Molecular-epidemiological studies on the risk evaluation of cancer induced by environmental carcinogen

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This study was performed to evaluate the risk of cancer induced by environmental carcinogens such as polycyclic aromatic hydrocarbons (PAH) which are contained in the automobile exhaust and the cigarette smoke. We selected both heavy smokers and coke-oven workers in an iron-steel factory as the PAH-exposed human populations. A small quantity of peripheral blood and spot urine was collected from these subjects. The level of exposure to PAH was estimated by determining urinary 1-hydroxypyrene (1-OHP) which is urinary metabolite of PAH. We measured DNA adducts levels in lymphocytes or total white blood cells using 32P-postlabeling method. The level of DNA adducts had a significant positive correlation with the level of exposure to PAH. In addition, the level of DNA adducts was influenced by genetic polymorphism of metabolising enzyme, CYP1A1, suggesting that the adduct level was higher in mutant type than in wild type of CYP1A1 polymorphism. On the other hand, no significant correlation was found between the level of exposure to PAH and the level of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) levels which is useful as a biomarker of oxidative DNA damage.In conclusion, the measurement of DNA adducts in lymphocytes and/or white blood cells may be useful for estimating the DNA damage induced by PAH exposure, and for evaluating an environmental cancer risk.