Preliminary study of children's exposure to PAHs and its association with 8-hydroxy-2′-deoxyguanosine in Guangzhou,China |
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| Institution: | 1. Department of Chemistry, Oregon State University, Corvallis, OR 97331, USA;2. School of Biological and Population Health Sciences, College of Public Health and Human Sciences, Oregon State University, Corvallis, OR 97331, USA;3. Department of Environmental and Molecular Toxicology, Oregon State University, Corvallis, OR 97331, USA;4. Department of Science and Engineering, Confederated Tribes of the Umatilla Indian Reservation, Pendleton, OR 97801, USA;1. International Laboratory for Air Quality and Health, Queensland University of Technology, Brisbane, QLD, Australia;2. National Research Centre for Environmental Toxicology, University of Queensland, Brisbane, QLD, Australia;3. School of Public Health and Social Work and Institute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, QLD, Australia;4. Centers for Disease Control and Prevention, Atlanta, GA, USA;5. Sullivan Nicolaides Pathology, Taringa, QLD, Australia;6. The Department of Environment, Canberra, ACT, Australia;1. School of Environmental Science and Engineering, Guangdong Provincial Key Laboratory of Environmental Pollution Control and Remediation Technology, Sun Yat-sen University, Guangzhou 510275, PR China;2. Shenzhen Center for Disease Control and Prevention, Shenzhen 518055, PR China;3. School of Geography and Planning, Guangdong Provincial Key Laboratory of Urbanization and Geo-simulation, Sun Yat-sen University, Guangzhou 510275, PR China;4. Wadsworth Center, New York State Department of Health, Department of Environmental Health Sciences, School of Public Health, State University of New York at Albany, Albany, NY 12201, USA;1. Key Laboratory of Ecology and Environmental Science in Guangdong Higher Education, School of Life Science, South China Normal University, Guangzhou 510631, China;2. Shenzhen Center for Disease Control and Prevention, Shenzhen 518055, China;3. Environmental Health Laboratory Branch, California Department of Public Health, 850 Marina Bay Parkway, Richmond, CA 94804, United States |
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| Abstract: | 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, 6–7 years old) from an elementary school situated near a heavy traffic road (polluted area) and (2) another group (n = 35, 4–6 years 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 ± 14.42 μmol/mol creatinine vs. 16.78 ± 13.30 μmol/mol creatinine). It may be that the potential co-exposure of the children to other pollutants affects 8-OHdG concentration besides the PAHs. |
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