首页> 外文期刊>International journal of occupational medicine and environmental health. >PRELIMINARY STUDY TO EXPLORE GENE-PM2.5 INTERACTIVE EFFECTS ON RESPIRATORY SYSTEM IN TRAFFIC POLICEMEN
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PRELIMINARY STUDY TO EXPLORE GENE-PM2.5 INTERACTIVE EFFECTS ON RESPIRATORY SYSTEM IN TRAFFIC POLICEMEN

机译:探索基因-PM2.5在交通警察中对呼吸系统的交互作用的初步研究

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Objectives: Traffic-related particulate matter (PM) is one of the major sources of air pollution in metropolitan areas. This study is to observe the interactive effects of gene and fine particles (particles smaller than 2.5 mu m - PM2.5) on the respiratory system and explore the mechanisms linking PM2.5 and pulmonary injury. Material and Methods: The participants include 110 traffic policemen and 101 common populations in Shanghai, China. Continuous 24 h individual-level PM2.5 is detected and the pulmonary function, high-sensitivity C-reactive protein (hs-CRP), Clara cell protein 16 (CC16) and the polymorphism in CXCL3, NME7 and C5 genes are determined. The multiple linear regression method is used to analyze the association between PM2.5 and health effects. Meanwhile, the interactive effects of gene and PM2.5 on lung function are analyzed. Results: The individual PM2.5 exposure for traffic policemen was higher than that in the common population whereas the forced expiratory volume in 1 s (FEV1), the ratio of FEV1 to forced vital capacity (FEV1/FVC) and lymphocytes are lower. In contrast, the hs-CRP level is higher. In the adjusted analysis, PM2.5 exposure was associated with the decrease in lymphocytes and the increase in hs-CRP. The allele frequencies for NME7 and C5 have significant differences between FEV1/FVC <= 70% and FEV1/FVC > 70% participants. The results didn't find the interaction effects of gene and PM2.5 on FEV1/FVC in all the 3 genes. Conclusions: The results indicated that traffic exposure to high levels of PM2.5 was associated with systemic inflammatory response and respiratory injury. Traffic policemen represent a high risk group suffering from the respiratory injury.
机译:目标:与交通有关的颗粒物(PM)是大都市地区空气污染的主要来源之一。这项研究旨在观察基因和细小颗粒(小于2.5微米-PM2.5的颗粒)对呼吸系统的相互作用,并探索将PM2.5与肺损伤联系起来的机制。资料和方法:参与者包括中国上海的110名交警和101个普通人群。连续检测24 h个人水平的PM2.5,并测定肺功能,高敏C反应蛋白(hs-CRP),Clara细胞蛋白16(CC16)以及CXCL3,NME7和C5基因的多态性。多元线性回归方法用于分析PM2.5与健康影响之间的关系。同时,分析了基因和PM2.5对肺功能的相互作用。结果:交警个人的PM2.5暴露水平高于普通人群,而强制呼气量在1 s(FEV1),FEV1与强制肺活量(FEV1 / FVC)和淋巴细胞的比率较低。相反,hs-CRP水平较高。在调整后的分析中,PM2.5暴露与淋巴细胞减少和hs-CRP增加有关。 NME7和C5的等位基因频率在FEV1 / FVC <= 70%和FEV1 / FVC> 70%参与者之间有显着差异。结果未发现在所有3个基因中基因和PM2.5对FEV1 / FVC的相互作用。结论:结果表明交通暴露于高水平的PM2.5与全身炎症反应和呼吸系统损伤有关。交警代表呼吸系统伤害的高危人群。

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