Differential Susceptibility: Implications for Epidemiology, Risk Assessment, and Public Policy
- 42 Downloads
In conventional toxicologic analysis for acute toxicity, differential susceptibility is assumed as the explanation for the dose-response relationship. For example, if susceptibility to the fatal effects of a chemical substance is distributed normally in a population, then the dose-response relationship will follow the cumulative normal distribution and will appear linear on probit graph paper. Some of the explanation for the spread in susceptibility can lie in genetic factors such as the presence or absence of detoxifying enzymes, while the remainder is usually assumed to be associated with age, body morphology, general health status, and other environmental factors. Chance is not often assigned a significant role in acute toxicity.
KeywordsBladder Cancer Phenotypic Variation Liver Cancer Differential Susceptibility Bladder Cancer Patient
Unable to display preview. Download preview PDF.
- Cartwright, R. A., Rogers, H. J., Barham-Hall, D., Glashan, R. W., Ahmad, R. A., Higgins, E. and Kahn, M. A., 1982, Role of N-acetyltransferase phenotypes in bladder carcinogenesis, a pharmacogenetic epidemiological approach to bladder cancer, Lancet, 842.Google Scholar
- Case, R. A. M., Hosker, M. E., McDonald, D. B., and Pearson, J. T., 1954, Tumors of the urinary bladder in workmen engaged in the manufacture and use of certain dyestuff intermediates in the British chemical industry, Brit. J. Indust. Med., 11:75.Google Scholar
- Evans, D. A. P., Manley, K. A., and McKusick, V. A., 1960, Genetic Control of Isoniazid Metabolism in Man, Brit. Med. J., 485.Google Scholar
- Glowinski, I. B., Radtke, H. E., and Weber, W. W., 1978, Genetic variation in N-acetylation of carcinogenic arylamines by human and rabbit liver, Mol. Pharm., 14:940.Google Scholar
- Knight, R. A., Selin, M. J. and Harris, H. W., 1959, Genetic factors influencing isoniazid blood levels in humans, in: “Transactions of the 18th conference on the Chemotherapy of Tuberculosis,” Veterans Administration, Washington, 52.Google Scholar
- Lower, G. M. Jr., Nilsson, T., Nelson, C. E., Wolf, H., Gamsky, T. E., and Bryan, G. T., 1979, N-acetyltransferase phenotype and rise in urinary bladder cancer: approaches in molecular epidemiology. Preliminary results in Sweden and Denmark, Environ. Health Perspect., 29:71.PubMedCrossRefGoogle Scholar
- National Cancer Institute, 1981, “Surveillance, Epidemiology, and End Results: Incidence and Mortality Data, 1973–1977,” NCI Monograph 57, U.S. Government Printing Office, Washington.Google Scholar
- Williams, G. M., Reiss, B., and Weisburger, J. H., 1985, A comparison of the animal and human carcinogenicity of environmental, occupational and therapeutic chemicals, in: “Advances in Modern Environmental Toxicology,” Vol. XII, W. G. Flamm and R. J. Lorentzen, eds., Princeton Scientific Publishers, Inc., Princeton, 207.Google Scholar