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Ambient Particulate Air Pollution and Circulating Biomarkers in Healthy Adults: the Health Volunteer Natural Relocation Study

机译:健康成人的环境微粒空气污染和循环生物标志物:健康志愿者自然搬迁研究

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Background: Ambient air pollution has been associated with activation of systemic inflammation and hypercoagulability and increased plasma homocysteine, but the chemical constituents behind the association are not well understood. Aims: We examined the relations of chemical constituents of fine particles (PM2.5) and biomarkers of inflammation, coagulation and homocysteine in the context of traffic-related air pollution. Methods: A panel of 40 healthy college students underwent biweekly blood collection for 12 times before and after relocating from a suburban campus to an urban campus with changing air pollution contents in Beijing. Blood samples were measured for circulatory biomarkers ofhigh-sensitivity C reactive protein (hs-CRP), tumor necrosis factor alpha (TNF-α), fibrinogen, plasminogen activator inhibitor type 1 (PAI-1), tissue-type plasminogen activator (t-PA), von Willebrand factor (vWF), soluble platelet selectin (sP-selectin), and total homocysteine (tHcy). Various air pollutants were measured in a central air-monitoring station in each campus and 32 PM2.5 chemical constituents were determined in the laboratory. We used mixed-effects models to estimate the effects of PM2.5 chemical constituents on circulatory biomarkers. Results:We found consistent positive associations between the following biomarkers and PM2.5 chemical constituents across different models: TNF-α with secondary organic carbon, chloride, zinc, molybdenum and stannum; fibrinogen with magnesium, iron, titanium, cobalt and cadmium; PAI-1 with titanium, cobalt and manganese; t-PA with cadmium and selenium; vWF with aluminum.We also found consistent inverse associations of vWF with nitrate, chloride and sodium, and sP-selectin with manganese. Conclusions: Our results provide clues for the potential roles that PM2.5 chemical constituents may play in the biological mechanisms through which air pollution may influence the cardiovascular system.
机译:背景:环境空气污染与全身炎症的激活和高凝和高凝血性和增加的血浆同型术,但结合背后的化学成分并不充分了解。目的:在交通相关的空气污染的背景下,我们检查了细颗粒(PM2.5)和炎症,凝血和同型半胱氨酸的生物标志物的关系。方法:40名健康大学生小组接受双周血液收集,前后从郊区校园搬迁到北京市空气污染内容的城市校园前后12次。测量高灵敏度C反应蛋白(HS-CRP)的循环生物标志物,肿瘤坏死因子α(TNF-α),纤维蛋白原,纤溶酶原激活剂抑制剂1(PAI-1),组织型纤溶酶原激活剂(T-)的血液样品PA),Von Willebrand因子(VWF),可溶性血小板选择(SP-SELETIN)和总同型半胱氨酸(THCY)。在每个校区的中央空气监测站中测量各种空气污染物,在实验室中测定32pm2.5化学成分。我们使用了混合效果模型来估计PM2.5化学成分对循环生物标志物的影响。结果:我们在不同模型中发现了以下生物标志物和PM2.5化学成分之间的一致阳性关联:TNF-α具有二次有机碳,氯化物,锌,钼和甾烷;纤维蛋白原与镁,铁,钛,钴和镉; Pai-1用钛,钴和锰; T-Pa用镉和硒; VWF与铝。我们还发现VWF与硝酸盐,氯和钠的一致逆关联,以及用锰的Sp-Selectin。结论:我们的结果提供了PM2.5化学成分在空气污染可能影响心血管系统的生物机制中发挥的潜在作用的线索。

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