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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 <or= 2.5 microm (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 microg/m(3) in PM(2.5) (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. 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 et al. (Sat,) studied this question.