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Aromatic compounds such as polycyclic aromatic hydrocarbons, arylamines and heterocyclic amines require metabolic activation to form metabolites able to bind to DNA, a process mediated by polymorphic enzymes. We measured aromatic DNA adducts in white blood cells by the32P-post-labelling assay in a sample of 296 healthy adults (147 men and 149 women) from five regions of Spain. We also analyzed functional polymorphisms in the metabolic genesCYP1A1,CYP1A2,EPHX1,GSTM1,GSTT1,NAT2andSULT1A1. A significant increased level of DNA aromatic adducts was found related to the fast oxidation–hydrolysis phenotype defined by the polymorphismI462VinCYP1A1, the allele A in IVS1−154C&gt;A ofCYP1A2and the combination Tyrosine–Arginine forY113HandH139RofEPHX1. Geometric means (adducts per 10−9normal nucleotides) were 2.17, 4.04 and 6.30 for slow, normal and fast phenotypes, respectively (P-trend = 0.01). Slow acetylation by NAT2 was associated with a significant decrease in adduct level; subjects with slow alleles*5Aand*7A/Bhad in average 1.56 × 10−9adducts, as compared with 5.60 for those with normal NAT2 activity (P-value = 0.01). No association was seen with polymorphisms of other metabolic genes such asGSTM1,GSTT1orSULT1A1. We concluded that the metabolic pathways of oxidation, hydrolysis and acetylation are relevant to the formation of bulky DNA adducts. This could suggest a potential involvement of aromatic compounds in the formation of such adducts; however, given lack of specificity of the post-labeling assay, a firm conclusion cannot be drawn.

Aromatic DNA adducts and polymorphisms in metabolic genes in healthy adults: findings from the EPIC-Spain cohort