Document pBpmkDoOQME6ZgmZe5a9aO907

ASBESTOSIS . J5SV. / />; A. J. LANZA, M.D. Assistant Medical Director, Metropolitan Life Insurance Company NEW YORK r Reprinted from The Journal of the American Medical Association February 1, 1936, Vol. 106, pp. 36S and 369 Copyright, 193tf, y American Medical Association 535 North Dearborn Street Chicago, III. i :r >m 'ft' /airiuil .''`'i .try /, !')So c >r;>- t /`J'v . f \f, / /*/. .-'M ; 1/,f ti .hi, ,./u \l, - < ; ' . K,, . i <>! ASl'.F.SToSIS A. .1. LAX/A. ,\f.L>. A?a:s::i: r Mr-iwal f)irc.!or, Metropolitan Lite Insurance Company Nr.W \"t<K Asbestosis is a pneumoconiosis caused by the inhala tion of asbestos dust. It is distinct trout silicosis in its pathology and clinically. Whether asbestosis will remain a distinct form of pulmonary dust disease or will prove 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, that has received any considerable amount of study from pathologist?, clinicians and industrial hygienists. Whereas silicosis has been recognized for many cen turies. asbestosis is a newcomer. Asbestos (_Canadian) is a hydrated magnesium silicate containing no free silica but about 44 per cent of combined silica, 43 per cent magnesium, nearly 13 per cent of water, and traces of iron and nickel. While asbestos was known to the ancients, the fabricating of asbestos on a large scale is comparatively new; it received a tremendous impetus from its use in connection with automobiles and as an insulating material and a heat resistant for a great variety of mechanical purposes. While Hoffman *1 called attention to the possible harmfulness of asbestos dust in 1918, it was not until February 1927 that asbestosis was, so to speak, officially recognized in this country by the filing of a disabilityclaim for workmen's compensation in Massachusetts. The claimant was a foreman in the weaving department of an asbestos plant, and the claim was upheld by the Massachusetts Industrial Accident Board. This was twenty-seven years after the first fatal case was reported in England by Dr. Montague Murray. In 1910 and Read before the Section on Preventive and Industrial Medicine and Public Health at the Eighty-Sixth Annual Session ot the American Medical Association, Atlantic City, N\ J., June 13, 1935. 1. Holman, F. L.: ' Mortality from Respiratory Diseases in Dusty Trades, Bull. 231, U. S. Department ot Labor, June 1918. c 9 again in 1934 a fatal case was reported in England, and in 1928 the British Factory Department conducted an investigation and enacted laws for the protection and compensation of the worker against this hazard. The whole subject in England has been summarized by Merewether.2 At the present time, as nearly as can be estimated, there are about 12,000 individuals employed in the chief asbestos plants in the United States, of whom 10,000 might be exposed to asbestos dust. In 1927 a fatal case of uncomplicated asbestosis was reported to the Medical Society of South Carolina,3 4 5 and since then, including this case, there have been eleven fatal cases reported in the United States, eight uncomplicated and three complicated by tuberculosis. These reports, together with the fact that asbestosis figured in the extraordinary occupational disease litiga tion that has spread over this country, resulted in both laboratory and field studies of this new hazard. Gard ner and Cummings * at Saranac Lake, N. Y., com menced animal experimentation with asbestos in 1928 and reported their observations in 1931. These two authorities in the Lhiited States and Glovne 3 in England have described the pathology. While silicosis is pre dominant!}' parenchymatous, asbestosis is mainly inter stitial ; nor is asbestosis characterized by the nodular formation so distinctive of silicosis. A search of all the death records on file in the Metro politan Life Insurance Company revealed that asbestosis had been given as a cause or contributing cause of death in only nineteen cases. The first case noted was in 1924. there were two in 1927, one occurred in 1931, and the rest have occurred since 1933. The diagnosis was supported by autopsy in only six. In one of the 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 contribut ing cause. Some of these cases were reported in the literature. 2. Merewether, E. R. A.: A Memorandum on Asbestosis. Tubercle 15:69 (Nov.), 109 (Dec.) 1933: 15:152 (Jan.) 1934. 3. Lynch, K. M., and Smith, \V. A.: Pulmonary Asbestosis, Am. Rev. Tuberc. 23: 643 (June) 1931. 4. Gardner, L. U.. and Cummings. D. E.: Studies on Experimental Pneumonokoniosis: VI. Inhalation of Asbestos Dust: Its Effect upon Primary Tuberculous Infection. J. Indust. Hvg. 13:65 (Feb.) 1931. 5. Gloyne, S. R.: The Morbid Anatomy and Histology of Asbestosis. Tubercle 14: 445 (July), 493 (Aug.), 550 (Sept.) 1933. 1 '1 -OVt* 'M " c* impt icnten by hoart < hsea-c wa- given cu;-c "i 'Icath in seven cases . T lie re were no : 'ic- *n 'ue.'C -even and pullll' in ary tuberculosis 'O' i iu -cveral 1 >v the attend!ng physician, erhap- i" o much Wei gilt cannot he given to these notes. Diabetes and pulmonary tuberculosis were also men::"ncd in the remaining six cases, in which there were no autopsies. All nineteen patients were males and with one exception all were white. In our studies of asbestos mines and fabricating plants.* the clinical picture of asbestosis was milder than that of silicosis. To be sure, the individual patient with marked asbestosis will greatly resemble the indi vidual with silicosis. There is the same dyspnea on exertion, the same dry cough, and the more or less indefinite physical signs elicited by the stethoscope. The patient with asbestosis is apt to have clubbed fingers-- not usually seen in silicosis--and he is apt to be pasty faced and even show a slight cyanosis, while the silicotic patient i> apt to be fairly robust looking. Of course, in each instance I refer to patients whose disease is not complicated by infection. We did not rind in communities in which asbestos was mined or fabricated the familiar picture of disa bility and tuberculous infection so characteristic of hard rock mining communities. Our observations were sup ported by the statements of physicians practicing in these communities. All the patients with asbestosis that we detected were, with one exception, working steadily at their trades. In only one case did we find evidence of active tuberculosis and that diagnosis was based only on the roentgen appearance. Several showed healed tuberculosis. Gardner and Cummings in their reports called attention to the difference between the action of asbestos dust and silica dust in relation to tubercle infection in experimental animals, and their observa tions tend to bear out our clinical study. In all. our clinical data are based on 126 physical examinations of asbestos workers, all of whom had more than three years' exposure and who were selected at random. Sixty-three of these presented a roentgen appearance which we thought indicated a pneumoconi osis, but the symptoms were indefinite and inconclusive.6 6. Lanza, A. J.: McConnell, W. J., and Fehnel. J. \V\: Effects of the Inhalation of Asbestos Dust on the Lungs of Asbestos Workers, Pub. Health Rep. SO: 1 (Jan. 4) 1935. r 4 We called these cases first stage. Four presenting evi dent pulmonary symptoms and corroborative roentgeno grams. we termed second stage. Of these sixty-seven patients, twenty had been exposed more than ten years and thirteen more than fifteen years. We are still con tinuing our asbestos studies and hope to secure additional information on the time element in develop ment and the tendency and rate of progress. One feature that has impressed us is that the British investigators found asbestosis more severe and more menacing than we did. This difference may be more apparent than real, but it is possible that the English factories may be more dusty than ours. There were not available any comparative dust counts, but this impression is based on their reports and on statements made to myself and my colleagues by persons familiar with the English conditions. One process, described in the British reports as "mattress making" and stated to be extremely dusty, does not appear to have a counter part in this country. In both countries, energetic steps have been taken to control the dust hazard in asbestos plants, so that it is probable that further cases of dis abling asbestosis will be rare. As in silicosis, the diagnosis centers on the roentgeno gram. However, the whole matter of attempting to interpret these films and correlate them with the clin ical evidence, if any. is difficult and elusive. If. in our studies, we had found a more clear-cut and severe type of pneumoconiosis with marked symptoms and dis ability as well a? a distinctive roentgen appearance, such as my colleagues and myself had been accustomed to find in our previous investigations of silicosis, our task in attempting to make a positive diagnosis and estimate the extent of the disease would have been easier. There is no d<>ubt that, especially in the begin ning. we were handicapped by endeavoring to evaluate asbestosis with a silicosis foot rule. The x-ray appearances are not clear cut or distinctive as in silicosis and do not lend themselves to ready grouping into progressive stages. There are less evident pathologic changes in these films and the shadows are finer, more granular and softer than in silicosis. The asbestosis film gives the impression of ground glass, and there is no nodulation with the consequent ten dency of the nodules to coalesce and give dense opaque areas in the films. The distribution of the shadows is i h-: th m- n:: in (i; I-"' ar pa- W! t>-ti te: pr pt: M.* pc th is li ar ey- v: K I) - ; C, .V si-mewhat different, occupying the louver third of the lung, except in far advanced cases, when tire shadows n ay occupy the major portion of the lung. We noticed frequently the well marked outline of the interlobar septum on the right side. We also noticed that a num ber of films in cases of asbestosis showed enlarged hearts, and this might be expected when one considers that the pathologic process tends to constrict the pul monary blond vessels as they ramify almg with the bn-nchioles/ It is possible that the x-ray appearance of asbestosis may not be distinctive of this disease alone but uniform in appearance with pneumoconiosis due to other silicate dusts. Much more investigation and study of roentgen ograms of industrial workers exposed to ail sorts of -ilicate and other dusts are needed before it will be possible to speak definitely on this, the most important phase of the diagnosis of pneumoconiosis. One thing is certain. The utmost care and patience are needed to elicit the occupational history of the patient and to correlate this and the clinical picture with the roentgenogram before a diagnosis of asbes tosis is justified. As noted in relation to other occupa tional health hazards, there is an all too frequent tendency to make a diagnosis of a specific occupational (disease because of presumptive or actual exposure with out the corroboration of other essential factors to a correct diagnosis. One is not justified in making a diagnosis of asbestosis any more than of silicosts in the presence of a roentgenogram showing no distinctive pulmonary pathologic changes. Associated with exposure to asbestos dust is the occurrence in the sputum and pulmonary tissues of a peculiar formation known as asbestos bodies. These asbestos bodies have been described by a number of observers and are due apparently to the action of the tissues on the asbestos fiber. Their exact significance is doubtful, but it is commonly agreed at the present time that they are not diagnostic of pulmonary fibrosis and indicate merely that the individual has been exposed to asbestos dust.'* Some observers believe that, when these asbestos bodies appear in the sputum in7 * 7. Dubrow, J. L., in discussion on McCann, W. S.; Hurtado, Alberto; Kaltreider, Xolan. and Fray, W. W\: The Estimation of Functional Disability in the Pulmonary Fibroses, J. A. M. A. 103:510 (Sept. 15) 1934, Merewetber.2 Wood, W. B., and Gloyne, S. R.: Pulmonary Asbestosis, Lancet 2: 1333 (Dec. 22) 1934. 6 clumps, they indicate actual disintegration of lung tissue. Dr. Miller 9 of the United States Public Health Ser vice describes the technic that he employs in the intraperitoneal injection of finely divided dusts in a state of suspension. Miller defined three types of reaction : absorptive, inert and proliferative. The first is pro duced by relatively harmless or inactive dusts, the sec ond by dusts that might cause pulmonary fibrosis, and the third as the typical reaction of silicosis. Recently Miller 10 described the effects of the injection of three varieties of asbestos; namely, chrysotile, crocidolite and amosite. Chrysotile is Canadian asbestos and. as pre viously stated, is largely magnesium silicate. Crocido lite and amosite contain only a small quantity of magnesium, containing instead iron silicate in approxi mately the same quantity. The three types of asbestos produced the same type of reaction : namely, the one described by this investi gator as inert. He states: We have been assuming that the dusts producing this inert reaction cause pneumoconiosis c>f tiie diffuse fibrosis type as distinct from the proliferative reacting dusts which cause nodular fibrosis. This assumption, as you know, has not been proven by corresponding animal experiments with the same dusts, but results from observation of pathologic materia! from autopsies. . . . I believe that the gross behavior of asbestos in the tissues has further strengthened the value of our classification of dusts and the intraperitoneal test as a means of determining the harmful dusts by its clinical correlation. Much work remains to be done before asbesto'sis ispoken of as authoritatively as is silicosis. In the mean time. asbestos plants are being cleaned up and the dust is being controlled. This, together with the smaller number of persons employed, implies that there wifi probably never be the wealth of clinical material that has been available in silicosis. It is by no means certain, that asbestosis progresses a.' does silicosis after with drawal from dust exposure, nor does infection seem, m be as closely and intimately associated with asbestos;. as with silicosis. The answer to these and other prob lems resulting from exposure to silicate dusts demandfurther study both in the field and in the laboratorv. Metropolitan Life Insurance Company. 9. Miller, f. \V.f and Sayers. R. K.r T,;-j Phjsiou^ica: ResT'-n^ the Peritoneal Tissue to Dusts Introduce! as Foreign Bodies. Pui>. Jl;a!: Rep. 49: 80 (Jan. 19) 1934. 10. Miller, T. W.r Persona! communication to the author.