Viehmann Anja, Hertel Sabine, Fuks Kateryna, Eisele Lewin, Moebus Susanne, Möhlenkamp Stefan, Nonnemacher Michael, Jakobs Hermann, Erbel Raimund, Jöckel Karl-Heinz, Hoffmann Barbara
Institute for Medical Informatics, Biometry and Epidemiology, University Hospital of Essen, Essen, Germany.
IUF-Leibniz Institute of Environmental Medicine Research and Medical Faculty, Deanery of Medicine, Heinrich Heine University of Düsseldorf, Düsseldorf, Germany.
Occup Environ Med. 2015 Sep;72(9):656-63. doi: 10.1136/oemed-2014-102800. Epub 2015 Jul 10.
In several studies, exposure to fine particulate matter (PM) has been associated with inflammation, with inconsistent results. We used repeated measurements to examine the association of long-term fine and ultrafine particle exposure with several blood markers of inflammation and coagulation.
We used baseline (2000-2003) and follow-up (2006-2008) data from the Heinz Nixdorf Recall Study, a German population-based prospective cohort of 4814 participants. A chemistry transport model was applied to model daily surface concentrations of PM air pollutants (PM10, PM2.5) and particle number on a grid of 1 km(2). Applying mixed regression models, we analysed associations of long-term (mean of 365 days prior to blood draw) particle exposure at each participant's residence with the level of high-sensitivity C reactive protein (hs-CRP), fibrinogen, platelet and white cell count (WCC), adjusting for short-term PM exposure (moving averages of 1-7 days), personal characteristics, season, ambient temperature (1-5 days), ozone and time trend.
We analysed 6488 observations: 3275 participants with baseline data and 3213 with follow-up data. An increase of 2.4 µg/m(3) in long-term PM2.5 was associated with an adjusted increase of 5.4% (95% CI 0.6% to 10.5%) in hs-CRP and of 2.3% (95% CI 1.4% to 3.3%) in the platelet count. Fibrinogen and WCC were not associated with long-term particle exposure.
In this population-based cohort, we found associations of long-term exposure to PM with markers of inflammation (hs-CRP) and coagulation (platelets). This finding supports the hypothesis that inflammatory processes might contribute to chronic effects of air pollution on cardiovascular disease.
在多项研究中,暴露于细颗粒物(PM)与炎症相关,但结果并不一致。我们采用重复测量的方法来研究长期暴露于细颗粒物和超细颗粒物与多种血液炎症和凝血标志物之间的关联。
我们使用了海因茨·尼克斯多夫召回研究的基线数据(2000 - 2003年)和随访数据(2006 - 2008年),该研究是一项基于德国人群的前瞻性队列研究,共有4814名参与者。应用化学传输模型来模拟1平方千米网格上PM空气污染物(PM10、PM2.5)和颗粒数的每日地面浓度。应用混合回归模型,我们分析了每位参与者居住地长期(采血前365天的平均值)颗粒物暴露与高敏C反应蛋白(hs-CRP)、纤维蛋白原、血小板和白细胞计数(WCC)水平之间的关联,并对短期PM暴露(1 - 7天移动平均值)、个人特征、季节、环境温度(1 - 5天)、臭氧和时间趋势进行了调整。
我们分析了6488条观测数据:3275名有基线数据的参与者和3213名有随访数据的参与者。长期PM2.5每增加2.4微克/立方米,hs-CRP调整后增加5.4%(95%可信区间为0.6%至10.5%),血小板计数增加2.3%(95%可信区间为1.4%至3.3%)。纤维蛋白原和WCC与长期颗粒物暴露无关。
在这个基于人群的队列中,我们发现长期暴露于PM与炎症标志物(hs-CRP)和凝血标志物(血小板)之间存在关联。这一发现支持了炎症过程可能导致空气污染对心血管疾病产生慢性影响这一假说。