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The metabolism of tobacco carcinogens was studied in a potential target for their carcinogenic effects. Rat buccal mucosa cells metabolized several polycyclic aromatic hydrocarbons, e.g., benzo(a)pyrene, benz(b)- and benz(j)-fluoranthene, dibenz(a,j)acridine, N,N-diethylnitrosamine and protein pyrolysate products, 2-amino-3-methylimidazo(4,5-f)quinoline, and 2-amino-3,4-dimethylimidazo(4,5-f)quinoline, as measured by binding of the carcinogens to cellular DNA. The highest level of binding was seen with the nitrosamine followed by the protein pyrolysate products. There was no significant difference in the binding levels between the different polycyclic aromatic hydrocarbons. Cells treated with a non-cytotoxic dose of the non-volatile condensate fraction of regular tobacco smoke increased metabolism as measured by binding to DNA of the protein pyrolysate products, whereas the pretreatment did not have any effect on the metabolism of benzo(a)pyrene, and N,N-diethylnitrosamine. However, the profile of benzo(a)pyrene metabolites released into the media changed. The results indicate that rat buccal mucosa cells metabolize several classes of tobacco specific carcinogens, and that the metabolism is modified by continued exposure to tobacco smoke components.