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Ambient Particulate Air Pollution and Circulating C-Reactive Protein Level: A Meta-Analysis

机译:环境颗粒物空气污染和循环C反应蛋白水平:荟萃分析

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Background: Ambient particulate air pollution is a major threat to the cardiovascular health of the population. Inflammation is an important component of the pathophysiological process linking air pollution and cardiovascular disease (CVD). A classical marker of inflammation-C-reactive protein (CRP), has been recognized as an independent predictor of CVD risk. Exposure to ambient air pollutants may cause systemic inflammatory response but the association with CRP has been inconsistently reported. Objectives: We aims to estimate the effects of short-term and long-term exposures to ambient particulate air pollution on circulating CRP based on previous epidemiological studies. Methods: A systematic literature search of the PubMed, Web of Science, Embase, Scopus databases for publications up to January 2018 was conducted for studies reporting the association between ambient particulate matters (PM2.5, PM10) and circulating CRP level. We performed metaanalysis for associations reported in individual studies using a random-effect model and evaluated the effect modification by major potential confounders. Results: This meta-analysis comprised 243,960 participants from 37 observational studies carried out worldwide. Long-term exposure to particulate air pollution was much strongly associated with CRP level than short-term exposure. A 10 μg/m3 increase of short-term exposure to PM2.5 and PM10 is associated with increases of 0.78% (95% CI: 0.22-1.33%) and 0.26% (95% Cl:-0.03%,0.55%) in CRP level, respectively; and a 10 μg/m3 increase of long-term exposure to PM2.5 and PM10 is associated with much higher increases of 18.49% (95%CI: 8.50-28.49%) and 11.10% (95%CI: 2.73-19.45%) in CRP level, respectively. Studies in Europe and North America showed stronger PM-CRP associations than studies in Asia. Conclusion: Exposure to ambient particulate air pollution is associated with elevated circulating CRP level.
机译:背景:环境中的颗粒物空气污染是对人群心血管健康的主要威胁。炎症是连接空气污染和心血管疾病(CVD)的病理生理过程的重要组成部分。炎症C反应蛋白(CRP)的经典标记已被认为是CVD风险的独立预测因子。暴露于环境空气污染物中可能引起全身性炎症反应,但与CRP的相关报道却不一致。目标:我们的目的是根据先前的流行病学研究,估计短期和长期暴露于环境颗粒物空气污染对循环CRP的影响。方法:对PubMed,Web of Science,Embase,Scopus数据库的系统文献检索进行了研究,以研究截至2018年1月的出版物,这些研究报告了环境颗粒物(PM2.5,PM10)与循环CRP水平之间的关系。我们使用随机效应模型对个体研究中报道的关联进行了荟萃分析,并评估了主要潜在混杂因素对效应的修正。结果:这项荟萃分析包括来自全球37项观察性研究的243,960名参与者。与短期暴露相比,长期暴露于颗粒空气污染与CRP水平密切相关。短期暴露于PM2.5和PM10的10μg/ m3的增加会导致0.78%(95%CI:0.22-1.33%)和0.26%(95%Cl:-0.03%,0.55%)的增加CRP水平;长期暴露于PM2.5和PM10中的量增加10μg/ m3,则分别增加18.49%(95%CI:8.50-28.49%)和11.10%(95%CI:2.73-19.45%)在CRP级别。欧洲和北美的研究表明,与亚洲的研究相比,PM-CRP关联更强。结论:暴露于周围的颗粒空气污染与循环CRP水平升高有关。

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