期刊
JOURNAL OF APPLIED TOXICOLOGY
卷 31, 期 2, 页码 131-138出版社
WILEY-BLACKWELL
DOI: 10.1002/jat.1572
关键词
air pollution; PM2.5; mutagenicity; Ames test; genotoxicity; DNA bulky adducts; 8-OHdG; A549 cells; human alveolar macrophages
类别
资金
- Region Nord-Pas de Calais [08070005]
- Ministere de l'Enseignement Superieur et de la Recherche
- European Funds (FEDER)
- Agence Francaise de Securite Sanitaire de l'Environnement et du Travail (AFSSET) [EST-2007-48]
Epidemiological studies have demonstrated the link between chronic exposure to particulate matter (PM), especially particles with an aerodynamic diameter lesser than 2.5 mu m (PM2.5), and lung cancer. Mechanistic investigations focus on the contribution of the various genotoxicants adsorbed onto the particles, and more particularly on polycyclic aromatic hydrocarbons or nitroaromatics. Most of the previous studies dealing with genotoxic and/or mutagenic measurements were performed on organic extracts obtained from PM2.5 collected in polluted areas. In contrast, we have evaluated genotoxic and mutagenic properties of urbano-industrial PM2.5 (PM) collected in Dunkerque (France). Thermally desorbed PM2.5 (dPM) was also comparatively studied. Suspensions of PM and dPM (5-50 mu g per plate) were tested in Salmonella tester strains TA98, TA102 and YG1041 +/- S9mix. Significant mutagenicity was observed for PM in YG1041 +/- S9 mix. In strain TA102 - S9mix, a slight, but not significant dose-response increase was observed, for both PM and dPM. Genotoxic properties of PM and dPM were evaluated by the measurement of (1) 8-OHdG in A549 cells and (2) bulky DNA adducts on A549 cells and on human alveolar macrophages (AMs) in primary culture. A dose-dependant formation of 8-OHdG adducts was observed on A549 cells for PM and dPM, probably mainly attributed to the core of the particles. Bulky DNA adducts were observed only in AMs after exposure to PM and dPM. In conclusion, using relevant exposure models, suspension of PM2.5 induces a combination of DNA-interaction mechanisms, which could contribute to the induction of lung cancer in exposed populations. Copyright (C) 2010 John Wiley & Sons, Ltd.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据