Exposure to polycyclic aromatic hydrocarbons could cause their oxidative DNA damage: a case study for college students in Guangzhou, China.

Human exposure to carcinogenic polycyclic aromatic hydrocarbons (PAHs) in cigarette smoking might result in generation of reactive oxygen species (ROS) and induce formation of 8-hydroxy-2'-deoxyguanosine (8-OHdG). This study was designed to examine whether levels of 8-OHdG are associated with levels of urinary metabolites of PAHs. Two groups (smokers and non-smokers) were recruited from college students in Guangzhou, China. Their urine samples were collected and analyzed for ten urinary mono-hydroxylated PAHs (OH-PAHs) and 8-OHdG by liquid chromatography equipped with tandem mass spectrometer (LC/MS/MS). Multiple linear regression analysis was performed to examine correlations between urinary levels of 8-OHdG and OH-PAHs. No significant difference was observed for creatinine-adjusted OH-PAHs between smokers and non-smokers. The levels of 8-OHdG between smokers and non-smokers were comparative. OH-PAH levels in this study were 2-50 times higher than those in populations from other countries and areas. The estimated daily intake (EDI; μg/day) of PAHs ranged from 0.02 to 371.4, which were far lower than the reference doses (RfDs) specified by U.S. Environmental Protection Agency (EPA). Though smoking was a main factor, which affected the PAH exposure, it was not a dominant factor in the exposure to PAHs of Guangzhou college students. The environmental exposure could not be ignored. The sum concentrations of OH-PAHs (∑OH-PAHs) had a dose-increase relationship with 8-OHdG both for smokers and non-smokers, especially for smokers. Though people in Guangzhou bore higher PAH hazards, the estimated environmental risk was still under safe ranges.