Exposure to polycyclic aromatic hydrocarbons could cause their oxidative DNA damage: a case study for college students in Guangzhou, China
2015
Li, Junnan | Fan, Ruifang | Lu, Shaoyou | Zhang, Dongru | Zhou, Yuanxiu | Lv, Yanshan
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.
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