Document KGwZDdev510070nJK6Rr4qQkK

4 Mortality Effects of Cigarette Smoking Among Amosite Asbestos Factory Workers * CLAIMED PRIVILEGED BY 0CF Irving J. Scllkoff, M.D.. 3 Hrt>*rt Sldman, 4 and E. Cuyl*r Hammond, Sc.D. *5 ABSTRACT--Nina hundrad and thirty-throe amoaita aabaatoa accumulating data to compare with our original obser factory worker* began work from June 1941 through Oacamoar vations. but we believe that this method has made the 1945. At 20 yaars from ortaat of amploymant (1961-65). 562 wara comparisons more secure. known to ba ativa and to hava had aabaatoa work axparianca We have been conscious of the fact that our findings solely at tha factory. Smoking habita wara aaoartainad at 20 yaara have been derived from one category of asbestos-exposed from onaat of amploymant and obaarvabon waa than maintainad individuals--asbestos, insulation workers. Whereas it proapactivaty through 1977: 304 daatha occurred. approximataty has been clearly established that these individuals have twica tha numbar axpactad. Tha axcaaa mortality waa largafy dua very significantly increased risks of death from asbestos- to malignant neoplasm* 116 naoplaama aa compfrad to 33 associated diseases (4, 5), there^emained the possibility axpactad. Sixty canear daatha wara from lung cancar and 14 that other factors in their work environment could mora wara dua to maaothalioma. Nevtrthaiess, had it not baan have interacted with their cigarette smoking exposure for cigaratta amoking. many of tha axcaaa daatha would hava and that some or all of their increased lung cancer risk baan avoidad. Aabaatoa alona would hava aecountad for much of could be so attributed. It has therefore been of interest tha incraaaa. including aoma axcaaa daatha from lung cancar. but to us to investigate the mortality .exfferience of anotberX not tor moat of tha daatha (60) from thia naoplaam. With tha uaa& group of asbestos-exposed workers who did no insuja- \ of smoking-specific mortality rates, It waa caicuiatad that thart tion work and who were not employed in the construe- \ combination of cigarette amoking and-aabaatoa axpoauro- tion industry. / ,A craaaad tha rtak of lung cancar daath about 60 tlmaa. Thua tha We now report resuluifom this study. We found that axparianca of tha amoaita aabaatoa factory workara agreed wtd| factory workers enjphSyed in a plant making a^nosite that of irtaulation workara and provide*avidanoa that tba aabaatoa^ asbestos ^credtrCfsfor shipyards and other industrial amoking Interaction ia epecifie for aabaatoa rather than othagF ' facilities had lung cancer mortality experience consis poaaibla influancaa in Industrial environments. ~JNCI 65: 507- tent with that of the insulation workers. Asbestos 513. I960. exposure alone increased the risk of lung cancer in the absence of cigarette smoking, but for reasons given, the It was shown in 1967 that asbestos exposure sharply increased the already high risk of death from lung cancer associated with cigarette smoking among asbestos total number of such cancers was not great. On the other hand, it appears that the remarkable increase in risk among cigarette-smoking asbestos workers is due insulation workers. (I). The limited data on which these observations were based were later extended and confirmed by much larger studies, which demonstrated Assxcviations used-. ACS "American Cancer Society: BE" best evi that between 1 in 4 and I in 5 deaths among these dence available; DC "death certificate information only. workers was due to lung cancer if they smoked cigarettes. In addition, as compared to other non- smokers. nonsmoking insulation workers also had an 1 Received August 21. 1979: revised February 29. 1960; accepted increased risk of lung cancer, but inasmuch as risk among nonsmokers has been relatively low. even multi plying this risk severalfold did not result in_many lung cancers (2, 3). 'Cancer of the esophagus was also considerably increased among smoking insulation work ers but not among theix' nonsmoking co-workers. However, pleural mesothelioma, peritoneal mesotheli oma. cancer of the stomach, and cancer of the colon March 17. I960. * Supported in pan by Public Health Service grant ES00928 from the Nauonal Institute of Environmental Health Sciences and by grant R-53 from the American Cancer Society. * Environmental Sciences Laboratory. Mount Sinai School of Medicine of the City University of New York. 10 East 102d St., New York- N.Y. 10029. 4 Department of Epidemiology and Stauruci. American Cancer Society. 777 Third Ave.. New York. N Y. 10017. and rectum occurred -with approximately equal excess ' We thank Mr. Ashley Bodden. Mr. David Newman. Mr. Edwin among both smokers-and nonsmokers (3). Silverberg. and Ms. Mane Corbo (or thetr assistance in processing the These studies were detailed and prolonged because we preferred to utilize only prospective observations made after establishing the smoking history from the individual concerned, with subsequent observation, and to compare observed deaths with those expected among men of the same age. in. the same years, with the same distribution of smoking habits, also observed irospectively. This situation led to some delay in dau: Ms. Dorothy Perron. Ms. Shirlev Levine. Mt. Rayla Margoles. and Mr. Otarles V. Nolan (or the held tnvesugauons of the men tn this study: Mr Frances Perez for management of specimens and Xrsvs; and Ms. Selma Annenberg. Mr. Sidney Sibel. and Ms. Judv Marmor (or preparation oi the manuscript. We acknowledge the help of the pathologists, clinicians, hospitals, coroners. State health departments, and other medical facilities providing detailed informa tion. records, slides, blocks, and roentgenograms. We also thank Dr. J. Churg. Dr. Y. Suzuki, and Dr. M. Kannertiein (or their help PLAINTIFFS EXHIBIT 507 JNCl VOL. M. NO J. SEPTEMBER I9 02 401 0395 508 ' Selikoff, Soldman, and Hammond to the exposure to the mineral dust rather than other factors, multiplying the already very high risk of cigarette smoking. MATERIALS AND METHODS In 1941. with the encouragement of the U.S. Navy, a factors' was established- in Paterson, New Jersey, to manufacture asbestos products for the armed forces and for industrial uses. We have ascertained that amosite asbestos was used almost exclusively (with very small amounts of chrysotile asbestos also being used). Our analyses of fiber retrieved from the factory's storerooms, filters from workers' dust masks, samples of the prod ucts made, and fibers extracted from workers' lungs at autopsy have confirmed this almost exclusive use of amosite asbestos and are consistent with the fact that the product specification called for such fiber, that the machinery was designed specifically for this purpose, and that the company that supplied the asbestos from its South African mine had provided only this fiber variety (6). This specificity is of some interest because it provides information concerning one of the three major fiber types. Insulation workers had been exposed only to chrysotile asbestos at first and later to both chrysotile and amosite (5). In 1941-45. 933 men began work in this plant. Some worked for a month or less and others until the plant closed in 1954. We have sought to trace the entire cohort of 933 men and to keep them under surveil lance. We have already found that this group has, overall, a significantly increased risk of death from asbestos-associated disease (7). Other studies have shown that the risk of death from neoplasms known to be associated with asbestos expo sure becomes considerable only after 20 yean from onset of exposure to asbestos. We therefore believed it useful to limit our analyses to the experience of the men who worked in this plant, suiting with their 20th year from onset of employment and excluding all experience subsequent to asbestos employment else where. For some men (those who began work in 1941) the experience was from 1961 onward. For othen, observation for current purposes did not begin until 1965 (i.e., men who began work in 1945). Of the original cohort of 933 men, 351 did ftOt qualify for this analysis. Of these 351 men. 39 had prior asbestos work employment elsewhejjt, 270 were dead, and 42 were lost to follow-up. Almost-aU of those lost to follow-up were lost immediately after termination of their factory employment Actually, this cohort exhibited decidedly unfavorable mortality even before the 20-year point (8, 9). Table 1 demonstrates that 582 -men came under surveillance at the 20-year point and that the ex perience for each man from that time to December 31, 1977, included 6.311 man-years of observation. Table 1 also gives the age distribution of these men. Most of the men in this factory had a history of cigarette smoking. Table 2 outlines the smoking habits of the 582 men we have studied; 430 (73.9%) had a CLAIMED PRIVILEGED BY OCF Table 1.--Number of men at t0-year point and man-yean observation. 1961-77. to or mart years from onset of employme 19U-IS. for S6S amoeite asbestos factory workers by apt Are group. yr 35-39 40-44 45-49 50-54 55-69 60-64 65-69 70-74 75-79 80-84 85+ Total No. of men 84 99 90 86 65 55 40 35 20 6 2 582 Ma'n-yr 150 663 1.062 1.192 1.037 787 560 406 266 126 62 6.311 history of regular cigarette smoking (and almost 85% c these were still smoking at onset of observation whereas 137 men had no such history. Of these 13 men, 59 (10.1%) had smoked pipes and/or cigars but n cigarettes, whereas only 78 (13.4%) had no history c any tobacco smoking. Smoking histories were unol tainable for 15 men (2.6%). __ The entire cohort has been under surveillance sine 1961. with the majority undergoing periodic clinic examination. For men for whom this periodic exam nadon was not possible, intermittent Contact w; achieved. Whenever a death occurred, all availab! clinical and pathologic material was sought and n viewed, including reports of personal medical attenc ants, hospiul records, and histologic material of uined at operauon and/or autopsy. For each death certificate of death was obtained. Each individual in the cohort remained in th analysis "at risk" from the point at which he reache 20 years from onset of employment during the perio 1961-65 until he took up other asbestos employment c otherwise until December 31, 1977, if he was still aliv or unul date of death if he died before then. The grou as a whole then included 6,311 man-years of observa don (table 1): 4.811 man-years for individuals with history of cigarette smoking, 868 for those who neve smoked regularly. 528 for those who had smoked pipe and/or cigars, and 104 for those whose smoking histor was unknown (table 3). Using the attained age of each man in each calenda year period after admission to the cohort following th TABLE 2.--Number of mm at t0~ysar point and man-years observation. 1961-77. tO or more years from onset of emptoymer 19il-iS. for SSt amosite asbestos factory workers by smokir habits at to-year point Smoking history History of cigarette smoking Current smokers Exsmokera No history of cigarette smoking Never smoked regularly Pipe and/or cigar only Smoking history unknown No. of men 430 359 71 137 78 59 15 Man-jr 4.811 3.993 818 1.396 868 528 104 JNCI. VOL 65. NO S. SEPTEMBER I960 02 401 0396 | t j* t i > ob s: Mortality: Smoking and Asbestos Factory Work 5 Table 3.--Number of men at tO-year point and man-years of observation. 1961-77. SO or more years from onset of exposure. 1911-15. for 58S amosite asbestos factory workers by smoking habits at SO-year point and by age 35-39 40-44 45-49 60-54 55-69 60-64 65-69 70-74 75-79 80-84 854Total History of cigarette smoking No. of men Man-yr 67 -80 70 70 62 38 25 19 7 1 1 430 121 529 837 942 814 630 433 287 148 49 21 4.811 Never smoked Pipe and/or Smoking history ________ regularlycigar onlyunknown No. of men Man-yr No. of men Man-yr No. of men Man-yr 10 19 3 64 4 10 80 9 39 0 15 16 140 3 64 2 21 8 166 6 67 2 17 6 132 3 69 4 CL <22-MED 8 93 8 47 1 PRIVTCLEGED 9 69 6 51 0 BV Vir-TT 7 67 9 52 0 4 56 8 62 1 0 1 37 3 39 1 l 0 9 1 32 0 0 78 868 59 528 15 104 20-year-from-onset point, 1961-77, we computed the number of expected deaths for this cohort for these periods of years. Calculations were made in several ways. First, ex. pected deaths were based on age-specific data of the U.S. National Center for Health Statistics for New Jersey white males (1965-66, 1967-71, and 1972-77) without regard to smoking habits. Expected deaths were also computed in relation to smoking habits on the basis of age- and smoking-specific experience (1963-66 and 1967-71) of white males in the ACS prospective study (70); this analysis was limited to the experience of men other than farmers with at most a high school education and a history of occupational exposure to dust, fumes, chemicals, gases, or radiation. The 1967-71 ACS study rates were extrapolated to 1972-77 according to changes in age-specific death rates among total U.S. white males between 1967-71 and 1972-77. Expected deaths for the few men with unknown smoking habits were computed on the basis of the age-specific and calendar-year-specific rates of all . the men (regardless of smoking history) in the ACS study. A third set of expected deaths was computed on the basts of the death rates of the amosite asbestos factory workers who never smoked regularly. To ensure more stable figures, we initially used age-specific death rates for all of the men with experience past 20 years from onset of employment (regardless of smoking habits). 1961-66. 1967-71, and 1972-77. The resulting expected deaths were then proportionately adjusted to levels such that totals of expected and observed deaths were equal for the workers who never smoked regularly. Observed deaths were then compared with deaths expected. We classified the causes of death in the , observed deaths in two ways, according to DC and according to BE. Some investigators may prefer to use the DC figures and argue that the deaths in the populations used as controls have not been subject to a review similar to that of the BE deaths. Their prefer ence assumes that whatever errors exist in the DC * figures are much the same in the population being investigated (factory workers) as in the control popula tions (ACS or U.S. National Center for Health Statis tics data). This procedure is certainly far less laborious. However, some serious difficulties arise. When the distributions of causes of death in the population being investigated and control groups are markedly' different, one might anticipate the distributions of error to be different. Mesothelioma and asbestosis Have been decidedly underreported on the death certificates of asbestos workers. However, because of the" infre quency of these conditions, they have not pose^corre sponding difficulties in the general population. Whatever one does, one cannot ensure strict compar ability between the cause-of-death classifications for the population investigated and the control populations. In the interest of showing as accurate results as we can for the population being studied, we have oriented the exposition in this paper to the BE findings. However, the DC results have also been shown in the tables for those who prefer such data. Paralleling the observations for insulation workers (3, II), some differences were observed among the various categories between cause of death as recorded on the death certificate and cause of death established after review (table 4). However, on the whole, this set of findings speaks well for the diagnostic acumen of the medical attendants of these men. RESULTS Three hundred and four deaths occurred among the 582 men observed sometime between 1961 and 1965 (the point at which each man reached 20 yr from onset of employment) to December 31. 1977. Cancer of one or another site accounted for 116 of these deaths (38.2%). and 18 deaths were due to asbestosis (5.9%). Table 5 shows that the following cancers in five areas caused most of the deaths: lung cancer (60 deaths): pleural mesothelioma (7 deaths); peritoneal mesothelioma (7 deaths): pasrrnimrsnnal nmvr inrlndino Mnnhj?m (16 deatnsi: ana cancers ot me oral cavity, pna.vngeal, and laryngeal tissues (5 deaths). Altogether, there were approximately three and one-half times as many cancer deaths as expected. The increase in cancer deaths. JNCl. VOL. 65. NO J. SEPTEMBER I960 02 401 0397 510 Scllkott, Saidman, and Hammond CLAI MEL' PRIVILEGED by ocf Table 4--CategonsaHm of SOI death*. 1961-77. to or mart year* from cmeet of employment 1911-15. for SSt amoeile aebeeto* ' ' factory worker* Cause of death Based on DC only All causes - -- Cancer, all sites - Lung Pleural mesothelioma Peritoneal mesothelioma Mesothelioma not spec- ified above Larynx, oral cavity, and pharynx Esophagus Kidney Colon-rectum Stomach Prostate gland Bladder Pancreas Other and unspecified Noninfeetious pulmonary diseases, total Asbestosis Cardiovascular diseases Other and unspecified ctuttt 304 103 62 1 0 3 3 1 2 11 4 4 2 6 15 29 8 130 42 Baaed on BE 304 116 60 7 7 0 6 1 2 11 4 4 2 4 9 24 18 122 42 Difference between BE and DC 0 +13 +8 +6 +7 -3 +2 0 0 0 0 0 0 -1 -6 -5 +10 -8 0 coupled with deaths due to asbestosis, serves to explain most of the virtual doubling of the expected deaths for these men over the period under study. In contrast to the insulation workers, the factory workers had an excess, though a limited one, in mortality from cardio vascular diseases (?, 11). Data in cables 6 and 7 are organized to shed some light on the excess deaths associated with amosite asbestos exposure, tobacco habits, and amosite asbestos plus tobacco exposures. _uable b). I his "observation shows me strong influence of amosite asbestos expo sure in itself. For the total cohort of asbestos factory workers, if expected deaths had been calculated on the basis of the experience of asbestos factory workers_who never smoked regularly, 'ifcould be estimated that~244 deaths would have occurred, whereas 91 deaths would have been anticipated for men- who had neither a history of tobacco smoking nor-asbestos employment (table 6). The influence of asbestos alone can be seen as the difference,.or 1-53 deaths. Similarly, if expected deaths were based on men with the same smoking habits, but not with a history of asbestos employment. 137 deaths would have occurred instead of the 91 (table 6). The influence of smoking alone would thus account for 46 deaths. The remainder of 14 when 91 + 153+46 is subtracted from the observed total of 304 deaths can be regarded either as the joint effect of asbestos and smoking or as discrepancies in data that do not purport to be absolutely consistent. The 304 deaths then are distributed as 30% neither asbestos related smoking related, 50% related to asbestos alone, related to smoking alone, and 5% remaining. Performing the same computations for the asbe factory workers who were cigarette smokers, we < mated that of the 214 deaths (table 6), 57 (27%) v neither asbestos nor smoking related. 115 (54%) v related to asbestos alone, 46 (21%) were related smoking alone, and --4 (--2%) were the remaind Although these data can hardly be regarded definitive, they do illustrate the general nature of composite effects evident for all causes of death. ~ composite effects include, among others, specific sm ing effects, asbestos effects-- pleural mesothelioma, p itoneal mesothelioma, asbestosis. and the excess dea from cancers of the stomach, colon-rectum, oral cav pharynx, and larynx as well as the limited number excess deaths from lung cancer among the nonsmo: Table 5--Observed and expected death*. 1961-77. ty or r year* from ontet of employment J9U-15. among 582 ante aebeeto* factory worker* by eeitee of .death" Cause of death Observed deaths "Heaths Y Smokin DC BE New Jersey* adjustec * ACS stuc All causae , Cancer, all sites Lung Pleural mesothelioma Peritoneal mesothe- lioma Mesothelioma not specified above Larynx, oral cavity. and pharynx Esophagus Kidney Colon-rectum Stomach Prostate gland Bladder Pancreas Other and unspecified Noninfectious pulmonary diseases, total Asbestosis Cardiovascular diseases Other and unspecified eftusef 304 304 103 116 52 60 17 07 30 35 *2 411" 2 5 15 29 1 2 . 11' 4 4 2 4 9 24 8 *18 130 122 42 42 15&6 V 33.4' 10.1 Fn e Fn e Fn e 1.6 - 'TT'\ 1.4 1.8 7.0 4.7 Fn e 95.3 25.2 137.1 29.8 10.1 Fn e Fn e Fn c 1.0 06 ~TTT 3.7 0.9 1.8 69 7.4 Fn e 81.2 18.7 * Expected deaths were computed on the basis of tge-*peei data of the U.S. National Center for Health Statistics for N Jersey white males (1963-66. 1967-71, and 1972-77) without ; gard for smoking habits. Expected deaths were computed on the basis of age- a smoking-specific experience (1963-66 and 1967-71) of white ma in the ACS prospective study. This analysis involved men with moat a high school education and with a history of oecupatior exposure to dust, fumes, chemicals, gases, or radiation: farm* were excluded from this group. The 1967-71 ACS study ra' were extrapolated to 1972-77 according to changes in age-s; cific death rates in total U.S. white males between 1967-71 a 1972-77. ` New Jersey and ACS study death rates are not available, t these diseases have been rare causes of death in the general pop lation. JNQ. VOL. 61. NO 3. SEPTEMBER 19S0 02 401 0398 Mortality: Smoking and Aabaatoa Factory Work 5 Table 6.--Obtervedfaiid expected total death*. 1961-77. to or more peart from oneet of employment. 19il-iS. among 582 amorite . __ atbeeto* factory workers by tmoking habit* at 20-year point Expected death* based on Smoking- history History of cigarette smoking Never smoked regularly Pipe and/or cigar only Smoking history unknown Total Observed deaths 2U 38 41 11 304 Amoaite asbestos factory worker* who never smoked regularly* 171.9 38.0 30.7 3.0 243.6 __________________ ACS study Men with matching history of smoking* Men who never smoked regularly' 102.3 16.6 18.1 \2 137.1 66.7 15.6 17.7 0.8 90.7 * Expected deaths were initially computed on the basis of age-specific experience (1961-66. 1967-71. and 1972-77) of all men in the cohort 20 or more yr from onset of exposure. The expected death totals were then adjusted proportionately to that the expected death total for the men who never smoked regularly equaled their observed death total. * Expected deaths were computed on the basis of age- and smoking-specific experience (1969-66 and 1967-71) of white male* in the ACS prospective study. This analysis was limited to men with at most a high school education and with a history of occupational exposure to dust, fumes, chemicals, gases, or radiation: farmers were excluded from this group. The rates in the ACS study (1967-71) were extrapolated to 1972-77 according to changes in age-specific death rates in total U.S. white males between 1967-71 and 1972-77. * As in footnote 6. except that expected deaths were computed on the basis of the experience of the men who had never smoked regularly. asbestos workers--and the very much larger increase in the lung cancer category as a result of the interaction between asbestos exposure and cigarette smoking. The last phenomenon, the remarkable multiplication of the already high lung cancer risk of cigarette smoking that occurs in asbestos workers, is clearly seen in table 7. The 0.2 deaths were expected to occur among the nonsmoking asbestos workers if their ex perience had been the same as comparable nonsmokers who had no history of asbestos work. However, 3 such deaths (BE classification) occurred among the 78 men in the group who had no history of regular cigarette smoking. This observation suggests that asbestos-expo sure alone produces an increased risk of lung cancer and agrees with observations in our cohorts of asbestos' insulation workers (5). In terms of total number of lung cancer deaths, the increase is limited although undesirable. However, the increase in number of lung cancer deaths among cigarette smokers is devastating. Among 430 men with a history of cigarette smoking were 55 men who died from lung cancer (BE), approx imately six times the number of other cigarette smokers without a history of asbestos employment and approx imately 80 times the number expected among men of Table 7.--Observed and expected lung cancer death*. 1961-77. to or mart peart from oneet of employment. J961-IS. among Sit amoeite asbestos factory workers by smoking habit* at to-year point - /' Expected deaths based on Smoking history C*teroriution Observed deaths Amosite asbestos factory workers who smoked rneegvuelrarly', ACS study Men with matching history of smoking* Men who never smoked regularly' History of cigarette smoking Never smoked regularly Pipe and/or cigar only -- Smoking history unknown Total DC 46 BE - 66 DC 6 BE 3 DC 2 BE 2 DC 0 BE 0 DC 62 BE 60 28.8 16.5 5.0 3.0 3.0 1.8 0.6 0.3 37.3 21.6 - 9.6 02 02 0.1 10.1 0.7 02 02 0.0 1.1 * Expected deaths were initially computed on the basis of the sge-speeific DC and BE experience (1961-66. 1967-71. and 1972-77) of all men in the cohort 20 or more yr from onset of exposure. The expected death totals (DC and BE) were then adjusted proportionately so that the expected death totals for the men who never smoked regularly equaled their observed death totals (DC and BE) Expected deaths were computed on the basis of aye- and smoking-specifie experience (1969-66 and 1967-71) of white males in the ACS prospective study. This analysts was limited to men with at most a high school education and with a history of occupational ex posure to dust, fumes, chemicals, gases, or radiation: farmers were excluded from this group. The rates in the ACS study (1967-71) were extrapolated to 1972-77 according to changes in age-specific death rates in total U.S. white males between 1967-71 and 1972-77. * As in footnote b. except that expected deaths were computed on the basis of the experience of the men who had never smoked regularly. cu^frc,,. JNd. VOL. U. NO S. SEPTEMBER 1900 02 401 0399 512 Sallkofl, Satdman, and Hammond the same age and same personal background but without a history, of either tobacco smoking or asbestos employment (077" expected and 55 observed). For other asbestos-related diseases, considerable in terest exists in whether the risks of death associated with asbestos exposure are also influenced by cigarette smoking. However, there are only a small number of deaths at hand'fSr use_in investigation of these diseases among the amosite asbestos factory workers, especially among the nonsmoking workers. Table 8 shows the data available for mesothelioma, gastrointestinal cancer, and asbestosis deaths among the factory workers (cigarette smokers and nonsmokers). To supplement these insubstantial findings, table 8 also gives corresponding data for the asbestos insula tion workers (Hammond EC Selikoff IJ, Seidman H: Unpublished data.) The BE classification of causes of death is used because all comparisons in table 8 are within the asbestos worker groups. Moreover, the DC classification does not provide results of any value with respect to the incidence of deaths from mesothelioma and asbestosis. We found no increased risk of death from mesothe lioma in amosite asbestos factory workers with a history of cigarette smoking compared with nonsmokers. The same was true for cancer of the stomach, colon, and rectum. These observations agree with those for the asbestos insulation workers. However, the factory workers do not show the strong influence of cigarette smoking on risk of death from asbestosis that was so striking in insulation workers (table 8). CONCLUSIONS The mortality experiences of amosite asbestos factory workers are much the same as those of asbestos-exposed insulation workers, i.e., remarkably increased risk of deaths from asbestosis and cancers of several sites (lung cancer; pleural mesothelioma; peritoneal mesothelioma; gastrointestinal cancer; and oral cavity, pharvngi and laryngeal cancers) (11, 12). Among men 20 or m years from onset of asbestos exposure, observed p spectivelv from a 20-year point reached 1961-65 December 51. 1977. 504 deaths were seen, approximai twice the number expected. Eighteen deaths fr asbestosis occurred. Excess deaths, however, were larg due to neoplasms. Neoplasms caused 116 deaths, th and one-half times the number expected. Sixty can deaths were from bronchogenic carcinoma and 14 mi were due to either pleural or peritoneal mesothelior. Nevertheless, had it not been for cigarette smokir many of the excess deaths would have been avoid' Asbestos alone would have accounted for an imporu increase, including some excess deaths from lu cancer, but not for most of the lung cancer deal! Here asbestos exposure greatly multiplied the alrea high risk that would have been present with cigare smoking alone. The combination of cigarette smokii and asbestos exposure among these amosite asbest factory workers was calculated to have increased the risk of lung cancer death alsout 80 times- as cor pared with like men of the same age_whfl_neith smoked cigarettes nor worked with asbestos. Th increased risk is very much the same as that see among asbestos insulation workers. Thi-observatic indicates that the increased risk of deatft from lur cancer among cigarette-smoking asbescos `.workers is specific interaction rather than coincidental, and no for example, the result of other agents in the enviror mem of the construction trades. The factory in which these men worked closed i 1954, and no further occupational exposure to asbestc occurred for most of the men. For most worker, asbestos employment ceased in 1945 at or before th end of World War II. In other studies (8, 9) we foum that cessation of occupational exposure to asbestos ir this factory was not accompanied by cessation of ris! of asbestos-associated disease, including mesothelioma Table 8.--Obterved and expected death* from teieeted causes (BE) tO or more year* from onset of employment far SSt amarite asbesic factory worker*. 1961-77, and It.051 aehtetae insulation worker*. 1967-76. for men with a history of making cigarette* compared, ml thorn who never rmoked regularly Causes of death or NSR* Mesothelioma Cancer of stomach, colon-rectum Asbestosis Cigarettes NSR Cigarettes NSR Cigarettes ' NSR Amosite asbestos factory worker* Observed deaths. BE Expected deaths. NSR* 9 14.8 3 3.0 9 10.1 3 3.0 11 - 10.0 2 2.0 Asbestos insula tion workers Observed deaths. BE Expected deaths. NSR' 105 108.8 IS 15.0 43 41.5 6 6.0 97 32 8 5 5.0 * NSR-never smoked regularly. * Expected deaths were initially computed on the basis of the age-specific BE experience (1961-66. 1967-71. and 1972-77) of all amosite asbestos factory worker* 20 or more yr from onset of exposure. The expected death totals were then adjusted proportionately sc that the expected death totals for the men who never smoked regularly equaled their observed death totals. * Expected deaths were initially computed on the basis of the age-specific BE experience (1967-71 and 1972-76) of all asbestos insu lation workers 20 or more yr from onset of exposure. The expected death touls were then adjusted proportionately so that the expected death touts for the men who never smoked regularly equaled their observed death touls. JNQ. VOL 65. NO i. SEPTEMBER I960 CU*vl`_rv-n 02 401 0400 Mortality; Smoking and Aab*to Factory Work 5 gastrointestinal cancer, and asbestosis. Thts?Knt!l| mak^ir aJf'thesnKnertece**ary<?u^ rrpeararrlrdmo&f ioiy preyit>u>Iymatk^^CAsbftf6r^orfaeiwha,inolt agamies should sioptunggkincinunediaielr. and (hos* who do not. smokryshouj^fcaevcfabegink: Furthermore*! all avoidable exposumjo aiihest'Sr must' be prevented* REFERENCES (1) Seukoff (J. Hammond EC Chukc J. Asbestos exposure, smoking and neoplasia. JAMA 1968:204:106-112. (?) Hammond EC Seukoff IJ. Relation of cigarette molting to rid of death of asbestos-associated disease among insulation workers m the United States. In: Bogovski P. Ctlson JC Timbrell V, Wagner JC eds. Biological effects of asbestos. 1ARC Sd Publ 1973:8:812-317. til Hammond EC Seukoff IJ, Seidman H. Asbestos exposure, cig arette smoking and death rates. Ann NY Acad So 1979:330: 473-490. H) Seukoff IJ, Chukc J, Hammono EC Asbestos exposure and neoplasia. JAMA 1964:188:22-26. (5) Scukoff IJ. Hammond EC Otuxc J. Mortality experiences of asbestos insulation workers In: Shapiro HA. ed. Pneumo coniosis. Proceedings of the intemauonal conference. Johan nesburg. Capetown: Oxford Univ Press. 1970:180-186. Id) Lances AM. Ruin- I. Seukoff IJ. Electron microprobe analysts of asbestos bodies. In: Shapiro HA. ed. Pneumoconiosis. Pro ceedings of the international conference. Johannesburg. Cape town: Oxford Unis Press. 1970:57-69. (7) Seukoff IJ. Hammond EC. Chlsc J. Carcinogenicity of amosiie asbestos. Arch Environ Health 1972:25:183-186. (S) Seidman H. Lius R. Seukoff IJ. Short-term asbestos exposure and delayed cancer risk. In: Nieburgs HE. ed. Prevention and detection of cancer. Vol I. New York: Marcel Dekker. Inc-. 1976:943-960. (9) Seidman H. Seukoff IJ. Hammond EC Short-term atbettoi work exposure and long-term observation. Ann NY Acad Set 1970: 330*1-89. <10) Hammond EC Gakftnkei. L. Seidman H. Lew Ea. Tar and nicotine content of cigarette smoke in reiauon to death rates. Environ Res 1976:12:263-274. (//) Seukoff IJ, Hammond EC. Seidman H. Morality experience of insulation workers in the United Sutes and Canada. 19431976. Ann NY Acad Sci 1979:330:91-116. (12) Seukoff IJ. Cancer risk of asbestos exposure. In: Hiatt HH. Watson JO. Winsten JA. eds. Origins of human cancer. New York: Cold Spring Harbor. 1977:1765-17W. privileged . B* OCF JNa. VOL &J. NO J. SEPTEMBER 1940 A* 02 401 0401