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暴露于环境空气污染与凝血标志物之间的关联,以及 DNA 甲基化的潜在影响。

The associations between exposure to ambient air pollution and coagulation markers and the potential effects of DNA methylation.

机构信息

Department of Occupational and Environmental Health, School of Public Health, Sun Yat-sen University, Guangzhou 510080, China.

Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, the University of Melbourne, Melbourne, VIC 3053, Australia.

出版信息

J Hazard Mater. 2024 Dec 5;480:136433. doi: 10.1016/j.jhazmat.2024.136433. Epub 2024 Nov 8.

Abstract

Previous studies have illustrated the pivotal role of coagulation biomarkers in the link between air pollution and cardiovascular disease (CVD). However, inconsistencies remain in the conclusions, with limited studies conducted in rural areas of China. We conducted a panel study in rural areas of Henan Province, China. Considering the potential effect modifications of atherosclerotic cardiovascular disease (ASCVD) risks, 104 participants were enrolled, comprising two matched groups: 52 with high ASCVD risks and 52 with low ASCVD risks. DNA methylation at CpG sites and coagulation indices were measured for all participants. Linear mixed-effect regression models were used to evaluate the associations between ambient air pollution, coagulation biomarkers, and DNA methylation. We observed that for every 5-day standard deviation (SD) increment of PM (11.91 μg/m³) and PM (13.65 μg/m³), fibrinogen increased by 7.70 % (95 %CI: 2.27, 13.12) and 8.50 % (95 %CI: 2.46, 14.55), respectively. SO (6.95 μg/m³) was associated with 40.25 % (95 %CI: 14.83, 65.67) increase in plasminogen activator inhibitor-1 (PAI-1). Decreased methylation at CpG sites was associated with exposure to air pollution. However, DNA methylation did not mediate the association between ambient air pollution and coagulation. Our study revealed the harmful impact of ambient air pollution on coagulation function but found no significant mediation effects of DNA methylation.

摘要

先前的研究表明,凝血生物标志物在空气污染与心血管疾病(CVD)之间的关联中起着关键作用。然而,结论仍存在不一致之处,且在中国农村地区的研究有限。我们在中国河南省的农村地区进行了一项面板研究。考虑到动脉粥样硬化性心血管疾病(ASCVD)风险的潜在效应修饰,我们纳入了 104 名参与者,包括两组匹配的人群:52 名 ASCVD 风险高的人群和 52 名 ASCVD 风险低的人群。所有参与者均进行了 CpG 位点的 DNA 甲基化和凝血指数检测。采用线性混合效应回归模型评估环境空气污染、凝血生物标志物和 DNA 甲基化之间的关联。我们观察到,对于 PM(11.91μg/m³)和 PM(13.65μg/m³)每增加 5 天的标准偏差(SD),纤维蛋白原分别增加 7.70%(95%CI:2.27,13.12)和 8.50%(95%CI:2.46,14.55)。SO(6.95μg/m³)与纤溶酶原激活物抑制剂-1(PAI-1)增加 40.25%(95%CI:14.83,65.67)相关。CpG 位点的去甲基化与暴露于空气污染有关。然而,DNA 甲基化并没有介导环境空气污染与凝血之间的关联。我们的研究揭示了环境空气污染对凝血功能的有害影响,但没有发现 DNA 甲基化的显著介导作用。

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