Air pollution and markers of coagulation, inflammation, and endothelial function: associations and epigene-environment interactions in an elderly cohort.
Air pollution and markers of coagulation, inflammation, and endothelial function: associations and epigene-environment interactions in an elderly cohort.
复制标题
DOI：
10.1097/ede.0b013e31824523f0
复制
发表时间：
2012-03
期刊：
影响因子：
--
通讯作者：
Schwartz J
中科院分区：
文献类型：
--
作者：
Bind MA;Baccarelli A;Zanobetti A;Tarantini L;Suh H;Vokonas P;Schwartz J
先前的研究表明，空气污染与血栓形成、炎症和内皮功能障碍有关。易感性的机制和来源尚不清楚。一种可能性是，这些关联可以通过DNA甲基化状态进行修改。我们进行了一项队列研究，重复测量纤维蛋白原，C反应蛋白，细胞间粘附分子-1（ICAM-1），血管细胞粘附分子-1（VCAM-1）在704名老年男性参加退伍军人管理局规范老化研究（2000-2009年）。我们研究了短期和中期空气污染对这些血液标志物的影响，以及Alu，LINE-1，组织因子（F3），Toll样受体2（TLR-2）和ICAM-1的DNA甲基化的表观基因-环境相互作用。我们发现颗粒数，黑碳，二氧化氮（NO2）和一氧化碳（CO）对纤维蛋白原的影响。臭氧是C-反应蛋白和ICAM-1的重要预测因子。颗粒数、黑碳、NO2、CO、PM2.5和硫酸盐与ICAM-1和VCAM-1相关。NO2 24小时暴露的四分位数范围增加;与1.7%的（95%置信区间= 0.2%至3.3%）臭氧导致纤维蛋白原增加10.8% C反应蛋白颗粒数增加（2.2%-20.0%），5.9%对于PM2.5，ICAM-1增加3.6%至8.3%;对于PM2.5，VCAM-1增加3.7%（1.7%至5.8%）。在Alu较高、LINE-1、组织因子或TLR-2甲基化状态较低的受试者中，空气污染的影响更强。我们观察到与交通相关的污染物对纤维蛋白原，交通和二次颗粒对C-反应蛋白，ICAM-1和VCAM-1的关联。DNA甲基化状态的修饰效应，表明表观遗传状态可以传递空气污染的易感性。
Previous studies suggest that air pollution is related to thrombosis, inflammation, and endothelial dysfunction. Mechanisms and sources of susceptibility are still unclear. One possibility is that these associations can be modified by DNA methylation states. We conducted a cohort study with repeated measurements of fibrinogen, C-reactive protein, intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) in 704 elderly men participating in the Veterans Administration Normative Aging Study (2000-2009). We investigated short- and intermediate-term air pollution effects on these blood markers, and epigene-environment interactions by DNA methylation of Alu, LINE-1, tissue factor (F3), Toll-Like Receptor 2 (TLR-2), and ICAM-1. We found effects of particle number, black carbon, nitrogen dioxide (NO2), and carbon monoxide (CO) on fibrinogen. Ozone was a significant predictor of C-reactive protein and ICAM-1. Particle number, black carbon, NO2, CO, PM2.5, and sulfates were associated with ICAM-1and VCAM-1. An interquartile range increase in 24-hour exposure for NO2; was associated with a 1.7% (95% confidence interval = 0.2% to 3.3%) increase in fibrinogen for ozone a 10.8% (2.2% to 20.0%) increase in C-reactive protein for particle number, a 5.9% (3.6% to 8.3%) increase in ICAM-1; and for PM2.5 a 3.7% (1.7% to 5.8%) increase in VCAM-1. The air pollution effect was stronger among subjects having higher Alu, lower LINE-1, tissue factor, or TLR-2 methylation status. We observed associations of traffic-related pollutants on fibrinogen, and both traffic and secondary particles on C-reactive protein, ICAM-1, and VCAM-1. There was effect modification by DNA methylation status, indicating that epigenetic states can convey susceptibility to air pollution.