Document 6bn1VdZ5b48jXx7oLOw30e1wo

f1 5 THE JOURNAL OF S'-- NDUSTRIAL HYGIENE and TOXICOLOGY EDITORS DAVID L. EDSALL, M.D., S.D., United States EDGAR L. COLLIS, M.D., M.R.C.S., Great Britain VOLUME 18 JANUARY, 1936--DECEMBER, 1936 PUBUSHED BY THE WILLIAMS & WILKINS COMPANY Baltimore, Md. n L.4 (w TO! / m.' m- f'^ t-'av:*. ~ =La. PULMONARY ASBEST0SI8: INCIDENCE AND PROGNOSIS* J. Don-nelly, M.D. Mecklenburg Sanatorium, Huntersville, N. C. ITHIN a comparatively short effective types of suction apparatus Wtime the occupational disease, now in use will remove a maximum . pulmonary asbestosis, has be- of not over 90 per cent of the dust, come a matter of considerable impor- but the remaining 10 per cent may be tance, not only to manufacturers of definitely injurious. In 1916 protec- asbestos products, but also to the tive devices of the suction type were workmen engaged in the industry, placed in a certain asbestos mill, and That the serious industrial hazard of yet 15 years later cases of asbestosis this type of work has not previously with fatal termination were reported received sufficient attention is becom- among workers from this plant. Since ing more apparent. The manufacture the most efficient type of protective of asbestos products has increased machinery known apparently does not more than four-fold in the last 20 completely protect, although the num- years, and hence, because of the ber of workers affected is probably greater number of workers exposed, somewhat reduced, and the time re- and the more frequent recognition S3 . quired for the production of an ad a pathological entity of the resulting vanced type of disease is probably pulmonary condition, the subject of lengthened, the problem becomes a asbestosis has rapidly assumed greater matter for serious consideration, importance. In the case of any industrial em It is indicated that the owners of ployee presumed to be physically asbestos plants, and the workers them- handicapped by any condition or dis- selves, are beginning to realize that ease, supposedly caused or aggravated exposure to asbestos dust is a serious by conditions under which he has occupational hazard, and it also is worked, there enters the question of apparent that these workers must be compensability. Pulmonary asbesto- protected against the hazard as effec- si3 has not as yet been widely recog- tively as is possible. That this pro- nized as a compensable disease in tection can be made complete seems states having laws governing the very doubtful. It seems to be the compensation of workers. If such opinion of engineers that the most cases are viewed as compensable un der the Industrial Compensation Law3, 1335BeceiV*d (0T publiestioa Jaauary 2* it will be necessary to decide the. Rend before tbe Industrial Hvgiene Sec- degree of disability in each individual ffilSuiaSSSS'iffiSSStoSIlt " "* "V b8 Milwaukee, Wis., Oct. S, 1935. made. 222 vul. 18, no. 4] . PULMONARY ASBESTOS1S 223 actically all writers on the sub ject are agreed that the principal symptom of the condition is a varying degree of dyspnea, and that the physi cal signs are those found in fibroid tuberculosis. Hence a definite diag nosis cannot be made by a physical examination alone. The x-ray film, however, is distinctive, in that it shows a picture of pathological changes in several particulars different from those found in the x-ray films of any Jther respiratory abnormality. The presence of the condition can be dem- mstrated by the x-ray film alone, but he degree of disability cannot be stimated unless the symptoms and hysical signs axe also considered, 'he dyspnea is usually out of propor- on to other symptomatic manifesta- ons, and is the one symptom which, i the more advanced cases, precludes ly form of muscular exertion. For lat reason, an asbestotic victim is lah'e to sell his labor on the open a , and must be rated as totally sabled. ' ' I. have seen no statistics in the erature in regard to the incidence asbestosis among the workers in the iustry. It would seem to be a itter of some importance to deter- ne the average number of employees .o may be now, or who are likely become, disabled by the condition, ave lately had occasion to review the ay films of 151 workers in asbestos Is. Of these, fifty-two showed mite evidence of asbestosis in ying degrees. Of the 151, eighty- had worked in asbestos for periods yiug from 4 to 20 years, and "in s group were found fifty-one of the itive cases, a percentage of 59.3. re was only one case with definite x-ray evidence of asbestosis who had worked less than 4 years in the indus try. Of the 52 workers with evidence of asbestosis only four had worked less than 5 years, forty-eight having been employed for 5 years or more. There were eleven with an advanced type, no one of whom had worked less than 8 years. One of these advanced cases had been exposed to asbestos dust for 8 years, two for 9, and one each for 10, 11, 12, 14, 15, 16, 17 and 20 years. Unfortunately I have no record of the length of service of these employees in the various departments of the mills, all of which are unquestionably dusty, but it is agreed that the carding room is the dustiest, and the weave room probably next. It is presumed that the dustier the work, the more likelihood there is that pathological changes in the lungs may result. It is noteworthy, however, that some employees work in asbestos plants for years without;suffering any pathologi cal changes in the lungs, as far as can be detected in the x-ray films. In this series of 151 employees, ninety-nine showed no positive evi dence of asbestosis in the films. Five had worked in asbestos for 6 years, three for 7, three for 8, four for 9, six for 10, one for 11, and one for 15 years. All the others had worked for periods varying from a few months to 5 years. Since the percentage of those in the series who were affected was so high, it seems remarkable that so many could be entirely free from the condition even after years of expo sure. Since this process is non-infectious, the term "physical resistance to disease" is not applicable. It is true that muscular development avails \ ( 224 JOURNAL OF INDUSTRIAL HYGIENE AND TOXICOLOCY [Apr., jm nothing as a protection against the disease, since well developed men are as frequently affected as those not so well developed. It is also possible that some individuals may be sus ceptible even though exposed to low concentrations of dust. It is the opinion of some writers that the inhalation of asbestos dust and the consequent production of asbestosis has a tendency to exacerbate old tuberculous lesions. This opinion is apparently not universal. Merewether (1) says "from a review of 42 fatal cases of confirmed asbestosis it appeals that asbestosis ... is less fre quently accompanied by tuberculosis than is silicosis." Gardner and Cum mings (2) state that "primary tubercu lous infection is influenced only to a limited degree by inhaled asbestos." Egbert (3), dn an analysis of 28 cases of pulmonary asbestosis with fatal termination as reported in the litera ture, found that tuberculosis was present in only 6 cases of the 28, and in only 3 instances was death due primarily to tuberculosis. . It is universally agreed that silicosis does tend to exacerbate old tubercu lous lesions. In fact more or less rapidly progressive tuberculosis is considered the most frequent and most serious complication of silicos'13. Boisliniere (4) says that silica is the only phthisis-producing dust. In ob servations for several years I have been unable to find evidence that the inhalation of asbestos dust, or the condition asbestosis itself, has any tendency to render active old, appar ently healed tuberculous lesions. In this series of 151 workers there were three who had a definite asbestosis in addition to an apparently healed tuber culosis. One bad heen working in asbestos for 10 years, another for 4 years, and the third for 2 years. There was no evidence in the films that the presence of asbestosis had yet had any tendency to activate the tuberculous lesion. The films of 23 workers showed evidence of tubercu lous infection without any pathological changes indicating asbestosis. Of these, eleven showed healed childhood type tuberculosis, but none of these had worked longer than 15 months in asbestos. Two workers showed healed childhood type tuberculosis with no asbestosis, one of whom had spent 8 years in the work and the other 6 years. There were 5 films showing apparently arrested adult type disease with no asbestosis. These films were of employees who had spent the following periods in this work: One each, for 4, 6, 7, and 9 years; and one, no term of sendee given. There was 1 case with an apparently healed and calcified miliary tuberculosis with a history of only S months' service in the industry. . In the 151 films there were only four which, from an x-ray standpoint, were diagnosed as probably active tuberculosis of the adult type. One of these had been in sendee for 5 months, and one each for 15 months, for 6 years, and for 10 years. Since 1 case had worked only 5 months and another 15 months, it would seem im probable that this type of work could be the cause of their, active disease, particularly as the films of both cases indicated a -chronic type of disease and apparently not an acute exacerba tion. There remain for consideration 2 active cases with 6 and 10 years' sendee respectively. Agreeing that rol. IS, <> -<1 PULMONARY ASBESTOSIS 225 .De work in asbestos may have aggra vated their pulmonary condition, 2 cases of active tuberculosis in 151 workers seems a decidedly low per centage, if thi3 type of industrial occupation has any tendency per se to exacerbate old tuberculous lesions. ..Tuberculosis of an active type may be found quite as frequently in the routine examination of workers in any industry, regardless of whether or not the occupation be dusty. Case X, The x-ray films of one man who has worked approximately 10 years in asbestos illustrates the fact that employment in this industry even for a long time does not tend always to re-activatc old tuberculous lesions. The first film, taken April 2, 1930, shows some fine fibrosis on both sides from the 6th to the 9th posterior ribs, thickened interlobular pleura with some involvement of the diaphrag matic pleura, and a slightly "shaggy" 1 ; outline, these pathological changes indicating a probable asbestosis which is not very far advanced. In addition to this condition the film shows a tuberculous infiltration in the right apex, which appears to be in a quiescent state. The second film, taken May 3, 1935, indicates that the tuberculous lesion still remains inac tive, although a period of 5 years has elapsed since the previous film was taken. This man left the asbestos industry for a while during this period, but returned to it about 2 years ago. One of the most important problems in the consideration of pulmonary as bestosis is whether or not the disease is progressive, even after an individual handicapped by it ceases to work in the industry. Information on this question is of considerable moment in rating the eventual degree of disability of a worker, either in the assessment of damages in civil suits or in claims under State Compensation Laws. Sparks (5) states that the disease is apparently progressive, not even the cessation of exposure to the dust checking its spread. Wood and Gloyne (6) state that once asbestosis bodies are found in the sputum the course of the disease appears pro gressively downward, and cessation of exposure then does not check the spread. Many writers consider that silicosis is a progressive disease, regardless of whether or not there has been cessa tion of exposure. However, Sayers (7) says that "a man suffering from simple silicosis generally improves when removed from the dusty atmos phere and placed in suitable surround ings." Boisliniere (4) says: "Silicosis by no means always progresses after the hazard has ceased, nor does it always produce tuberculosis." It is reasonable to assume that the eventual effect of the inhalation of a dust which sometimes contains as much as 99 per cent silica might be somewhat more severe than that caused by a dust which contains a maximum of only 2.6 per cent. It seems to be true, however, that the fibrosis in asbestosis is produced by a much shorter exposure than is' the rule in silicosis. Gardner and Cum mings (2) say: "The particles and elongated fibers of asbestos dust do not, during this period (2 years and 5 months), penetrate so deeply into the air passages of the lung as do the other dusts previously studied. The major portion is held up and pbagocytosed in the lumina of respiratory ', v ^ . ip .. W-. 3- rss-:.- . 'Mriurajtv .t 226 JOURNAL OF INDUSTRIAL HYGIENE AND TOXICOLOGY [Apr., ms bronchioles and the alveoli given off Case III. C. A. B., white male. from their walls." Since the condi Quit his work in the card room of an tion is not an infectious process, it asbestos plant in June, 1931, after should not continue to progress on re having worked continuously for 8 moval of the causative factor. Gard years. The first film was taken June ner and Cummings (2) state that the 13, 1931; the second film, January 30, asbestosis body and the production 1935. The first film shows a bilateral of fibrous tissue in the lung is caused fibrosis over the lower two-thirds of by hydrolysis of asbestos fibers in the the lungs, the usual "shaggy" heart tissues. Theoretically, then, extension outline and adhesive pleurisy. This of the pathological process should case was diagnosed well-advanced as continue until all asbestos fibers re bestosis. The last film shows an maining in the lung are hydrolyzed, extensive progression of the condition, which may require a considerable time. the fibrosis having extended into the Several of my cases seem to indicate apices, and also become more dense. that the rapidity of progress of the In spite of the fact that this man ha3 fibrotic change in the lungs after had no exposure for a period of 3J- cessation of exposure is dependent to years, the condition has steadily be some extent on the amount of involve come more extensive. At the time ment which occurred before the indi this is Written he has begun to show vidual ceased work. To illustrate this symptoms of progressive heart failure, point, consideration of additional x-ray and a fatal termination seems in films of 3 cases reported in 1933 may evitable. . be of interest. . ' ' * Case IV. R. Gj J.; white male. Case II. D. S. W., white male. Quit his work in the card room of an Ceased work in card room of asbestos asbestos plant in April, 1930. The plant in January, 1929, after working first film was taken April 23, 1930, only IS months. The first film was and shows fine fibrosis and mottling taken June 13, 1931, and shows a over the lower lung fields with soma fairly extensive fine fibrosis, a "shagginess" of the heart outline' and "shaggy" heart outline and some pleural adhesions. The next film, involvement of the pleura. The sec taken September 2, 1931, 16 months ond film was taken on March 8, 1935, after the first film, shows some in approximately 4 years later. Com crease in the pulmonary fibrosis. This parison of the two films indicates man, under rest treatment, improved that in the 4 year interval the densi his general physical condition ma ties at the hila have increased notice terially. He was advised r.ot to return ably, the pulmonary fibrosis has ex to work in an asbestos plant, but ha tended toward the apices, and the did not heed this advice because he hypertrophy of both the right and felt that he must make an attempt' left heart has increased. Symptomat to care for his family. He started to ically, the dyspnea has noticeably work again in May, 1933, and con increased within the last year. The tinued until October, 1934, when he man has not been exposed to asbestos was forced again to leave his job: dust since January, 1929. The final film, taken August 30, 1934, ;*" 2'v-'-'-v- : rot. JS, no. 4) cates extensive progression of the fibrosis well up into the apices, and a _definitely hopeless outlook. In fact this man is beginning to manifest the physical signs and symptoms of pro gressive cardiac failure, which, in my opinion, is the terminal result most frequently met with in pulmonary asbestosis. - " ' The rate of progress of the condition in Case II, and the extensive progress in`Case III, even though there was cessation Sf exposure in both cases, qualifies the statement of Wood and Gloyne (6) that "once asbestosis bodies are found in the sputum the course of the disease appears progres sively downward." Asbestosis bodies were not found in the sputum of Case II, but were found in that of Case III. The sputum of Case IV was at first negative for the bodies, but they are present since the condition has become far advanced. Inciden ts1 ' lireful examination of the spu tum A cases with definite asbestotic involvement in the lungs frequently fails to exhibit asbestosis bodies. The high percentage of pulmonary isbestosis (34.4) found in this series af 151 workers, indicates unquestion ably the need for more complete irotection of employees in asbestos nilIs. Sufficient evidence has been produced to prove that the inhalation asbestos dust is productive of serious mpairment of health. In fact, the ictim of asbestosis, as a rule, eventuJly becomes totally disabled from ngaging in any form of labor. The iost prominent and lasting symptom f this disease is dyspnea, and this ; out of all proportion not only to he physical signs found in the lungs, at also to the pathological changes depicted in the x-ray films. It is this symptom which very frequently pre cludes any form of physical exertion. Furthermore, even in those cases in which the x-ray films show a negligible increase in the pathological process over a period of years, there is no indicated improvement in the dyspnea. Serial x-ray films indicate that the condition is slowly progressive even when exposure has been discontinued for several years. The prognosis for extension of life after cessation of exposure in the cases in which iuvolvementis not far advanced is encourag ing, but the hope for amelioration of the dyspnea is not encouraging. industrial worker is entitled to every protection that may safeguard his health, so that he may earn a livelihood for himself and family for at least a reasonable period of years in the work in which he is most skilled. If he is prevented from con-, tinuing in such'work because of im pairment of health through no fault of his own, he is entitled to some remuneration for his loss of earning power. That protection of asbestos workers has been woefully lacking in the past has been definitely shown. It is imperative that such protection, as nearly complete as possible, be provided by mill owners. Efficient protective devices will be far less expensive in the final check up than the aggregate of numerous claims for compensation and frequent damage suits77 That complete protection can he afforded by the devices in use at the present time seems to be somewhat doubtful, but workers are entitled to the highest type of protection which the engineers familiar with the hazard can provide. 22S JOURNAL OF INDUSTRIAL HYGIENE AND TOXICOLOGY [Apr., 1039 BIBLIOGRAPHY 1. Merewether, E. R. A.: A memorandum on asbestosis. Tubercle, IS, 69, 109, 132 (1933,1934). 2. GABKfEit, L. U., and CmiMixcs, 1). E.: Studies on experimental pneumoconio sis. VI. Inhalation of asbestos dust; its effect upon primary tuberculous infection.' This Jour., 13, 65 (1931). 3. Egbert, D. S.: Pulmonary asbestosis: Report of a case with necropsy find ings. Am. Rer. Tuberc., 31,23 (1933). 4. Boislimeae, L. C.: Silicosis end s'tlico- tuberculosis. J. Missouri State Med. Assoc., 30, 309 (1933). 5. Spares, J. V.: Pulmonary asbestosis. Radiology, 17, 1249 (1931). 6. Wood, W. B., asd Glovne, S. R.: Pul monary asbestosis. Lancet, 218, 443 (1930). . 7. Savers, R. R.: Silicosis--Review of history, pathology, and prevention. U. S. Pub. Health Repta., 49, 393 (1934).