Chronic residential exposure to particulate matter air pollution and systemic inflammatory markers

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Background: 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. Methods: 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 (PM 2.5 )] 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 PM 2.5 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. Results: In the adjusted analysis, a cross-sectional exposure difference of 3.91 μg/m 3 in PM 2.5 (interdecile range) was associated with increases in h s -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. Conclusions: Our study indicates that long-term residential exposure to high levels of PM 2.5 is associated with systemic inflammatory markers in men. This might provide a link between air pollution and coronary atherosclerosis.




Hoffmann, B., Moebus, S., Dragano, N., Stang, A., Möhlenkamp, S., Schmermund, A., … Jöckel, K. H. (2009). Chronic residential exposure to particulate matter air pollution and systemic inflammatory markers. Environmental Health Perspectives, 117(8), 1302–1308.

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