Personal exposure to particulate PAHs and anthraquinone and oxidative DNA damages in humans

• Published in: Chemosphere (Oxford) Vol. 81; no. 10; pp. 1280 - 1285
• Main Authors: Wei, Yongjie, Han, In-Kyu, Hu, Min, Shao, Min, Zhang, Junfeng(Jim), Tang, Xiaoyan
• Format: Journal Article
• Language: English
• Published: Kidlington Elsevier Ltd 01.11.2010; Elsevier
• Subjects: 8-OHdG (8-hydroxydeoxyguanosine); Air Pollutants - analysis; Air Pollutants - urine; Air Pollutants, Occupational - analysis; Air Pollutants, Occupational - urine; Air. Soil. Water. Waste. Feeding; Animal, plant and microbial ecology; Anthraquinone; Anthraquinones - analysis; Anthraquinones - urine; Applied ecology; Biological and medical sciences; Deoxyguanosine - analogs & derivatives; Deoxyguanosine - urine; DNA Damage; Ecotoxicology, biological effects of pollution; Environment. Living conditions; Fundamental and applied biological sciences. Psychology; General aspects; Humans; Inhalation Exposure - analysis; Medical sciences; Occupational Exposure - analysis; Oxidative Stress; PAHs; Particulate Matter - analysis; Particulate Matter - urine; Personal exposure; PM 2.5; Polycyclic Aromatic Hydrocarbons - analysis; Polycyclic Aromatic Hydrocarbons - urine; Public health. Hygiene; Public health. Hygiene-occupational medicine; Oxidative stress; PAHs; Anthraquinone; Personal exposure; PM 2.5; 8-OHdG (8-hydroxydeoxyguanosine); Human; Ecotoxicology; Hydrocarbon; Toxicity; Genotoxicity; Polycyclic aromatic compound; Mutagen; Persistent organic pollutant; Carcinogen; Health and environment; Fine particle; DNA; Aerosols; Air pollution; Damage; PM; Public health; Organic compounds
• ISSN: 0045-6535; 1879-1298; 1879-1298
• DOI: 10.1016/j.chemosphere.2010.08.055

Recent studies suggest that DNA oxidative damage be related to the chemical constituents of ambient particles. The purpose of this study was to examine whether particulate polycyclic aromatic hydrocarbons (PAHs) and quinone-structure chemicals increase body burden of oxidative stress in human exposed to heavy traffic volume. We recruited two nonsmoking security guards who worked at a university campus gate near a heavily trafficked road. Each subject wore a personal air sampler for 24 h per day to estimate exposures to 24 PAHs and anthraquinone (AnQ) in PM 2.5. Daily pre- and post-work shift spot urines were collected for 29 d from each subject. Urine samples were analyzed for 8-hydroxy-2′-deoxyguanosine (8-OHdG). Additionally, using 19 organic tracers other than 24 PAHs and AnQ, a receptor source apportionment model of chemical mass balance was applied to determine the contributions of sources on the PM: gasoline vehicle, diesel vehicle, coal burning, vegetable debris, cooking, natural gas and biomass burning. The relationship among urinary 8-OHdG, individual PAH, and AnQ was demonstrated as follows: the average urinary concentration of 8-OHdG was increased more than three times after 8-h work-shift than those before the work shift. All the 24 PAH and AnQ levels were positively and significantly associated with the post-work urinary 8-OHdG. The results from source apportionment suggest vehicular emission to be the dominant source of personal exposure to PM 2.5. Our finding indicates that personal air exposures to 24 individual PAHs and AnQ originating from traffic emissions are important in increasing oxidative burdens in human body.