Estimation of Unit Risk for Coke Oven Emissions

In 1984, based on epidemiological data on cohorts of coke oven workers, USEPA estimated a unit risk for lung cancer associated with continuous exposure from birth to 1 μg/m3 of coke oven emissions, of 6.2 × 10−4. This risk assessment was based on information on the cohorts available through 1966. Follow-up of these cohorts has now been extended to 1982 and, moreover, individual job histories, which were not available in 1984, have been constructed. In this study, lung cancer mortality in these cohorts of coke oven workers with extended follow-up was analyzed using standard techniques of survival analysis and a new approach based on the two stage clonal expansion model of carcinogenesis. The latter approach allows the explicit consideration of detailed patterns of exposure of each individual in the cohort. The analyses used the extended follow-up data through 1982 and the detailed job histories now available. Based on these analyses, the best estimate of unit risk is 1.5 × 10−4 with 95% confidence interval = 1.2 × 10−4−1.8 × 10−4.

[1]  A. Ciocco,et al.  Long-term mortality study of steelworkers. I. Methodology. , 1969, Journal of occupational medicine. : official publication of the Industrial Medical Association.

[2]  Lloyd Jw,et al.  Long-term mortality study of steelworkers. V. Respiratory cancer in coke plant workers. , 1971 .

[3]  C K Redmond,et al.  Long-term mortality study of steelworkers. VI. Mortality from malignant neoplasms among coke oven workers. , 1972, Journal of occupational medicine. : official publication of the Industrial Medical Association.

[4]  C. Redmond,et al.  An Epidemiological Study of Exposure to Coal Tar Pitch Volatiles Among Coke Oven Workers , 1975 .

[5]  H. Rockette,et al.  Long-term mortality study of steelworkers. , 1976, Journal of occupational medicine. : official publication of the Industrial Medical Association.

[6]  C. Redmond,et al.  CANCER EXPERIENCE AMONG COKE BY‐PRODUCT WORKERS , 1976, Annals of the New York Academy of Sciences.

[7]  R. Doll,et al.  Cigarette smoking and bronchial carcinoma: dose and time relationships among regular smokers and lifelong non-smokers. , 1978, Journal of epidemiology and community health.

[8]  S. Moolgavkar,et al.  Two-event models for carcinogenesis: incidence curves for childhood and adult tumors☆ , 1979 .

[9]  S H Moolgavkar,et al.  Mutation and cancer: a model for human carcinogenesis. , 1981, Journal of the National Cancer Institute.

[10]  J. Kalbfleisch,et al.  The Statistical Analysis of Failure Time Data , 1980 .

[11]  S H Moolgavkar,et al.  Two-event model for carcinogenesis: biological, mathematical, and statistical considerations. , 1990, Risk analysis : an official publication of the Society for Risk Analysis.

[12]  L. Ellwein,et al.  Cell proliferation in carcinogenesis. , 1990, Science.

[13]  Recent developments in the multistage modeling of cohort data for carcinogenic risk assessment. , 1991 .

[14]  E G Luebeck,et al.  Multistage carcinogenesis: population-based model for colon cancer. , 1992, Journal of the National Cancer Institute.

[15]  D Krewski,et al.  Radon, Cigarette Smoke, and Lung Cancer: A Re‐analysis of the Colorado Plateau Uranium Miners' Data , 1993, Epidemiology.

[16]  C. Redmond,et al.  Design, analysis and interpretation of long-term mortality studies of coke oven workers : Epidemiological studies of industrial pollutants , 1993 .

[17]  E G Luebeck,et al.  Growth kinetics of enzyme-altered liver foci in rats treated with phenobarbital or alpha-hexachlorocyclohexane. , 1995, Toxicology and applied pharmacology.

[18]  C. Redmond,et al.  Occupationally Related Cancer Risk Among Coke Oven Workers: 30 Years of Follow-Up , 1995, Journal of occupational and environmental medicine.

[19]  M. Little,et al.  Are two mutations sufficient to cause cancer? Some generalizations of the two-mutation model of carcinogenesis of Moolgavkar, Venzon, and Knudson, and of the multistage model of Armitage and Doll. , 1995, Biometrics.

[20]  C. Muirhead,et al.  Modelling lymphocytic leukaemia incidence in England and Wales using generalizations of the two-mutation model of carcinogenesis of Moolgavkar, Venzon and Knudson. , 1996, Statistics in medicine.

[21]  M. Little Generalisations of the two-mutation and classical multi-stage models of carcinogenesis fitted to the Japanese atomic bomb survivor data , 1996 .

[22]  W. Heidenreich On the parameters of the clonal expansion model , 1996, Radiation and environmental biophysics.

[23]  E G Luebeck,et al.  Quantitative analysis of enzyme-altered liver foci in rats initiated with diethylnitrosamine and promoted with 2,3,7,8-tetrachlorodibenzo-p-dioxin or 1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin. , 1996, Toxicology and applied pharmacology.

[24]  F. T. Cross,et al.  Two-stage model of radon-induced malignant lung tumors in rats: effects of cell killing. , 1996, Radiation research.

[25]  W F Heidenreich,et al.  Some Properties of the Hazard Function of the Two‐Mutation Clonal Expansion Model , 1997, Risk analysis : an official publication of the Society for Risk Analysis.

[26]  Sylvia Richardson,et al.  Markov Chain Monte Carlo in Practice , 1997 .

[27]  E. Luebeck,et al.  Analysis of the incidence of solid cancer among atomic bomb survivors using a two-stage model of carcinogenesis. , 1997, Radiation research.