Differences in cytotoxicity versus pro-inflammatory potency of different PM fractions in human epithelial lung cells

被引:190
作者
Gualtieri, Maurizio [1 ,2 ]
Ovrevik, Johan [1 ]
Holme, Jorn A. [1 ]
Perrone, M. Grazia [2 ]
Bolzacchini, Ezio [2 ]
Schwarze, Per E. [1 ]
Camatini, Marina [2 ]
机构
[1] Norwegian Inst Publ Hlth, Div Environm Med, N-0403 Oslo, Norway
[2] Univ Milano Bicocca, Polaris Res Ctr, Dipartimento Sci Ambiente & Terr, I-20126 Milan, Italy
关键词
PM10; PM2.5; PM chemical composition; PAHs; Cytotoxicity; Inflammation; Mitotic arrest/delay; POLYCYCLIC AROMATIC-HYDROCARBONS; ATMOSPHERIC PARTICULATE MATTER; DIESEL EXHAUST PARTICLES; OBSTRUCTIVE PULMONARY-DISEASE; AMBIENT AIR PARTICLES; IN-VITRO; DNA-DAMAGE; COARSE PARTICLES; DAILY MORTALITY; PHYSICOCHEMICAL CHARACTERISTICS;
D O I
10.1016/j.tiv.2009.09.013
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
Air pollution in Milan causes health concern due to the high concentrations of particulate matter (PM10 and PM2.5). The aim of this study was to investigate possible seasonal differences in PM10 and PM2.5 chemical composition and their biological effects on pro-inflammatory cytokine release and cytotoxicity. The PM was sampled during winter and summer seasons. The winter PMs had higher levels of PAHs than the summer samples which contained a greater amount of mineral dust elements. The PM toxicity was tested in the human pulmonary epithelial cell lines BEAS-2B and A549. The winter PMs were more cytotoxic than summer samples, whereas the summer PM10 exhibited a higher pro-inflammatory potential, as measured by ELISA. This inflammatory potential seemed partly due to biological components such as bacterial lipopolysaccharides (LPS), as evaluated by the use of Polymixin B. Interestingly, in the BEAS-2B cells the winter PM2.5 reduced proliferation due to a mitotic delay/arrest, while no such effects were observed in the A549 cells. These results underline that the in vitro responsiveness to PM may be cell line dependent and suggest that the PM different properties may trigger different endpoints such as inflammation, perturbation of cell cycle and cell death. (C) 2009 Elsevier Ltd. All rights reserved.
引用
收藏
页码:29 / 39
页数:11
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