Long-term residential exposure to urban air pollution, and repeated measures of systemic blood markers of inflammation and coagulation

纤维蛋白原 全身炎症 C反应蛋白 人口 医学 白细胞 炎症 免疫学 内科学 环境卫生
作者
Anja Viehmann,Sabine Hertel,Kateryna Fuks,Lewin Eisele,Susanne Moebus,Stefan Möhlenkamp,Michael Nonnemacher,Hermann Jakobs,Raimund Erbel,Karl‐Heinz Jöckel,Barbara Hoffmann
出处
期刊:Occupational and Environmental Medicine [BMJ]
卷期号:72 (9): 656-663 被引量:140
标识
DOI:10.1136/oemed-2014-102800
摘要

Background

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.

Methods

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 km2. Applying mixed regression models, we analysed associations of long-term (mean of 365 days prior to blood draw) particle exposure at each participant9s 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.

Results

We analysed 6488 observations: 3275 participants with baseline data and 3213 with follow-up data. An increase of 2.4 µg/m3 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.

Conclusions

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.
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