Smokers with at least one of the variant alleles CYP1A2 −3860A and −2467 delT showed a significantly increased CYP1A2 CMR (−3860 G/A versus G/G, p < 0.05; −2467 delT/delT versus T/delT and T/T, p < 0.01). Multiple regression analysis showed that the increase in CYP1A2 CMR (ln values) was again significantly related to the presence of CYP1A2 variants −2467delT and also to variant −163A (p < 0.05), but moderately to −3860A (p = 0.084). No influence of the number of cigarettes smoked per day by each subject was found. Heavy smokers (n = 48, with urinary nicotine plus its metabolites ≥0.69 mg/mmol creatinine) with variant allele −2467delT or −163A had significantly increased urinary mutagenicity (p < 0.01 and <0.05).
CYP1A2 genetic polymorphisms are shown to influence the CYP1A2 phenotype in smokers, −2467 T → delT having the main effect. This information is of interest for future studies assessing the possible role of tobacco smoke-inducible CYP1A2 genotypes as individual susceptibility factors in exposure to carcinogens.