Document 1ewprD871ZYMrg1QX0n37GVa

V'* r :r-. . Asbestos Disease in the United States 1918-1975 Irving J. Selikoff, M.D. Mount Sinai School of Medicine of the City University of New York / 0 `i PLAINTIFF'S EXHIBIT ST0065928 ^v^&^C^JiCorapafatively few studies were undertaken in the United States com ing asbestos-associated disease until the 1930's, despite the consid able use of asbestos. The first medical reference to disease among asbestos workers r.ay be found in the rich monograph of Frederick L. Hoffman ''Mortality from Respiratory Diseases in the Dusty Trades. In organic Dusts." published by the U.S. Bureau of Labar Statistics in 191S.^ Ho noted that insurance company records showed increased mortal ity ar.ong asbestos workers and commented that these companies were re luctant to insure such workers. In the same year, there was tlie finding by Par.roast, Miller and Landis of fine fibrosis in the chest x-rays 2,3 of 15 asbestos workers. In retrospect, these early scientific reports should perhaps have attrac-- ed more attention. There are unpublished data indicating that both compensation awards and insurance claims reflected disability among 4 asbestos workers, for example. The first published case report ox 5 fatal asbestos disease in the United States appeared in 1930. 6 **12 The brilliant series of British reports 1927-1929 concerning asbes-- - -* tosis attracted much attention in the United States and stimulated the initiation of important research studies. In 1929, the U.S. as'oestcr industry commissioned a survey of asbestos health hazards in the United States and Canada, which was conducted from October 1929 to .Tar.uary 1231. P;c-sen tea at the Conference on Asbestos Disease, Rouen, Franc a. Octobe; 27, 1975. t *"..1 ' 1 -? - i-t ( H . * * .-T r, . . .T*` - ' \ 7! * .-i .. .. .> "VffW-i- ` ~a- ST0065929 ' , 'V - 2 13 The results were reported in 1935. A serious situation had been fau: Of 126 workers employed three years or more, selected at random, 106 had abnormal findings, with only 25 of 121 asymptomatic. Meanwhile, independent surveys had been undertaken, and had shown 14-17 nifleant prevalence of asbestosis in factories. iVhen an extens investigation by the U.S. Public Health Service confirmed these fi it became widely known and appreciated that asbestos exposure commo resulted in a serious pneumoconiosis. Although industrial hygiena were scant, the U.S. Public Health Service proposed a "tentative standard," to be revised when better information became available. In 1935, Lynch and Smith suggested that lung cancer could also be 19 associated with asbestos exposure. Thus, by 1935, the main directions of the problem were known. Chrysotiie J*u ' , sgSHy asbestos, virtually the only fiber then used, could produce widespread disease, this disease could be fatal and malignancy night be a result^Jj^^m-;/- of exposure. With this background, it is difficult to explain the curious quiafc*' 20 hiatus of the next 25 years. Little was done, regulations were * _* - and government inspections and supervision were infrequent. for ex- _ ample, in a clinical survey of 1,117 asbestos insulation workers conducted by us, each worker was asked about dust counts he had seen. 21 Their employment covered the span 1910-1952. In approximately 3,500,000 working days, seven dust counts had been observed; tost, in relation to recent Workmen's Compensation claims. . rue ST0065930 3 Towards the end of this "silent era" some disquiet appeared concerning the question of asbestos-induced cancer, and was augmented by an obser vation reported by O'Donnell and Mann in 1957, from a hospital in a city in Pennsylvania with an asbestos factory, that of 27 cases of 22 asbestosis seen by them, 13 had had lung cancer. It is worthy of note that during these years of inattention, years in which the use of asbestos grew approximately five-fold in a rapidly expanding industry making thousands of products, approximately one million"United States men and women began work for shorter or longer periods, unwarned and largely unprotected, a fact for which our scientists can take little pride and little credit. This is especially true because many of the cases of asbestos disease now being seen in the United States had their origin in uncontrolled excessive exposures 23 during this time. *********** Fifteen years ago, asbestos disease in the United States began to attract much more attention. A. number of studies appeared which identified three major problems, which we have not solved and with which we are now con cerned. First, although the frequent prasence of pulmonary asbestosis among workers in the asbestos trades had been demonstrated 40 years ago, this knowledge has not resulted in an important reduction in its prevalence among such groups of workers nor in the prevention of its more serious consequences, cor pulmonale and respiratory insufficiency. In one study of asbestos insulation workers, for example, of 1,249 men who had been members of the insulation worker's union in the New York metropoliton 4 area at any tine from Januaiy 1, 19:13-.r)ecember 31, 1962, 1,117 -.ere 21 x-rayed during 1963. 542 had abnormal x-rays. Notable was the fact that of the 725 wit;h less than 20 years from onset of exposure, only 203 were abnormal. On the other hand, of the 392 men with longer durations from onset of exposure, 339 had abnormal roentgenograns (Table 1). ST006593I Moreover, it was found that in many groups of workers from 5 to 7" of deaths were due to cor pulmonale and respiratory insufficiency. 2~~`,5 Identification of the problem 1930-1935 had not been sufficient to prevent the occurrence of the disease. ********** Second, and perhaps more important, although the persistence of asbestosis as an inportant industrial hazard was rediscovered, it soon be came evident that it v.as not the principal hazard of exposure to the fiber. The principal difficulty was clearly cancer. Two critical studies showed this to be true, both in the factory production of 27 24 asbestos products and among workers using these materials. In our experience, approximately 40% of deaths among asbestos insulation workers in recant years have been due to malignancy. In one study, we have followed a cohort of 632 asbestos insulation workers from January 1, 1943 to December 31, 1974; they continue under observation. Alto gether, 305 deaths were expected. 451 occurred. The excess was largely due to cancer. Age, year ancl sex specific analysis indicated that 52 such deaths vea- to have been expected -- 200 occurred. Specifically, analysis of the cur-.cev deaths by site indicate that 12 lung ere:. d-.-e `hr. ror likely to have occurred; 509 were fernn! i. 5o"o 5 two or three times as many cancers of the esophagus, stomach, colon and rectum occurred as expected. There were also 35 deaths of mesothelioma, 10 pleural and 25 peritoneal. Of course, no deaths of this rare dis ease were expected (Table 2). ST0065932 It was of interest to find that, among the mesothelioma deaths, there were more peritoneal reaotheliomas thin pleural. This observation is 28 consistent with that made by Entickre? and Smithcr among workers in an asbestos factory in London, and is in contrast to the location among patients with mesothelioma derived from environmental contact with 29 asbestos. Perhaps differences in intensity and in nature of exposure are responsible for this variation. Direct occupational exposure, with .its exposure to large numbers of fibers including, perhaps, ingestion as well as inhalation, may be more likely to increase the risk of peritoneal mesothelioma while the far fewer fibers in environmental circumstances, tend not to lead to such disease. Similar findings have been obtained in other studies. In one, we have been following all members of the insulation workers' union in the United States and Canada (International Association of Heat and Frost Insu lators and Asbestos Workers, AFL-CIO, CLC). On January 1, 1967 there were 17,800 such men. By the end of 1973, 1,577 deaths had occurred. Again, there were approximately three times as many cancers as ex pected (Table 3). And again, lung cancer, r.esothcl ir.mn and gastro intestinal cancer were the principal categories of such excess neo plastic deaths. 67 deaths of lung cancer wore an L i c ipat ed; 321 occurred. There were 103 deaths oi r>o.-othcl: o.\. (again, \. ifch a pre ponderance of peu i toneal sites of origin) and a - U ; increase of -6 - cancer of the esophagus, stomach, colon and rectum. it was of interest that cancers of other sites were also, in the aggregate. Increased (103 expected, 165 observed). While increased risk of cancer of a number of t, 30 ' 3i v' ' v"' othef sites exists (larynx, oro-phavynx, and others) the infrequency of such neoplasms in general makes it advisable to seek further experience before a firm opinion is expressed concerning the extent of such increased risk. ST0065933 We have considered the possibility that the complex environment in which these insulation workers are employed (industrial construction) might in some way influence their mortality risks. V.'e therefore under- . took to investigate the workforce of two factories making insulation materials, exposed to asbestos but not to many of the other r.aterials found at construction worksites. The first was a plant which made aiiiosite asbestos insulation materials (pipe covering, block, asbestos mattresses, etc.). Introduced in the late 1930's, their use increased during World War II. A factory making the products started production in an eastern U.S. city in 1941. From June, 1941 to the end of 1945, 933 men began work at the plant. Some worked for as little as one day, others for one or more months and a number for some.hat over 13 years, until the plant ceased oper ations in November 1954. We have traced this group of workers to December 31, 1974, Table 4 includes their mortality experience, start ing five years from onset of work. It will be noted that their experi ence was very much like that of the construction workers who used the product:: made io thi* >ry. there was *hr-s* '.ir.es increase of cancel- ol .-11 sites (00 anticipated. ' r-7 . hs . r\:!') . Too, 7 lung 'career, gastrointestinal cancer and mesothelioma were the major categories with excess neoplastic deaths. These experiences confirm 32 earlier observations of neoplastic risk associated with this work. STOOG5934 In an investigation of workers in another asbestos factory (the largest in the United States) we had less opportunity of focusing on the pro duction of insulation materials, since many other products were made.Nevertheless, the results are again of interest. On January 1, 1959, there were 689 production employees in this factory (including 611 males) who had begun work before January 1, 1939. We have studied the male mortality experience January 1, 1959-December 31, 1973. There was little difference from our findings in other cohorts. Again, can cer proved to be the major asbestos hazard (although asbestosis, as in the other cohorts, was an important cause of death). Oi the cancer categories, bronchogenic carcinoma, mesothelioma and gastrointestinal cancer took pride of place (Table 5). ********** A third major difficulty now with us is derived from the appreciation that it may take much less asbestos to cause cancer than to result iu asbestosis -- sometimes, very little indeed. We learned this first 29 33 from the work of Wagner and his colleagues and Ne.vhouse. So alerted, we have become concerned not only with asbestos workers, but with widespread dissemination of asbestos from the primary worksite, exposing both other workers nearby as well as individuals not associatod with the work at all, but exposed to asbestos as a result of environ mental pollution. Examples include household contamination by dust brought hor.te by workers to their households .and asbestos air pollution ST 00G5935 -8 - from asbestos-using facilities, contaminating surrounding neighborhoods and, to a lesser extent, the general environment. Such indirect exposure of workers has been particularly important in the United States in the construction industry and shipyards, in the former, since 1959, a particular hazard has resulted from the use of sprayed 34 35 asbestos fireproofing. This is now strictly controlled. 36 Anderson and his colleagues have also demonstrated that family contact asbestos disease, among wives and children of asbestos workers, is much more common than originally auspected. 326 household contacts of workers employed in the amosite asbestos factory for shorter or longer periods 1341-1954 were examined in 1974-1975. Approximately one-third had characteristic parenchymal and/or pleural x-ray abnormalities (Tables 6 and 7). At further remove from occupational sources of asbestos contamination, there has also been concern with asbestos pollution of general community 37 air. There are numerous sources for such asbestos air pollution in 38 the United States. In recent months an additional source has been 39 identified: air within buildings fireproofed with asbestos. Con comitant with such environmental contamination has been the frequent finding of chrysotile asbestos fibrils in the lungs of urban dwellers. ********** 9 Current United States Approaches to Control of Asbestos Disease Perspectives which provide a background to approaches designed to control or eliminate asbestos disease in the United States are largely derived from experiences such as those above and are reflected irTproposed regu- 41 35 ' . lations, either in occupational or environmental circumstances. 1. Asbestos-associated cancer of primary concern. Control measures are now based on the realization that it is necessary to prevent 41 asbestos-associated cancer, as well as asbescosis. In general, this Implies that permissable asbestos concentrations need be significantly lo.ver than those calculated to minimize the rick of asbestos alone. ST0065936 2. Long period of clinical latency. In seeking to prevent cancer, it is appreciated that the long period of clinical latency of asbestos cancer must be taken into account. Our studies and those of others have demonstrated that cancers associated with asbestos exposure frequently do not become clinically evident for at least 20 years after onset of exposure. Often, the elapsed period is 30, 40 or more years. V.e have analyzed deaths of lung cancer in our cohort of 17,800 asbestos insulation workers in the United States and Canada, from January 1, 1967 to December 31, 1972. Table 8 demonstrates that there were no deaths of lung cancer among individuals with less than 10 years from onset of exposure. A small increased risk v.as found in the period 10-14 years from onset but the major impact of the increased lung cancer risk was observed 20-40 years from the beginn? ny. of work -j. 10 It is likely that "duration from onset of exposure" is, in some instances at least, a composite effect and includes both the in fluence of total exposure and that of the passage of time from first exposure (or, more accurately, from the time sufficient exposure has occurred to result in increased cancer risk - "affective exposure";. Brief (excessive) exposure may produce later disease. Even brief 42 exposures -- a day, a week, a month -- if excessive, can later result in disease. The inhaled fibers remain in the lung. Thus, the men erployed in the areosite asbestos products factory mentioned above 1941-1945, worked for varying periods of tine. Approximately one-third worked for three months or less, one-third for a year or more. Even less than three months of work resulted, during the next 30 or so years, in significantly increased cancer risk (Table 9). Nevertheless, those with longer periods of work had even greater risk. CO --I O CD CO cn CD CO --I Multiple facter interaction -- cigarette smoking. In 1967, it was found that the risk of the most important occupational asbestos cancer, bronchogenic carcinoma, did not depend upon asbestos exposure alone. Rather, if there were absence of concordance of two agents, cigarette smoking and asbestos, there did not seem to be a signifi- 25 cantly increased risk. In the first cohort study detailed above (Table 2), on January 1, 1963 there were 370 survivors of the group whose observation had begun in 1913. Vhen these ren we:-:- o\ '.mined, each was asked of his ` wiki nr habits. 87 r.ien had no history of cigarette smoking and 2S3 had such history. By April 30, 1957, it was anticipated that \ ircually no ii. - deaths would have occurred among the non-snokers. Not one did occur despite their long years of asbestos work. On the- ocher r.sni, 3 deaths of lung cancer had been anticipated among the 2S3 smokers. 24 were observed. It was calculated from these data that asbestos workers who smoke cigarettes have approximately 92 times the risk of dying of lung cancer, compared to men of equal age who r.either 25 smoke nor work with asbestos (Table 10). 0CGG9OO1S The cigarette sroking-asbestos interaction has beer, cor.jtmed in 43 _ a larger study. Among 2,056 non-smoking asbe.-trs uor.-ttrs i.ol deaths of lung cancer were expected from January 1. 1357 through 1972 on the basis of rates derived from the general nazulai; or. of the United States. 2 deaths occurred. On the other hard, r-.rzr.g 9.59* men with a recorded history of cigarette smoking, 31.:? deaths, of lung cancer were expected, and 179 were observed fable ll't . No clear association with risk of mesothelioma has been observed, nor of cancer of the stomach, colon or rectum. Asbestos workers who do not smoke may still die more frequently than expeate-o of these diseases, or of asbestosis. Nevertheless, if they do smoke cigarettes, our data indicate that their risk of death of lung cancer is approximately eight times that of other smokers. Cose response relationship. There is little foul", that a dose response relationship exists for the several aebc-s tos-associated diseases. This is well demonstrated by the exrc-: fence of the aru'itc asbestos factory tor! ers referred : 'i~` ' "ah 1 ; and 9;. Cere, v orkers were exposed to the sn fiber. a '--7 th` sure pox i .<*1 of time, ia.ki.ng the same products, ir. tr.;- '.r.e c:v. : tr.-ey 12 varied, however, with regard to their total exposure. Such variations were reflected in differences in the risk of death of both asbestosis and asbestos-associated cancer. 6CGS9001S It may be that risk also varies with other factors, such as intensity of exposure, peak exposure, type of fiber, individual susceptibility, 44 etc. Insofar as fiber type is concerned, Wagner has proposed that crocidolite has a greater potential to cause mesothelioma than do other fiber types. Our own studies provide little information con cerning this hypothesis. Chrysotile has long been the principal fiber type used in the United States. Comparatively little crocidolite 31 was imported into the United States until World War II, and it has not been used in insulation materials utilized by the asbestos insulation workers investigated in our studies. Our data do not allow comparisons, therefore, between crocidolite and chrysotile risks. Amosite was also imported in the United States in scant quantities until the last part of the 1930Ts and the 1940's. While 24 1940 and 1950 deaths among insulation workers are unlikely to have been influenced by amosite exposure, it would be difficult to separate the influence of amosite from chrysotile since that time, since exposure to both fiber types could have occurred and sufficiently long in the past to effect analysis of deaths 1960-1975. An unresolved question related to the p;oblc r. of "dose-disease response" relationships is whether or not a "safe" exposure level exists, whether there is, for asbestos, as for any carcinogen, a t-1; e .U`I le.cl. 1.. . : :v1 : i L; t.nt s , . 45 - 1 a i 1 --e to find evidence for a th; ush .>1 d close of t.sbos t-v- 'or mesothelioma. 13 - Fro.a >. practical point of view, one might consider the observations of a continuous reduction in identifiable cancer risk with decrease in levels o!f exposure suggest that it may be feasible to reach levels at which it will not be possible to statist!cally ine V increased risk of cancer of those sites known to be associated with a neoplastic effect of asbestos. ST 0061591|0 6. Industry efforts to control exposures. In the last several years, there has been sharp increase in the scope and intensity of industry efforts to control factory exposures, and the importance of avoidance of cigarette smoking is also now being stressed. .7. End product vso major unresolved pi~ab1em. Still unresolved is the control of exposures encountered in the use of asbestos products. This is not only true in the construction industry, shipyards and poter plants, but in such uses as brake repair ana brake maintenance, as well as in the end product use of some asbestos materials by the general public. Attention has recently been called to one such use, the home utilization of taping and spackle compounds needed for home repairs and rebuilding. Analytical studies showed that many con tained asbestos, without warning labels or instructions for the 46 use of special protective precautions. 8. Demolition, waste disposal, maintenance and repair. Waste disposal, demolition of asbestos-containing structures and the necessity for repair of facilities contain'ng asbestos material? are thorny prob lem?. So far, lit'.ir research has been dove tod to Ibis question. 14 - 47 although some notable efforts have recently been made, and the U.S. Environmental Protection Agency is seeking to establish regu- lations aimed at minimizing environmental pollution from these r? i;v- . ' ' .-Ay.. *'i .. " % ' . -35 sources. - -v/rw: . . ST006594I 9. Environmental exposure; conjugal, neighborhood and general community disease. Although family contact and neighborhood residence have been clearly demonstrated to carry a risk of asbestos disease, the magnitude of this risk has not been established quantitatively. Indeed, although it is known that mesothelioma may result in such circumstances, there is no information whether other asbestosassociated cancers might also occur in excess among people so ex posed. It is unlikely that extensive asbestosis, sufficient to result in death of cor-pulmonale, will often occur although I have seen cases of moderately extensive pulmonary fibrosis (2/2 in the ILO-U/C classification) among wives of asbestos workers. Studies are currently underway in our Laboratory to provide information on the extent of asbestos-associated disease other than mesothelioma, among family contacts and neighborhood residents. There is no evi dence at present that asbestos exposure of the community at large ("general asbestos air pollution") has been associated with disease risk, although attention has been called to the fact that meso theliomas not known to be associated with asbestos exposure (approximately 15% in the series of Greenberg and Lloyd Davies 42 48 and Webster ) have also been increasing incidence. 10. Asbestos contamination of piiblic water supplies. Asbestos may be found in some food and beverages, presumably as the result of the filtration of these products through asbestos filters or as the Z'lGG9U01S 15 result of use of water contaminated by asbestos. V.'ater may naturally contain fibers as the result of ground waters coursing 38 through geological formations containingasbestos minerals. In dher instances, there is the possibility that water being traps-- ported through asbestos cement pipe could, in some circumstances, 50 51 be contaminated by the asbestos cement material. ' There are, at present, few data that would allow appropriate evaluation of a potential hazard, especially since the question of asbestos 52 disease resulting from ingestion of the fiber is still unresolved. It has also been found that wide contamination of public water supplies may result from disposal of asbestos-containing waste, as in the contamination of Lake Superior by mining operations."* Ineffective therapy. To the present, little has been achieved in terms of improved survival of asbestos workers suffering from asbestos-induced cancer. (Insofar as asbestosis is concerned, much can be done to lengthen life by appropriate medical surveillance.) In our studies of asbestos insulation workers in the New York metropolitan area, we observed 1,249 men from January 1, 1963. 370 men had long experience, having been members of the insulation workers' union in 1943. By December 31, 1974, 7 pleural meso theliomas, 21 peritoneal mesotheliomas and 49 lung cancers were observed. All 28 men with mesothelioma are dead and 4S of the 49 individuals with lung cancer. Among the 879 r.c-r, v ho were admitted to the union between 1913 and 19G2, 2 pleural mesotheliomas occurred, and 1 peritoneal . All 3 i n r.re chad. F<r:: 1 10 instance; or lung cancer were seen by December 3! , 19/1; i. .<' the 10 arc doi-ci. 16 Epilogue: It is sobering to consider that the asbestos disease and asbestos-* associated deaths that have Recently bedti 3`e^h' in the Unltddy^ietes are largely related to the Inadequately controlled use of asbestos 1930-1940, when some 200,000-300,000 tons per year were usedyin the United States. At present, approximately 650,000 tons per annum are used (Table 12). To the extent that this use is inadequately con trolled, we will see deaths of asbestosis and cancer in the year 2000, and later.55 ST 0065943 nnGssioois Table 1 X-ray Changes in Asbestos Insulation Wo; -21 Onset of ex osure (vrs.) 40-130-29 20-29 10-19 0-9 No. 121 194 77 379 346 % Norma 5.3 12.9 27.2 55.9 89.6 % Abnormal Asbes tosis (grade) 12 3 94.2 35 51 28 87.1 102 49 18 72.S 35 17 4 44.1 15S 3 0 10.4 . 36 0 0 1,117 51.5 48.5 365 126 50 Table 2 ST0065945 Expected and observed deaths among 632 N.Y.-h'.J. asbestos Insulation workers. January 1, 1943-D8cen]Mr 31, 1974 Total deaths, all causes Total cancel* - ell sites -Lung cancer Pleural mesothelioma Peritoneal mesothelioma Cancer of stomach, esophagus Cancer of colon Asbestosis All other causes Expected* Observ* 305.20 451 52.02 200 12.20 ** ** 6.46 7.64 89 10 25 20 23 ** 37 253.18 214 *632 members were on the union's rolls on January 1, 1943. 9 died before reaching 20 years from first employment. All others entered these calculations upon reaching the 20-year from onset of first exposure point. Expected deaths are based upon white male age-specific death rate data of the U.S. National Office of Vital Statistics from 1947-73. Rates were extrapolated 1943-48 from rates for 1949-55, and for 1974 from rates for 1969-73.** **U.S. death rates not available, but these are rare causes of death in the general population. * * a o p ft 03 sr a K* a 0p + rt sr 5* OH P ft o9 3 o H S3 P0 H* rt 0 P O ; * Hi Hi 3 w OH o X H O rt- TJ 3 co Mo <0 M a ft co p o oo a rt a t to P H* 1 a <0 H* O o -o o Hi p CO -4 rt * CO rt sr O p 53 ci w P o rt 03 O c* p ss > i-* 0 rt V o 1 o y- o u > cr o ft o H* > M H* o p 9 n p 9 o p s *0 o 0 H* O r 5 o O o H* c G4 0 o O o ft 5 ft H H O p o sr 0 H* p o O O0o 9 H Hi Hi Hi p 3 o H* o o O P o o o m ct 3 0 S3 a o g o ft *rj c 9* o 9* p p o o * p o rt M *5 c V 9* Q H- o O H* 3 o H* p ft o o ft p H* o p S3 o o *t 1 p H* u H* rt O H rOt P M a o p rt sr a p == o a H* O rt a H* pP c H* Oc <+ O* 9 0 H* M o Po oO 9 cc rt rstr X H p rt H Op P Hi oq a Hi o fto H* 1 H* O *p o o CO CO H* 00 A * ic H* O CO CO H* H* A X *; !- O CO O O CO P Q A A co o CO H* rt O sr o Cl 00 * * CO CO H* o 0*1 CO * CO -4 M o * c. rt o <0 C o a cn a Hi H* o p H o M P Hi Hi < H* oO i ft H P H* s*r O H* -4 03 ft CO ct O ' 0o0 o MM H* 03 CO CJ1 u H* CO M a CO CO A CO o -4 CD H* a Cl 09 H* O 4 -0 a o o c* po fstr 3 < o o. QP Hi ft 3 O 1 H* P ffl oPg; O H* 3 ft O H- H Oa P CD a o H rt P -4 O fStr 53 M CO H* H* P CO H P ft oa Cl 03 1 i ~j H* CO H A o CO t l o A CO O GO o CD cr> cn v> H* 0 ft H w 0" -o X o 0 00 n c: o a c rt CO o pa p cr p <D 9 9 O a a M co H* 2. uP H p c+ P- CO -0 9 C Ho- n P CO P 5 c+ Hy *< w O M1 * p oo M *i 3 O w rj <33 o Table 4 Deaths among 933 workers employed in an amosite asbestos factory, starting five years from onset of work 1941-1945 to December 31, 1974 ST00G59U7 Cuu.se of death All causes Cmcer - nil sites Lung cancer C. .1. cancer Pleural mesothelioma. Peritoneal mesothelioma "Asbestos" cancer Other cancer Asbcntosis All other causes Deaths 1946-1974 ** Expeoted Observed Ratio 285,62 50,10 12,45 12,05 *** **/* 24,50 25,60 * 23) 152 483 157 63 24 5 5 117 40 26 298 1.69 3.13 6.67 1.99 **. 4.78 1.56 * 1.27 * 128 workers were omitted from these calculations: 33 had prior asbestos exposure; 38 died in the first five years after onset of employment. 49 were not completely traced; and eight had other asbestos employment after the five year from onset point. ** Expected deaths are based upon white male age-specific death rate data of the U.S. National Office of Vital Statistics, 1949-1973. Rates were extrapolated for 194G-1948 from rates for 1949-1955 and .for 1974 from rates for 1959-1973. U.S. death rates not available but these are rave causes of death in the general population. E x p e c te d and o b s e rv e d num ber o f d e n tli? nr.topg G il Now J e rs o v a s b e s to s fa c to ry em ployees 1 J a n u a ry - MI iJecem bcr 1073 tw e n ty o r wore years a fte r o n se t o f f ir s t exposure to asbes to s cr n I o H <n in Po o cm CO H CO n Ci N 01 P d H cm CM L4 H CM H CM O o *h in o ri H O a r- -.1- ' CO H XI CM h o CO rot 03 n OO 03 ri CM CO CM c* o H H -Oi O P ,o jj CO r* (0 w xi in oo - o (O o CO Cl a k 00 o c 00 wl H in o CO roH a c CM CO cn ri Co ri H ri G p >' .. o .i O o *H VI Vf o o ' - 4* S0 -a <0H 00 CO CO o CM P t i 00 m o CM CO V oc as H Cl <0 ts ri ri CM o co p* .H I *o o 00 V in pH Cl i cm 00 ol CO ri 10 , i CM 00 rH 00 00 CO c.1 o X n C* Cn t d a a Cl O in COMT rH 00 CJ w Cl CrHM c o pH G CM *c iH0 P 00 00 CM 03 1 CO Cl CM Ci CM 00 0? rH CM CM H CM o ri 1 V o CM CM tfi x> o CM CO CM rOi CO 1 1 CM o C~ CO pH %* Ci ri a o CM 00 X d C3 f* 00 00 CM V CO . rt o CM w CM o CO pH d co pH CO e 00 CO o H CM <0 o o P cri O CO CO o CO a ri CM CM V* V* CO o rH 1 H rH ri CM <n 5 O 01 pH r4 rH CO ^3* 00 CM * a N CO o X rH 03 d G CM CM CM ci w CO CM d C o o CO CM G CM C3 HO Prt > U o <n i 0 SH eo <n E c; o >i t a o ol ds= 01 O o <D d T-t m 01 rH Cj 3 cc u in O p rCl rH P in 3 & G m tH o rH p pH H a si p G OI O a jr:i e IT. G a 0*. i pH <A r a o 0E ;i V rH t' fj 001 3 P Oa - o u L, 1h oO o P r, c ti rH Cl V, LrI ci G P c: o *o r*< n i U o c c rH o c) G r* to z> rH c. cl t, ?; H G i r-4 C, r GH CO G v4 * r* Sh 0- o pH jG* o 0 a o p--i f--> G It PG 01 Or 0. r-- r-t po *" c o p c a: cc 3> O P o c p o P kcn ,c P c o O P <H a o D. I o atc O rH a E a> p rf j: c o c. 3 G o: c pO ot. rH c; l cr. sz p H d 0 *c cr. o G 4HJ p G --i GP cz rt +* o: A>. o o6 p X o Li o > 0 1 JS O U a >, or* Sh k o rH .3 O rH P .2 > C P o c o hi a r* + a o o Vh o w o m 3 G U o 01 G P. Lh G <0H 0 P P c; a G pH P3 C5 P. Lt O a O H rH Cl H U G0 Gc Cl o be n c GO CD CO cn CO "v" CO Table 6 Distribution of 326 household contacts of acosite asbestos workers by relationship to worker 6 isGC900iS Chi 1'Iren Sibs Others Relationship Wives Daughters Sons Sisters Brothers Mother Father Cbusins, etc. Number 83 - s 7 3 23 13 oi1 ` r-t Percent 25" 5S~- 7n Table 7 X-ray abnormalities among 326 household members of amosite asbestos workers STO065950 X-ray findings Number of household members Pleural thickening the only abnormality 42 (13%) Pleural calcification the only abnormality 7 ( 2%; Pleural thickening and pleural calcification 3 ( 1%) Irregular opacities the only abnormality 35 (11%) Irregular opacities, pleural thickening and/or pleural calcification 27 ( 8%) Total 114 (35%) Table 8 tV'! ' -'L -':7'/v5 v''"` - ' - Deaths frcm lung cancer among 17,800 asbestos insulation workers in the (1.8. and Canada January 1, 1967-December 31, 1972; relation to elapsed period from onset of work exposure Years fro:', onset < 10 10-14 15-19 20-24 25-29 30-34 35-39 40-44 45-49 50-r Lung cancer Expected Observed deaths deaths Ratio 0.56 0 -- 1.97 5 2.5 5.87 23 3.9 9.55 34 3.6 10.70 56 5.2 8.20 60 7.3 4.68 29 .2 4.84 27 5.6 4.51 19 4.2 4.97 22 4.4 Total 55.87 275 4.9 Expected deaths are based upon age-specific white male death rate data of the U.S. National Office of Vital Statistics. Rates for 1972 were extrapolated from data for 1967-1971. V' - I S6S90U1S E xpected and observed deaths subsequent to f i r s t y e a r a fte r o n se t o f e m p lo y mfei nr ts at m ong 8 7 0 a m o s i,te a s b e s to s l a c t o r y w o r k e r s e m p lo y e d 1 9 4 1 -4 5 a n d `o b s e r v e d to December 31, 1973. D is tr ib u tio n b y d u ra tio n o f em ploym ent. w 10 Cl CM m o t- 03 00 CM IN I .I CM CD H 01 M 00 N 5 ns C* ft HxJ o X in in oOl opH 09 H pH d CC CO r~ NID d iVnO e c pH CD C H 01 V* o 03 s oo c * r-i CM V 00 I <o oO I n I CM w i W x+xj EO O' og O sc in oa ph p> t* O ^ pH M rH I'4-* o V* CO a CO oo o a pH d c r- r^ d CO G -i CO in fi K o m t- a w rH poH P d cs Cr--Of n in fCO p-H pH CO 1 1 1 1 CO 00 o 1 1 o to i o o rH pH B N 03 O O pH `O* pH CO H CO H CO to xi jC O 4-> Go T3 s CO O , in CO CO Cl pH 4 to 00 d d TJ* CO d CO d CO ci to Vf n a pH CO (3 CO Cl *H W CO n o w 3 dW oo M pH H rH cn Ci pH ri pH W x: v> 1 d '0 o o rH 3 aa CJ +j Pf < d B o d H r-l 0 Si ^H 4 pH +i 0 XX o IA 4- C) a u o 0 EJ w 0 tA d g 0 o e d 4-> d O in d pH o ci d o u dp o H C, G 3 r--' o d c< p* O 6 3 v o o h 3 O rH o o u 01 CJ H u r 0 ci +J o in o A* 0t < in 01 3 d o fn X* 4 a rH r-l < p .r> ji a 3 UA o vi mfl t* to o x o j&; J*?L 00 o . 0. J;S po 2u o o in Cl O W CO o Cl CO N in d 0 wH Vr>t > r-t o IT. X Wc o <H .u* 0 0 c. t* k d V4 0 0 5*. u 1 Cl Cl Xr;l y5. '-- n3 o + a3 5a . *3 m a < 6 r-i It J +> rl O t< o p co ci< oe a hp u tl p JZ vi p a s< p O > <1 33 c o u o r? tl C "O l *3 O W r-i r-i JSOX1 3 O 00 O - Vi r5-1i o pH 0 r-i OX rj c H oo e. vi oK -SO I *3 P rM c o til V* O 1-1 ci cs E CO P H ?> r0-i &o P 3z rH CS a rt C- P E ea Cl V o x VI o po H o u * d tn pH ,3 d >o-> vo> Vi 3 pOH 3 o 3, 55 m od 3 +01* Xw2 o *o -P d H d xs o (4 w VI o V* v d bC c pH C H O N I d Cl 3WO V 0 0 3 WO CU -r4 X H H *Q X CS *d -| w *3 pH *3 O <0 d H Cl 3 C o +* M o a * V* a +* o m ci P P, 0 d <H C. P G o e 3 X w ca O o au: *H d 01 +J d CO O fs o 4H ii H c *E > 'a H in 0 a rl o 3: o (h *w c. H o lH 3 Ol in rH 'a ci OQ o 4- o Cl o tv X XX w m H 1 0 d o <H CO oCl VI tv o r-l v> 01 01 pH Cd rH yl r* d o rH 3 * r1 0o d It fi 0 v! U! in rl -.1 ^5 ci r_, X! 3 V 'd o d rj H X 01 01 ?. o *-f d -< & OP. a dU o c to G -rl CS O TJ V4 0 01 w 3 cl U d u d tfl 3 .O Xd* d 3do c in -oM ci fn Ci tD * \ CO --i CD cn cn \o cn f\? ix'l i.v ST0065953 Table 10 Lung cancer among 370 NY-N-J asbestos Insulation workers, January 1, 1963-April 30, 1957 No history of cigarette smoking History of cigarette smoking Number of men 87 283 Expected lung cancer'- 0.15 2.98 Observed lung cancer 0 24 Hammond, E.C. Smoking in relation to death rates of 1,000,000 men and women. In: KCI Monograph 19, 19GS, p. 127-204. -';.s-: -ty.v;.w-:'p_jv, - ?r : \. ST0065954 Table 11 Expected and observed deaths of lung cancer among IV,800 U.S. and Canada asbestos insulation workers, January 1, 1967-December 31, 1972; Relation of cigarette smoking Smoking habits not known History of cigarette smoking No history of cigarette smoking Never smoked History of pipe and/or cigar only No. of persons 6,14-1 9,590 2,066 1,457 609 Deaths from lung cancer x E.vpcc tec! Observed Ratio 16.76 31.60 7.51 4.40 3.11 94 179 2 1 1 5.6 5.7 0.3 0.2 0.3 * Expected deaths based upon age-spccific U.S, mortality rates for white males disregarding smoking. Lung cancer estimates based upon U.S. rates for cancer of lung, pleural, bronchus and trachea, categories 162 and 163 of the International Classification of Diseases and Causes of Deaths, 7th Revision. Table 12 U. :. Cons'.anpticn of Asbestos SS6G90U1S 1930 1340 1950 1950 1973 Tons 120,000 262,COO 727,000 710,000 862,000* *Chry5otile S39,20C tons, anosice 4,273 ^ons, crocidolica 17,90S tons and anthophyll.'te 1,162 tons, (fourne U.S. Bv.rei" of I'.ir.cs.; BIBLIOGRAPHY ST00G5056 1. Hoffman, F.L. Mortality from respiratory diseases in dusty trades. Inorganic dusts. Bull, of the U.S. Bureau of Labor Statistics No. 231. (In- . dustrial Accidents and Hygiene Series: No.17) pp.458. Washington, D.C. June 1918. 2. Pancoast, H.K., Miller, T.G. and Landis, H.R.M. A roentgenologic study of the effects of dust inhalation upon the lungs. Amer. J. Roent. 5: 129-138, 1918. 3. Pancoast, H.K. and Pendergrass, E.P. A review of our present knowledge of pneumoconiosis, based upon roentgenologic studies, with notes on the pathology of the condition. Amer. J. Roent. 14(5):381-423, November 1925. 4. Lanza, A.J. Asbestosis. J. Amer. Med. Assoc. 106:368-369, February 1, 1936. 5. Mills, R.G. Pulmonary Asbestosis. Report of a case. Minnesota Med. 13(7):495-499, July 1930. 6. Cooke, W.E. Pulmonary asbestosis. Brit. Med. J. 2:1024-1025, December 3, 1927. 7.. Oliver, T. Clinical aspects of pulmonary asbestosis. Brit. Med. J. 2:1026-1027, December 3, 1927. 8. Seiler, H.E. A case of pneumoconiosis. Result of the inhalation of asbestos dust. Brit. Med. J. 2:982, December 1, 1928. 9. Bridge, J.C. Remarks on occupational dust. Brit. Med. J. 2:1143-1147, December 21, 1929. 10. Haddow, A.C. Clinical aspects of pulmonary asbestosis. Brit. Med. J. 2:580-581, September 28, 1929. 11. Wood, W.B. Pulmonary asbestosis. Radiographic appearances in skiagrams of the chest of workers in asbestos. Tubercle 10:353-363, April 1929. 12. Merewether, E.R.A. and Price, C.V. Report on effects of asbestos dust on the lungs and dust suppression in the asbestos industry. Part I. Occurrence of pulmonary fibrosis and other pulmonary affections in asbestos workers. Part II. Processes giving rise to dust and methods for its suppression. H.M.S.O., 1930. 13. Lanza, A.J., McConnell, W.J, and Fehnel, J.W. Effects of the inhalation of asbestos dust on the lungs of asbestos workers. Pub. Health Rep. 50(1): 1-12, January 4, 1935. 14. Donnelly, J. Pulmonary asbestosis. Am. J. Public Health 23:1275-1281, December 1933. 15. Fulton, W.B., Dooley, A., Matthews, J.L. and Houtz, R.L. Asbestosis. Part II. The nature and amount of dust encountered in asbestos fabricating plants. Part III. The effects of expsoure to dust encountered in asbestos fabricating plants on the health of a group of workers. Department of Labor and Industry, Bureau of Industrial Standards, Cotir.onwealth of Penn., Harrisburg, Pa. Spec. Bull. No. 42, September 20, 1935. 1G. S-.'ill, -T.r. Asb-vs cosis . A rosns-gv-ologic I'cvii ' of 71 cases. ?.''lo:o^7 27(G) :27S.-pt-n kc-- i?g:. 17. J.!cFhaete<s, S.E. A surrey of u ft-..up of e. .ployec-s exposed to J. Indr.rt. Hyg S: Toxicol. Iti 1) : 2u9----..*9, April tas du 1.?. Dressso.-, W.C., L'alliv.lie, J.'i. , Md-.arc'.s, T.I., Miller, J.Vf. and 3 V'ers, R.ii. with Eo.tO", E'.F. c.n.d Tr; ce, V.r. A study of ask^stosis la the asfc-rs tos textile incurs try . rub. Htulxh. Bull. ~'2 1 . August 1935, Vesiiing to-. D.C. J.jar..! Foi.'n, lung in a,,be.i ;;o i cc> 1; ru'.T.cmry asbestoses TIf: Care iron:: of the A-:-.-.-. -J. Cancer 21 ( .):5S-Si May i?3Cs. T u- -A-ii. V.M. Sore f? ct.s oi: the pre-.-elonso of si`icesi3 ir. the U.S. A.M.A. Arch. Tr.-ius c . Hit1'.. 1-1:379-385, October 1333. .21 Selikoff, I. J , C.-urg, J. zrJ Htrror.d, E.C. TUe ccc of as.be? ` anori-i iiisulat *o > - :rs it. the '."ite-J Su^-s. A >*. Y. Acad. 3ui. 132:13 3-155, 1953. ST00G5957 O' Donnell, V> .f.i. a ad Minn, R. r. Asbestos: r.n o::u r sic factor- in. ch-2 pithoconesin of bvjr-u! jgr.n Lc rcvcinor-[Abstract] A-.c-r. J. Vai/a. 33(3): bl j Mj -Jens 12 77. C-.ru'C.- if . -1 ' 7-1 ' .3 , Au*v - lr 3 f. S'.Iik- ff, I.J., Bad..-, R.7., .lad nr, M.E., Cbuuy. J. a-.! Ear- E.C. Editorial: Asbestos, it and r.,-unl:=Ln. At :* r. J. ".-e-c . -M: (-.1}: 43 7--'Po , 1 S'~7 . 24. Iclikcff, I.-I., Chu.-g, J. .'"-J Krn--on<?, E.C. AsV-:-tos exposure ar.d nenplrsia, r. Ar - r r 133:22-36 25. Selikoff, I.J., Kanrrr.f, E.C. and Ca'-irg, J. Arbas tos exposiu-o, snaking and neoplasia. J. Aeer. Mod. Arroc. 201(2):105-112, April 193S. 26. Selikoff, I.J., Kain:iond, E.C. and Seid'-nn, H. Cunce- risk of insulation workers in the United States. In: Biological Effects of Asbestos, Ed. P. Bogovski et al. IAF.C Sc. Pub. No. S, Lion, Franco, 1973. pp. 209-216. 27. Mancuso, T.F. raid Coulter, E.J. Methodology U- an lustri^l hoalt'a studies. The cohort approach, with special reference to cn asbestos company. Arch. Envir. Hlth. 6(2):2l0-223, February 1903. 23. Enticknap, J.B. and Suit her, V,'. J. For] toner 1 i'.rrojrs ir. asbsstosis. Brit. -J. Indust. Med. 21:20-21, 193], 29. Wagner, J.C., Sleggs, C.-\. and Mai-ch.-c.-'., P, Hi .ffuse- pU-u>-dl n>-v-c.thelia"<a and asbestos rx ;in the Morch We., to t ; C-.p: V. .-'ret, F.: it. J. i. Med. 17:250-2 71, 19- i. 30. Stoll, P.M. and McGill, T. Asbestos and 1 a r -e -1 cn : ci m-.an . 1,erect 2:41C--117 , August 25, 197 3. 7.1. Selikoff, I..J. , Kr:--'o-:P, E.C. no c_ y - asl-o;in-, ilil ion . "k In: AO- - Mop. I 97-: . . - . . . 7 r - r - , O : ... ' M . 9 . i . 7 , ' 1 . t3 Sol ir ~ I !, I .J. , p E.C. i;:d Chur* , J. Corci i-cg'Viici ty of r. V. . J 10 . U* F-'.vi:. 2:.: KiC-lE-'o, S.' p :.''j,^r 5 <- r1 > i f- JTerl-rJse, M. L , *a*I The tp.-on, K. 1 'c*of pleura and perl to -.or-. fol loving errosurto a ,!.o^ to?; in t..o Iordan area. Brit. J. I;.du> t. Mod. 22:231-369, Ooii'.ev 19",3. r Mt/C , . ,1 . , 0 ..: . ' ' v, B.A. r. Scltboff, I.-J. Apnli- cation of sprayed m.-.*. f i. 3 ' - * CO td.ini.nz a;sb = v <;: - ccc.-i.-wci-oaui :j.v.i. A.-:.*:*. f.'iaus r . *g. Assoc. J 1372. 35, Ir.-.tArdvrs Ai . PeJ lilt: C.toLe.' 14, If 7:3 . febir.il Register 40! LS3) :-i3E91-4S311, Anderson, H. . I.li1--., R. , Z S.M., Fir-ebb noo; se .i ccr.tac t cstos c r.eorl: stic riid. pro-s) A.E., ar.d SeL-Aorr, r.J. A. A. Acad. Sci. (i:> non. Acer. _ . ,.o a. . n.vii. 26:1-13, July lo.'l. A-. vested air pollu- ~r 35, Airborr.s A.--i. :;s - . A re-tori prana rod by Kr.z Co: 1:-:? on Eiolcyle Effects of At. Pel 'i u l cl- , Division r ' V Sc Le.iCc;.:; '.l L v_a F.er-cerc'.i Co'-;:.eil, a.; . .Ac d. 3c:. bc-sb 1 ng fc :.n, P.C. 1571. * 33, Nl-jLoISc.O. , ' . j . . . u *. bv.iidin~ a: r ';;! v Engineers ( i.' pres >} conl3rn. ^ a::c?l Electronic CO ZD On o CH CD 10. Render, a.M. . SolA.-A-, I , J. r <! Sir: o--, A lun^u of peiso nr> ir: :! Vo 'I: Ci . A: / '. : March 1971. 41. Occupational E .vposr: ? 47665, October 9, IS/5 42 . Greerberg, M. and I.loyi Brit. J. Indus i. Med. : 43. Haramond, E.C. and Suit of death of asbestos-r United States. Ir: Bii al. IARC Sc. Pub. Mo. i * Vagner, J.C. A nbestoOss oauccr :e sraoKirr to rts! , r r. r- h --nes''.os, Ed. P. Eogovs'-.i et France, 1273. pc .3V2-3] 7 . J. N : l. Car. 7 c . CO:v-ix, 1971. 45. Vagner, J.C., B c v ry, 0 i*o. J.V,', ai'-i *i v.brel1 , V. The effects of the irhul.it lor. of -r: : for in o1- 29*2ll-9( 137 P.ohl, A.y., L : *ic.r-1', A.::., E'e''l 1.3. -nd 3 ; rr - * rr , Vl.-T. !" v. - to asbe? io*. in tb. . of cour.u* c.* rpar M 1 r*y , p*- r*;-; and t a piny: cc.:- pounds . S co 1M v i- 3j) : 0.71-0 > t (Ar yi1 i .1 f> > 1 ` *V .'. Sawyer, vMo r> pas t, p' Osc- 1 rad ! 1 Lni; i ,l"i ; r =. (j .* li.. . V. a *ci ' `.'-c an. la: V' .-..a. r . .to'h i Li oM.: d i i : - . V. i oc: f rvui , 4.S. Veb^L'^r, r . A?'fo: tos cud ; 1 i cnar.r y. S, Arr. A''-:!. J. 4 ( 9) : 105-1 '* 11 ' Fcrrucry 3, lii". 49. Por.tt-f i net, R.T). :*.'*'. *'-;i.>.r., H.'f. Pc-octrn tics of ashes to 3 thro'*.?', the tract of r.i ; . Nature 2 S3 : 352 -A53, Juno 8, 1973. ^ o j. k.c.y, C . :T, Asaes i - *.n dr. e .*i j water*. *7 . .-c: ;i*, *, -t-^r >.or*.-.-- .kssoc . 65<9) :513-51-1, 107-:. 51. Klvor.jra, C.H.J. -J.*. , 7?y-:r, r*.B., stu-upi i us, J. A prsliniaa rj* in ves r l v<tion tata th*.- ?par.*.. .:-.ce of asbc-s V?; la D'itch tirir.ka::^ a.rter, hnO 7 (!,') ; JO 3 -: -* , 1-/-1. 6SCS9001S Environ. Hlth. Pcrap, 9:1-192, Decent, sc 15 71. 53. Cook. Giaa.-. C-. E. ar-'i Tuck-;:*, J.h. As k>sc iforra attchihole nine'.air,: detente' r, on-.i rurons.-Oi of hi.rh conceit ra ticn-s ia .* c:ici n r I water_ Ei.,itlios . \ c?.n Ot- 1 r : &..--o r* a , a y* e.. " - * r -- *r' ' ~ * * 5 i. Cook, P.M. , r:.:'*>Li*, i.-., '.;ioi*o, C.J. ar.d Nicholson, V.'.J. M-roy di 11 rac r 2on and ;] ..ctron br: **. r.t;*> Lysi s of a-.' fare rirer.i s in Lake Screricr .-.ace . In; Trans. Inat. K: ~:*l.-..cl Fleet ran. * c X:*.: ir.er * ? (i.a p.or-i). 5 5 . Solikoff. I.J. and LI'J, ~.C. l;-v-L.:c.;rvl. ta' r rearer ir. the year 2005 7th N. tiC..-il Ca;.'*<. . Conf, F.roc. los 7rv .,'.*.?, 7270. rr .Cki-OOG.