| 南京市大气PM2.5无机组分及对A549细胞的毒性效应 |
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| 引用本文： | 刘慧灵,毋赟,陈敏东,聂东阳,李文婧,张凯,葛鹏翔. 南京市大气PM2.5无机组分及对A549细胞的毒性效应[J]. 环境科学研究, 2018, 31(10): 1736-1742. DOI: 10.13198/j.issn.1001-6929.2018.04.16 |
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| 作者姓名： | 刘慧灵 毋赟 陈敏东 聂东阳 李文婧 张凯 葛鹏翔 |
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| 作者单位： | 南京信息工程大学环境科学与工程学院, 江苏省大气环境监测与污染控制高技术重点实验室, 江苏省大气环境与装备技术协同创新中心, 江苏 南京 210044 |
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| 基金项目： | 国家自然科学基金项目（No.91543115，21577065）；国际科技合作项目（No.2014DFA90780） |
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| 摘 要： | 为研究不同来源的大气颗粒物中PM2.5对人体的健康毒性效应，于2016年1-3月在南京市交通源区、化工园区、生活区等代表性站点分别采集PM2.5样品，分析其水溶性离子和金属元素含量，并以PM2.5对人体肺上皮细胞A549染毒24 h，研究暴露于不同来源颗粒物后的细胞活性和氧化损伤程度.结果表明:交通源区和化工园区日均ρ（PM2.5）远高于生活区，3个区域均含有大量二次污染物，其中SO42-、NO3-和NH4+占PM2.5总离子质量的80.6%~85.0%.交通源区PM2.5中w（Zn）较高，主要来源于燃料燃烧和柴油发动机排放；而化工园区PM2.5中w（Cu）、w（Pb）和w（Mn）均高于其他站点.将PM2.5染毒剂量设定为50、100、200、400 μg/mL，各站点颗粒物均显著抑制A549细胞的存活率，并呈剂量-效应关系，化工园区对细胞存活率的半抑制浓度（IC50=229.1 μg/mL）最低，而在高暴露浓度（200 μg/mL）下化工园区诱导产生的活性氧（ROS）最少.因此，南京地区主要受二次污染影响，机动车污染正在加剧；化工园区的颗粒物具有较大的细胞毒性，而较低的氧化损伤程度可能与该站点颗粒物中较低的w（Zn）以及测试暴露时间有关.
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| 关 键 词： | PM2.5 来源 A549细胞 细胞活性 氧化损伤 |
| 收稿时间： | 2018-01-21 |
| 修稿时间： | 2018-04-26 |
Characteristics of Atmospheric PM2.5 in Nanjing City and Its Cytotoxicity in Human Lung Epithelial Cells A549 |
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| LIU Huiling,WU Yun,CHEN Mindong,NIE Dongyang,LI Wenjing,ZHANG Kai and GE Pengxiang. Characteristics of Atmospheric PM2.5 in Nanjing City and Its Cytotoxicity in Human Lung Epithelial Cells A549[J]. Research of Environmental Sciences, 2018, 31(10): 1736-1742. DOI: 10.13198/j.issn.1001-6929.2018.04.16 |
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| Authors: | LIU Huiling WU Yun CHEN Mindong NIE Dongyang LI Wenjing ZHANG Kai GE Pengxiang |
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| Affiliation: | Jiangsu Key Laboratory of Atmospheric Environment Monitoring and Pollution Control, Collaborative Innovation Center of Atmospheric Environment and Equipment Technology, School of Environmental Science and Engineering, Nanjing University of Information Science & Technology, Nanjing 210044, China |
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| Abstract: | Air pollution is one of the most pressing public health issues in China, especially the pollution caused by fine particulate matter (PM2.5). PM2.5 is a mixture of multiple chemicals, the composition of which is greatly influenced by the source types, locations and atmospheric conditions. Furthermore, the health effects of PM2.5 vary according to its chemical composition. In order to investigate the toxic effects of atmospheric PM2.5 from different sources, PM2.5 samples were collected from three sites (a traffic site, an industrial site and a residential site located on campus) in Nanjing City. The sampling was conducted from January through March 2016. The contents of particulate-bound water-soluble ions and metal elements were analyzed by ion chromatography and inductively coupled plasma mass spectrometry, respectively. Cytotoxicity and PM2.5-induced oxidative stress in human lung epithelial cells (A549 cells) were also determined. The results showed that the daily PM2.5 mass concentrations in both traffic and industrial sites were much higher than the National Standard of the People's Republic of China Ambient Air Quality Standard (NAAQS) (GB 3095-2012) Grade Ⅱ 24-h standard (75 μg/m3). SO42-, NO3- and NH4+ were the main water-soluble inorganic ions, which accounted for 80.6%-85.0% of the total ions. PM2.5 samples from the traffic site showed much higher concentrations of Zn, while the industrial PM2.5 samples had higher concentrations of Cu, Pb and Mn than in other sites. Particles from all sites inhibited the cell activity over our dosage range (50, 100, 200 and 400 μg/mL), and presented a linear dose-response relationship. The cell viability of A549 was the most sensitive to PM2.5 samples from the industrial site, with an IC50 value of 229.1 μg/mL. In contrast, the industrial PM2.5 samples induced the lowest contents of ROS, which may be caused by relatively low Zn contents or the exposure time used. Our results indicated the importance of secondary air pollution and vehicle exhaust in Nanjing. There was notable variation in both the inorganic composition and the cytotoxicity of the three different sources. In the future, the contributions of each component to particulate toxicity should be further studied. |
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| Keywords: | PM2.5 source A549 cells cell viability oxidative damage |
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