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细颗粒物2.5的成分与人类DNA氧化损伤

PM2.5 constituents and oxidative DNA damage in humans.

作者信息

Wei Yongjie, Han In-Kyu, Shao Min, Hu Min, Zhang O Junfeng, Tang Xiaoyan

机构信息

State Key Joint Laboratory of Environmental Simulation and Pollution Control, College of Environmental Sciences and Engineering, Peking University, Beijing 100871, China.

出版信息

Environ Sci Technol. 2009 Jul 1;43(13):4757-62. doi: 10.1021/es803337c.

DOI:10.1021/es803337c
PMID:19673262
Abstract

Previous studies suggested that certain constituents of ambient PM2.5 can induce or increase oxidative stress in biological systems. The present study is designed to examine whether exposure to traffic generated particles increases the burden of oxidative stress in humans and to identify specific PM2.5 constituents responsible for pollution-induced oxidative stress. We recruited two nonsmoking security guards who worked at a university campus gate by a heavily trafficked road. Pre- and post-workshift spot urines were collected on each of the 29 days of measurement. Concentrations of PM2.5 mass and 126 chemical species were measured at the worksite and a campus background site simultaneously. Urine samples were analyzed for 8-hydroxy-2'-deoxyguanosine (8-OHdG). Factor analysis and linear mixed-effects regression models were used in statistical analyses. Three clusters of PM2.5 species were identified, including PAHs, metals, and polar organic compounds. Urinary concentrations of 8-OHdG increased by > 3 times following an eight-hour workshift in participants. Pre-workshift urinary concentrations of 8-OHdG were associated with PM2.5 concentrations at the background site. Post-workshift 8-OHdG concentrations were significantly and positively associated with PM2.5 mass, PAHs, and metals, but not polar organic species, measured at the worksite. Our findings provide direct evidence in humans that PM compositions are important in increasing oxidative stress burdens. Our results support that PAHs and metals are biologically active constituents of PM2.5 with regards to the induction of oxidative DNA damages in the human body.

摘要

以往的研究表明,环境细颗粒物(PM2.5)的某些成分可在生物系统中诱导或增加氧化应激。本研究旨在探讨接触交通产生的颗粒物是否会增加人类氧化应激负担,并确定导致污染诱导氧化应激的特定PM2.5成分。我们招募了两名在大学校园门口一条交通繁忙道路旁工作的不吸烟保安。在测量的29天中,每天工作班前和班后采集即时尿样。同时在工作场所和校园背景站点测量PM2.5质量浓度和126种化学物质的浓度。对尿样进行8-羟基-2'-脱氧鸟苷(8-OHdG)分析。统计分析采用因子分析和线性混合效应回归模型。确定了三类PM2.5物质,包括多环芳烃、金属和极性有机化合物。参与者经过8小时轮班后,尿中8-OHdG浓度增加了3倍以上。班前尿中8-OHdG浓度与背景站点的PM2.5浓度相关。班后8-OHdG浓度与工作场所测量的PM2.5质量、多环芳烃和金属显著正相关,但与极性有机物质无关。我们的研究结果为人类提供了直接证据,证明PM成分在增加氧化应激负担方面很重要。我们的结果支持多环芳烃和金属是PM2.5的生物活性成分,可诱导人体氧化DNA损伤。

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