Personal exposure to particulate PAHs and anthraquinone and oxidative DNA damages in humans.
Personal exposure to particulate PAHs and anthraquinone and oxidative DNA damages in humans.
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DOI：
10.1016/j.chemosphere.2010.08.055
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发表时间：
2010-11
期刊：
影响因子：
8.8
通讯作者：
Yong-jie Wei;In-Kyu Han;Min Hu;M. Shao;J. Zhang;Xiao-yan Tang
中科院分区：
文献类型：
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作者：
Yong-jie Wei;In-Kyu Han;Min Hu;M. Shao;J. Zhang;Xiao-yan Tang
近年来的研究表明，DNA氧化损伤与环境颗粒的化学成分有关。本研究的目的是研究微粒性多环芳烃（PAHs）和醌结构化学物质是否会增加高交通流量暴露的人体氧化应激负担。我们招募了两名不吸烟的保安，他们在一条交通繁忙的道路附近的一所大学校园门口工作。每个受试者每天佩戴个人空气采样器24小时，以估计PM2.5中24种多环芳烃和蒽醌（AnQ）的暴露量。收集每个受试者每天工作前和下班后的尿样，持续29d。尿样分析8-羟基-2 ' -脱氧鸟苷（8-OHdG）。此外，采用除24种PAHs和AnQ外的19种有机示踪剂，建立化学质量平衡受体源分配模型，确定汽油车、柴油车、燃煤、蔬菜碎屑、烹饪、天然气和生物质燃烧等源对PM的贡献。尿8-OHdG、个体PAH和AnQ之间的关系如下：8-OHdG在轮班8小时后的平均尿浓度比轮班前增加了3倍以上。所有24种PAH和AnQ水平均与工作后尿8-OHdG呈正相关。来源解析结果表明，机动车排放是个人PM2.5暴露的主要来源。我们的研究结果表明，个人空气暴露于24种不同的多环芳烃和来自交通排放的AnQ是增加人体氧化负担的重要因素。
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 24h per day to estimate exposures to 24 PAHs and anthraquinone (AnQ) in PM2.5. Daily pre- and post-work shift spot urines were collected for 29d 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 PM2.5. 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.