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Influence of short-term exposure to ultrafine and fine particles on systemic inflammation
Sabine Hertel, Anja Viehmann, Susanne Moebus, Klaus Mann, Martina Bröcker-Preuss, Stefan Möhlenkamp, Michael Nonnemacher, Raimund Erbel, Hermann Jakobs, Michael Memmesheimer, Karl-Heinz Jöckel and Barbara Hoffmann
European Journal of Epidemiology
Vol. 25, No. 8 (2010), pp. 581-592
Published by: Springer
Stable URL: http://www.jstor.org/stable/40802359
Page Count: 12
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Daily to monthly variations in fine particulate matter have been linked to systemic inflammatory responses. It has been hypothesized that smaller particles resulting from combustion processes confer higher toxicity. We aim to analyze the association between short-term exposure to ultrafine and fine particles and systemic inflammation. We use baseline data (2000-2003) of the Heinz Nixdorf Recall Study, a population-based cohort study of 4,814 participants in the Ruhr Area in Germany. A chemistry transport model was applied to model daily surface concentrations of particulate air pollutants on a grid of 1 km 2 . Exposure included particle number (PN) and particulate matter mass concentration with an aerodynamic diameter < 2.5 μm (PM 2.5 ) and < 10 μm (PM 10). Generalized additive models were used to explore the relation of air pollutants using single day lags and averaging times of up to 28 days with high-sensitivity C-reactive protein (hs-CRP). We adjusted for meteorology, season, time trend, and personal characteristics. Median hs-CRP level in the 3,999 included participants was 1.5 mgA. Median daily concentration of PN was 8,414 ÷ 10⁴/ml (IQR 4,580 ÷ 10⁴/ml), of PM 2 .5 14.5 μg/m³ (IQR 11.5 μg/m³) and of PM ₁₀ 18.5 μg/m³ (IQR 13.9 μg/m³). A positive association between PN and hs-CRP could be observed only for single day lags and for averaged PN concentrations with higher estimates for longer averaging times. The highest hs-CRPincrease of 7.1% (95%-CI: 1.9,12.6%) was found for the 21-day average. These results support the hypothesis that shortterm exposure to traffic-related particles might lead to detrimental cardiovascular health effects via an inflammatory mechanism.
European Journal of Epidemiology © 2010 Springer