Seasonally varied cytotoxicity of organic components in PM2.5 from urban and industrial areas of a Chinese megacity

Seasonally varied cytotoxicity of organic components in PM2.5 from urban and industrial areas of a Chinese megacity
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中国大城市城市和工业区 PM2.5 中有机成分的细胞毒性随季节变化。

DOI:
10.1016/j.chemosphere.2019.04.226
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发表时间:
2019-09-01
期刊:
影响因子:
8.8
通讯作者:
Jin, Ling
Jin, Ling
中科院分区:
环境科学与生态学2区
文献类型:
--
作者:
Chen, Qi;Luo, Xiao-San;Jin, Ling

文献摘要

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大气细颗粒物(PM2.5)以氧化应激和促炎反应等形式对人体健康产生重大负面影响。有机污染物是PM2.5中重要的有害和有毒成分,其风险通常呈现时空变化。为了研究空气中有机污染物对人体肺上皮细胞A549的毒性作用,在中国东部南京市的城市和工业区收集了PM2.5样本,每个月采集一次。暴露于PM2.5中提取的有机成分后,测定细胞活力、乳酸脱氢酶含量、氧化应激指数水平和炎症因子表达水平。在多环芳烃(PAHs)和正构烷烃浓度的支持下,结果表明,寒冷季节(冬春季)PM2.5的有机成分对细胞膜、细胞氧化和炎症损伤的影响较为明显,而温暖季节(夏秋季)城市样本对细胞活力的影响更为显著。从空间上看,工业源样品的毒性总体强于城市源样品,但城市源样品对细胞膜的破坏程度明显强于工业源样品。多环芳烃、正构烷烃含量与毒性参数的相关性表明,机动车尾气和煤炭燃烧产生的空气中有机成分可能是主要的毒源。(C) 2019 Elsevier Ltd.版权所有。
The atmospheric fine particulate matters (PM2.5) induce significant negative effects on human health, such as in the form of oxidative stress and pro-inflammatory response. Organic pollutants are important harmful and toxic compositions in PM2.5, risks of which usually show temporal and spatial variations. To investigate the toxic effects of airborne organic pollutants on human lung epithelial cells A549, the PM2.5 samples were collected monthly from both urban and industrial areas during a whole year in Nanjing, eastern China. After exposure to organic components extracted from these PM2.5, the cell viability, lactate dehydrogenase content, oxidative stress index level and inflammatory factor expression level were measured. Supported by the concentrations of polycyclic aromatic hydrocarbons (PAHs) and n-alkanes, results showed that, organic components of PM2.5 from cold season (winter and spring) typically influenced cell membrane, cell oxidation and inflammatory damage, while the urban samples of warm season (summer and autumn) impacted cell viability more prominently. Spatially, the toxicity of samples from industrial sources was generally stronger than that from urban source, but urban samples induced much stronger damage to cell membranes than industrial one. The correlations between the PAHs, n-alkanes contents and toxicity parameters indicated that, the airborne organic components derived from motor vehicle exhaust and coal combustion were possibly the key toxic sources. (C) 2019 Elsevier Ltd. All rights reserved.