Document yrNoYQ6j1RdkN0zxYoROw36D

FILE NAME: RT Vanderbilt (RTV) DATE: 1990 DOC#: RTV 103 DOCUMENT DESCRIPTION: NIOSH Health Hazard Report - RT Vanderbilt Co. Hazard Evaluation (HHE) report and any recommendations made herein are for the specific facility evaluated and may not be universally Any recommendations made are not to be considered as final statements of N IO SH policy or of any agency or individual involved H E reports are available at http7/www.cdc.gov/niosh/hhe/reports Ji Mtnim id Hm Mi nPduMlMi Hvn u tM AHNitD*H*U IMmANM tuKmRtoVrICOCIm U.i. DCPAHTMINT O f H IALTH C w w i 1er DhM Cwnml Health Hazard Evaluation Report HETA 90-390-2065 MHETA 86-012-2065 R.T. VANDERBILT COMPANY GOUVERNEUR, NEW YORK ll^0 PREFACE Ihe Hazard Evaluations and Technical Assistance Branch of HIOSH conducts field investigations of possible health hazards in the workplace. These investigations are conducted under the authority of Section 20(a)(6) of the Occupational Safety and Health Act of 1970, 29 U.S.C. 669(a)(6) which authorizes the Secretary of Health and Hunan Services, following a written request from any employer or authorized representative of employees, to determine whether any substance normally found in the place of employment has potentially toxic effects in such concentrations as used or found. The Hazard Evaluations and Technical Assistance Branch also provides, upon request, medical, nursing, and industrial hygiene technical and consultative assistance (TA) to Federal, state, and local agencies; labor; industry and other groups or individuals to control occupational health hazards and to prevent related trauma and disease. Mention of company names or products does not constitute endorsement by the Rational Institute for Occupational Safety and Health. BETA 90-390-2065 MHETA 86-012-2065 SEPTEMBER 1990 S.T. VANDERBILT COMPANY GOUVERHEOR, NEW YORK HIOSH INVESTIGATORS: David P. Brown, M.P.H. Wayne Sanderson, C.I.H. Lawrence J. Fine, M.D. I. SUMMARY The study conducted for this health hazard evaluation adds eight years of observation to the mortality study of miners and millers at the Gouvernenr Talc Company (GTC) that was published by HIOSH researchers in 1980. The current study was based on 710 white male workers who were employed any time at GTC between 1947 and 1978 and whose vital status was determined as of 1983. When compared to O.S. white male mortality rates, there were statistically significant increases in all causes combined (SMR=128, 161 oba.), all non-malignant respiratory disease (SHR=251, 17 obs.), and lung cancer (SME=207, 17 obs.). The SMR for lung cancer was slightly higher for the workers with tenure of employment less than 1 year (SMRs222, Cl 96, 438) compared to workers with tenure greater than one year (SMR=194, Cl 89, 369). The lung cancer risk was higher in those with 20 or more years of latency (SMR=58, Cl 137 , 441) than in those with less than 20 years of latency (5MR=126, Cl 34, 322). The SMR for non-malignant respiratory disease was significantly elevated among those with more than one year of tenure (SHR=290, Cl 144, 518). The magnitude of the risk for both lung cancer and non-malignant respiratory disease indicate that the workplace exposures at GTC are, in part, associated with these excesses in mortality. Possible confounding factors, such as cigarette smoking and other occupational exposures from employment elsewhere, may have contributed to these risks as well. Although the contribution of these confounding factors could not be totally quantified in this study, it is unlikely that they, alone, could account for the observed excess risks. The principal limitations in this study are; (1) the size of the cohort (especially for those workers with long tenure), (2) the inability to precisely characterize past occupational exposures at GTC or occupational exposures from employment elsewhere, and (3) the lack of reliable smoking data. The elevated risks observed in this study are similar to those in one other study of talc miners in Hew York State. Keywords: (SIC 1499) talc, amphiboles, cohort mortality study, mining, lung cancer, non-malignant respiratory disease. Page 2 - Health Hazard Evaluation Report Ho. 90-390 and MHETA 86-012 II. i m O D O C T I ON Researchers from the Rational Institute for Occupational Safety and Health (lTIOSH) have previously conducted studies of mortality and morbidity patterns and occupational exposures among talc miners and millers.'1'8 ^ In February 1980, HIOSH researchers published a Technical Report entitled "Occupational Exposure to Talc Containing Asbestos"^1), vhich dealt specifically with talc ore mined by the Gouvemeur Talc Company (GTC) in the Gouvemeur Talc District in upper Hew York. This report was divided into three sections (1. Environmental, 2. Cross-sectional morbidity, and 3. Retrospective cohort mortality), which were subsequently published elsewhere (2-4,6). Additionally there have been three other mortality studies of GTC workers, all of which were based on the same basic data set. (9-11) The interpretation of the epidemiologic findings of these studies; and the controversy about the mineralogical composition of the talc and its contaminants at this mine has been the subject of numerous publications.(i2--23) Authors of the previous mortality studies differ in their conclusions about the excess risk of lung cancer observed in the GTC workers. The 1980 cohort mortality study published by HI0SH researchers concluded, "exposures to asbestifoxm tremolite and anthophyllite stand out as the prime suspect etiologic factors associated with the observed increase in bronchogenic cancer and non-malignant respiratory disease among this study cohort."(1) Brown et al., also concluded that "exposures to talcs from the Gouvemeur mining area are associated with an increased risk of bronchogenic cancdr and non-malignant diseases of the respiratory system."(*) Stille and Taberahaw concluded there were "elevated mortalities but no significant increases in the numbers of deaths from lung cancer, from non-malignant respiratory disease, and from all causes."(5) Lamm concluded that the increased lung cancer risk "is most likely due to risk acquired elsewhere, such as prior employments, or to differences in smoking experience or other behavioral characteristics."(U ) On Hovoober 9, 1985, R.T. Vanderbilt, Inc., requested that HI0SH conduct a Health Hazard Evaluation (HHE) to update the 1980 HI0SH study qf employees at their Gouvemeur Talc Company in Balmat, Hew York, particularly that portion of the study that dealt with the mortality experience of the cohort. In response to this request HI0SH updated the vital status of the cohort through 1983; and evaluated exposure-response by latency using tenure as a surrogate of exposure. Page 3 - Health Hazard Evaluation Report Ho. 90-390 and MHETA 86-012 III. METHODS Cohort Definition Since the entire working population ia white and ninety five percent ale, the atody cohort was defined as all white sales who worked at least one day at GTC between the beginning of operation in 1947 through 12/31/78. This definition did not include any criteria for a minimum length of employment in order to be consistent with the mortality study published in 1980.(*) The demographic and work history data on the cohort were obtained from R.T. Vanderbilt, Inc., and were originally i" ' ' ~ 'onal Medical Associates Data on this tape (referred to as the ~DRDS master file") were collected from plant personnel records and include GTC job histories (date of hire; age at hire; type, location and duration of each job held while working at GTC; date of termination) and demographic information. To assure completeness of the cohort and accuracy of work history information, comparisons were made between the "DRDS master file", Social Security Administration (SSA) quarterly reports (1962-1983), separate lists of employees kept by GTC (one from 1947-1962 and one from 1947-1966), and the master file used in the 1980 study. Any differences in job history comparisons were resolved using company personnel records. Vital status was determined as of 12/31/83 for all white male workers in the cohort. If the vital status could not be determined by the SSA or IRS, then verification was determined by telephone follow-up to next of kin. Death certificated were obtained for all deceased persons in the cohort and compared with name, SSN, and date of birth information in the "DRDS master file" to assure a correct natch. The underlying cause of death was coded by a nosologist according to the Eighth Revision of the International Classification of Diseases (ICD). The person-years analysis consisted of a comparison of age-time-adjusted death rates in the study cohort with the mortality experience of D.S. white males. Standardized mortality ratios (SMR's) were computed by the modified life-table technique described by Monson(24) ttsing the 0CKAP computer program. (25) Computation of expected number of deaths from the external population rates were Adjusted by the 0CMAP program for comparability to the Eighth Revision of the ICD using comparability ratios developed by the national Center for Health Statistics. SMR's were calculated by dividing the observed deaths by expected deaths and multiplying by 100. A statistical test to determine whether the SMR was significantly different from 100 was used, and the observed number of deaths was assumed to have a Poisson distribution.(26) Page 4 _ Health Hazard Evaluation Report Ho. 90-390 and MHETA 86-012 Person-years (PI) were calculated beginning with initial date of employment and accumulated till death or end of follow--up (12/31/83), whichever occurred first. The FYs for all workers were distributed in 5 year age groups and 5 year calendar tine periods, for calculation of expected deaths. PIS also were distributed by tenure and tine since first employment, in order to examine risk by these variables. Tenure was used as a surrogate of exposure, being defined as calendar tine spent in all jobs between date of first hire and termination of employment or date of record collection. Latency was defined as time from first employment to time of observation. IV. RESULTS There were 710 white males who had worked one day or more between 1947, the beginning of construction of GTC, and 1978. Vital status (alive or dead) was determined for the entire cohort. The cause of death was determined for all but 5 (0.7X) individuals. Follow-up was ascertained through 1983, at which tine 161 (27X) members of the cohort were dead. Table 1 provides descriptive data on the cohort. There were a total of 15,294 FT at risk. The average age at hire was 30, and the average age at death was 56. Almost half of the cohort (322/710), half of the deceased members of the cohort'(79/161), and half of the lung cancer cases (8/17) had worked at GTC less than one year. Table 2 compares the observed number of deaths to the number of deaths expected for this cohort based on U.S. white male mortality rates. The following causes of death had SMRs that were significantly elevated above 100: all causes of death (128), all malignant neoplasms (145), lung cancer (207), and non-malignant respiratory disease (251). Table 3 provides the distribution of lung cancer deaths by tenure and latency. Thw lung cancer SMR for the latency group with 20 or more years was 258 (Cl 137, 441); over half (8/13) of the lung cancer cases in this latency group occurred in the less than 1 year tenure group where the SMR was 357 (Cl 154 , 704). Those workers with greater than 20 years latency and with greater than 1 year tenure also demonstrated an increase in risk (SMR, 178), however, the excess was not statistically significant. Table 4, all causes, malignant neoplasm, lung cancer, and non-malignant respiratory disease mortality are stratified by workers with leas than one year tenure and workers with greater than one-year tenure. After stratification, all cause mortality for workers with Page 5 - Health Hazard Evaluation Report Ho. 90-390 and MHKTA 86-012 less than one-year tenure was significantly elevated; non-nalignant respiratory disease mortality vas significantly elevated among workers with greater than one-year tenure. Other increases did not achieve statistical significance. V. DISCUSSION This is a small cohort (710 workers), of which 161 (22.7X) are deceased. The SMS analysis (Table 2) indicates a statistically significant excess of lung cancer and non-malignant respiratory disease in this cohort. In a previous update of this cohort(9), which determined vital status as of 12/31/78, ten lung cancer deaths had been identified. This update adds eight new lung cancers to the study. The SMS for lung cancer vas uniform across tenure strata and increased vith increasing latency (Table 3). There vas a statistically significant excess in lung cancer in those with 20 years or more latency and vith less than one year employment. Those in this latency group with greater than one year duration also exhibited an increased risk but it vas not statistically significant. The increased risk of lung cancer among those vith short duration also vas observed in the 1980 analysis^). There are several possible explanations for this observation. First, cohort members may have been employed in other New York State talc mines and mills where there may have been additional exposures to the same or to similar types of mineral dust. This potential confounding variable is difficult to quantify. Based on limited information U . 2 7 ) ft is known that as many as half of the lung cancer cases worked in other talc mining operations. In addition, there may have been exposure to other lung carcinogens from employment previous to 6TC. Second, some of those in the short duration group may have had very high exposures, especially in the early years of the mining operation. This, too, is impossible to quantify, especially for the oldest exposures. Third, the smoking habits among the employees may have been different from the reference population. Although several diseases associated vith cigarette smoking are nonsignlfieantly elevated, smoking alone does not account for the excess observed in the cohort. At the time of the morbidity study by Camble(l), which vas conducted in 1975, the smoking patterns among GIC workers vere not much different from those of U.S. white males. Among those in the cross-sectional study the distribution vas: non-smokers (2IX) ex-smokers (31X) and smokers (48X). The distribution, in 1976, among white males 20 years and over In the U.S.(28) vas: non-smokers (28.2X), ex-smokers (30X), and smokers (41.2X). For those in the age group, 20-44 years old, which is more comparable to the cross-sectional study group, the smoking prevalence rate for U.S. white males was approximately 47X. Using an adjustment for smoking as suggested by Axelson^29); even if 100X of the cohort vere smokers, the risk for lung cancer vonld have been Increased only by 60X or an SMS of 160. Page 6 - Health. Hazard Evaluation Report Ho. 90-390 and HHETA 86-012 A combination of these factors, mentioned above, may account for the lack of a positive association between lung cancer risk and duration of employment. It also should be noted that the group with less then one year duration represents half of the person-years of the cohort and although those with longer duration also had an increased risk for lung cancer, the number of workers within each strata, by duration of employment greater than one year, was small and the power to detect a significant risk within these strata was limited. The excess for nonmalignant respiratory disease was more consistently associated with an occupational exposure at GTC. There was a larger excess risk in those with duration of employment over one year compared to those with less than one year. To evaluate the consistency of the results of the current analysis with prior research at GTC, SMR's for all causes and for lung cancer were compared between three previous mortality studies of this cohort and an earlier proportionate mortality study of Hew Tork talc workers (Table 5). The earliest report was of talc workers with >15 years tenure in the northern part of Hew York State, presumably in the Gouvernenr talc district.(30,31) The talc contained asbestos amphibole and serpentine minerals.(32) The proportionate mortality ratio (FMR) for lung cancer was about 3 times expected. (31) The remaining SMR studies (1 9 H ) involved essentially the same cohort as in this study, i.e. white male employees who ever worked at GTC since it began operations. The results are consistent across studies in that both overall mortality and lung cancer mortality were elevated; the SHR for lung cancer in the 20 or more year latency group was 2.6 to 4.6 times expected. Among employees with greater then 20 years latency, the lung cancer SHR was about 2 times greater for employees with less than one-year tenure compared to those with greater than one-year tenure. However, these differences are based on small numbers. In conclusion, the results of this updated study support the findings of an excess risk for lung cancer and non-malignant respiratory disease which was observed in these workers by HI0SH researchers in 1980. The recommendations for control of exposure made in the 1980 report remain appropriate. VI. REFEREHGES 1. Dement JM, Zumw&lde SD, Gamble JF, Fellner W, DiHeo MJ, Brown DP, Wagoner JK. Occupational exposure to talc containing asbestos-morbidity, mortality and environmental studies of miners and millers. Cincinnati, Ohio: national Institute for Occupational Safety and Health, 1980; DREW (HX0SH) Publication Ho. 80-115. Page 7 - Health Hazard Evaluation Report Ho. 90-390 and MHETA 86-012 2. Dement JM, Zumvalde RD. Occupational exposures to talcs containing asbestiform minerals. In: Lernen R, Dement JM, eds. Dusts and disease. Park Forest: Pathotox Publishers Inc., 1979:307-16. 3. Gamble J, Fellner V, DiHeo HJ. An epidemiologic study of a group of talc workers. Am Rev Reap Dis 1979;119:741-53. 4. Gamble JR, Greife A, Hancock J. An epidemiologic-industrial hygiene study of talc workers. Ann Occup Hyg 1982; 26:841-59. 5. Gamble Jr, Greife A. Health studies of miners and millers exposed to talc. In: Wagner WW, Rom WH, Merchant JA, eds. Health issues related to metal and nan-metallic mining. Boston: Butterworth Publishing, 1983. 6. Brown DP, Dement JM, Wagoner JR. Mortality patterns among miners and millers occupationally exposed to asbestiform talc. In: Lernen R, Dement JM, eds. Dust and disease. Park Forest: Pathotox Publishers Inc., 1979:317-24. 7. Selevan SG, Dement JM, Wagoner JK, Froines JR. Mortality patterson among miners and millers of non-asbestiform talc: preliminary report. In: Lernen R, Dement JM, eds. Dust and disease. Park Forest: Pathotox Publishers Inc., 1979:379-388. 8. Wegman DH, Peters JM, Boundy MG, Smith TJ. Evaluation of respiratory effects in miners and millers exposed to talc free of asbestos and silica. Brit J Ind Med 1982;39:233-8. 9. Stille WT, Tabershav IR. The mortality experience of upstate Hew York talc workers. J Occup Med 1982;24:480-4. 10. Itamra SH, Starr JA. Analysis of epidemiologic mortality study: Hew York talc workers at Gouverneur Talc Company. Presented to OSHA, April 30, 1984. 11. Lamm S, Levine M, Starr J, and Tirey S. Analysis of excess lung cancer risk in short-term employees. Am J Xpid 1988;127:1202-1209. 12. Brown DP, Beaumont JJ, Dement JM. The toxicity of upstate He York talc. [Letter to the editor]. J Occup Med 1983;25:178-9. 13. Tabershav IR, Thompson CS. Authors response (Letter to the editor). J Occup Med 1983;25-179-81. 14. Dement JM, Brown DP. The forum [Letter to the editor]. Am Ind Hyg Assoc J 1982;43:A25-A25. Page 8 - Health Hazard Evaluation Report Ho. 90-390 and MHETA 86-012 15. Thompson CD. Consequences of using improper definition for regulated minerals. In: Levadie B, ed. Definition for asbestos and other health-related silicates. Philadelphia: American Society for Testing and Materials, ASTM special technical publication no. 834:175--83. 16. Taylor LD. The forum [Letter to editor). Am Ind Hyg Assoc J 1981;42:A26. 17. Broun DP. Review of Analysis of R.T. Vanderbilt Talc Employees, Memo to R.A. Lemen, August 18, 1983. 18. OSHA, Post-Hearing Coaments of R.T. Vanderbilt, Inc., November 1, 1984. 19. Campbell VJ, Steel EB, Virta RL, Eisner MH. Characteristic of cleavage fragments and asbestiform amphibole particulates. In: Lemen R, Dement JM, eds. Dust and disease. Park Forest: Pathotox Publishers Inc., 1979. 20. Campbell VJ, Huggins CW, Wylie AG. Chemical and physical characteristics of amosite, chrysotile, croddolite, and nonfibrous trcmolite for oral ingestions studies by the national Institute of Environmental Health Sciences, Bureau of Mines, 1980;. Research Investigation Ho. 8452. 21. Campbell VJ. Identification of selected silicate minerals and their asbestiform varieties. Proceedings of the workshop on Asbestos: definition and measurement methods held at HBS. Gathersburg: HBS Special Publication 506:1978. 22. Graf JL, Ase PR, Drafts RG. Preparation and characterization of analytical reference materials. Cincinnati, Ohio: Rational Institute for Occupational Safety and Health, 1979; DHEW (HI0SH) publication no, 79-139. 23. HI0SH testimony to the D.S. Department of Labor (OSHA): proposed rulemaking for asbestos, June 19, 1984. 24. Monson RR. Analysis of relative survival and proportional mortality. Computers Blamed Res 1974;1:325-32. 25. Harsh GW, Privlnger H. OCKAP: A user oriented occupational cohort mortality analysis program. University of Pittsburgh, Pittsburgh, PA., 1981. 26. Bailar JC, and Ederer F. Significance factors for the ratio of a poisson variable to its expectation. Biometrics 1964;20:639. Page 9 - Health Hazard Evaluation Report Ho. 90-390 and HHETA 86-012 27. Gamble J. Unpublished data. 28. U.S. Department of Health and Human Services, FHS, HCHS. Health United States 1981. DHHS Publication Ho. (PHS) 82-1232, Hyattsville, MD. December, 1981. 29. AxeIson, 0. Letter to the Editor: Aspects on confounding in occupational health epidemiology. Scand J work environ and health. 4:85-89, 1978. 30. Kleinfeld M, Messite J, Zaki H. Mortality experiences among talc workers; a follow-up study. J Occup Med 1974;16:345-9. 31. Kleinfeld M, Messite J, Kooyman 0, Zaki H. Mortality among talc miners and millers in Hew York state. Arch Env Hlth 1967;14:663-7. 32. Kleinfeld M, Messite J, Langer AM. A study of workers exposed to asbestiform minerals in commercial talc manufacture. Env Res 1972;6:132-43. VII. AUTHORSHIP AHD ACKNOWLEDGEMENTS Report Prepared By David P. Brown, M.P.H. Wayne Sanderson, C.I.H. Lawrence J. Fine, M.D. Originating Office Hazard Evaluations and Technical Assistance Branch Division of Surveillance, Hazard Evaluations and Field Studies The authors acknowledge Dr. John Gamble for preparation of the data. VIII. DISTBIBPTIOH AHD AVAILABILITY OF REPORT Copies of this report are currently available upon request from HIOSH, Hazard Evaluations and Technical Assistance Branch, 4676 Columbia Parkway, Cincinnati, Ohio 45226. After 90 days, the report will he available through the national Technical Information Service (HTIS), 5285 Port Royal, Springfield, Virginia 22161. Information regarding its availability through HTIS can be obtained from HIOSH Publications Office at the Cincinnati address. Copies of this report have been sent to: 1. R.T. Vanderbilt Company 2. United Steelworkers of America 3. OSHA Region II 4. HIOSH Boston Region For the purpose of informing affected employees, copies of this report shall be posted by the employer in a prominent place accessible to the employees for a period of 30 calendar days. Aae G r o w Age at Hire n IX) Age at Oeath 1947-59 Person-years (Pt) by Tiae Period 1960-69 1970-79 1980-83 Total Pt <20 20-29 30-39 40-49 50-59 60-69 70-79 80 107(15) 311(64) 184(26) 64(9) 32(4) 11(2) 11) O(-) O(-) 5(3) 12(8) 31(19) 52(32) 36(22) 21(13) 4(3) 47 1050 1302 657 165 86 12 5 Total 710 161 3324 Average 30 yrs 56 yrs 37 543 1446 1364 624 150 54 3 4221 41 864 1063 1605 1304 476 119 21 5493 0 212 462 492 642 352 72 24 2256 125 2669 4273 4118 2735 1064 257 53 15294 Table 2 Cause - Specific Mortality of Cohort, 1 M 7 - 1 9 B Couvemeur Talc Company HRETA 86-012 Cause of Death (ICO - 8 1 * Huaber Observed Huaber Exoected SMR All Causes (1-999) 161 125.5 128** Respiratory Tuberculosis (010-019) 3 0.7 619 All Malignant Reoptasa (160-209) 36 Digestive Organs and Peritoneua (150-159) 8 Esophagus (150) 1 Stoaach (151) 2 Liver (155-156) 2 Pancreas (157) 2 Respiratory Systea (160-163) 18 Larynx (161) 1 Lung(162-163) 17 Prostate (185) 1 Bladder (188) 1 Kidney (189) 1 Brain and CMS (191-192) 1 Lyaphosarcoaa and Reticulosarccaa (200) 1 Hodgkin's Disease (201) 2 Leukeaia (206-207) 2 Lyaphatic (202-203/820.8) 1 26.8 6.5 0.6 1.2 0.6 1.3 8.7 0.6 8.2 1.3 0.7 0.6 0.9 0.6 0.6 1.0 0.6 165* 167 167 171 500 156 207** 250 207** 77 163 167 111 167 500 200 167 All Diseases of Circulatory systea (390-658) 68 60.7 112 All Ron-Malignant Respiratory Disease (660-519) 17 Pneuaonia (680-686) 6 Eaphyseaa (692) 3 Other Mon-Malignant Respiratory (660-679, 8 687-691, 693-519) 6.8 250** 2.5 260 1.7 176 2.7 296* All Disease of Digestive Systca (520-577) 8 6.7 119 External Causes (800-998) Accidents (800-969) Suicide (9SD-959) 18 16.7 108 15 11.2 136 3 3.8 79 All Other 11 International Classification of Oisease, Eighth Revision 95* Confidence Interval for SKR * p<0.05 ft* p < 0 .0 1 95* Cl**' 109-150 86-1226 102-210 53-262 6-963 21-616 58-1729 18-566 123-328 7-1502 120-331 2-638 6-866 6-865 3-625 6-969 62-1857 23-699 6-911 87-162 166-601 90-536 37-523 130-596 51-235 66-171 75-221 16-231 Years since date of hire 0-<1 Tabic 3 Lung Cancer Mortality by Latency and Tenure 19*7-1983 6ouvemeur Talc Company KRETA 86-012 Tenure-Yeare 1-9 10-19 20-36 0-<10 10-19 20-36 95X 0/E sm PY 0/E SMR PY 0/E SMR C.I. PY 0/.5 -- 3612 0/.B -2229 8/2.2 36*** (156,706) 1870 1/.7 1*3 327 2/.5 *00 1203 1/1.2 83 (2,*57) 821 0/0 -- 0 1/.7 167 12*7 2/.5 *00 (5*,1611) 289 0/0 -0 0/0 -0 2/1.1 182 (21,636) 751 Total 0/E 8/3.5 SMR 229 PY 7711 */2.* 167 5297 3/1.2 250 1536 2/1.1 182 751 * p < .05 ** p < .01 Mean latency: 22.9 (range: 5.5-3*.3) Mean tenure: 6.3 (range: 0.003-23.5) Total 1/1.2 83 6885 3/2.0 150 *680 13/5.0 260 (137,**1) 3731 17/8.2 207** 1529* Table 4 All Cause, All Malignant Neoplasa, lung Cancer end All Respiratory Disease Mortality by Tenure Couvcmeur Talc Coapany MNETA 86-012 Cause of Death Uorkers Uith less Than 1 Tear Tenure All Causes All Malignant Neoplasa Lung Cancer All Non-Maligrant Respiratory Disease uorkers Uith Greater Than 1 Tear Tenure All Causes All Malignant Neoplasa lung Cancer All Mon-Malignant Respiratory Disease Nuaber Observed Muaber Exoected SMB 79 56.0 H I ** 112-176 15 11.1 135 76-223 a 3.6 222 96-438 6 3.1 194 72-428 82 69.5 118 94-147 21 13.8 152 93-230 9 A.6 196 89-369 11 3.8 289** 145-518 * p<0.05 * p-c0.01 Rafaranca Klatnfald^^ 1967 lrown<7 > 1960 t m <10) 1982 lamm<12> 1986 Thli Study Tabi 5 tunmaryi HortiUty Studi of Nu York Tale Uorkri flouvarnaur Tale Company HKETA 86-012 Cohort ilijlbllItyi pariod of mployitant >15y tanura imployad 1940-1969 End of follou-up Stia of Cohort (n) 1969 260 All Cauaa Hortalltv OBS RR 108 -- luno Canctr Mortali tv All >20 vr Latncv OBS RR OBS RR 13 324 1/1/47-12/31/59 6/30/75 398 74 121 9 273* 1/1/48-12/31/77 12/12/78 65$ 113 106 10 157 1947-12/31/77 12/31/78 605 118 141* 12 240 1947-1978 12/31/83 710 161 128** 17 207* 13 258 * p< .05 ** p< .01 OBS Obaarvad numbar of daatha RR PMR or SUR