Document 2Ja1EjVmB0M74akDrwR8M2546

/. i i i * l* i <* * tK ' LJ . tomy is still in its infancy. Postoperative observations may be changed as the survival period increases, which, if it does, will alter.the surgical indications and the selection of cases. Close cooperation between laboratory investigators,. elinidahs and neurosurgeons is imperative in order to make the best selection of cases for surgery and to evaluate accurately the results obtained, whether they are failures or successes. ASBESTOSIS ,,: . A. J. LANZA, US). . Assistant Medical Director, Metropolitan life Insurance Company ' MEW Y0BX Asbestosis Is a pneumoconiosis caused by the_inhala tion of asbestos dust It is distinct from silicosis in its pathology and clinically.. Whether asbestosis trill remain a distinct form of pulmonaiy dust disease or trill 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 pathologists, dinidans 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 2c3al*led 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 disability daim for workmen's compensation in Massachusetts. The claimant was a foreman in the wearing department of an asbestos plant, and the daim was uphdd by the Massachusetts Industrial Acddent 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 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.* 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,* and since then, including this case, there have been eleven fatal cases reported in the United States, right 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 Rcad before (be Section on Preyentire and Industrial Medicine and Public Health at the Eixbty-Sixth Annual Session of the American Medical Association, Atlantic City, N. Jane 13, 1935. 1. Hoffman, F. L.: Mortality from Respiratory Diseases ta Dusty Trades, Bull. 211, U. S. Department of labor, Jane 1910. 2. Mercwetber. E., R. A.: A Memorandnm on Asbestosis, Tubercle 16s 69 (Not.). 109 (Dee.) 1933: 1511S2 Can.) 1936. . 3. Lynch, K. M., and Smith, W. A.: Pulmonary Asbestosis, Am. Rct. Tnbcrc. 28: 643 (June) 1931. . . . r m................ . , 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 United States and Gloyne * in England have described the pathology. While silicosis is pre dominantly 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. Asbestosis complicated by heart disease was given as the cause of death in seven cases. There were no autopsies in these seven and pulmonary tuberculosis was diagnosed in several by the attending physician, so perhaps too much weight cannot be given to these certificates. .. Diabetes and pulmonary tuberculosis were also men tioned 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 dinical 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 dubbed fingers-- not usually seen in silicosis--and he is apt to be pasty faced and even show a slight cyanosis, while the silicotic patient is 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 find in communities in which asbestos was rained or fabricated the familiar picture of disa bility and.tuberculous infection so characteristic of hard rock mining communities. Our observations were sup ported .tty 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 dinical study. In all, our dinical 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- 4. Gardner, L. U,, and Cummings, D. E>: Studies on Experimental Pactxmonoiconioeis: VI. Inhalation of Asbestos Dust: Its Effect upon Primary Tnberenloas Infection, J. Xndast. Hy*. 13163 (Feb.) 1931. 5. Gloyne, S. R.: The Morbid Anatomy and Hitttdofy of Asbestosis, Toberde 14t44S (Jobr). 493 (Ant.)', 550 (Sept.) 1933. 6. Inn, A. T.; McConnell, W. J.. and Febnd, J. W.t Effects of the Inhalation of Asbestos bast on the Lanes of Asbestos Workers,. Pub. Health Rep. 60s 1 (Jan. 4) 1935. . . -- t E HO 03173 Vol( ji New__ f ASBEi )sis--. LANZA 369 osis, but the symptoms were indefinite and inconclusive. patient and to correlate this and the clinical picture .... We called these cases first stage. Four presenting evi- . with the roentgenogram before a diagnosis of asbes ( " dent pulmonaiy symptoms and corroborative roentgeno- tosis is justified. As noted in relation to other occupa '" grams, we termed second stage. Of these sixty-seven tional health hazards, there is an all too frequent patients, twenty had been exposed more than ten years tendency to, make a diagnosis of a specific occupational and thirteen more than fifteen years. We are still con disease because of presumptive or actual exposure with tinuing'our asbestos studies, and hope , to secure out the corroboration of other essential factors to a additional information on the time element in develop correct diagnosis. One is not justified in making a ment and the tendency and rate of progress. . diagnosis of asbestosis any more than of silicosis in the One feature that has impressed us is that the British presence of a roentgenogram showing no distinctive investigators found asbestosis more severe and more pulmonaiy pathologic changes. menacing .than we did. This difference may be `more Associated with exposure to asbestos dust is the apparent than real, but it is possible that the English occurrence in the sputum and pulmonary tissues of a factories may be more dusty than ours. There were peculiar formation known as asbestos bodies. These not available any comparative dust counts, but this asbestos bodies have been described by a number of impression is based on their reports and on statements observers and are due apparently to the action of the made to myself and my colleagues by persons familiar tissues on the asbestos fiber. Their exact significance with the English conditions. One process, described in is doubtful, but it is commonly agreed at the present the British reports as "mattress making'' and stated to time that they are not diagnostic of pulmonary fibrosis be extremely dusty, does not appear to have a counter and indicate merely that the individual has been part in this country. In both countries, energetic steps exposed to asbestos dust.* Some observers believe that, have been taken to control the dust hazard in asbestos when these asbestos bodies appear in the sputum-in plants, so that it is probable that further cases of dis clumps, they indicate actual disintegration of lung abling asbestosis will be rare. . tissue. . As in silicosis, the diagnosis centers on the roentgeno Dr. Miller* of the United States Public Health Ser gram. However, the whole matter of attempting to vice describes the technic that he employs in the intra- interpret these films and correlate them with the din- peritoneal injection of finely divided dusts in a state - ical evidence, if any, is difficult and elusive. If, in our of suspension. Miller defined three types of reaction: C studies, we had found a more dear-cut and severe type absorptive, inert and proliferative. The first is pro of pneumoconiosis -with marked symptoms and dis duced by relatively harmless or inactive dusts, the sec ability as well as a distinctive roentgen appearance, ond by dusts that might cause pulmonary fibrosis, and such as my colldigues and myself had been accustomed the third as the typical reaction of silicosis. Recently to find in our previous investigations of silicosis, our Miller*109described the effects of the injection of three task in attempting to make a positive diagnosis and varieties of asbestos; namely, chrysotile, croddolite and estimate the extent of the disease would have been amosite. Chrysotile is Canadian asbestos and, as pre easier. There is no doubt that, especially in the begin viously stated, is largely magnesium silicate. Croddo- ning, we were handicapped by endeavoring to evaluate lite and amosite contain only a small quantity of asbestosis with a silicosis foot rule. magnesium, containing instead iron silicate m approxi The x-ray appearances are not dear cut or distinctive mately the same quantity. ' as in silicosis and do not lend themsdves to ready The three types of asbestos produced the same type grouping into progressive stages. There are less evident of reaction; namely, the one described by this investi pathologic changes in these films and the shadows are gator as inert He states: .' finer, more granular and softer than in silicosis. The We have been assuming that the dusts producing this inert asbestosis film gives the impression of ground glass, reaction cause pneumoconiosis of the diffuse fibrosis type as and there is no nodulation with the consequent ten distinct from the proliferative reacting dusts which cause nodular dency of the nodules to coalesce and give dense opaque areas in the films. The distribution of the shadows is. somewhat different, occupying the lower third of the lung, except in far advanced cases, when the shadows may 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 C hearts, and this might be expected -when one considers that the pathologic process tends to constrict the pulmonaiy blood vessels as they ramify along with the bronchioles.* `` ` ' 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 all sorts of silicate and other dusts are needed before it will be possible to speak definitely on this, the .most important phase of the diagnosis of-pneumoconiosis. . fibrosis. This assumption, as you know, has not been proven by corresponding animal experiments with the same dusts, but results from obsovation of pathologic material 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 asbestosis is spoken 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 will probably never be.the wealth of clinical material that has been available in silicosis. It is by no means certain that asbestosis progresses as does silicosis after with drawal from dust exposure, nor does infection seem to be as closely and intimately associated with asbestosis as with silicosis. The answer to these and other prob lems resulting from exposure to silicate, dusts demands further study both in the field and in the laboratory. One thing is certain. The utmost care and patience Metropolitan Life Insurance Company. are needed to elicit the occupational history of the 7. Dubrow, J. L, in diicockm on McCann* W S.; Hurtado, Alberto: Kaltreider, Nolan, and Fray. W. W: The Estimation cf Functional Disability in tbe Pulmonary Fibroses* J, A. M. A. 103* 10 (Sept. IS) ,8. Mtrewetlier.* Wood, W. B.. and Glojroe. S. R-: Pulmonaiy Asbestotis. Lancet 2: 1383 (Dec 22) 1934. 9. Miller* J. W.* and Sayers, R. R.: Tbe Fhysiolofical Response of tbe Peritoneal Tissue to Dusts Introduced as Forezs Bodies. Pub. Health Rep. 40180 (Jan. 19) 1934. . 10. Miller* J^W.: Personal communication to tbe author. " EM00317A