A variable but often significant proportion of urinary bladder cancer can be attributed to occupational and cultural (smoking) situations associated with exposures to carcinogenic arylamines. The variable N-acetylation of carcinogenic arylamines by human hepatic enzyme systems, the known genetic regulation and polymorphic distribution of this enzyme activity in humans, and the known enhanced susceptibility of individuals with the genetically-distinct "slow acetylator" phenotype to various arylamine toxicities, has prompted examination of possible correlations between human-N-acetyltransferase phenotype and susceptibility to urinary bladder cancer. The hypothesis being tested is that slow acetylators, by virtue of their lesser abilities to detoxify arylamines by N-acetylation, might be more susceptible to occupation- and smoking-related urinary bladder cancer and might, therefore, be found in greater percentage in bladder cancer populations than in nationality-matched, disease-free control populations. Sulfamethazine phenotyping will be employed to examine well defined Japanese bladder cancer populations with and without histories of cigarette smoking, and with and without documentable occupational exposure to 4,4'-diamino-biphenyl (i.e., benzidine) or 2-aminophthalene (i.e., beta-naphthylamine). The results of these studies are expected to allow assessment of the existence of a relationship between arylamine-induced bladder cancer and the slow acetylator phenotype as a determinant of susceptibility, assessment of the involvement of arylamines in tobacco smoke-related bladder cancer, and assessment of the feasibility of identifying highly susceptible individuals in high risk populations.