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C. ASBESTOSIS
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A. iF. Ia&Z&| mt Pt Assistant Medical Director Metropolitan Life Insurance Company
Asbestosis is a pneunoconiosis caused by the inhalation of asbestos dust. It is distinct froa silicosis in Its pathology and clinically. Tihether asbestosis will remain a distinct fora of pulaonary dust disease or will- provery to be of a type common to a number of dusts remains to be seen. So far, It is .. the only pneumoconiosis, other than silicosis, which has received any consider able amount of study froa pathologists, clinicians, and industrial hygienists.
Tihereas silicosis has been recognised for cany centuries, asbestosis is a newcomer. Asbestos (Canadian) Is a hydrated magnesium silicate containing no free silica, but about lAf: of centimes silica, 43, magnesium, nearly 13> of water, and traces of iron and nickel. ITnile asbestos was known to the ancients, the fabricating of asbestos on a large scale is comparitively new and received a tremendous innetus from its use in connection'with automobiles and as an insul
ating material and a heat resistant for a great variety of mechanical purposes. YFhile Hoffman, in his celebrated Bulletin on Mortality froa Resoiretory (1) *
Diseases in Dusty Trades, called attention to the possible harmfulness of asbes tos dust in 1913, it res not until February, 1927 that asbestosis was, so to speak, officially recognised in this country' by the filing of a disability claim for workman's compensation in Massachusetts. The claimant was a foreman in the weaving d|martment of an asbestos plant and the claim was upheld by the Massachuscttsj^dustriel Accident Board. This was twenty-seven years after the first
fatal case was reported in England by Dr. Montague Murray. In 1910 and again in 1934, a fatal case was reported in England, and In 1923, the British Factory
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Department conducted an investigation and enacted laws for the protection and
conpensatioa of the worker cgainst this hazard. The whole subject in England
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has been very well summarised by Mere-ether in a series of articles in Tubercle.
At the present tine, as nearly as can be estimated, there are about 12,000
individuals eaployed in the chief asbestos plants in the United States of whoa,
10,000 might be exposed to asbestos dust.
In 1927, a fatal case of uncoanlicated asfcestosis was reported to the
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Kedical Society of South Carolina and since then, including this case, there
have been eleven fatal cases reported in the United States, eight uncoaplicated
and three complicated by tuberculosis. These reports, together with the fact
that esbestosis figured in the extraordinary occupational disease litigation
that has spread over this country, resulted in both laboratory and field stud
ies of this new hazard. Gardner and Cursings at Saranac Lake commenced animal
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experimentation with asbestos in 1923 and resorted their findings in 1931.
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These two authorities in the United States and Gloyne in England have pro
duced masterly descriptions of the pathology, while silicosis is predominantly
pareuchyjzatous, asbestosis is mainly interstitial, nor is asbestosis character
ized by the nodular formation so distinctive of silicosis.
A search of all the death records on file in the Metropolitan Life
Insurance Company revealed that asbestosis had been given as a cause or.con
tributing cause of death in only nineteen cases. The first case noted was
in 1924, two in 1927, or.e in 1931> amd the rest since 1933. The diagnosis was
supported by autopsy in only six. In one of these six, the primary cause of
death was carcinoma; in another, glioma of the brain; and in another, pulmonary
tuberculosis. In the other three, asbestosis was given as the primary cause
with cardiac failure as the contributing cause. Some of these cases were re
ported in the literature.
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# l* Asbestos is complicated by heart disease ras given as tte cense
of death in seven cases. There sere no autopsies ir these seven and pul-
nonary tuberculosis rss diagnosed in several by the atbeding physician,
so perheps too much seight cannot he given to these certificates.
Diabetes and pulrcr.ery tuberculosis sere also mentioned in the
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remaining six cases, in which there rere no autopsies. All these nineteen
cases cere rales and all cere white with one exception.
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In our studies of asbestos sines end fabricating plants, the clini
cal picture cf asbestesis was nilcer than that cf sillcisis. To be sure, the
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individual patient with narked asbestesis rill greatly resemble the individual
trith silicosis. There is the sane <5yspr.es on ererticn, the str.e dry cough,
the nore or less indefinite physical signs elicited by the stethescope. The
patient with csbsstcsis is apt to have clubbed fingers - not usually seen in
silicosis - end* he is apt to he pasty faced and even shrr e slight cyanosis,
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(r:v while the silicotic is apt to he fairly robust locking. Of course, in each
instance I refer to pstiehts where disecso is not complicated by infection.
YTe did not fir.d in ccnnunities where asbestos was mined or fabri
cated the familiar picture of disability and tuberculous infection so char
acteristic of hard rock mining ccnmunities. Cur pers'-rrj. observations rere
supported by the statements cf physicians practicing in these ccmnunitieo.
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. All the ceses of astect:5i3 re dtected rere, with ohs czcepticn, working
steedily at their trades. Ir. only one did re find evidence of active tubercu
losis end tbe.t diagnosis ras based on X-ray appearance-only, end shored heeled
tuberculosis. Gardner End Cumirgs in their reports cslled attention to the
difference between the action of asbestos dust end silica dust in relation to
tubercle irfecti.cn in experimental animals and their findings tend to beer
out our clinical observation.
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la all, cur clinical data aro "based on 126 physical examinations of asbestos workers, all of when had core than three years' exposure and who were selec ted at random. 65 of these shored an X-ray eppe6rez.ee which re thought indi cated a pneumoconiosis but their synptocs were indefinite and inconclusive. Tie called these cases first stage. 4, with evident pulconary synptocs and corrobative X-ray, re termed second stage. Of these 67, 2D hsd over ten years' exposure, end 13 had over IS years. Tie ere still continuing our asbestos .stud ies and hops to secure additional information on the tire element in develop-
cay he core apparent than reel but it is possible that the English factories
.My be core dusty than curs. There rere not available my comparative dust
counts but this impression is based on their reports ted statements cade to
ayself and colleagues by persons familiar with the English conditions. One
process, described ir. the British reports as "mattress raking" and stated to
be extremely dusty, docs not appear to have a courterpert in th<s country,
In 'both countries , energetic steps have been taken to control the dust hazard
in asbestos plant s so that it is probable that further oases of disabling as-
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bestosis will be rare.
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. As in silicosis, the diagnosis centers upon lie X-ray film. How
ever, the whole natter of attempting to interpret these files and correlate
then with the clinical evidence, if any, is difficult cod elusive. If, in
our studies, we had found a core clear cut ar.d severe type of pne*~*oconiocis
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trith narked symptoms and disability as cell as a distinctive X-ray appearance,
such as ny colleagues ar.d cyself had teen accustomed to find in our previous
investigations of silicosis, eta* task in attenpting to sake a positive diag
nosis and estimate the extent of the disease would have teen easier. There
is no doubt that, especially in the beginning, we were handicapped by endeev-
'oring to evaluate ashestesis with a silicosis foCt-rule.
. The X-rcy appearances ere not clear cut nor distinctive, as in sili
cosis end do net lend themselves to ready grouping into progressive stages.
There is less evident pathology in these films, the shsccrs are finer, core
granular, end softer, then in silicosis. The rstestosis film gives the im
pression of ground glass and there is no nodulaticn with the ccsseqvsnt ten
dency of the nodules to coalesce and give dense eparue areas in the films.
The distributicn cf the shadows is semewhat different, occupying the lever
third of the lung, except in far advanced cases when the shadows may occupy
the najer portion of the lung. T?e noticed fre^uswtly --2 well marled outline
of the interloper se;tun on the right side. e else noticed that a number of
the' films of cases of ashestosis had enlarged hearts, and this might be expec
ted when one ccnsif.ers that the pathological process'tends to constrict the
(7) pulmonary bleed vessels and they ramify along with the hror.chicles.
It is possible that the X-ray appearance cf ashestesis nay not be
distinctive of this disease clone but uniform in appearance with pneumoconi
osis due to other silicate dusts. Much mere investigation and study of X-ray
films of industrial workers exposed to all sorts cf silicate and other dusts
are needed before it will be possible to speak definitely cn this, the r.cst
important phase of the diegnosis of pnemmcccr.icsis.
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. One thing is certain. The utaost care and patience are needed to
elicit the occupational history of the patient end to correlate this and the
clinical picture rith the X-ray filn before a diagnosis of asbestcsis is Just
ified. As noted in relation to' other occupational health hazards, there is an
ell too frequent tendency to sake a diagnosis of a specific occupational dis
ease because of presumptive or actual exposure without the corroboration of
other essential factors to a correct diagnosis, Tie are not Justified in
leaking a' disgnesis of asbestcsis, any cere then of silicosis, in the pres
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ence of an X-ray.file shoring nc distinctive p-pnor.ary pathology.
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. Associated cith exposure to asbestos dust is the occurrence in the
sputua and pulmonary tissues of a peculiar formation hr.cnu as asbestos bodies.
These asbestes bodies'have been described by a number of observers r.nd^ar'e
due apparently to the action of the tissues upon the asbestos fibre. /Their
exact significance is doubtful but it is ccur.only agreed at the present tine
that they are r.ot dicgnostic of pulr.carry fibrosis rr.d indicate merely that
the ir.divid'.u.i' has'\oer. exposed to asbestos dust.
Sene observers believe
that rhere these rsbestes bodies appear in the sputum in clumps, they indi
cate actual disir.tegrticn of lung tissue.
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Dr. Miller cf the United States Public Health Service, ir. the
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Public Health ?.sports, describes the technique trhich he employes in the ir.tr?.-
pcritoneal injection of finely divided dusts in a state of suspension. Miller
defined three types of reaction - Absorption, Inert, end Proliferative. The
first is produced by relatively harmless-or inactive dusts; the second by
dusts rhich could cause pulmonary fibrosis; and the third is the typical re
action of silicosis, P.ecer.tly, in a personal communication, Miller described
the effects of the injection of three varieties of asbestos, namely chrysotile,
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crocidolite, cr.d anosite. Chrysctile is Car.ediaa asbestos and, es previously
stated, is largely naguesiun silicate. Crocidelite end ancsite contain only
a very snail quantity of raghesiua, containing instead iron silicate in approx
imately the sane quantity.
The three types of asbestos produced the sene type of reaction -
nanely the or.e described by this investigator as inert. "TTe have been assun- *
lng," he states, "that th9 dusts producing this..inert..reaction cause pr.euno-
coniosis of the diffuse fibrosis type as distinct iron the proliferative re
acting dusts rrhich cause nodular fibrosis. This essunptica, as you hr.cr, has
not been proven by corresponding aninal experiments rith the sene dusts, but
results fron observation of pathologic naterial iron autopsies. He further
states, "I believe that the gross behavior cf asbestos in the tissues has fur
ther strengthened the value of cur classification of dusts and the intraperi-
toneal test as e nears of detemining the harnful dusts by its clinical correl
ation."
" '. lluch verb renains to be done before rehear speah as^authcritatively
about asbestos as re do about silica. In the r.sar.tire, esbestps rlrr.ts ere
being cleared up and the dust controlled. This, together rith the snail nvnher
of persons enplcyed, in-lies that re rill probably^never have the re rith ef
clinical ncteriel that has been available ir. silicosis. It is by no nears cer
tain that asbestesis progresses as dees silicosis after rithdre.rtl fren dust
exposure, nor does infection seen to be as closely cr.d intinately associated
rith f.obcctcsis r.s rith silicosis. The ansrer to these end other prcblens
resulting fron exposure to silicate dusts deuands further study both in the
field and in the laboratory.
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BIBLIOGRAPHY
CD MORTALITY FROM RESPIRATORY DISEASES UT BUSTY T7JLBSS - Frederick L.
Hoffr.m - U. . Bspartr.snt of Labor - Bulletin of tie U. S.
Bureau of Labor Statistics, IIo. 31, Jure, 1913.
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Inspectors of Factories (Greet Britain) - Tubercle - Ucvenber,
* 1953; Becenter, 1333; Jcr.uary, 1934.
(5) PUIAICMARY ASSESTCSIS - Xametb M. I^nch ar.d Ulllian Ataor Sniti -
Anerican Rereiu of Tuberculosis, Vcl. Hill, "o. 6, June, 1331.
(4) studies cn empeeittutal piietmcuciioitcsis, vi. utalaticm or asezstcsis
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Gardner and Donald Z. Cunnings - .Tie Journal cf Industrial Hygiene,
Vol. XIII, Mo. 2, February, 1931.
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(5) THE
AMATCMY AMD HIST9I00I 0? ASBESTOSES - S. Roadhouse Gloyne, .
U. D., D. ?. H., - Tubercle - Vol.- XIV, To. 10, July, 1333; Mo. 11,
August, 1933; Vs. 12, Sep.ter.oer, 1035.
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Asst. Medical Uircctcr; end J. Ml11inn Fsbnsl, Cksnist; - Metro
politan Life Insurance Co., Public Health reports, Vol. SO, Mo. 1,
Janyor,- 4, *<c5#
(7) EISCUSSIC:: - Jarx3 L. Dubro-U- - Journal of tie Anoricer. Medical Arscci:-
ticn - Vcl. 103, Mo. 11, September 13, 1934 (y.314)
(3). PULMCDAEY ASBESTOSES - X. Burton TTscd, M. B. Coni., M.R.C.P. lend.,
B.P.H. and S. Rscdicure Gloyne, !!. B. Leeds, B.P.E. - Tie Lance:,
Becenber 2?., 1334.
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0) THE PHYSIOLOGICAL RESPONSE 0? TIT PZE.ITOITAl TISP7T TO BUSTS IT'"'"
AS FCrSITV BOBUS* Join ~. Miller, Acting Assistant Sur,,s
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R. R. Sayers, Suryeen, J. S. Public Health Service- Public "
Reports, Vcl. 49, Me. 3, January 19, 1934.
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