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首页> 外文期刊>Particle Fibre Toxicology >Chemical constituents of ambient particulate air pollution and biomarkers of inflammation, coagulation and homocysteine in healthy adults: A prospective panel study
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Chemical constituents of ambient particulate air pollution and biomarkers of inflammation, coagulation and homocysteine in healthy adults: A prospective panel study

机译:健康成年人中环境空气污染物的化学成分以及炎症,凝血和高半胱氨酸的生物标志物:一项前瞻性面板研究

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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. We examined the relations of various 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 their relocation from a suburban campus to an urban campus with changing air pollution contents in Beijing. Blood samples were measured for circulatory biomarkers of high-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 three different mixed-effects models (single-constituent model, constituent-PM2.5 joint model and constituent residual model) controlling for potential confounders 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. Two positive associations of zinc with TNF-α and of cobalt with fibrinogen, and two inverse associations of nitrate with vWF , and of manganese with sP-selectin, were independent of the other constituents in two-constituent models using constituent residual data. We only found weak air pollution effects on hs-CRP and tHcy. 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:背景技术环境空气污染与全身炎症反应和高凝性的激活以及血浆同型半胱氨酸的增加有关,但这种关联背后的化学成分尚未得到很好的了解。在交通相关的空气污染的背景下,我们研究了微粒的各种化学成分(PM 2.5 )与炎症,凝血和高半胱氨酸的生物标志物之间的关系。方法一组40名健康的大学生在从郊区校园搬迁到城市校园之前和之后,每两周接受一次血液采集12次,之后北京的空气污染含量不断变化。测量血液样本中的高敏感性C反应蛋白(hs-CRP),肿瘤坏死因子α(TNF-α),纤维蛋白原,纤溶酶原激活物抑制剂1型(PAI-1),组织型纤溶酶原激活物(t -PA),von Willebrand因子(vWF),可溶性血小板选择素(sP-selectin)和总高半胱氨酸(tHcy)。在每个园区的中央空气监测站中测量了各种空气污染物,并在实验室中确定了32 PM 2.5 的化学成分。我们使用了三种不同的混合效应模型(单成分模型,component-PM 2.5 联合模型和成分残差模型)来控制潜在的混杂因素,以估算循环生物标志物上的PM 2.5 化学成分。结果我们发现以下生物标志物与不同模型中的PM 2.5 化学成分之间具有一致的正相关性:TNF-α与次级有机碳,氯化物,锌,钼和锡;含有镁,铁,钛,钴和镉的纤维蛋白原; PAI-1,含钛,钴和锰;含镉和硒的t-PA;带铝的vWF。我们还发现vWF与硝酸盐,氯化物和钠以及sP-选择素与锰具有一致的逆相关性。锌与TNF-α的两个正相关,钴与纤维蛋白原的两个正相关,硝酸盐与vWF的两个负相关,以及锰与sP-选择素的两个反向相关,在使用成分残留数据的两成分模型中与其他成分无关。我们仅发现空气污染对hs-CRP和tHcy的影响微弱。结论我们的结果为PM 2.5 化学成分可能在空气污染可能影响心血管系统的生物学机制中发挥潜在作用提供了线索。

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