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The acute effects of fine particulate matter constituents on circulating inflammatory biomarkers in healthy adults

机译:细颗粒物成分对健康成年人循环炎症生物标志物的急性影响

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Background: Systemic inflammation is considered one of the key mechanisms in the development of cardiovascular diseases induced by fine particulate matter (PM_(2.5)) air pollution. However, evidence concerning the effects of various PM_(2.5) constituents on circulating inflammatory biomarkers were limited and inconsistent. Objectives: To evaluate the associations of short-term exposure to a variety of PM_(2.5) constituents with circulating inflammatory biomarkers. Methods: We conducted a panel study from May to October 2016 among 40 healthy adults in Shanghai, China. We monitored the concentrations of 27 constituents of PM_(2.5). We applied linear mixed-effect models to analyze the associations of PM_(2.5) and its constituents with 7 inflammatory biomarkers, and further assessed the robustness of the associations by fitting models adjusting for PM_(2.5) mass and/or their collinearity. Benjamini-Hochberg false discovery rate was used to correct for multiple comparisons. Results: The associations of PM2.5 were strongest at lag 0 d with tumor necrosis factor-α (TNF-α), at lag 1 d with interleukin-6, interleukin-8, and interleukin-17A, at lag 02 d with monocyte chemoattractant protein-1 (MCP-1) and intercellular adhesion molecule-1 (ICAM-1). After correcting for multiple comparisons in all models, Cl~-, K~+, Si, K, As, and Pb were significantly associated with interleukin-8; SO_4~(2-) and Se were marginally significantly associated with interleukin-8; SO_4~(2-), As, and Se were marginally significantly associated with TNF-α; and Si, K, Zn, As, Se, and Pb were marginally significantly associated with MCP-1. Conclusions: Our results suggested that some constituents (SO_4~(2-), Cl~-, K~+, and some elements) might be mainly responsible for systemic inflammation triggered by short-term PM2.5 exposure.
机译:背景:全身性炎症被认为是由细颗粒物(PM_(2.5))空气污染引起的心血管疾病发展的关键机制之一。但是,有关各种PM_(2.5)成分对循环炎症生物标志物影响的证据有限且不一致。目的:评估短期暴露于多种PM_(2.5)成分与循环炎症生物标志物的关联。方法:我们于2016年5月至2016年10月在中国上海的40名健康成年人中进行了一项小组研究。我们监测了PM_(2.5)中27种成分的浓度。我们应用线性混合效应模型分析了PM_(2.5)及其成分与7种炎症生物标记的关联,并通过拟合调整PM_(2.5)质量和/或它们的共线性的模型进一步评估了关联的鲁棒性。 Benjamini-Hochberg错误发现率用于校正多个比较。结果:PM2.5与肿瘤坏死因子-α(TNF-α)滞后0 d,白细胞介素6,白细胞介素8和白细胞介素17A滞后1 d,单核细胞滞后02 d的相关性最强。化学吸引蛋白1(MCP-1)和细胞间粘附分子1(ICAM-1)。在校正了所有模型的多重比较后,Cl〜-,K〜+,Si,K,As和Pb与白介素8显着相关。 SO_4〜(2-)和Se与白细胞介素8的相关性很小。 SO_4〜(2-),As和Se与TNF-α的相关性很小。 Si,K,Zn,As,Se和Pb与MCP-1的相关性很小。结论:我们的结果表明,某些成分(SO_4〜(2-),Cl〜-,K〜+和某些元素)可能是由短期暴露于PM2.5引发的系统性炎症的主要原因。

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