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Preliminary study of children's exposure to PAHs and its association with 8-hydroxy-2′-deoxyguanosine in Guangzhou, China

Fan, Ruifang, Wang, Dongli, Mao, Chuanwei, Ou, Shangkang, Lian, Zhixia, Huang, Shaoling, Lin, Qiongshan, Ding, Runhao, She, Jianwen
Environment international 2012 v.42 pp. 53-58
DNA damage, air, automobiles, biomarkers, carcinogenesis, children, cigarettes, combustion, creatinine, elementary students, kindergarten, metabolites, oxidative stress, pollutants, polycyclic aromatic hydrocarbons, t-test, traffic, urine, China
Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous air pollutants generated mainly from incomplete combustion such as automobile exhaust and cigarette smoke. Oxidative stress is believed to be involved in carcinogenesis, and urinary 8-hydroxy-2′-deoxyguanosine (8-OHdG) was used as the biomarker to assess such DNA damage. The children's urinary PAH metabolite (OH-PAHs) level were explored in Guangzhou and their associations with 8-OHdG. Two groups of subjects were selected: (1) one group (n=39, 6–7years old) from an elementary school situated near a heavy traffic road (polluted area) and (2) another group (n=35, 4–6years old) from a kindergarten situated in a corner of the main campus of a big university (non-polluted area). Urinary 8-OHdG and nine urinary monohydroxylated PAH metabolites were measured, including 2-hydroxynaphthalene (2-OHN), 2-hydroxyfluorene (2-OHF), 2-, 3-, 4-, 9-hydroxyphenanthrene (2-, 3-, 4-, 9-OHPhe), 1-hydroxypyrene (1-OHP), 6-hydroxychrysene (6-OHChr) and 3-hydroxybenzo(a)pyrene (3-OHBaP). All other PAH metabolites were detected in urine samples from both children groups except for 6-OHChr and 3-OHBaP. Levels of 2-OHN, 2-OHF, 3-OHPhe, 9-OHPhe and 1-OHP were significantly different between two groups (P<0.05, T-test). The elementary school children from the polluted area had higher urinary levels of 2-OHN, 2-OHF, 2-, 3-, 4-OHPhe and 1-OHP ((9.10±7.39, 3.72±2.91, 0.32±0.50, 0.37±0.28, 0.23±0.29 and 0.64±0.07 μmol/mol creatinine, respectively) than those from the control group. The results suggested that heavy traffic pollution led to higher PAH body burden. There existed no significant difference for urinary 8-OHdG concentration between two groups (p>0.05, T-test), and no strong correlations between the individual OH-PAHs and 8-OHdG. However, the urinary 8-OHdG concentration in the elementary school children from the traffic polluted area was slightly higher than those in the non-polluted area (20.87±14.42μmol/mol creatinine vs. 16.78±13.30μmol/mol creatinine). It may be that the potential co-exposure of the children to other pollutants affects 8-OHdG concentration besides the PAHs.