestos Dust - Recommended Control Procedures.
Asbestos International Association, 1978.
8o5
HM Factory Inspectorate.
British Occupational
HM Factory
THE ENVIRONMENTAL DATA BASE FOR PREVENTION STUDIES IN QUEBEC
Graham W. Glbbs
Occupational Health and Safety Unit,
Department of Epidemiology and Health,
McGlll University,
Montreal, Quebec, Canada
The setting of alr-quallty standards In the workplace to
reduce the risks of asbestos-related diseases to levels which
are acceptable to the worker and society requires a knowledge
of the relationship between exposure and response.
While In-
dices of "health effect" are In need of refinement and standardisation to permit valid comparisons between the health experience
of various occupational groups, I will restrict my discussion
today to the problem of exposure assessment.
The main factors Involved In the production of health effect
are the quality and quantity of dust, the duration and pattern of
exposure, and individual factors.
By quality of dust I refer to fibre type, fibre dimensions,
shape, surface characteristics, other minerals, trace, elements
and organic contaminants.
The quantitative aspects of
exposure will be discussed later.
Duration of exposure Is an Important Index of exposure, but
of limited usefulness on Its own, unless the other parameters of
exposure are static.
The pattern of exposure (e.g. short period high v s long term
low) may be Important, especially when lung clearance mechanisms
might be overwhelmed.
Time since first exposure Is Important, but alone does not
8o7
provide Information which can be used to prevent health effects.
Individual factors and susceptibility include age, other
diseases, particle clearance rates, and other host factors as
well as variations in level of exposure related to work practices.
The latter is of increasing importance in considerations of exposure assessment.
Other agents or factors include smoking habits, general air
pollution, etc.
which might influence particle behaviour or
effects.
That all varieties of asbestos present the same level of
health risks for the same level of exposure is logically unlikely.
Fibre types differ chemically, mineralogically and in physical
dimensions, and specific health effects do occur at different
rates for persons exposed to different fibre types.
In order to provide information on one variety of asbestos
(chrysotile), an epidemiological investigation of the relationships
between exposure and mortality, pulmonary function, symptoms and
radiological changes in Quebec asbestos miners and millers was
initiated by Dr. J. C. McDonald in 1966. The methods and results
of these studies have been published elsewhere.
However, the
environmental data used in these epidemiological studies provide
one example of how indices of exposure can be developed, their
problems, limitations and validity.
Considerations in the selection of an appropriate index of
dust exposure are threefold!
1)
To derive a numerical value for levels of exposure
808
which produces various risks of health effect, It is
necessary to base the index on measurement of environmental conditions.
Measurements of personal exposure
would be ideal but are rarely available for the past.
2) The index of exposure should have a good chance of relating to the measured health effect.
3) As the health effects being measured probably result
from exposures 20-30 years ago, it is necessary to be
able to assess the levels of past exposure.
Asbestos has been implicated in lung fibrosis, in producing
increased risks of lung cancer, gastro-intestinal, and laryngeal
cancers, and, except for anthophyllite, is associated with malignant mesothelioma.
It is therefore quite possible for different
health effects to be related to different parameters of the asbestos
dusts to which workers are exposed.
Indeed primary malignant meso-
thelial tumours may be related to the presence of fibres of certain dimensions in the inhaled dust cloud.
In the Quebec chrysotile asbestos mining industry, measurements of airborne dust were made by the same observer since the
late 1940's using the midget impinger method.
This method of
dust measurement, which formed the basis for standards in the asbestos industry in North America for almost 30 years, is inefficient
for
the collection of fibres, the count being based main-
ly on particles. As particles observed are essentially greater
than 1.0 AM in diameter, it is likely that counts reflect the
8o9
airborne respirable mass concentration but this remains to be
demonstrated.
Although some counts of fibres using the midget
impinger were made in the past, the low efficiency of the impinger for fibres at the time of the Initial studies forced us
to rely on the particle counts in million particles per cubic
feet.
As measurements were made at some mills before dust
controls were installed, they provided a useful bench mark for
assessment of earlier levels of exposure in the industry.
Based
on the midget impinger measurements, discussions with older employees and management, dates of ventilation improvements and
process changes, we constructed a table of dust levels for each
area in which workers might be employed.
From a description of
the time spent in various locations, we derived for each job,
for each year since the industry began in 1878 an index of
dust exposure.
Using the work history records for each employee
(some 28,000) taking account of the Job and hours of work, we calculated for each worker a dust index expressed as the product
of exposure time and dust concentration for all jobs on which
men had worked.
We also calculated dust indices weighted for
physical effort, physical application and weighted by the time
that the dust had been able to act on the lung.
Some of the limitations in the data were as follows i
Dust surveys were conducted at irregular intervals.
Individual
work practices may have permitted exposure above or below the
ambient concentrations.
While the conditions under which the
surveys were conducted were reasonably well documented, the
measurements were not made primarily for health studies, but for
81 o
evaluation of environmental quality.
The irapinger samples were
collected over relatively short periods (10 minutes), and the
lmpinger is known to be inefficient for the collection of fibres.
It was necessary to assess levels in periods prior to measurements
being made.
Nevertheless, the patterns of dustiness as recorded
by the midget lmpinger coincided with the known level of environmental control and provided a useful data base for the establishment of an index of exposure.
The validity of an exposure index is checked by its ability
to predict health effects.
In the study of mortality of Quebec
miners and millers, the relative risk of death from respiratory
cancer showed an extremely good relationship to dust exposure level.
In the case of radiological changes, the age-standardised prevalence of irregular small opacities (1/0 or more), in workers
in one mining area (Thetford Mines) showed a gradient with dust
exposure, but the highest correlation coefficient was only 0.27.
In the other asbestos mining area there did not appear to be any
meaningful relationship.
The weighted indices produced only
minor improvements in correlations with some abnormalities.
In
a longitudinal study Liddell et al., also found that associations
between radiological responses and measures of asbestos exposure
were weak.
Whether this is due to an inappropriate index of
exposure, individual differences in level of exposure or susceptibility factors is not known.
Breathlessness related reasonably well to the dust index,
and certain pulmonary function changes were also sensible related
to exposure.
811
It therefore appears that the dust index based on midget
impinger measurements reflects in some way the parameters related
to increased risk of mortality from lung cancer among Quebec
chrysotile mines«
Environmental standards for asbestos are now almost universally based on fibre counts using the membrane filter method*
is also so in the Quebec asbestos mines and mills.
This
It was there-
fore important to examine the relationships between fibre exposure
and indices of health in that industry to determine the validity
of using fibre counts for the prevention of asbestos-related
disease.
A study is now underway to examine the relationships between
mortality from mesothelioma, lung cancer, gastro-intestinal
tumours, cancer of the larynx, penunoconiosis and fibre exposure
as measured by the membrane filter method.
We are also examining
the relationships between radiological outcome and fibre exposure.
This presents a special difficulty as the membrane filter method
was not introduced until the 1970s and no single conversion factor
was found between midger impinger and membrane-filter fibre counts
for the Quebec mills.
We have therefore compiled all fibre measu-
rements and midget impinger measurements with a view to determining appropriate conversion factors for certain work areas and in
conjunction with environmental control data and midget impinger
counts to assess past fibre exposures.
The case control approach
permits us to work with a relatively small number of persons (1500)
from whom we have checked occupational histories, and to examine
exposures for each individual.
812
In some instances, past dust measurements do not exist.
Another approach to the assessment of past exposures has been
used in a study of employees in a textile manufacturing plant.
In order to assess the past exposure of employees we asked five
members of management and five employees with long services in the
industry to rank on scale 0-9 the relative dustiness of the environment in the workplace at 5 year intervals since the plant began
production.
These rankings were performed independently.
There
was reasonably good agreement when conditions were dusty but
poorer agreement for more recent conditions.
In order to get an
idea of what the various categories might mean in terms of fibre
concentration we conducted environmental surveys at the plant.
We then attempted to relate the categories of dust
exposure with
the measurements of fibre for the various locations and found that
for the first 3 categories the actual measured airborne fibre concentrations were not too different from one another, but that measure
ments of fibre concentration did increase in a meaningful way for
the next two categories. As there were no present-day operations
ranker as category 6 or greater, we do not know what these concentrations were.
However, the main interest Is the health risks for
persons exposed at the lower end of the scale as it is recognised
that health risks are elevated In high exposure situations. Although the rating of exposures by workers is subjective, backed up
by environmental survey to check actual airborne fibre concentrations, such an approach may be useful In some situations.
In conclusion studies in the Quebec Mining and Milling Industry
have shown that indices of dust exposure based on the midget im-
813
plnger can relate well to lung cancer mortality and demonstrate
clearly exposure-response relationships.
Whether membrane filter
counts relate as well remains to be demonstrated.
may improve the prediction
(symptoms and function).
Fibre counts
of radiological and other changes
For the studies of the Incidence of
radiological changes, more detail concerning individual differences
in exposure will be necessary before reaching conclusions that
"individual susceptibility" Is the main rason for poor relationships with exposure.
The relationships between exposure and res-
ponse In the Quebec asbestos mining Industry may not be extrapolatable to other work environments where fibre type, associated
dusts and fibre characteristics may be different.
The Quebec
study has Indicated that a single Index may not satisfactorily
relate to all health effects. There Is a need for uniformity In
the measurement and recording of environmental data and a critical
evaluation of the Indices used In epidemiological studies.
In-
vestigators should be encouraged to examine other. Indices of dust
exposure In parallel with those based on the membrane filter
method.
The validity of the dust or fibre Index should be evaluated
on Its ability to predict health effects and to reduce health
risks.
This should not be overlooked In providing the environ-
mental data base for future epidemiological surveillance or studies
of asbestos-exposed workers.
814
PROTECTION AGAINST QUARTZ AND ASBESTOS DUST EXPOSURES AT
WORKPLACES
Regulations and Guidelines in the Federal Republic of
Germany
A. Schütz
Dust Research Institute of the Central Association of
Industrial Injuries Insurance Institutes, Bonn, Federal
Republic of Germany
Among occupational diseases, the lung conditions silicosis
and asbestosis, caused by quartz and asbestos dusts, are still
widespread.
Asbestos dust is also capable of provoking carci-
noma and mesothelioma.
Table 1 shows the development of these
diseases in the Federal Republic of Germany since 1950. The
number of silicosis and silicotuberculosis cases
has continuous
ly decreased since theni at present their number is only about
one sixth of the cases compensated in 1950. The total number
of asbestosis cases is essentially lowerj since 1950, however,
an increasing trend can be noted.
Particularly, the number of
cases of lung cancer and mesothelioma due to asbestos dust has
increased.
Table li Annually compensated cases of occupational diseases
caused by quartz and asbestos dust
Year
1950
1960
1965
1970
1972
1975
1976
1977
Quartz Fine Dust
Silicosi s Silicotuberculosis
6616
3791
2416
1295
1272
1088
976
1052
924
454
393
227
256
221
184
155
Asbestos Fine Dust
Asbestosis
Lung Cancer+
Mesothelioma
5
23
47
63
77
75
87
62
815
.
3
2
7
15
20
26
In order to protect employees against quartz and asbestos
dust, extensive regulations and guidelines have been established
in the Federal Republic of Germany.
They apply to every factory
handling materials containing quartz or asbestos that may release
fine dust.
1.
The following regulations are the most importanti
Enlisting of factories and exposed employees
Every factory handling materials containing asbestos or more
than 2% of quartz is obliged to inform the authority responsible for occupational health. This information is not
required if the treatment of these materials does not induce
dust production.
For the purpose of enlisting factories and
exposed employees handling asbestos a central office was established by the Industrial Injuries Insurance Institutes.
According to the present survey about 50,000 persons from
about 5,000 factories are exposed to asbestos dust in the
Federal Republic of Germany.
2.
Measurement and evaluation of dust exposure
Table 2 shows the currently admissible limit values for quartz
and asbestos fine dust.
Concentrations of respirable dust are
restricted to a total value of 4,0 mg/m
at workplaces where
the fine dust includes quartz or
asbestos proportions. The
3
quartz fine dust concentration must not exceed 0,15 mg/m i for
the asbestos modifications chrysotile and amosite the value must
3
be below 0,10 mg/m . Besides, the asbestos fibre concentration
3
must not be above 2 f/cm .
816
Table 2i Threshold limits for quartz and asbestos
Material
Threshold limit
rag/m3
Quartz fine dust
Asbestos fine dust
(Chrysotlle, amoslte)
Fine dust (In total)
(f/cm 3 ) + )
0,15
0,10
4,0
2,0
' fibre length> 5jura and
fibre diameter < 3 /jm
Measurements of the fine-dust mass concentration of quartz
and asbestos are carried out at workplaces by means of special
dust sampling equipment and subsequent radiographic or lnfraredspectrographlc analysis In laboratories«
Assessments are made by
comparison between measuring results and the corresponding allowable
threshold limits*
In order to obtain uniform information regard-
ing the question of exceeding or falling short of limit values,
criteria for sampling and analysis, employee exposure monitoring
programs, and statistical evaluation of the measuring results were
established in a guideline by the Industrial Injuries Insurance
Institutes.
For example, this guideline includes instructions
regarding sampler position, frequency and duration of the required
measurements as well as confidence Intervals for random samples.
3. Medical surveillance
The employer is obliged to provide medical surveillance for
each employee exposed to quartz or asbestos dust. Exemptions
from this obligation are only possible if it has been ascertained
817
by special measurement techniques or medical surveillance tests
that there are no health risks»
The extent of the medical sur-
veillance was fixed in a guideline of the Industrial Injuries
Insurance Institutes.
-
One has to distinguish betweeni
Pre-employment medical examinations i They should be carried
our before employment starts»
The employer is allowed to en-
gage an employee only If no objections against employment are
raised by the physician.
-
Periodic medical examinations i They are to be performed at
maximum intervals of 3 years.
In particular cases these in-
tervals may be shortened (or prolonged) if this appears necessary because of the employee's physical condition or exposure
conditions.
Follow-up medical examinations i They are carried out only
in case of asbestos exposure after termination of exposure
at five years' Intervals.
4.
Substitutes for asbestos and quartz
Within the framework of preventive measures the prime question
is the replacement of quartz or asbestos-containing materials by
less harmful substances, of course. According to the existing
regulations and codes of practice it has to be checked always
whether substitutes are available.
In several cases this could
be achieved by intensified efforts.
-
Some examples arei
blasting agents, polishing and grinding materials, moulding
sands which are free from quartz or have
proportions.
818
only low quartz
Insulating and filter materials free from asbestos.
In the Federal Republic of Germany the use of quartz sand
for blasting has been prohibited.
At present, certain restrictions
for the use of asbestos are discussed by experts in the European
Community.
5.
Technical and personal protective measures
According to the existing regulations and guidelines the
following order of priority for preventive measures has to be observed«
change of process to prevent dust occurrence at workplaces
or non-employment in critical areas (e.g. wet instead of dry
processing, automatisation).
installation of devices on dust producing machines and equipment
to avoid dust spread at workplaces (e .g. complete enclosure
of equipment and operation under negative pressure, complete
dust exhaustion at the source)
ventilation of the entire work room or workplace, use of dusttight cabins
use of respirators (filter or closed-circuit breathing aparatus)
As respirators always mean an additional strain for the wearer
they can In general only be used for short periods of time and for
special purposes like repair work.
They must not replace technical
prevention measures.
There are special regulations for exhaust air contaminated
by quartz or asbestos dust.
This air has to be sufficiently cleanee
and eliminated in a manner that excludes health hazards.
Each re-
circulation of cleaned air into the work rooms for processing or
819
energy-saving reasons requires a permission.
Permission is grant-
ed if It is proved that the fine dust concentration of the return
q
air is below 0,1 mg/m .
6.
Checking of protective devices
Devices which are used frequently and in large numbers for
the protection against quartz and asbestos dust require type
testing.
This kind of testing is performed fort
small dust collectors attached to machines as independent units
which return the cleaned exhaust air directly to work rooms i
-
mobile vacuum cleaners and vacuum sweepers particularly used
for floor cleaningi
respirators.
The requirements to be met for these devices are fixed in
special guidelines.
For instance, the filter material used in
fine dust collectors must show a filtering efficiency of>99%
for the use in factories handling quartz and>99,5% for factories
handling asbestos«
2
hour by 1 m
Besides, the air quantity to be cleaned per
3
filter surface is limited to 120 m . Certain insti-
tutes, e.g. the Oust Research Institute, are authorized to perform these tests. The approved devices are provided with a test
certificate and are particularly recommended for the use in
factories.
Conclusion
The present regulations and guidelines applicable in the
Federal Republic of Germany for the protection against quartz
82o
and asbestos dust have primarily been elaborated by the Industri.
Injuries Insurance Institutes! Their application in the field
is controlled by the Technical Inspection Service of the Industrial Injuries Insurance Institutes.
The Dust Research In-
stitute has the task of developing dust measuring and evaluation
methods, of carrying out measurements, of advising plants about
protective measures and of checking protective equipment.
821
References
(1) Verordnung zur Änderung der 7. BerufskrankheitenVerordnung. 8. Dez. 1976, Bundesgesetzblatt I,
S. 3329/3337
(2) Geschäfts- und Rechnungsberichte der gewerblichen
Berufsgenossenschaften für das Jahr 1977
(3) Unfallverhütungsvorschrift VBG 119 "Schutz gegen
gesundheitsgefährlichen mineralischen Staub" vom
1.4.1973
(4) Verordnung über gefährliche Arbeitsstoffe vom 8.9.1975
(5) Regeln zur Messung und Beurteilung gesundheitsgefährlicher mineralischer Stäube (ZU 1/561). Herausgegeben vom Hauptverband der gewerblichen Berufsgenossenschaften (1977), Carl Heymanns Verlag, Köln
(6) Berufsgenossenschaftliche Grundsätze für arbeitsmedizinische Vorsorgeuntersuchungen. Herausgeber: Hauptverband der gewerblichen Berufsgenossenschaften, Bonn;
A.W. Gentner Verlag, Stuttgart
(7) Atemschutzmerkblatt ZH 1/134. Carl Heymanns Verlag,
Köln
(8) Einrichtungen zum Abscheiden gesundheitsgefährlicher
Stäube mit Rückführung der Reinluft in die Arbeitsräume. ZH 1/487, Herausgeber: Hauptverband der gewerblichen Berufsgenossenschaften (1973), Carl Heymanns Verlag, Köln
P?2.
IX/6
EFFICACITE DCS MASQUES ANTIP0IJ3SIERES VIS-A-VIS DE L'AflIANTE
COMPARAISONS'DES DIFFERENTES TECHMIDIIES DE COMPTAGE
DFS FIBRES D'AMIANTE
B. CARTON.
E. KAUFFER, 3.C. VIGNERON st fi. VILLA
I.N.R.S.
Vandoeuvre - lea - Nancy
France.
1.- INTRODUCTION
En France une norme AFNOR (NF S 76-101 et 201) décrit les
caractéristiques minimales des demi-masques antipoussieres:
efficacité* mesurée au bleu de méthylène meilleure que 85%,
colmatage meilleur que 400 mg de silice a 1 mbar et pertes
de charges inspiratoires et sxpiratolres inférieures (a
quatre débits de mesure) a certeines limites.
A intervalles réguliers, une campagne de mesure de la conformité des modeles commercialise'*en FRANCE est faite par
l'INRS.
Ainsi en 1976 sur 71 modeles testés, 27 étaient
conformas a la norme.
Il a paru intéressant, compte tenu du danger particulier
des poussières d'amiante, de compléter ces mesures par une
évaluation de la permeance aux fibres d'amiante. La mesure a
été faite dans deux atmospheres industrielles.
2.- METHODE DE MESURE
2.1 Le montage
Trois prélèvements sont faits simultanément a 1,50m
du sol:
823
- un orélevement d'ambiance selon la méthode l/min
classique associant le ROTHEROE MITCHELL régla a
2 l/min et la filtre MILLIPuRE 0,8 pm;
- deux prélèvements sur chacune des deux tetes. On
fixe de facon Stanche le demi-masque étudiéjl'air filtré
par le masque est refiltrô par un filtre SART0-
RIUS 0,8 pm, la débit ast continu.
Chaque masure est répétée deux fois dans des conditions
identiques.
Les trois surfaces de filtration (deux mas-
ques et la filtre d'ambiance) sont aussi proches l'une
de l'autre qu'il est possible.
2.2 Ambiance
La premiara série a été faite dans l'atelier des dalles
d'une entreprise fabriquant du revêtement de sol. L'amiante utilisé est le Chrysotils, la moyenne des Concansa
trations mesurées est de 1,25 fibre /cm
avec un écart
type de 0,5 fibre/cm .
La deuxième série a été faite dans un atelier d'une autre société du même type que la précédente.La encore le chrysolite
est utilisé; la moyenne des concentrations mesurées
est de 1,25 fibre/cm
avec un écart type de 0,5 fibre/cm .
2.3 Choix des débitas
On a renroupé les modeles de facon que les vitesses frontales de nassane de l'air sur le médium filtrant soient
aussi peu dispersées Q U O possible et comparables a celles
de l'essai au bleu de methylene.
L'essai dure 30 minutes
(tableau 1 ) . Lo volume d'air passant a travers le masque
est de plusieurs metres cubes.
824
3
• -p.ETEnniNATION
PES^KRfíZMCZS,
Elle passe par la mesure de la concentration C n initiale et
de la concentration C. derrière le masque. La permeance est
le rapport CQ/C., complément a 1 de l'efficacité.
On peut évaluer CQ et C. soit par microscopie optique a contraste de phase après transparisation, soit par microscopie
électronique (balayage ou transmission).
On a donc mesura plusieurs permeances:
-
une permeance "optique" ou C„ et C, sont évaluées
par comptage en microscopie optique (n„n) des fibres
de longueur supérieure à 5 pm;
une permeance "microscope électronique a balayaqe"
(n___) ou C-, et C, sont évaluées au P1EB a un grossissement de 500 "fraticule" de même surface qu'en microscopie optique et en comptant les fibres de longueur
supérieure a 5 pm;
-
une permeance "microscope électronique a transmission"
par comptage sur photographie de toutes les fibres
(n „p.- totale). Dans ce dernier cas on compte les fibriles élémentaires si elles ont une longueur suffi*
sante da l'ordre du micrometre).
(suite tableau No.l)
825
Tableau 1 - MODELES TESTES
SURFACE
(cm 2 )
270
415
450
5D0
530
530
560
600
710
760
760
104 0
530
|
VITESSE
(cm/s)
PERMEANCE
AU BLEU DE
METHYLENE
~~7T~
7
2,4
0,5
0,3
0,3
2,1
0,4
0,9
1,5
6,6
3,7
0,5
5,0
7,6
7
6
6
5,5
5
5
4
4
4
3
5
44
33
20
14
16
11
11
4
4
4
2
2
27
30
50
77
64
<U
100
250
250
270
4500
50
-J.
4,6
2,3
0,7
4,7
2,0
1,9
1,5
14,9
2,0
2,4
0,3
0,3
.
826
MEDIUM FILTRANT
i
Ì
1
.
, .
papier épais
épais
papier
papier épais
papier plissé
feutre
papier épais
papier épais
papier plissé
papier plissé
papier plissé
papier plissa
papier piissé
foutre
matériau ouaté
matériau ouaté
matériau ouaté
matériau ouaté
matériau ouaté
feutre
J
feutre
! panier épais
j panier épais
i papier épais
! papier épais
i napier plissé
_,
i
;
',
¡
!
;
!
;
j
4.- MODELES TRAITES
CG sont les modeles conformes en 1976 aux normes AFNOR
n'ont J'efficacité mesurée au bleu de méthylène est dont
meilleure que 855?.
Au total, 22 media filtrants ont été testés dans deux
entreprises. Chaque essai a été doublé.
La liste des modeles av/ec le numéro de code correspondant
finure dans le tableau 1.
5..- RESULTATS
5.1 Remarque préliminaire
L'exploitation des essais n'a été maná« a bien qu'après passage au four a ozone. L'ensemble dea filtres
SARTORIOS situés derrière les masquas afits'calciné
at le comptage par microscopie optique s'est révélé
comparable au comptage par microscopie a baleyaqe
ce qui est normal pour la mame catégorie d'objetä
comptés et le même protocole de comptage.
5.2 Permeance ; fibres de longueur supérieure a 5 pu
Dans la grande majorité des cas, la permeance optique
est tres proche de la permeance mesurée au microscope
à balayage, les moyennes sur l'ensemble des mesures
sont comparables. On peut donc calculer une permeance moyenne
exprimée en pourcentage de fibres de
lonnueur supérieure a 5 pm traversant le médium filtrant qui est faible, en général inférieure a 1 #.
82?
5.3 Permeance :_ toutes fibres
Apres calcination, on a compta avant et apres la
masque le nnmhre de fibres présentes, quels que
soient leur longueur et leur diamètre. Une fibre
est un objet de rapport lonnueur sur diamètre au
moins égal a trois, on a compté sur photographia
les fibrilles élémentaires de longueur supérieure
a 1 pm (photonraphie prise a 660 et agrandie 4
fois).
Les résultats figurent sur le tableau II, la permeance mesurée de cette facon est supérieure a la
permeance mesurée en comptant les fibres de longueur
supérieure a 5 pm de fa^on significative.
6.- DISCUSSION
6.1 La cohérence entre les deux séries de mesures est
acceptable pour tous les types de comptage.
U v a
trois exceptions (numéros 20 - 12 et 64) ou les résultats d'une série a l'autre sont tres différents;
il est possible que les chiffre élevés soient dus
a une mauvaise étancheité du masque.
Dans trois cas, la mesure a été faite sur petit et
nrand support : les résultats obtenus sont en bon
accord:
De nlus len numéros 51 et 49 sont constitues du mame
matériau filtrant; la encore les résultats sont en
bon accord.
828
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- 0',t
0,9
-0,6
0,C
1.4
- 0,7
»•*.:.',;
1,8
- 1,2
0,85 - î , 3 5
•-. ° « 4 '
•
0,7
2.0
1
-7
1
1,1
1.6
"'
1.15
2,¡"< i •
i
•
1.3
1.5,--/; .1 1,6 ' - f ^ 1 :
* apraa c a l c i n â t Ion
_-*
829
i
•1
y
^
!•)'
6.2 Si on porte par exemple la moyenne n des permeances
mesurée (fibres rie lonnueur supérieure a 5 pm) en
fonction de la vitesse frontale da passaqe de l'air
a travers le medium filtrant : on s'aperçoit que la
permeance a tendancB a croître quand la vitesse de
filtration, a debit égal, est la plus faible.
6.3 Les permeances mesurées sont nettement inférieures
aux permeances mesurées au bleu de méthylène. Neuf
modelas sur 10 ont une permeance inférieure a 2%, ce
qui vaut dire qu'ils ne laissent passar que 2 fibres
sur IDO de lonqueur supérieure a 5 pm au maximum.
PTBS de un modele sur 2 a une permeance "toutes fibres" inférieure a 2 #.
CONCLUSIONS
On a mesuré la permeance des media filtrants conforme a
la norme A FM PR. Le résultat est exprimé en % du nombre
dn fibres. Aucune mesure de la perte de charge, n'a été"
faite. L'essai est comparable à l'essai au bleu de méthylène prévu par la norme AFNOR pour ce qui est des vitesses de filtration.
La permeance mesuran aux fibres d'amiante est plus fnible
nue la permeance mesurée au bleu de methylene. On peut dire nue les masques conformes a la norme NFS 76-2P1 arrêtent
au moins 95 fibres rie lonnueur supérieure a 5 nm sur 1PP.
Il n'y a pas d'autre liaison entre l'efficacité a l'amiante
et l'efficacité au bleu de methylene.
La tres bnnne efficacité mesurée ne fait pas de ce moyen
rie protection individuelle la nanacée. L'étanchRité au visant: midinern desriemi-masquRn(le projet rie norme du Comité européen de normalisation autorise 5'', de fuite) ne
permet pas rie les recommander nnur le travail dans des
83o
ambiances nolluécs par l'amianto mnme si l'efficacité du
médium filtrant sembla tras bonne, flieux vaudrait dann ces
conditions utiliser des masoues a adduction d'air ou a ventilation assistée.
Las résultats obtenus sont valables oour le Chrysotils. Pour
les fibres plus rinides (verre ou amosita), on peut s'attendre a des résultats comparables.
831
IX/7
CAS D ' A P P L I C A T I ™ D E LA C O N V E N T I O N OE L'CJIT ( M O . 139)
LE C A N C E R P R O F E S S I O N N E L , 1 9 7 4 , EN R E L A T I O N A V E C
SUR
LE F L O C A G E
A L ' A M I A N T E D E S S T R U C T U R E S NFTALLIOIIES E T D E S T U Y A U T E R I E S
D'UN
I N N E U B L E EN C O N S T R U C T I O N A G E N E V E
Dirscteur de l'Office d'inspection du travail de la République et Canton de Geneue, Suisse.
A. Degoumois
1ère étape - 1968 - Construction de l'immeuble de la télévision SuU_SB_ fran£ai_se à jGeneve.
Projection d'amiante sur la charpente métalliaue et les tuyauteries de chauffane, ventilation et eaux (prévention contre les incendies).
-
Plainte des voisins de l'immeuble en construction qui
constatent que des poussières d'amiante (duvets) se déposent sur les rebords dBS fenêtres et pénètrent a l'intérieur des locaux d'habitation et de travail.
Intervention de l'inspection du travail qui s'adresse à:
l'inspection de la construction pour que la projection d'amiante s'accompaqne d'une aspiration des poussières a la source.
la caisse de sécurité sociale pour faire porter aux
travailleurs exposés aux poussières des masques de
protection.
2eme étape - jna_rs_ 1978 - Les occupants de 1 ' immeuble tel évision
constatent la présence de duvets d'amiante derrière les radiateurs des locauj» de t r a v a il, en partie climatisés.
Plainte déposée a l'inspection du travail et traitée oar
un inspecteur du travail, docteur on physique et spécialiste
833
des problemas de toxiques et de poussières.
-
L'inspecteur prélevé des duvets d'amiante et les fait
analyser par le laboratoire de toxicologie industrielle.
-
Résultat de l'analyse: crocidolite (amiante bleu).
Quantitativement, la valeur maximale admise de 2 fibres/cm-' lors d'un prélèvement d'air n'est pas atteinte:
Décision de l'inspecteur du travail :
Exige de la direction de la télévision
>uisse - Française
(employeur), sur la base des articles 50 et SS de la Loi
sur le travail et de la convention 139 de l'OIT, et cela,
bien que la valeur limité ne soit pas atteinte:
-
Le nettoyage complet de tous les locaux de travail, étage
par étage.
-
L'enlèvement du revêtement d'amiante sur les poutres métalliques et les tuyauteries qui peuvent entrer en contact avec l'air respiré par les travailleurs ou le recouvrement de l'amiante par une peinture de fixation, innifune, de longue durée de résistance.
Copie de la décision est adressé aux syndicats des travailleurs.
3eme étape - juin 1978 - Réaction du directeur de l'inspection
du travail et de l'entreprise.
-
Réaction du directeur de l'inspection qui s'assure, pour
sauvegarder les dispositions du secret administratif
(article 41LT) que les svndicets ne réunissent que des
travailleurs de l'entreprise, ce qui est le cas.
834
-
Réaction de l'entreprise qui convoaue une conférence a
laquelle assistent:
l'inspection du travail (directeur et médecin-inspecteur) des spécialistes de toxicoloaie industrielle
des spécialistes de l'association
Suisse des fabri-
cants de produits a base d'amiante
-
la direction de l'entreprise
Lors de cette séance, le directeur de l'inspection du
travail soutient totalement la décision de l'inspecteur
du travail, ajoutant qu'il n'a aucune crainte relative a
un recours de droit public contre cette décision.
£5J!Le- étape - Décision de 1*entreprise
L'entreprise renonce a recourir et assume ses responsabilités face aux exiqences de l'inspection du travail.
-
Elle procede immédiatement au nettoyaoe complet des locaux.
Elle étudie présentement la meilleure solution pour éliminer le risque de désaqrôqation du revêtement d'amiante.
-
L'inspection du travail se met au service de l'entreprise
pour effectuer des mesures de quantité d'atniante sur les
lieux de travail.
coût de l'opération évalué a 1/2 million de
francs suisses
5eme étape - Information des travailleurs
Selon l'article 4 de la convention No.139, les travailleurs
qui sont ou qui furent en contact avec une substance concériqene doivent recevoir une information sur les conséquences qui peuvent résulter de cette contamination.
835
Si l'on peut, sans difficulté, donner cette information
aux travailleurs de l'immeuble de la télévision, le problème est plus difficile pour les travailleurs qui durant
les années 1967 et 1966 se trouvaient sur le chantier en
contact avec les poussières d'amiante.
L'inspecteur du travail est actuellement occupé a obtenir
la liste des entreprises qui ont construit l'immeuble pour
connaître les noms de leurs travailleurs a l'époque de la
construction et signaler a ces dernière qu'ils ont été en
contect avec un produit cancérigène.
La question que l'on peut cependant se poser est la suivante :
Est-ce qu'il conviant, après que dix ans ont passé depuis
cette exposition a l'amiante, de renseigner les travailleurs du chantier de construction de3 risques qu'ils courant?
836
I N D T C C
X. I.
S r e; s T
n
**' X
D.Ascarrunz ,
Rappor t.Bur
X. I I
V.V.Tkatchev.
Two-stage gravimetric method of dust concentration
measurement and its application In ore mines.
X. Ill
C.flmoudru
Problèmes méthodologiques actuales de la lutte contre
les Pneumoconioses dans les charbonnages français
X. IV
N.'dlles., F.Falrclouçih
Thu prevention and prevalence of Pneumoconiosis im
nei» south wales coal mlnlnq
X. V
V.S.Nikitin
Modern methods of dust control in oßen-pit mines in
the Soviet Union.
837
CONTROL Y SUPRESIÓN DE POLVO EN MINAS
Ing: Douglas Ascarrunz Eduardo.
Dirección General de Higiene y Seguridad Ocupacional.
Ministerio de Trabajo y Desarrollo Laboral.
La Paz - Bolivia.
ANTECEDENTES
Desde luego que las altas incidencias de silicosis, que se
presentan en la mineria boliviana no son justificables desde
ningún punto de vista. Sin embargo, se impone una explicación,
porque es inconcebible que no se tomen medidas más drásticas p¿
ra reducir el impacto de esta enfermedad.
Como historia, diríamos que,es posible que la silicosis se
manifestaba ya durante el Imperio de los Incas, sin. embargo no
se tienen citas específicas a éste respecto, lo.que indica que
no era un fenómeno muy aparente, máximo cuando se sabe que los
incas tenían una actitud muy avanzada, en lo que hoy se denomina
Salud Ocupacional. Se sabe, por ejemplo, que .al enterarse de
que la explotación de las minas de sinabrio suponía un riesgo probado, se prohibió la explotación de éstas. También se sabe que los incas compensaban el servicio en minas con privilegios
especiales, por ejemplo, se distribuía coca entre los mineros
para ayudarles a sobrellevar el rudo trabajo en regiones de
gran elevación y bajas'temperaturas. La coca, sabemos, estaba reservada a los nobles y altos funcionarios del gobierno imperi
al.
La conquista española trabajo un incremento descomunal en
el laboreo de minas y el sistema de encomiendas que en principio no suponía un regimen de abuso; pues conformaba hábilmente
con los sistemas incaicos de servicio gratuito al gobierno y sil
ponía solo un servicio de 5 años de trabajo en minas; se convirtió en un sistema de explotación inhumano en manos de los aventureros que se instalaron en el Nuevo Mundo como propietarios de minas.
839
Posteriormente en las denuncias que hicieron de éste siste
ma los propios españoles, no se menciona especificamente como un problema la enfermedad que deviene de respirar polvo. Es muy
posible que los problemas de seguridad así como otnos abusos re
legaban la silicosis a un plano secundario. Por ejemplo, I03
servicios de encomienda.debían durar solo 5 años, sin. embargo,
se dilataban mañosamente hasta el doble o triple de éste período. En algunos casos los turnos de trabajo se extendían por semanas enteras en que los mineros vivián bajo tierra. Tal situación es explicable que relegue la silicosis a un plano secundario. .Además, la expectancia de vida de la época debió ser b a s tante baja de modo que la silicosis no-llegó.a. ser un impacto disernible en la población minera de la época.
La República trajo la abolición de la encomienda y por ende los abusos a que ésta.daba lugar. Además, como la mano de
obra dejó de ser gratuita, por primera vez se empezó a aplicar
métodos más eficaces de explotación minera, empero, el problema
de la silicosis tampoco se destacó, posiblemente porque las cori
diciones generales cambiaban muy paulatinamente.
En realidad, el problema en Bolivia no se hizo aparente
hasta que la expectancia de vida hubo experimentado un inerea¡eii
to y los métodos de minería sufrieran un notable cambio con la
introducción de los métodosrieumáticos,de perforación, incre-mentando de éste modo el riesgo silicógeno. De ésta época datan
las primeras menciones del "mal de mina." cuya presencia se va
haciendo más importante con el paso del tiempo.
En la época de la segunda guerra mundial las exigencias de
producción llevaron a investigar las razones.del bajo rendimien.
to del minero boliviano y se identifican las condiciones de higiene y seguridad como factores predominantes. Desde entonces se emprenden los trabajos que permitirían puntualizar el p r o blema.
840
Como la silicosis no es una enfermedad.deformante o particularmente dolorosa, es en realidad un estado con el que es relativamente fácil de vivir. Tampoco es la silicosis una enfermée
dad mortal, sino que más bien acorta la vida natural, no se han
extremado acciones preventivas como ha ocurrido con otras enfer
medades.
ESTABLECIMIENTO DE CONTROLES
Las acciones de prevención se fijaron desde.un principio en el método más expedito, menos costoso y relativamente simple.
La distribución de mascaras contra el polvo, en el caso, de Boli
via. Estas eran particularmente inaprepiadas, pues a las defic¿
encias por demás conocidas, debe añadirse el hecho de que la re
sistencia que causa en la respiración la hace inútil a gran ele
vación. No obstante, ésta era la única acción preventiva estatuida en los primeros años de la nacionalización de la gran mi«
neria boliviana.
El principio de abatir polvo y ventilar minas es el objeti
vo de la empresa minera estatal (COMIBOL), pues ésta es la única forma efectiva de reducir el polvo silicógeno. Este objetivo tiene limitaciones generalmente de orden económico. El estado al hacerse cargo de minas con gran desarrollo en las que no
se contemplo la ventilación forzada, encontró que debía hacer grandes inversiones que no podían pagarse bajo las condiciones
imperantes. Muchas de las minas de Comibol son marginales y se
las mantiene en trabajo solo por razones sociales.
La presión para ventilar las minas en escala integral es cada vez más fuerte y proviene del sector técnico, laboral, seguro social e incluso de las autoridades de gobierno.
841
Los logros alcanzados hasta ahora son muy dispares y van
ligados a la economía de la empresa, así también como la del
trabajador. Este último punto merece una explicación.
Las minas que explotan minerales de alta ley manejan volúmenes menores de carga produciendo menos polvo, pero lo más
importante es que pagan mejor a sus trabajadores y éstos es-tan dispuestos a usar como única medida de "protección., la mas
cara, ya que un sistema de ventilación integral vendría de he
cho a disminuir sus ganancias. Resulta entonces que cuando
una mina mejora sus leyes los incentivos para mejorar la protección del ambiente disminuyen en la misma proporción. Por otro lado la explotación de filones de baja ley requieren ma^
yor movimiento de carga con el inconveniente de que las ganan
cias son reducidas, en éste caso el trabajador insiste y pro^
mueve el sistema de ventilación integral, porque no tiene mucho que perder y por otra parte la ventilación integral la
permite mover mayores volúmenes de carga para poder compensar
sus bajas ganancias. Tal es el caso de la explotación en block
caving en la mina Siglo XX, en la que a insistencia de las
trabajadores se instaló el primer sistema de ventilación forzada en Comibol.
Como se presentan las cosas en el momento actual, la veri
tilación forzada tiene que imponerse aunque en forma paulatina y desigual, pues en algunas minas, la preparación de éstas
ya incluía un sistema integral de ventilación como ocurre con
mina Matilde que es una de las instalaciones mas modernas de
Comibol.
La mayor parte de las minas de Comibol dependen de la
ventilación natural, es decir se aprovechan las depresiones naturales que existen entre sus comunicaciones al exterior.
Este es un sistema limitado e inflexible. La tendencia actual
es optimizar estos sistemas y tratar en lo posible de estable
cer la ventilación forzada donde pueda ser financiada. Esto se manifiesta en una de las conclusiones del último seminario
gerencial minero de Comibol.
842
En'el desarrollo de la minería en general se distinguen tres etapas en la lucha contra la neuraoconiosis. Primero, se trabaja sin conocer el efecto que tiene el polvo contra la salud. Segundo, se detecta la causa y se emprunue un reconocimien.
to del problema y una evaluación de ambientes riesgosos. Tercj;
ro, se procede a establecer controles sistemáticos.
La segunda etapa suele ser la más larga y ésto se debe g¿
neralmente a que la supresión del polvo y la ventilación integral significan inversiones de importancia que debemos asegurarnos que la mina pueda pagar.
En la empresa privada esto se reduce a una cuestión conta
ble. En la empresa minera pública de Bolivia, las minas sin ejn
bargo pueden trabajar a pérdida durante largos periodos ya que
su cierre significaría un problema social mayor al de la silicosis.
Se puede decir que Bolivia esta francamente en el camimo
de intensificar controles de silicosis en todas sus formas de
explotación minera, ya sea pública, privada o en cooperativas.
Todos están concientes de ésta necesidad y esto se demuestra en las evaluaciones epidemiológicas más recientes que acusan niveles inferiores a los anteriores.
MEDIDAS DE CONTROL DE POLVO
Una de las primeras medidas, que se establecieron exitosa
mente como control dé la producción de polvo fué la prohibición
de perforar en seco.
La práctica de perforar en seco se prohibió def initivameri
te en el Reglamento Básico de Higiene y Seguridad Industrial promulgado en 1951, Pero anterior a ésta fecha, muchas de las
minas grandes ya no perforaban en seco por propia iniciativa,
sin embargo hasta 1965 se podían encontrar situaciones en las
que se contravenía esa disposición. Hoy podemos decir que las
843
contravenciones a ésta disposición son muy raras y ocurren scio
en minas muy chicas y por cortos períodos de tiempo.
La práctica de la perforación en húmedo es la primera med¿
da de control de silicosis que se puede decir que se ha impuesto en la minería boliviana en forma exitosa y definitiva.
Hasta el presente se sabe que el agua es el mejor medio de
abatir el polvo en su lugar de origen. Pero, la mejor forma de
usarla es una cuestión que depende de su disponibilidad, del
efecto que pueda tener en los estratos de la mina, en el traspoi*
te de carga y aún en el tratamiento metalúrgico del mineral;
por tanto su uso en la supresión del polvo se convierte en un problema técnico de bastante sofisticación.
La práctica actual en Bolivia, en aquellas minas que dispjj
nen de abundante agua, se reduce a mojar la carga quebrada, esto impide la resuspensión del polvo acentado, pero no tiene mucho efecto en el polvo en suspensión que es el que verdaderameri
te importa.
En diferentes épocas se han descrito y propuesto muchas
formas de usar el agua para abatir el polvo, estas propuestas van desde la dosificación de detergentes, el variado diseño de
atomizadores de agua, el uso de vapor de agua, la disposición de grandes bolsas de polietileno llenas de agua cerca de los lu
gares de disparo, de modo que la expansión subdita de los gases
se encargue de atomizarla y dispersarla conjuntamente con la nu
be de polvo.
En Bolivia no se ha practicado estos sistemas, porque sus
ventajas nunca se probaron a satisfacción o porque requerían
planificación técnica que resultaba poco práctica su generaliza.
ción.
844
El uso del agua, donde se puede usarla, no esta racionalizado y se reduce a instalar aspersores que no siempre son los apropiados, porque suprimen el polvo visible, es decir, el de gran tamaño de partícula y no. aatuan sobre el polvo de pequeño
tamaño de partícula, creando así una falsa seguridad. Consecueri
eia de éste factor es la recomendación enfática de no usar lava
dores de airé, que en algunas épocas se veía en algunas minas de Bolivia y que hoy se han descartado.
A través de la larga experiencia que se tiene evaluando ajn
bientes polvorientos en minas, se ha podido descubrir que cuando las condiciones de humedad del ambiente están en el punto de
rocío o muy cerca de éste, el polvo es suspensión es notablemeri
te reducido, en ocasiones, hasta podría decirse inexistente. EJJ
ta premisa se cumple independientemente de la temperatura ambieri
te y la elevación de la mina.
VENTILACIÓN
La ventilación tiene la enorme ventaja sobre la supresión
del polvo con agua de que su control puede ser más grosero, la
ventilación arrastra con todos los tamaños de polvo y por tanto
no se corre el riesgo de producir situaciones de falsa seguridad,
con la facilidad con que se producen en el abatimiento con agua.
En la ventilación de minas en Bolivia los primeros ventiladores se instalaron en mina Pulacayo desde la segunda década de
este siglo. El uso se debía, sin embargo, a las altas temperaturas que existían en las zonas de trabajo más que al control de silicosis.
La utilización de ventiladores de tamaño pequeño, nunca mayores a los 20.000 pies cúbicos por minuto se precticaba exclus^
vamente en minas con problemas de calor.
845
La mina Siglo XX fué la primera en usar ventiladores para
reducir el polvo en el trabajo de block caving.
En e-ste aspecto cabe mencionar también que la empresa pri
vada fué pionera en la instalación de ventilación forzada. Por
ejemplo, Mina Matilde fué la primera mina grande dotada de un
sistema integral de ventilación forzada, antes de producirse su reversion al estado. En- Mina Chojlla se instalaron ventila«
dores que contribuían al flujo natural de aire en forma muy
efectiva, y ésta es una mina privada.
La característica principal de la ventilación minera en Bolivia, al iniciarse esta práctica, es que no se dimensionaban técnicamente los ventiladores para los problemas existentes y a menudo se pecaba por exceso o defecto.
En Siglo XX, por ejemplo, se usaron los ventiladores que
sobraron cuando se cerro mina Pulacayo. Hoy se tiende a racionalizar la técnica de la ventilación poro por las razones anotadas al principio de esta síntesis su implantación es muy len
ta.
PROBLEMAS ESPECIALES DE LAS MEDIDAS DE CONTROL
La experiencia acumulada hasta ahora permite vislumbrar,
un efecto sinergético de la gran elevación sobre los factores
silicógenos, ésto tal vez no se debe a la gran elevación como
tal, sino al efecto de baja humedad relativa que reina en la generalidad de los ambientes de gran elevación.
Las instituciones dedicadas a la investigación de estos problemas tienen gran interés en descubrir y puntualizar los factores responsables de la notable incidencia de silicosis en
la minería boliviana. Desgraciadamente el accionar es siempre
lento y limitado a la disponibilidad de fondos para este estudio.
846
A manera de ejemplo a continuación anotamos una serie de
recomendaciones dadas a una empresa minera de tamaño grande, que son producto de un trabajo de evaluación de sus condiciones
y ambiente de trabajo:
a) Debe estudiarse los sistemas de preparación de cabos,
de ataque de taladros y/o de voladura de minerales a fin de re
ducir el actual consumo de explosivos a cantidades que fluctúen entre 0.5 - 1.0 libras/TMS. Con tal fin deberá llevarse un
control estricto del consumo, para evitar peligros en las labo
res vecinas la sustracción de este material por parte del personal, la generación innecesaria de gases, polvos producidos y
la pontecialidad de accidentes.
b) Debe racionalizarse la obligatoriedad del empleo de a.gua en la perforación para-cualquier actividad minera que gene
re polvo, las máquinas perforadoras deberán contar en sus sistemas de agua, con presiones mayores de tres (3) kilogramos/
centímetro cuadrado de sección hueca del barreno y una cantl-dad minima de 0.5 litros por segundo.
Debe educarseli personal en iniciar la perforación en húmedo.
Esta recomendación está relacionada con el mayor riesgo y
mayor número de perforistas y ayudantes encontrados enfermos.
c) Debe racionalizarse la obligatoriedad de emplear agua
en las operaciones de remoción, carguío, transporte y descarga
de material a fin de precipitar in situ gases y polvo remanentes, atrapados.
Esta recomendación está relacionada con el mayor riesgo y
elevado número de otras actividades con población afectadas,
(ver cuadro N°. 12).
847
Con tal fin, deben instalarse además, atomizadores hidroneumáticos en todos los puntos de generación de polvo.
d) Las recomendaciones B y C tienen de por sí, alta prioridad de ejecución inmediata en razón del alto contenido de ai.
lice libre encontrado en la roca madre (37»3Í)¡ la medida geométrica del diámetro de las partículas (1.35 micrones), todas
ellas inhalables y generadoras de silicosis.
e) Lo señalado en la recomendación D, aunadas a las condì
ciones gaseosas del aire ambiente producidas por un déficit de
ventilación de los lugares de trabajo, hace imperiosa la necesidad de instalar un ventilador principal del tipo axial de
100.000 pies cúbicos/minuto de capacidad, para reducir las cori
diciones riesgosas imperantes.
Debido a que volúmenes sustanciales de aire se pierden en
parajes abondonados tales lugares deberán sellarse hermética—
mente como medidas coadyuvantes a fin de hacer más efectivo lo
propuesto líneas arriba.
En la continuación de trabajos de desarrollo en frentes ciegos deberá instalar ventiladores auxiliares axiales de unos
3.000 pies cúbicos/minuto, que venzan una presión de ocho(8) pulgadas de agua, y con motores de ocho (8) caballos de fuerza.
El aire fresco deberá ser conducido a todo frente de trabajo,
por medio de mangas de ventilación.
Las características de estos sistemas auxiliares están
contempladas dentro del Informe. Se deberá capacitar adecuadamente una cuadrilla de ventilación, compuesta cuando menos, de
cinco (5) personas.
Para que el personal de interior mina no deteriore el equipo instalado, deberá cambiarse la denominación del "Bono de
Riesgo" por el de "Bono de Mantenimiento de Equipo".
848
Con el fin de iniciar los estudios preliminares de venti
lación el Departamento de Seguridad deberá desarrollar cuatro
aforos de ventilación natural(Marzo-Junio-Septiembre-Diciem-«í
bre), a fin de evaluar la influencia de las estaciones en la
ventilación de interior mina. La información recolectada se vaciará en planos de ventilación.
f) El Departamento de Seguridad no cuenta con personal suficiente para desarrollar acciones inherentes a la actividad, lo que le impide cumplir con sus funciones; efectuar acciones de Higiene Industrial Minera, desarrollar normas de S¿
guridad y Control; de Capacitación de Personal y Promoción de
la Seguridad; de Protección de Planta; y de Prevención de Per
didas; con tal fin es conveniente dotar a dicho Departamento
con personal profesional dedicado a tiempo completo en el desarrollo de las acciones señaladas en este inciso para el logro de sus fines.
Con el objeto de mejorar la inter-comunicación de los d.i
ferentes niveles, dicho personal deberá dirigir sus programas
educativos de expresión oral y escrita tanto en quechua como
en español.
CONCLUSIONES
1.- Todo el progreso que se hace en la implantación de controles, no satisface a ninguno de los involucrados, pero tampoco surgen claras pautas para incrementar y apurar ese
progreso, especialmente en el campo de la financiación de la
investigación, evaluación e instalación de controles.
2.- La supresión y control de polvos en las minas requie
re desarrollo de proyectos integrales, los cuales por las especiales características de los yacimientos, demandan costos
altos para su ejecución. En tal virtud los organismos estatales encargados de las tareas de prevención se hallan negocian
do fuentes de financiamiento blando, destinados a la compra de equipos de ventilación mecánica y otros sistemas de control.
849
Tema 1
FACTOBES MEDIÛ-AMBIENÏALBS Y SILICOSIS SM BOLIVIA
Resumen
El estudio en sus aspectos ambientales e s t á basado en l o s parámetros a l t i t u d i n a l e s , de temperatura, humedad r e l a t i v a , concentración de
polvo y tamaño de partículas de s í l i c e , referidos a nueve empresas de l a
minería e s t a t a l , privada y cooperativas. Las a l t i t u d e s van entre 2.150 y
4.800 metros S.N.H., l a s temperaturas entre 2° y 34° centígrados, una humedad r e l a t i v a entre ¿0 y 100$ y que en 1.612 muestras de polvo eilicógeno
e l promedio obtenido es de 11.30 m.ppp.c. para ocho horas/día de trabajo.
Se otra parte se muestra que e l CH ( c o e f i c i e n t e de riesgo) es dos veces
más a l t o que e l l í m i t e permisible, con un 62.36çé d e l t o t a l de muestras que
corresponden a l de partículas de s i g n i f i c a c i ó n b i o l ó g i c a .
Relacionado con e s t o s hallazgos en base a estudios clínico—radiol ó g i c o s de t i p o "inasivo-eelectivo" para e l decenio 1961-1970 en 24.955
mineros se encuentra una prevalencia de 22,13$ de s i l i c o s i s y 2.28$ de
silicotuberculosis.
El grupo e t a r i o más afectado es e l de 40-45 años y l a s ocupaciones
más expuestas en orden decreciente son l a de barretero, p e r f o r i s t a , ayudante perforiBta y p a r r i l l e r o s , con un tiempo promedio de exposición de
9 años para adquirir l a enfermedad. Para e l decenio 1971-1975 en muestra
s i g n i f i c a t i v a de 6.558 mineros l o más ILamativo e s un 12.1$ de S i l i c a t i c o s
y un '¿.alfa de s i l i c o t u b e r c u l o s i s con un desplazamiento al grupo e t a r i o de
50-59 anos de edad y pequeño incremento de l a s i l i c o t u b e r c u l o s i s .
Un estudio de incidencia en 6.174 trabajadores (28.36$ del t o t a l de
trabajadores mineros) y aplicada una muestra de s i g n i f i c a c i ó n e s t a d í s t i c a
se demuestra l a incidencia en 400 casos nuevos año de neumoconioais.
Complementariamente y desde e l punto de v i s t a negativo, a travéB de
l a s evaluaciones de incapacidad (año 1973-1974) se aprecia una mayor f r e cuencia debida a enfermedades p r o f e s i o n a l e s , caso de l a C.N.S.S. y que
representan 274 casos frente a l a s evaluaciones por incapacidad por accidentes
del trabajo que representan apenas 34 c a s o s .
85o
TWO-STAGE GRAVIMETRIC METHOD OF DUST CONCENTRATION MEASUREMENT
AND ITS APPLICATION IN ORE MINES
V. V. Tkatchev, Institute of Industrial Hygiene and Occupational
Diseases, USSR Academy of Medical Sciences, Moscow, USSR
In the Soviet Union the first maximum allowable concentrations (MAC) of airborne dust were proposed In the form of gravimetric Indices In 1931. During the following years new MAC
levels were proposed In the form of gravimetric Indices In the
course of occupational morbidity studies and experimental studies
of aerosol biological effects. Therefore, during several decades
the gravimetric method has been used to measure the total airborne
dust concentration without preliminary Isolation of any fraction
during monitoring of airborne dust In the working evlronment.
In this case dust particle-size distribution Is taken Into account
(mostly by microscopy and
measurement of particles), but during
routine measurements this Is not always done.
Is carried out In two steps. At first
The measurement
dust Is collected on the
highly effective aerosol filter made from FPP-15 material and
then the filter Is weighed.
At the same time It was recognized that human respiratory
diseases caused by industrial dust depend not only on the duration
of exposure, amount and composition, but also to a considerable
extent on the mass of particles of definite size (1). It was
also recognized that, In the process of respiration, coarse
851
particles and a small amount of
fine particles are retained in
the air passages of the respiratory system, and that only fine
particles, mainly less than 7yvn in size, reach the alveoli and
can be contained in alveolar air.
It is considered that the first
induces the development of dust bronchitis and the latter the development of pneumoconiosis, keeping in mind the biological correlation of the two.
In order to have an opportunity to differen-
tiate these dust effects, the airborne dust concentration should be
taken into consideration.
Industrial dust particle-size distribu-
tion is rather changeable and depends not only on the type of dust,
but also on the dust formation process, climatic conditions and many
other factors. The reduction of the airborne dust concentration
by various dust control measures (water spraying, fog formation,
inertial dust separation, etc.) has much less influence on concentrations of fine dust.
On the basis of many studies curves were elaborated distinguishing the coarse dust fraction from the fine one or, as it is
called abroad, from the "respirable" (2,3,4).
These curves (the
most well-known are the Johannesburg and the Los-Alamos curves) are
used as characteristics to make coarse dust fall out in a preseparation chamber of a precipitator sampler.
In this case only
the "respirable" dust is usually measured.
As the result of the joint USSR-GDR scientific studies on
a unified method to measure the airborne dust concentration, the
Institute of Industrial Hygiene and Occupational Diseases of the
USSR Academy of Medical Sciences and the Institute of Occupational
852
Medicine of the GDR Ministry of Health have developed basic
standard requirements for a two-stage gravimetric method of dust
concentration measurement.
In 1975 the USSR
Ministry of Health
adopted the new "Methodological instructions on measurement of
airborne dust concentrations in industrial environment".
The
same requirements were adopted in the German Democratic Republic
as TGL 32601/01 (group 963601)i Labour hygiene, mainly fibrogenous
action aerosol MAC in industrial working environment. Measurement method"¡ "Air in the industrial working environment .
General sanitary and hygienic requirements".
In accordance with the new Instructions it has been recommended that for the measurement of airborne dust concentrations devices
or apparatus should be used which measure the bulk of the total
airborne dust (general concentration according to the USSR State
Standard 12. 1005-76) and differentiate between fine and coarse
fractions. The fine fraction Is that part of the airborne dust
mass which passes through the preliminary separator of the twostage device. This part of the dust may be retained in the alveoli in the process of a healthy human being's respiration.
The coarse fraction is that part of the airborne dust mass which
is isolated from the air passing through the preliminary separator
and may be retained in the air passage of the respiratory system
while the aerosol passes to the alveoli.
The Methodological instructions on two-stage measurement do
not apply to dusts containing mainly asbestos and other fibrous
particles.
Measurement of these dusts is performed according to
the previous instructions.
853
Sampling is to be performed in existing typical occupational
conditions taking into account the principal technological processes, working equipment and sources of dust emission.
Airborne
dust monitoring is to be conducted at the workplace, preferably
in the breathing zone.
The duration of sampling depends on the objectives of monitoring.
When the dust concentration is measured to check whether
it conforms to the MAC level or to evaluate the effectiveness of
dust control measures, mean short-time (maximum one-time) dust
concentrations are determined (C k ).
measured to determine the
If the dust concentration is
dust load, an average-shift dust con-
centration is measured (C d ).
The periodicity of the C^ and C.
measurements is fixed in the departmental instructions.
The C^ measurement should last 30 minutest during this time
several successive measurements can be performed.
action instruments are used, discrete sampling
When rapid-
(not less than
5 measurements) at equal time intervals is permitted, followed
by averaging of indices and indication of minimum and maximum
concentrations.
The time interval is to be selected in such way
that C^ covers the period of the highest dust concentration in
a work shift.
When C . is measured during a shift, continuous sampling may
be performed, or such a number of successive samplings at intervals may be carried out, in spite of discrepancies between the
concentrations actually measured, would permit to obtain a statistically significant mean dust concentration.
854
When the dust con-
centration Is less than 0.5 MAC, it is permissible to prolong
sampling beyond the limits of one work shift in order to cover
several shifts.
The differentiation of dust fractions is considered to be
effective if the fine fraction contains not less than 85%
particles of 2 >um in size, 40-60% particles of 5>ura, and not more
than 5% particles of 10 /jm (Fig- 1). This effectiveness of separation has been achieved by the ZAM-10 ordinary cyclone developed
and studied in the GDR (5, 6). Contrary to impingement separators
designed to make particles of more than 7AM in size to fall out
in the laminar air flow, the cyclone offers the opportunity to
collect and analyse coarse dust.
The Methodological instructions also contain basic requirements for the analysis of dust samples, including permissible
relative errors in dust sample weighing, and for the order of
fibrogenous dust component identification and recording.
They
include basic requirements for sampling pumps and balances and
refer to recommended methods for identifying fibrogenous components of dusts.
It is important to note that the new instructions do not
abolish the present one-stage gravimetric measurement of the
total mass of airborne dust without its separation into fractions.
Their introduction Into the dust monitoring practice alms at
obtaining additional Information about the partlcle-slze distribution of industrial dust.
At present work is being done to
design and produce the corresponding apparatus.
A number of basic principles of the two«tage gravimetric
855
method were adopted at the first (German Democratic Republic,
Berlin, 1973) and developed at the second (People's Republic of
Bulgaria, Sofia, 1976) meetings of experts from Socialist countries'
Institutes of industrial hygiene and occupational diseases (7).
Unlike the gravimetric method used in the USA, United Kingdom,
FRG and other countries since 1970 and permitting to measure only
the "respirable" fraction, the two-stage method, as it was already
mentioned above, provides for simultaneous determination of the
total mass of airborne dust with its corresponding differentiation.
The "respirable" fraction share in the total mass of airborne
dust can differ within wide limits from industry to industry.
For instance, in highly mechanized stopes of coal mines it is
sometimes equal to 1% (8).
It is not difficult to calculate that
a dust concentration of 4.0 mg/m , e.g. in FRG (coal dust standard),
will correspond, with this type of measurement to a concentration
of 400 mg/m
when the total mass of airborne dust is measured by
the one-stage gravimetric method traditional in the USSR.
After development and adoption of the new measuring method,
studies aimed at its perfection and at the exploration of industrial
aerosols were continued in the USSR and GDR.
In the Soviet Union
these studies were performed in modern ore mines with different
dust concentrations.
In these mines, as in all others with posi-
tive air and rock temperatures, a modern and highly efficient
complex of dust control measures, based on the use of water and
ventilation, Is applied (1).
Sampling was carried out with the SPG-10 two-stage gravimetric apparatus designed and constructed in GDR.
856
The apparatus
Is so calibrated that its permanent working characteristic is
3
9.5 m of air per hour. To separate fine dust a ring-shaped
fibrous filter is used to which high voltage is applied through
electrodes.
After sampling the apparatus is disassembled and the
cyclone is cleared of the dust precipitated.
The filter with fine
dust is specially processed to separate the dust particles from
it.
Both dust fractions can be studied
qualitatively and quanti-
tatively.
Simultaneously with the SPG-10 apparatus sample collection,
sampling was carried out by the traditional method based on
filtering mine air through aerosol filters.
Filters were located
at a distance of not more than 0.5 m from the SPG-10 apparatus
inlet.
Besides, conimetric sampling was carried out periodically
with aerosol filters, and after filter clearing with dimethylbenzene vapours the particle number and size were determined by
microscopy (9).
52 two-stage dust samples and more than 300 one-stage
dust samples taken with aerosol filters were collected in the
mine workings. The two-stage sampling time was within the limits
from 85 to 465 min.
During this time several samples were collect-
ed with aerosol filters at small intervals necessary to change
filters.
All samples were collected at workplaces after the be-
ginning of mining operations (drilling, loading, dumping).
When
workbreaks exceeded 15 minutes (equipment breakdown, absence of
cars), sampling was stopped and continued after work had been
resumed.
857
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858
4)
Particle Size ( 0 = 1.0 g/cm-3), microns
Fig. 1. Selection Curves of Particlest
1 - Regulated with the two-stage method, shaded zone
permissible deviations
2 - Pulmonary deposition
3 - AEC penetration
4 - BMRC penetration
859
The results of the two-stage measurements are shown in Table 1.
As we can see from this Table, the particle-size distribution of
ore mine dust differs according to the main operations. The
highest gravimetric percentage of the fine fraction in the total
airborne dust was observed during ore loading in stopes.
scraping it was within the limits of 77.3 - 92.3%.
During
In this case
the high fine fraction content was evidently due to good ore
moisture, efficient ventilation of the scrapers' workplace, and
its remoteness from the source of dust emission.
It is interesting to note the good correlation of the overall concentrations of airborne dust measured with the SPG-10
apparatus and with the AFA aerosol filters.
The obtained ore mine dust samples were quantitatively analysed for free silica content according to Prof. Polezhaev's
chemical method and by x-ray diffractometry.
shown in Table 2.
The results are
It can be seen that the free silica content
in the fine fraction is usually less than in the coarse fraction
and in the total airborne dust.
The difference can be considerable.
TABLE 2
FREE SILICA CONTENT IN ORE MINE DUST
Total airborne dust
X
42.8
S
x
13.5
Fine fraction
X
S
x
6.0
13.6
S
x
7.0
S
x
3.1
The analysis of the results has also shown that the information about the particle-size distribution of ore mine dust
86o
obtained with che SPG-10 apparatus differs significantly from the
results obtained by conimecric
measurements.
The microscopic
dust examination did not permit to determine essential differences
In particle-size distribution during various mining operations.
In conclusion it is necessary to note that the introduction
of two-stage measurements into the practice of dust monitoring
will permit to compare measuring results and will contribute to
a further reduction of pneumoconiosis cases among workers.
From our point of view the best prospects of industrial environment dust monitoring are connected with the creation, in the
near future, of apparatus for three-stage gravimetric measurements
of the whole airborne dust.
In this case it will be necessary
to distinguish between the following dust fractions i fine, coarse
and gross. The first two were already mentioned above.
The
gross fraction Is that part of the total airborne dust which
falls out in nasopharynx of a healthy human being when breathing
Industrial dust.
861
REFERENCES
1.
Khukhrlna, E. V.,
Pnevmokoniozy 1 Ih profllaktlka.
Tkatchev, V.V.,
Moskva, -Meditsina", 1968
Meeting of experts on the preven-
2.
tion and suppression of dust in
mining, tunnelling and quarrying,
.Geneva, December 1952» Record of
proceedings.
International Labour
Office, Geneva, 1954.
3.
Walton, W. H.
Überlegungen zur Frage von Schwebestaubmessungen In britischen Kohlengruben.
4.
Breuer, H.
Staub 29 (1969), S.113-118
Entwicklungen zum -gravlmetrlschen
Staubmessverfahren.
Glückauf, 109
(1973), No. 7, S.390-395
5.
Thürmer, H.
Ein Vorschlag zur Kallbrlenung von
zweistufigen gravlmetrlschen Staubmebgeräten. Informationen ZAG. 14.S.
14-19
6.
Beck, B.,
Zum Stand der arbeitshygienischen
Ouwe, K.,
Messung und Bewertung nichttoxischer
Irmscher, G.,
Staube In der DDR - Inform. No. 14,
Thürmer, H.
ZAG die Ges. Arbeitshygiene DDR.
Berlin 1974
862
Vorontsova, E. I.,
Vtoroe soveschanie spetsiallstov
Tkatchev, V.V.
sotsialisticheskih stran pò unlfikatsii norm i metodov Izmerenlva
fibrogennoy pyli (Bolgariya,
Softya, May 1976). Published In
"Gigiena truda 1 professlonalnye
zabolevanlya", Moskva, USSR, No.12
1976, p. 57-58
Zaburdyaev, G. S.
Opredelenle dlspersnogo sostava
pyll v rudnlchnoi atmosfere.
Published In "Borba s slllkozom",
"Nauka", Moskva, 1977, Vol. e,
X, p. 141-144
VronskL, A.I.,
Metodlka opredelenlya zapylennostl
Latushklna, V.B.
vozdukha s lspolzovaniem analitichesklh aerozolnyh flltrov.
Published In Metody Izuchenlya
proizvodstvennoy pyll 1 zabolevaemosti pnevmokonlozami.
"Medlt8lna", Leningrad, 1965,
p. 10-19
863
X/3
PROBLEMES METHODOLOGIQUES ACTUELS DE LA LUTTE CONTRE
LES PNEUMOCONIOSES DANS LES CHARBONNAGES FRANCAIS
C. AMOUDRU
Médecin Chef, Charbonnages de France, Paris, France.
Lors de l'initiation d'un programme de lutte contre les
pneumoconioses dans une situation d'endémie sévère, il peut
suffire, d'une part, de dépister les sujets atteints pour les
soustraire aux risques majeurs,d'autre part, de développer
par tous les moyens la lutte contre les poussières. Puis vient
un moment où il apparaît indispensable de quantifier avec précision les différents paramètres,à la fois pour définir mieux
les objectifs et pour contrôler les résultats. Les principaux
types de problèmes méthodologiques sont alors:
- la quantification de l'endémie,
- la quantification des empoussiérages,
- la définition des concentrations maximales admissibles.
a) La quantification de l'endémie.
Deux types de statistiques sont simultanément utilisés
en France:
- statistiques médico-légales,
- statistiques radiologiques.
Le dénombrement des images radiologiques est fait en fonction de la Classification internationale BIT des U/C 1971 radiographies de pneumoconioses. Cette approche est le meilleur
outil de contrôle de l'efficacité de la prévention technique,
puisqu'il y a une relation statistique démontrée entre le poids
des poussières retenues dans les poumons et le score radiologique.
865
Mais ce classement des images radiographiques suppose une organisation particulière de leur lecture pour assurer la fiabilitô
des interprétations :
- constance de la technique radiographique
- lecture collégiale pour chaque grande zone de
dépistage
- échange interrégional et international pour
assurer l'homogénéité des interprétations et
éviter les dérives.
Par ailleurs, on sait qu'il n'y«pas de bonne corrélation entre
score radiologique et insuffisance respiratoire. Donc les enquêtes radiologiques ne suffisent pas à elles seules à représenter le vécu de la maladie. Il est donc nécessaire d'établir parallèlement la statistique des patients indemnisés selon les
taux d'incapacité permanente médico-légales ne permettent pas
de comparaison à l'échelon international du fait des différences de légalisation entre les différents pays, alors que ces
comparaisons peuvent être réalisées pour les enquêtes radiologiques basées sur la classification BIT U/C de 1971.
b)
Quantification des poussière«.
Les Charbonnages français ont maintenant adopté la
méthode gravimétrique; l'appareil standard de prélèvement est
le CPM 3 du CERCHAR; les conditions de prélèvement ont été définies et rendues obligatoires par instruction ministérielle.
Les valeurs constatées sont tributaires de cet appareillage et
des règles observées pour le prélèvement; elles ne sont donc pas
comparables à des valeurs trouvées dans d'autres pays qui utiliseraient un autre type d'appareil et/ou une autre tactique de
prélèvement. Enfin, le dosage de la silice lui-môme doit être
standardisé, quelle que soit la méthode analytique employée
(dlffractrométrie aux rayons X ou dosage dans l'infrarouge) et
l'on doit utiliser partout le même quartz-étalon.
866
c) Quantification dee valeurs admissibles.
Différente pays ont proposé des limites exprimées en
mg/nr de poussières respirables en fonction de la teneur en silice libre. Or - et c'est là le point essentiel de cette brève
communication - dans les houillères françaises, il est observé,
depuis de nombreuses années, des niveaux d'endémie très différents
suivant les exploitations, alore même que les concentrations en
poussières respirables et les teneurs en quartz sont très voisines. Il existe donc une nocivité spécifique des gisements et
celle-ci semblerait d'autant moindre qu'il y existe des minéraux associés contenant par exemple soit du fer, soit de l'aluminium, mais les raisons exactes de ces différences de nocivité
sont encore pleines d'inconnus. Force est cependant d'admettre
au moins pour les houillères françaises qu'il n'y a pas de valeur admissible unique exprimée par le seul poids des poussières en suspension et leur teneur en quartz. En attendant le résultat des recherches en cours, cherchant à mettre en évidence
par la voie épidémiologique ou par la voie expérimentale les facteurs supplémentaires de nocivité ou de non-nocivité des poussières de mines en suspension, il a été considéré que l'on pouvait
procéder a une évaluation globale du danger de l'«mpoussiérage
propre à chaque grande unité d'exploitation : unité géographique
ou unité technique, une nouvelle réglementation (1975) a donc
été formulée, qui oblige l'exploitant à définir par une méthode
épidémlologique et, pour chaque secteur homogène de l'exploitation, la valeur de "l'empoussiérage-seuil E o" pour lequel le risque de-pneumoconioBe est sensiblement nul en fin de carrière. En
pratique, on établit les courbes successives des prevalences radiologiques en fonction du temps d'exposition au risque et pour
différentes teneurs en poussières; ces courbes ôpidémiologiques
sont établies pour chaque unité d'exploitation. Par le calcul,
867
on peut alors définir la valeur E qui amènerait l'incidence au
niveau minimal souhaité.. Cette valeur E 0 ainsi déterminée varie
suivant les Bassins de 2 mg/nr à 10 mg/m-5 (ou même plus dans certaines exploitations à risque très faible).
Cette méthode a le mérite de fixer des cibles individualisées en fonction du risque local effectif. Cependand, elle nécessite, de la part des médecins et des hygiénistes industriels,
un important travail de collation des données et son renouvellement périodique pour contrôler et mettre a Jour les premières
propositions. D'autre part, si cette méthode est bien adaptée à
des Bassins importants et anciens à risque relativement homogène,
pour des raisons de technique statistique, elle pose de difficiles problèmes pour les exploitations nouvelles ou/et petites et
pour celles où les risques individuels sont très diversifiés.
Enfin, pas plus qu'aucune autre méthode, elle ne tient compte des
facteurs personnels ou prédispositions particulières de certains
travailleurs. Or, plus la prévention progresse,plus le role de
sensibilités personnelles prend une place appréciable dans l'endémie résiduelle.
En outre, des études récentes ont montré que des sujets ayant
quitté la mine, alors qu'ils n'avaient pas d'images pneumococoniotiques, voient apparaître parfois au bout d'un très long intervalle
libre des images de pneumoconiose caractérisée et évolutive. Il
s'ensuit que les valeurs seuil, calculées sur le seul personnel
en activité, sont probablement surestimées et qu'il faudrait
pouvoir étendre les statistiques au personnel retraité pour introduire le facteur correcteur nécessaire. Mais cette proposition
pose des problèmes très difficiles de mise en forme; car si on
peut saisir assez exactement le nombre des pneumoconiotiques hors
de l'effectif actif, la population de référence (retraités exmineurs) est pratiquement impossible à connaître avec la précision
convenable.
868
Force est donc do reconnaître que les concentrations maximales admissibles telles qu'elles sont actuellement définies par
la rêglamentation, ne peuvent être considérées que comme "valeurs
d'essai" et qu'elles devront être corrigées au fur et à mesure de
l'évolution des courbes êpidêmioloqiques.
Dans un tout autre domaine qui est celui du reclassement
des sujets atteints, nous constatons que l'efficacité de l'éviction du risque comme moyen de prévention de l'aggravation est
très loin d'être parfait. En effet, chez les agents reclassés
à la surface dans des emplois non empoussiéres, alors qu'ils
présentaient des images liminaires ou discrètes (forme 1 ou 2 ) ,
on constate, dans un nombre de cas non négligeable, des évolutions radiologiques parfois importantes, y compris vers les formes confluentes (forme A et -f- ). L'aggravation spontanée des
pneumoconioses reste donc un problème d'une extrême gravité et
pour lequel nous ne possédons actuellement aucune solution. En
revanche, les complications tuberculeuses autrefois gravissimes
sont maintenant moins fréquentes (incidence 0,5 % contre 1 % il
y a dix ans) et leur pronostic a été transformé par les antibacillaires récents. Mortelles autrefois, elles sont guéries dans
78 % des cas dans les enquêtes récentes.
En résumé, on peut considérer que la situation française
est actuellement la suivante: des progrès importants ont été réalisés dans le domaine de la prévention des nouveaux cas. Par
exemple, dans le plus grand Bassin français qui est le plus touché par l'endémie pneumoconiotique (NORD-PAS-devCALAIS), les empoussiérages ont été diminués de 10 fois depuis 20 ans et l'incidence de 3 fois dans le même laps de temps. Cette constatation
tend à valider une loi statistique précédemment établie par nos
services de recherches et qui peut grossièrement se résumer ainsi:
869
si on diminue de K fois l'empoussiérage, on diminue V K
la
prevalence. De plus, l'âge moyen d'apparition a été sensiblement
décale puisqu'il est maintenant de 50,5 ans: les formes macronodulaires sont devenues très exceptionnelles. Mais à l'inverse,
l'avenir demeure inquiétant pour les pneumoconioses déjà existantes alors qu'elles restent encore nombreuses; en particulier
l'incidence de la fibrose massive progressive dans cet effectif
varie suivant les classes d'âge de 1 % à 11 % par an, or, nous
restons encore dans l'ignorance du déterminisme de ce type dévolution qui est la cause principale de l'invalidité respiratoire
et du décès. La prévention de la fibrose massive progressive et
de l'insuffisance respiratoire est donc la préoccupation médicale principale, tandis que la prévention des nouveaux cas de pneumoconiose simple reste l'apanage de la prévention technique.
87o
THE PREVENTION AND PREVALENCE OF PNEUMOCONIOSIS IN
NEW SOUTH WALES COAL MINING
N. Wiles,Chief Medical Officer,
Joint Coal Board, Sydney, New South Wales, Australia
F. Fairclough, Deputy Chief Mining Engineer,
Joint Coal Board, Sydney, New South Wales, Australia
Introduction
In the last thirty years the underground coal mining Industry
in New South Wales has undergone a revolution in production methods
A perspective of the changes which have occurred may be gained from
the following statistics for underground operations in New South
Wales i
Underground Production (tonnes)
Number of Employees
Number of Mines
O.M.S. (raw tonnes per man
shift overall)
Year 1948
Year 1977
10,466,800
37,014,000
17,283
15,038
138
71
2.97
10.2
Coal workers pneumoconiosis, which had a substantial prevalence in the New South Wales industry 25 years ago, is no longer
a major problem.
Since the Joint Coal Board medical scheme be-
came fully operative in 1948 no man who has entered the industry
since that date! without previous dust exposure and with a clear
chest x-ray has developed a disabling degree of pneumoconiosis.
Table 1 shows the method of coal winning in underground
mines in New South Wales.
The figures are average daily production
for each of the main production areas in the State.
The table
shows the marked alteration in mining methods and highlights
871
the importance of continuous miners as coal producing machines.
Historical Review
The development of dust standards and dust sampling
practice in New South Wales has been very fully described by
J.J. Grierson and T. M. Clark, in papers given at the First
Australian Pneumoconiosis Conference held in Sydney in 1968.
The Royal Commission, under Mr. Justice Davidson, reported
on the Safety and Health of Workers in Coal Mines to the New
South Wales Legislative Assembly in 1939. The Report recognised
that certain chest conditions occurred in mineworkers after their
constant exposure to high concentrations of coal dust over long
periods.
Methods to reduce the incidence of dust diseases were
suggested in the Report.
Following the recommendations of the Commission, a committee
was formed to consider dust prevention and to determine a suitable standardt the first meeting of the committee was held in
1941.
The committee had the standard which had been recommended
by the Davidson Commission, quantitative results from New South
Wales collieries and reports and results of current overseas
practice to assist it in its deliberations.
The First Dust Standard and Later Revisions
The first dust standard was proclaimed in 1943 and followed
the committee's recommendation.
The increasing use of roof bolting
practice used in con-
junction with continuous miners created the need to drill in
the stone roof which contained considerably higher concentrations
872
Tabic 1
Himion or MINING COAL -
UNUIJÌCHOUND MINIS NI;W SOUTH KALIS
Average Daily rrotìuclioii
(tonnes)
South
Maitland
Singleton
NorthWest
Newcastle
West
Murragorang
Valley
South
Coast
i of
N.S.W.
total
prodn.
COAL WON IIV HAND
OR CRUNCHED
Year 1945
Year 1950
.. at June 1957
I960
1965
1970
1975
1977
1978
9,137
1,920
1,200
462
-
. f\n c<
* oz. 5* —
- 66.7Í1,477
1,120
933
517
740
984
1,105
2,609
1,501
723
500
895
1,458
1,153
.
81.5Í
74.1*
1,118
^
6S0
186
947
106
0
0
0
-
-
• :><•'• Sfi>
3,442
2,537
1,497
400
23
21
-
17,783
7,75S
4,539
2,826
1,764
2,463
2,25S
63.1
60.0
27.2
10.9
4.6
1.8
1.1
1-5
1.3
CONTINUOUS
HINHt
As at June 1945
1950
1957
I960
1965
1970
1975
1977
1978
Nil
Nil
4,394
9,286
9,830
7,496
6,491
6,166
4,713
10,630
13,953
14,896
16,560
1,669
5,641
21,882
53,065
46,991
45,125
47,490
340
550
2,904
6,768
13,876
16,427
19,585
11,619
21,912
22,253
23,603
23,053
7,536
17,372
26,326*
36,669
40,359
42,278
43,353
9,545
27,957
76,730«
138,874
144,925
145,825
152,968
14.6
39.2
77.7
87.O
93.0
90.8
90.O
LONGWALL
As at June 1945
I95O
1957
I960
1965
1970
1975
1977
1978
r<
7.4S9
3,902
8,767
7,160
¿
7.4S9
3,902
S, 767
7,160
Nil
Nil
Nil
Nil
Nil
4.7
2.5
5.3
4.21
COAL WON HÏ
COAL CUTTERS
Tear 1945
Year 1950
As at June 1957
I960
1965
1970
1975
1977
1978
6,103
7,183
627
5S4
457
~
- 37.5*—
. 33-3Í
—
1,949
2,368
1,086
457
-
14,447
15,603
10,747
7,412
3,928
3,523
4,015
18.5%
25.9%
5,450
5,239
3,818
1,562
36O
337
-
* Includes mechanised longwall.
^ Included with continuous miner.
873
49.756
- 6S.9S
10,141
5,181
1,250
-
384
509
-
35,090
35,574
17,52S
10,399
5,254
3,860
36.9
39.4
53.2
49.9
17.7
6.5
3.4
2.4
2.4
of silica than the normal coal seam.
The dust from this required
recognition that it created an additional hazard.
At this time
it was being realised that only particle size of less than 5
microns was significant with retentive dust.
In 1957 a new
standard was proclaimed which recognised both these criteria.
The physical difficulties of counting the small particles
and the appreciation of the importance of gravimetric results
caused a further revision of the standard in 1967 when the particle
size limits were established to be 1 to 5 microns.
Correlation studies made at the time of introduction of each
new standard showed the new standard to be a stricter requirement
than the one it replaced.
As required by the Coal Mines Regulation Act which controls
coal mining in New South Wales, dust sampling is carried out as
a regular procedure! a brief description of the procedure is
given below.
The coal mines are divided into four areas.
The
District Mining Engineer in each area programmes the Dust Sampling Officer to sample every working place on a regular basis.
Practice has shown that maintenance of dust suppression standards
is influenced by the regularity of sampling and care is taken to
ensure that every machine producing dust is sampled on a routine
basis.
A copy of the result of each individual sample is made
available to the colliery, to the Department of Mines Inspector
and to the District Check Inspector.
Any sample which exceeds
the proclaimed standard is resampled. Mining Engineers regularly visit production units and any adverse trends disclosed by
874
sampling are Investigated during these inspections.
The continuing use of the Owen's dust counter and the use of
a particle count standard may be criticised as being outdated.
It must, however, be remembered that these form only part of the
dust prevention system which Is In operation In New South Wales,
the effectiveness claimed for the system Is shown later In the
paper.
Trials are being undertaken to find an effective gravimetric
instrument suitable for application with continuous miners working
in pillars.
Gravimetric Instruments which measure the dust make
over a known time period have been used.
Attempts to fix this
type of instrument to the continuous miner have proven unsuccessful. More recently trials with personal samplers have been undertaken. These Instruments have disclosed problems In variations In
air flow rates and It would appear that the pumps require calibration and adjustment at frequent intervals.
Dampers have been
fitted to the Instruments to equalise air flow rates.
There have also been problems with the selection of suitable
cyclones.
Tests are proceeding to find the Instrument which Is
most suitable to the needs of the New South Wales Industry.
Correlation tests of particle count to gravimetric standards
have not been completed and will only become effective when a
selection of the gravimetric sampler to be used Is finally made.
The shortcomings of the Owen's dust counter are well known.
However, the Instrument Is light in weight, easy to operate and
has the characteristic of being able to determine high dust make
levels.
By Its use conditions which create high dust levels are
quickly discovered.
875
Efforts can then be made to reduce or avoid these high dust
levels in the mining system»
feature of the
instrument.
This has been found to be a useful
The sampling procedure using the
Owen's dust counter is given in Proclamation) N.S.W. Gobernment
Gazette 12th May 1967, which is appended.
Standing Committee on Dust Research and Control
The Joint Coal Board, with the concurrence of the Minister
for Mines, established the Standing Committee in 1954. By its
creation a permanent body was established which would give an
oversight to all dust problems in a constantly changing Industry.
It would develop expertise in dust suppression to enable it tò
advise the Minister, and it provides a forum for all interests
in the mining community to meet and discuss problems affecting
the incidence of pneumoconiosis.
The Committee is comprised of representatives of the following organisations iDepartment of Mines
Division of Industrial Hygiene of the Health
Commission
Miners' Federation
Combined Colliery Proprietors' Association
Australian Coal Industry Research Laboratories Ltd.
Australasian Institute of Mining and Metallurgy
Joint Coal Board
These are all authorities and organisations actively interested
876
In Che
coal industry and particularly in research into the
control of coal dust.
The Joint Coal Board provides the administrative and
secretarial services and facilities to permit the Committee to
function effectively.
In view of the Board's responsibilities
with regard to dust control this close tie has been found to be
most desirable. The Committee makes recommendations to the
Minister for any necessary variation of the Coal Mines Regulation
Act dealing with dust suppression.
The Standing Committee has three sub-committees which advise
it on particular areas of expertise.
The function of each of
these sub-committees is explained below.
Medical Sub-Committee
The members of the committee are medically qualified with
experience of working in the medical section of the Joint Coal
Board.
The Chairman of the committee is the Board's Chief
Medical Officer. The committee's principal task is to consider
trends in pneumoconiosis prevalence in New South Wales coal
miners and advise the Standing Committee on actions to be taken.
Sub-Committee on Atmospheric Dust and Ventilation Reports
The function of this committee Is to supervise the statistical correlation of all dust counts taken in the mines.
It
reports to the Standing Committee of any engineering reason
which may be the cause of any count not complying with the
standard.
The committee supervises the monitoring of any new
877
mining system to prevent excessive dust make.
Sub-Committee on Dust Counting Instruments and Size Frequency
Distribution of Airborne Dust
The committee advises of any developments in dust sampling
instruments and sampling methods.
dust sampling instruments.
It supervises the testing of
It is presently Involved with the
trials to determine a suitable gravimetric instrument and subsequently will become involved in the correlation work to determine
a gravimetric standard.
Table 2 shows the Average Dust Concentrations in N.S.W. Coal
Mines and is compiled from statistics available from Joint Coal
Board Annual Reports. The results are given for each of the Board's
four areas» commencing in 1957. The revision of the standard in
1967 had the effect of slightly increasing the later counts.
The Intake dust count and Total dust count are determined by
sampling, from these the Make dust count is found by subtraction.
The Intake dust count is taken in a predetermined position so that
it will capture the dust make from all operations which create
dust on the intake side of the machine being tested.
The total
dust count measures the actual dust concentration at the machine
being tested, the measuring point being at the known most dusty
point which is usually at the operator.
This count is taken to be
the measure of the most dusty condition at the working place being
sampled.
The Make dust count is taken to be representative of the
dust created by the machine at the time when the sample is taken.
The statistics include the results of all places which have
required resampling because of readings in excess of the standard.
878
Table 2
AVERACE DUST CONCKNTRATIQN'S N.S.W. COAL MINES
Number of Particles per cubic centimetre 1 to 5 microns in size
(counts taken in coal only)
South Haitiana
& Singleton
North West
Newcastle
West
South Coast
Rurragorang
Valley
37
45
97
12
26
21
21
39
46
118
18
15
10
15
75
46
69
19
33
32
25
116
70
133
54
112
74
58
0-5
0-5
0-5
1-5
1-5
1-5
1-5
microns
microns
microns
microns #
microns
microns
microns
IOS
84
111
20
51
43
44
114
91
93
29
26
23
38
116
71
124
42
69
58
47
228
150
276
65
75
78
64
0-5
0-5
0-5
1-5
1-5
1-5
1-5
microns
microns
microns
microns *
microns
microns
microns
145
126
196
41
65
5"
5i
15?
135
220
54
39
34
52
189
116
199
60
102
90
72
336
237
402
121
168
145
117
0-5
0-5
0-5
1-5
1-5
1-5
1-5
microns
microns
microns
microns *
microns
microns
microns
Intake
1957
I960
1965
1970
1975
1977
I97S
Hake
1957
i960
1965
1970
1975
1977
1978
Total
1957
I960
1965
1970
1975
1977
197S
* Standard changed 12.5-1967
879
In this way operations known to be dusty are sampled more frequently so that the results In the table do not attempt to show average
conditions In the mines. When a particular problem arises there Is
a concentration of effort to solve the problem.
This effort usual-
ly requires the taking of additional samples and these are Inevitably higher than normal.
Therefore In some short-period com-
parisons the dust count at a mine can be adversely affected by one
problem area and the long-term effect on the statistics Is to raise
the average result.
All production seams have been sampled to determine silica
levels.
At any production place which is cutting stone In associa-
tion with coal mining at the time when a regular sample Is being
taken, the Dust Sampling Officer will also take a sample to determine the silica content.
Respirators are available to all miners
at all times, and miners working In conditions where associated
stone Is being .cut are
expected to wear respirators.
Experience has shown that there are many reasons for failure
to maintain the standard.
The principal causes, however, are
cutting In stone and mining whilst ahead of auxiliary ventilation.
Efforts have been made to Increase Industry awareness of the
dangers of pneumoconiosis and prevention campaigns are directed
towards ultimate eradication.
Booklets In which are described the
dangers of dust In mines are distributed to all new entrants.
Films explaining the damaging effect of pneumoconiosis are shown
at medical centres to all new entrants and to mlneworkers who are
attending for routine medical examinations.
880
The decrease in the prevalence of coal miners pneumoconiosis
can be related to improvement in the health of miners which has
resulted from better working conditions apparent in the years
since the second world war.
The medical scheme run by the Joint Coal Board has been
operating since 1948.
It followed the results and recommendations
of an inquiry, established by Commissioner Davidson, into the
health of coal miners conducted by Drs. Cilento and Murray, and
Mines Inspector Brewster.
is given.
The reference of the Inquiry's Report
One of its main recommendations, adopted by the Board,
was a scheme that included pre-employment and medical examination
of all mine workers and similar periodic checks thereafter.
One
of the Board's main responsibilities is the investigation and
diagnosis of coal workers pneumoconiosis by the Medical Division.
Prevalence studies of pneumoconiosis amongst working miners
have been carried out at regular intervals since 1948, the most
recent study being for the period 1973/76.
The results were based
on the 1971 ILO U/C International Classification, as was the
previous study.
The 1968 classification had been used for all the
preceding studies.
Table 3
I.L.O. Scale
l.L.O. U/C Scale
Categoi•y
0 (Z
0/-
o/o
Category
1
Category
2
Category
3
0/1 1/0 1/1 1/2 2/1 2/2 2/3 3/2 | 3/3 3/4
881
Table 4 shows the prevalence for 1973-76 compared with
previous studies«
Table 4
1957-60
1960-63
1963-65
%
f
%
%
16
3.6
3.5
3.0
4-5
2.9
Cat. 2 or more
4.5
1.0
0.6
0.4
0.13
0.08
P.M.F.
0.7
0.02
0.01
0
0
0
Percentage of workforce examined
10
85
85
60
96
100
1948
All pneumoconiotics
*
1970-73
1973-76
% »
%
Commencent ent of 19 71 ILO V/ C International Classification
The stage has now been reached where a new worker in the
coal industry will be unlikely to sustain a severe degree of
pneumoconiosis in his working life time. This achievement has
been made possible by the success of dust suppression measures
in the coal mining industry.
In 1948 only 12 percent of the
work force were in mines that had water reticulated to the coal
face and many of these only used a hand held hose to suppress
dust.
Satisfactory suppression was only found in 6 percent of the
coal faces.
By 1955 dust suppression measures were effective in
99 percent of the work places.
The present system can be claimed to be successful.
It ha9
been shown that it can alter with changing circumstances of production and that standards have led to the eradication of pneumoconiosis.
The maintenance of results within the standard when
using the new methods and systems of mining, and the higher
882
productive capacity machines, has been made possible by better
ventilation at the face, use of greater quantities of water,
and improved control of sources of dust behind the actual mining
machine.
The longwall system is the only exception in which one
installation does not achieve the standard on a regular basis.
Trials have been in progress for some time to select the
gravimetric sampler which will be used in New South Wales.
This
presumes the acceptance of a gravimetric standard which will
come in the future. The particle based standard has served the
industry well, it has wide acceptance and any change in standard
will have to be shown to be an improvement.
The prevalence of pneumoconiosis can be shown to have been
dramatically reduced, but it can also be seen clearly that
constant vigilance is required to ensure a continuation of this
trend.
883
References
(1) Dust Sampling and Control in Coal Mines in New South Wales Part I
by J. J. Crierson.
(2) Dust Sampling and Control in Coal Mines in New South Wales Part II
by T. M. Clark,
(3) Royal Commission N.S.W. 1939Appointed to inquire into and
report upon the Safety and Health of Workers in Coal Mines.
(4) Coal Mines Regulation Act No. 37.
(5) Report of a National Survey of the Health of Coal Miners.
Canberra, Australia, 1945.
Sir R. Cilento, H.M.L. Murray and D. T. Brewster.
884
v. s . HIKITTT
Vico Director dol Instituto Contrai ""do
Invooticadonea Olenti fiera do Soeurlund dol Tmbajo
Consejo Centrnl do l o s
Soviéticos (URSS)
MCToros H0nsrai03
CE
Sin¿lentoa
EMMISACIOH
cAtiTCHi>3 DE LA mais
PE POLVO Ht LAS
/»VIATICA,
Durante loa Ultimos nfloa ol dosnrollo de lo indùstria alncra en l a
URSS so realizaba principalmente ncdlnnte ci crcclcnto
uao dol bono f í -
elo de recurooo naturales a d o l o abierto, e l cnal resulta nflo eficaz
7
procredvo. P"ra e l oflo 1930 a trovos de Sato DtHodo co producirá on 1«
Unifia Sovietica alrededor dol 75 5» del volunen total de recureoo naturnloo. El crcclnlonto de la oscnln de utilización do túcaicpo no dorna a
do alta iroductivided y el peso al benofíelo do profundas enana horlzontalea
colocaron frente a l a clónela 7 ln practica un nuevo problema do
eran dsiifleado auaonltarlo, social, economico 7 ecologico.
8a trata
do lo eliminación dol polTO de la otmooforo en la explotación de contorne, 7a quo cl equi;» que se usa es una fuente productora de polvillo.
El alto contenido do polvo en lao cantero« provoca pneuBoconlosla,
Influye de nanom nociva en loa trabajedorco do plantas industriales sdtundao cerea de laa con terna 7 en loa habitan tee do ¿wblndos vecinos. SI
polvo acolore ci doacooto do lea piezaa que ce encuentran en contacto
( en ¡particular, Irò do notorea y coapreoorco ) 7 puedo lndicir al cose
do la extracción 7 doscubrlalento.
Ln inpodbiUJlad de aprovechar en l e o canteras loa mloaoo aótodoo
que oc uoan en loa alnas para la lucha contra e l polvo obligaba a tosar
885
decídenos, on principio, nueva» quo tonaura en consideración las particularidades del bene l i d o a d o l o attorto y ana graa variedad
da
equipos 7 esquena» tecaologleoe. Adsnfto deberían da tenerse ea enante
la« propiedades da loa recursos an cuesto»,
condlolonea aetereolOgtcas,
ella« local, ate,
Las Investigaciones planifloadaa y aapllaa,ea «ata eaapo, o« lia»
van a cabo m la Onto» soviética dead« el aio 1996 bajo la dirección genera! dal aeadsaloo A.A. awchlaaky, por varíe« colectivo« dentificos
da la Aosdeata da Oseada» y do laatltatoa da Investigado» pertenedentea a las raaaa corraspoadleatas do la Industri». En ala do 20 anos
Aste personal ha reali nado sn conjunto do estados varieos y asparla«»»
talea« en al eaapo do la seguridad do trabajo o» lao canteras« qaa la*
cloy« l a higiene pabilo», proaloaaa do Ingsaerta, aotereologta, ete.
j
Loa reaultedoe do éetae Inveetlgaeloses ostia resoaldoa a» ato do 1.500
publlcacloneo, «atro loo cualea al 30 * o s t i dedicado a l a lucha coate»
el polvo a» l a s oxplotadoaeo a cielo abierto.
La clónela sovietica y sus aplleaelonoo prácticas, en este nueva
roa» de alaorta, ha aleaaaado grandes «altos y la prioridad ds resola don de Buenos probi nasa, ea cuanto a la ellalnadon da polvo en lao cantores, porteaoea o loo Investigadores soviéticos.
Los estudios en el eaapo do la higiene publie» pusieron ea e video d a las principales fuontes de tornado» da polvo en las canteras,
loo
valorea de eu contenido ea datiate« bases do trabajo y loa factoreo «os
influyas OB Astea coneontradenca. Eotoa estudios doaoetraroa que per falte de los oedloe pare luchar contra el polvo la eontealnsdoa de la stadere re, prácticamente ea todas las basée de trabajo,
pueda superar loa al*
volea poraldbles. Bata contrtUnn clon pueda extenderse s todo el
886
terrl-
tarla :!c Ir centers 7 r Src-ns .-Miynesntos, cu casule .ORCO ^otor-colù Tiene 'ïeafrvoroblco 0 en Ion cooos
en que c l • teori'cniii-iionto do r-olvo
por /orto do l o tioquinArla ooo do u.-yor In tea d'i ed. "."lovoóoo contonl:Ioo de polvo co obocrvra on Inn contcr.no do eualqulcr profundidnd, I n clusemi* Ino poco -rofunc'ao, ddndo 30 extrocn
l o o ^ao vrrladoa
recar-
l o alnerolos.
t o
cantidad de polvo r e s u l t a , pnrticularxicnto, m?s a l t o cn l a o
contorna dìodo oc u t i l i z a c i transporto de canlones y trabo Jan 08 quinas
perforadoras, cortadoras de piedra y excavadoras potentes, Kl beneficio
de l o o 9 ri do o 00 accoppila por e l saxiso dosprendlnlonto de polvo,
l o o cm terno ni tue io o en s l t l o o de e l i a n seco y cnlurooo,
Fa
ónde Ina v e -
l o c i dodo e del viento alcanzan 3 - U motros "or corundo o l papel afte i a portnnta l o Juega e l -rocoso de lcvnntn-jlcnto de -otvo, cuyo f jmaclOB
sc obnervo no '-8I0 en l a s operaciones tccnolS^icaa alno durante In d i s .jrecsciSn no turni de l a roca, bo Jo l o rcclSn de nütoblca difurencios
de tenders turre. .Tara suchos conteras el'contenido de polvo en l a
o.t-
ndsforn durante o l Invierno reculto don o t r o s vecos aha nltn que durant e e l verano. Por l o tanto
Ir lucha contro e l polvo debe de e f e c t u a r -
se durante todo e l P Í O , en cualquier proceca
Industrial que se aeon -
peflo co cu desprendlalento.
too entudion tcSrlcoo y oxforlnontaloa permitieron croar una adecuada clorjificociSn de esquenas cn cuento a l a contaManddn de d i s t i n tas brocs de trabajo, de (liferentco Areno de l a centers y de ou t e r r i torio cn ta t r i . ¿ìobro In bone de é s t o s estudian so hon obtenido cxnrealonoc - n o U t i c o o que pcnsltea, oân durante l o nroyocclSn y explota c l i n de contem,
dor un prondstlco ea cuanto a In contonlnoclSn
ao-
b l c n t a l . Loo Jotos I n i c i ó l e o prra óectoa c á l c u l o s non l o e d,'¿uicnteoj
discnoirjncs ¡jcoaétrlcae de l a cantera, particulariúadoo dol e l l o s l o c a l ,
887
cantidad de máquinas y equipos en funcloanmiento, Intensidad de Xa for«
nación de poltro.
Se han propuesto» •denla, l a s formulas que sirven para evaluar la
eficacia de técnicas y aedioa para ellaiaar ol polvo» calcular la cantidad nocooarla de loa equipo»» cuyo uao peralte aoraallsar la coaposlclon del aabiente en cuanto al faotor polvo.
El estudio dol fen&aeao físico déla dlfusl&n de tapnrsasa en régl•en turbulento peraltlo la elaboración de las técnicas para deteralaar
e l contenido do polvo en la atadafera de locales donde están instaladaa
esquinarlas do distia tos tipos,
s i igual qus Isa teealcaa para evaluar
la intensidad del deepreadialsnto de polvo por parto del equipo situada
en la cantera«
Aprovechando ésta aetodologta as ka llegado a la eoncluatoa de q«e
la latonsidad del despannrfiaelnto do polvo di rente e l funelonaaiento
do Isa atqulnas do perforado*» sin hacsr nao do l o s aedioe para luchar
ê
contra ol polvo» alcanna en laa can tersa de carbón 1.200 ng/sag» aleatras on laa cantoras ainoraleo llega a 43.000 ag/seg. La utllisaclftn do
l a s inotalaclonea abaorbeatea o aodloa huaidificadorea peralto rebajar
estos valorosi
on la peraoracloa do posoa llegan a 60 ag/sog , para
los cantoras de carbon» y hasta 250 ag/oeg en laa canteras donde se ext r a « Dinerales.
Las excavadoras de un cucharon y de rotaclta en las canteras de
carbi* ain la humectoelön se caractnrlaaa por intenaidndea do fonación do polvo del orden ontre W30 y 12.000 ag/ceg|
en las cantoras de
•Inórales éstos valores oscilan entre 100 y 800 ag/oeg. La huaeetaclAa
disminuye dichos Índices hasta 1?0 -
2.000 y 60 - 300 ag/ oeg ree pes-
t i vonen te.
•
La lntcnaldcd do formación de ;x>lvo rjuc oo produce por el tráfico
RRñ
do Ion caniancc volquctao sobre los corlaos naturales dentro do los conteras v r t a entro 3.000 y 15.000 aß/ceß i el trataalonto de lo ouporflcio dol camino con oodioa adecuados baja cetas concentrecionca haota
80 - 2.000 oß/oeß.
Los dedntocrodores cayo productividad oo fio o ta de 1.000 tonolados
por bora sin humectación se caracterizan porua Intensidad de formación
de polvo corea de 350 ng/oog, mientras que pr.ra laa maquinas cortadoras
do piedra ó a too intensidades occllsn entra 1M> y 1.200 mg/oeg.
/l baso de estudios teóricos canflrmadoo por datos experimentales
sa han propuesto las expresiones que peralten proveer las Intoned, dp de o
coperados para lo formación do polvo y de ou contonldo en los lócalos
dónde, Gccûn cl proyecto, deben Instalarse naovas maquinas de olta pro«
ductivldod y ol equipo para beneficiar los ¡dinerales a ciclo abierto.
Los investigaciones llovndoo a cabo donoatrrron que loo nótodos de
huaoctr.ciSn do distintos tipos rceultan convenientoo para loo algulentos
caeos do lo oxplotoclfin do conterasi perforación do pozos, trabajos con
excavadoras, bulldozers,
cal como en las lábaros do oxplosloD.
Bañándose en condderacionoo teóricas se ha elaborado una actodolocla que peralte évoluer la humectación necesaria de la roca o del ascino
Dontaflooo volado. Co ¿sta aonora so calcula lo eficiencia de 6llmlnaclfia
de polvo que al mismo tiempo resulto tccnolÔglCRacnte óptima y oconòmlennento Juotlftcda.
T.oe cotuiilos clúntíficos que oo hen llevado a cabo por porte do orCnnicnoB do proyecto y construcciones dieron COBO rcsultndo la olnboracidn de tAcnlcas de buaectnclfin y el dlocflo de lnotnlsciones para absorber cl polvo seco producido en los procesos do perforación. En In perforación
de distinto profundidrd, ollalnnado loo redd:ioo cedíante laa
S89
mezcla« coapaeotaa por al«» y ogua, loa gastos as flete altln» constltnyon ds 10 a 60 da^/sla, lo qu» dépends de la productividad do la aaqulno y de laa proplededoa ds la« rosas porfoaadaa. Bi le teaporade lavaras!
cuando la temperatura ansíente eas basta £0°C bajo cero, as aplican as»
ludonsa salinas i cloruro ds magnesio, clorar» ds sodi» y clorar» ds
calcio.
Para la ollalnaclta de polvo producido por trabajo ds explosiones
en crup» os asan, antes ds efectuar la operación» principalmente tres
aétodosi 1. Irrigado» del bloque a «ola» y ds l a s ftrsaa adynoeatss i
2.
Baaeetadoa femada del »acino a «»lar i
3 . Baasctocloa por liar»
filtrado» dal agua quo proviene de nanjas a&taada» on la onperficls dal
ascino a volar.
O rosadla prelininar »o afectas aediants trenes aidrsnlieo» y
aaqulnaa regadoras, sayo» gastos de agua ata do 10 da* por 1 a de arsa.
ai s i eaa» dohmestaeioa del aaoino a volar e l regedlo se efectoa aediante conpreoioa « filtrada» libra, satos gastos oscilan entóneos entro
20 y 200 dar por I r *
rosa, segna laa propiedades ds data.
Loe gaoto» de agua para la Impregnación interna son Iguales a 50 70 da3 por cada pono engendrado por l a explosion.
La humectado» tomada eoa agua o con soluciones calinas, al igual
que m libre OÍ trocid», adema* de eliminar el polvo durante los traba«
Joo de explosion, paraît» dieainuir el desprendimiento de polvo « l a s
ulteriores operaciones tecnológicas, que son perte de la extracción ds
recursos naturales por el metodo a cielo abierto. Cuando estos métodos
roooltan Insuficientes
pnre la huaectacl&n de la naos producida al vo-
lar lao rocas, o cuando dotas técnicas no se usaron en absoluto, entonces, pore bajar el contenido de jolvo durante explosiones en grupo su»-
R9o
le
copleorso c l regadío de dicha ans« usendo treaco hidráulicos, n i q u i -
noa recodoroo
o instalaciones de husiectociSc f i j o s . Ectoa nisnoa nôtodos
co usrn nom oreveer o l deoprendl.-d.cnfco de polvo cuando l o o r f c i z o e se beneficimi
en
y
"»" decacnuzorse previamente por ciedlo de explosiones, a3Î COBO
Ina labore3 do
carca
7
durnnts c l funcionnniento
do dzcovadoros
bulldozers.
G-iotos e s p e c í f i c o s del agua
por 1 O'5 do l e roe« per-
de unoo 300 ai
ni ton dlsoinuir o l contonido de polvo bosta 5 - 1 3 mg/o , Poro bonerielar
l a a canteros Se han dloeftado
huacetndoros e n n e c i ó l e s , cuyo alcance eo
de
15 - 32 raôtroo y l a productividad de unoo 200 - 390 -Jravmin, con una presión del aijun do t» ntDOsfcras. Las Boquinas rsendorno y monitores hidráulicos
instalados «so*ro camiones o trenes gprmtíztm
toclfin
un oleruce de busec-
do 30 c e t r o s , con un casto do hasta ?50 nr de agua por hora.
So han dlocflndo ooquenno y equinos pora 1« hiracctnclSn do l a s capas
do cortón y de t i e r r a roturada en l o s canteros, a l Igual quo técnicas que
reducen l a cmtldad do polvo levantado durmte o l funcionnniento de l a
Bwqulnírlo. T'ora e l l minor e l polvo iroducldo por BÄq ¡Inas que cortan p i e dra ce han elaborado i n s t a l a c i o n e s do huaectr.clfin Cuyo uso ;-eralto bajar b
concontrnclones correoponSientos
hootn 3 - 5
ne/a*.
Para reducir e l dooprendlnicnto de nolvo en l o s caninos dentro do l a
conten», proteger su revootinlento y diooinuir
l o o gastos do tratamientos
oe opiles» c r i o s ( cloruros de e s l c i o o s o d i o ) , colaciones que contienen
eotíin o c l e s , uolitciouco de Béselos nulfctonlcohQlicos, o oaulciones de l a s
nlcRos, potrfilco crudo o naeût. Con c^ictoo de cloruro de c a l c i o entre 0 . 3 - 0.7 Its W I B
do s u v e r t i d o dol canino, no nlccns?, con un nolo t r o -
tnalento, In eliminación de polvo por un Intervalo do .? a h rilo o. El t r n toalonto con coluclonos quo contienen e l 30?! do cloruro do c a l c i o o aozcla
891
oulfatoalcohdlica
.emite disminuir cl deoprondi.iiento de polve durent*
5 - 10 cHeo (potando 1.5 - 2 d«" d* arterial por l a
de la superficie.
r
El copleo de petróleo o aaatt, gastando 0.8 - X. por 1 •
de eael-
no y recubriéndolo luego coa gravili*, cesa la foraacloa de polvo por ua
intervalo de 20 - JO tiles. Con e l nao de emisiones, coa gastos comprendidos entre 3 • 5 da' por 1 a de oaaiao. so rednee el contenido de polvo
ea el aire basta lea concentraciones teenologlcaaeate peralaLblea por 60 90 dlaa, l o q*e depende de la intensidad dal trftfloo de caadoaes volquetes
y do las condiciones aeterealogleaa.
Para prevea» la contaalaaclon de la cantera eoa e l ¡»Ivo que proviene de eseorlalea y bordes, lea euperfldea correspondiente* se fijan por
aedlo de agontea antloroalvoa» La* partea horlaontalea dal eaeorial a*
fijan Bedlant* lapregneeloa eoa soluclaa da pollecrlloaltrllo al 0.5 %,
loa gaotoa de liquido son de 10 da* par 1 a . la« partas verücalea y
bordo* de cantera ola bcae flelar ae iapregnaa coa enulaloa tattaalBoaa al
15 % ( betfia HB-SH - 50*, silicato de sodio * »,
kldrdxldo da sodio -
o.15«, ngaa - «»7.85 * ) . Loa gaetoe de aateriel ooa da 10 da" por cada a y
el trataaiento ae repita aaa vaa ea doa o tree aftoa*
Para eupriair e l polvo eaependido ea el aira y pera la aeración de
dlfcrentaa partea de la eantera ae nan diseñado y ae oxplotaa eoa éxito
lnotalacloaea de aeración y huaoeaacioa alaulteneaa(de tipo OV 7. La l a oalACloa ceta acatada sobre el chasis de un cánida y puode producir ua
chorro serohldrlulioo cuyo e n u Joe son de PJtO a'/eeg de air* y ? a'/aora
de a g i s .
Para le aeración conerai do canteras so ha dinanado una serie de inetnleclonoa ventilodorna que coplean notoros de turbina y de propulr.i&h a
chorro, con une potencia do 15.000 cnb'Uoe do fucrea. Sus flujos de aire
cn la oocciSa prS::ima ri chorro al cansa 1.300 a /oep 7 1" velocidad sedia
892
en do unoo f r . 5 a/noc.
T,o lntro-1'jcclön del conjunto do nertlo/j cJeocrttoo, p.irn la rllnln*
clîln do '>ol»o on loo contorno rdderÄrRicna y t»rtn\1\rrïcpB, hn -vraltldo
roducir oun conecntrnclonee hont« loe lini toa :x>mlrdblco por IB higiene ~8bllCB.
893
I »! D ! C
r
S r <? S ! P N
/Î
fl. Pulmer.
Developments In dust control end dust 9uppression In mininq,
tunnelling and quarrying, engineering control, organisational
asoects, medical prevention.
1
L . L R bouffant., J.C. martin., H.Oanlel
rFfet dus aero9ol9 da S B I S D'alumlniun oour la prevention
traitement de la Silicose. Ctude expérimentale.
et le
1 ffl.L.fl. Flindt.
Prévention of illnes9 dua to allergenic
[l
du9t9
<ll.T.Ulmer.
Coal iuorkers'Pneumoconio9Í9
lonq-tima treatment and ita outcome
D.Clse., Namcy W . C a r o .
Problems associated »ith the U9e of helf-ma9k respirators
dusty environments of developing
895
countrie9
in
Developments In dust control and dust suppression
In mi.ni.ng, tunnelling and quarrying, engineering
control, organisational aspects, medical prevention A. Bulmer, Safety and Engineering Department, National
Union of Mineworkers, Great Britain.
1.
Introduction
Research over many years in the coal mining industry shows
that the mass concentration of "respirable dust" measured by selective sampling in accordance with the Medical Research Council/
Johannesburg selection curve provides a good correlation with the
incidence of pneumoconiosis*
The product of average respirable
dust concentration and duration of exposure can, therefore, be
used to measure the hazard.
There is no evidence to show that
high respirable dust concentrations for short periods increase
that risk, but exposure to high concentrations over several
years does increase the risk of the incidence of pneumoconiosis
as a result of fine dust being deposited and remaining in the
lung.
The effects of exposure to dusts encountered In other
mines, tunnelling, quarrying and some Industrial undertakings
create very similar problems, and the steps to be taken to counter
the hazard are also similar.
The report does not, however, attempt to deal with fibrous
dusts, such as asbestos, or indeed toxic dusts.
Because of the hazard created by airborne dust, the workforce must be made aware of the possible consequence of failure
to properly control the working environment.
The following points
must receive constant attention.
1.
Production and dispersal of respirable dust must be kept
to a minimum.
897
2.
Steps must always be taken to capture that dust which is
dispersed*
3.
There must always be provisions to protect the workforce
from any harmful dust which remains when the foregoing
requirements have been complied with.
Requirements 1 & 2 can only be achieved if an effective re-
liable means of measuring is systematically carried out.
2.
Engineering Control
(a) Minimising production and dispersal of respirable dust
Producing mineral by mechanical means or explosives, crush-
ing and transporting the said minerals creates dust particles of
all sizes from the very smallest respirable sizes to the large
sizes which cause other problems.
One of the earliest methods of reducing respirable dust at
source is wetting by infusing water into the mineral in situ prior
to getting.
This method is very effective when the right conditions
exist, but many coal seams cannot be effectively infused, e.g. in
the United Kingdom where coal seams are generally too homogeneous
to be injected uniforally.
When dust problems arise from floor
or roof of a coal seam, or mid seam dirt bands exist, infusion has
little effect on airborne dust production.
Machines for the mechanised production of mineral or for
driving underground roadways normally achieve this by rotating
cutting tools or cutting tools mounted on cutting chains. Cutting
tools must always be maintained in good condition because blunt
tools increase the force required to cut, reduce the depth of cut
898
and produce much more fine dust.
The number of cutting tools
should also be kept to a minimum necessary to produce a given
volume of mineral.
Excessive numbers of tools means excessive
work is being done on the mineral and excessive fine dust is produced.
Similarly tool
speeds should be kept to the minimum which
will effectively break down the mineral.
A minimum number of well maintained cutting tools rotating
at low speed increase depth of cut and considerably reduce the
make of fine dust.
Further gains can be achieved by the use of water.
Water
sprays have been used for many years on machinery producing mineral
but experience has shown that external . sprays contribute little
to the reduction of fine dust.
Water is much more effective if
introduced ahead of the cutting tools« and this method is now
common practice in the United Kingdom.
Success in the use of
wetting agents in the suppression of dust has been reported in
Germany and Poland, but experiments and trials in the United Kingdom have been disappointing, showing no advantage to date. Experiments with the use of foam in both the United States of America
and the United Kingdom have shown it is only effective for
suppressing dust when excessively large quantities are applied
to cutting tool machines. Machines operating on longwall coal
faces can also derive benefits from the use of cowls to partly
screen the dust source from the ventilating current.
Passing
water and air through drill roads Is very effective during
drilling operations.
899
Respiratile dust produced and dispersed from shotflrlng
operations can be kept to a minimum only by ensuring that the
holes are correctly placed and charged in relation to the pull
or burden.
Such operations can also often take place when
workmen have been withdrawn, remaining in a clean environment
until fumes and dust have cleared«
Crushing operations or industrial processes again produce
respirable dust, but dispersal can be prevented or minimised by
complete enclosure and the application of finely atomised water
droplets within the enclosure.
Transfer of minerals from one
transport system to another can cause degradation, producing
fine dust and/or dispersing such dust previously settled out.
Enclosures and properly engineered and constructed equipment,
chutes, wetting of conveyor belts etc., can keep this source to
a minimum.
Air velocities of more than four metres per second
can raise dust previously settled out and should be avoided
wherever possible.
b.
Capture of airborne respirable dust
Many types of filter units or dust collectors are currently
available falling into two basic categories, i.e. dry filters
and wet-type dust collectors.
Dry filters are generally more efficient that the wet type,
but are not suitable, with certain exceptions, for use in the
mining situation because of their size, dust dispersal, etc.
Consequently, the dry type of filter is normally used in conjunction with enclosed extractor installations.
9oo
Wet-type dust collectors are used more effectively In the
mining heading or cul-de-sac situation.
Free standing filter
units situated In. .mine roadways and passing a large proportion
of the total quantity of air In the ventilating current can substantially reduce the total dust content, Including respiratale
sizes.
When mine roadways or tunnels are being formed by mechanised
means» overlap ventilating systems which Incorporate dust collection
can be Integrated Into the total system successfully.
Such systems
can operate with main forcing ventilation provisions.
Research and development has also taken place In the Un