Chronic residential exposure to particulate matter air pollution and systemic inflammatory markers.
Chronic residential exposure to particulate matter air pollution and systemic inflammatory markers.
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DOI：
10.1289/ehp.0800362
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发表时间：
2009-08
影响因子：
10.4
通讯作者：
Jöckel KH
中科院分区：
文献类型：
--
作者：
Hoffmann B;Moebus S;Dragano N;Stang A;Möhlenkamp S;Schmermund A;Memmesheimer M;Bröcker-Preuss M;Mann K;Erbel R;Jöckel KH
长期暴露于城市空气污染可能会加速动脉粥样硬化的形成，但其机制尚不清楚。低级别全身炎症状态的诱导是一个合理的机制途径。目的：我们分析了住宅长期暴露于颗粒物（PM）和高流量与全身炎症标志物的关系。我们使用的基线数据来自德国海因茨尼克斯多夫回忆研究，这是一项基于人群的前瞻性队列研究，共有4,814名参与者，始于2000年。根据小规模分散和化学传输模型，将细颗粒物[空气动力学直径≤ 2.5 μm（PM2.5）]暴露分配给每个家庭地址。我们计算了住宅和主要道路之间的距离。长期暴露于空气污染（每年PM2.5和高交通量的距离）和炎症标志物[高敏C反应蛋白（hs-CRP）和纤维蛋白原]的浓度在基线访视当天进行了分析，性别分层多元线性回归，控制个人水平的风险因素。在调整后的分析中，PM2.5（十分位数范围）中3.91 μg/m3的横断面暴露差异与男性hs-CRP升高23.9% [95%置信区间（CI），4.1至47.4%]和纤维蛋白原升高3.9%（95% CI，0.3至7.7%）相关，而我们发现女性中没有相关性。慢性交通暴露与炎症标志物无关。短期暴露于空气污染物和温度没有显着影响的结果。我们的研究表明，长期居住暴露于高水平的PM2.5与男性的全身炎症标志物有关。这可能提供了空气污染和冠状动脉粥样硬化之间的联系。
Long-term exposure to urban air pollution may accelerate atherogenesis, but mechanisms are still unclear. The induction of a low-grade systemic inflammatory state is a plausible mechanistic pathway. Objectives: We analyzed the association of residential long-term exposure to particulate matter (PM) and high traffic with systemic inflammatory markers. We used baseline data from the German Heinz Nixdorf Recall Study, a population-based, prospective cohort study of 4,814 participants that started in 2000. Fine PM [aerodynamic diameter ≤ 2.5 μm (PM2.5)] exposure based on a small-scale dispersion and chemistry transport model was assigned to each home address. We calculated distances between residences and major roads. Long-term exposure to air pollution (annual PM2.5 and distance to high traffic) and concentration of inflammatory markers [high-sensitivity C-reactive protein (hs-CRP) and fibrinogen] on the day of the baseline visit were analyzed with sex-stratified multiple linear regression, controlling for individual-level risk factors. In the adjusted analysis, a cross-sectional exposure difference of 3.91 μg/m3 in PM2.5 (interdecile range) was associated with increases in hs-CRP of 23.9% [95% confidence interval (CI), 4.1 to 47.4%] and fibrinogen of 3.9% (95% CI, 0.3 to 7.7%) in men, whereas we found no association in women. Chronic traffic exposure was not associated with inflammatory markers. Short-term exposures to air pollutants and temperature did not influence the results markedly. Our study indicates that long-term residential exposure to high levels of PM2.5 is associated with systemic inflammatory markers in men. This might provide a link between air pollution and coronary atherosclerosis.
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影响因子：
10.4
作者：
Rückerl R;Greven S;Ljungman P;Aalto P;Antoniades C;Bellander T;Berglind N;Chrysohoou C;Forastiere F;Jacquemin B;von Klot S;Koenig W;Küchenhoff H;Lanki T;Pekkanen J;Perucci CA;Schneider A;Sunyer J;Peters A;AIRGENE Study Group
通讯作者：
AIRGENE Study Group
影响因子：
5.4
作者：
Forbes, Lindsay J. L.;Patel, Minal D.;Anderson, Ross H.
通讯作者：
Anderson, Ross H.
代谢综合征和对长期颗粒空气污染物的炎症反应。
影响因子：
10.4
作者：
Chen, Jiu-Chiuan;Schwartz, Joel
通讯作者：
Schwartz, Joel
动脉粥样硬化的炎症。
DOI：
10.1161/atvbaha.108.179705
发表时间：
2012-09
期刊：
Arteriosclerosis, thrombosis, and vascular biology
影响因子：
--
作者：
Libby P
通讯作者：
Libby P
DOI：
10.1038/sj.jea.7500408
发表时间：
2005-07-01
期刊：
JOURNAL OF EXPOSURE ANALYSIS AND ENVIRONMENTAL EPIDEMIOLOGY
影响因子：
--
作者：
Liao, DP;Heiss, G;Salomaa, V
通讯作者：
Salomaa, V