Department of Environment Health, School of Public Health, the Key Laboratory of Public Health Safety, Fudan University, Ministry of Education, Shanghai 200032, China.
Occup Environ Med. 2013 Jun;70(6):426-31. doi: 10.1136/oemed-2012-100864. Epub 2013 Jan 15.
Ambient fine-particle particulate matter (PM2.5) exposure is associated with the decline in pulmonary function, prevalence of coronary heart disease and incidence of myocardial infarction. The study is to observe the effects of ambient PM2.5 on the cardiovascular system and to explore the potential inflammatory and immune mechanisms.
The subjects included 110 traffic policemen in Shanghai, China, who were aged 25-55 years. Two-times continuous 24 h individual-level PM2.5 measurements were performed in winter and summer, respectively. The inflammatory marker (high-sensitivity C-reactive protein, hs-CRP), immune parameters (IgA, IgG, IgM and IgE) and lymphocyte profiles (CD4 T cells, CD8 T cells, CD4/CD8 T cells) were measured in blood. The associations between individual-level PM2.5 and inflammatory marker and immune parameters were analysed by multiple linear regression.
The average concentration of 24 h personal PM2.5 for participants was 116.98 μg/m(3) and 86.48 μg/m(3) in winter and summer, respectively. In the main analysis, PM2.5 exposure is associated with the increases in hs-CRP of 1.1%, IgG of 6.7%, IgM of 11.2% and IgE of 3.3% in participants, and decreases in IgA of 4.7% and CD8 of 0.7%, whereas we found no statistical association in CD4 T cells and CD4/CD8 T cells. In the adjusted model, the results showed that the increase of PM2.5 was associated with the changes of inflammatory markers and immune markers both in winter and summer.
Traffic policeman have been a high-risk group suffering inflammatory response or immune injury because of the high exposure to PM2.5. These findings provided new insight into the mechanisms linking ambient PM2.5 and inflammatory and immune response.
环境细颗粒物(PM2.5)暴露与肺功能下降、冠心病患病率和心肌梗死发病率有关。本研究旨在观察环境 PM2.5 对心血管系统的影响,并探讨潜在的炎症和免疫机制。
研究对象为中国上海的 110 名交通警察,年龄在 25-55 岁之间。分别在冬季和夏季进行了两次连续 24 小时的个体水平 PM2.5 测量。在血液中测量了炎症标志物(高敏 C 反应蛋白,hs-CRP)、免疫参数(IgA、IgG、IgM 和 IgE)和淋巴细胞谱(CD4 T 细胞、CD8 T 细胞、CD4/CD8 T 细胞)。采用多元线性回归分析个体水平 PM2.5 与炎症标志物和免疫参数之间的关系。
参与者 24 小时个人 PM2.5 的平均浓度分别为冬季 116.98μg/m3和夏季 86.48μg/m3。在主要分析中,PM2.5 暴露与参与者 hs-CRP 增加 1.1%、IgG 增加 6.7%、IgM 增加 11.2%和 IgE 增加 3.3%相关,而 IgA 减少 4.7%和 CD8 减少 0.7%。但我们未发现 CD4 T 细胞和 CD4/CD8 T 细胞有统计学关联。在调整模型中,结果表明,PM2.5 的增加与冬季和夏季炎症标志物和免疫标志物的变化有关。
由于交通警察 PM2.5 暴露水平较高,他们已经成为易受炎症反应或免疫损伤的高危人群。这些发现为环境 PM2.5 与炎症和免疫反应之间的联系机制提供了新的见解。