gms | German Medical Science

Background: Experimental and epidemiological evidence shows that short-term exposure to elevated levels of particulate matter (PM) is associated with an activation of the inflammatory cascade, which might contribute to the increased cardiovascular morbidity and mortality observed during periods of high air pollution. However, uncertainty remains regarding possible inflammatory pathways of long-term exposures on the development and progression of atherogenesis. We examined the relationship between long-term exposure to urban air pollution and markers of inflammation.

Methods: We used baseline data from the Heinz Nixdorf Recall-Study, an ongoing population-based, prospective cohort study. We assessed residential long-term traffic exposure (distance to a major road with mean daily traffic counts of 10,000-130,000) and assigned annual mean background PM2.5 concentrations to each residence, using the EURAD dispersion model. We evaluated the association between the two different measures of air pollution and high sensitive C-reactive protein (hs-CRP) and fibrinogen with linear regression, controlling for factors associated with the exposure and the outcome.

Results: Of the 4323 participants included in the analysis, 652 (15%) lived within 200 m of a major road. Quartiles of PM2.5 exposure were 22.05 (Q1), 22.59 (Q2) and 23.75 (Q3) µg/m3. An exposure contrast in PM2.5 from the 10th to the 90th percentile (4.09 µg/m3) was associated with an increase in hs-CRP and fibrinogen of 17.8% (95% CI 7.8-28.8%) and 2.9% (95% CI 1.0-4.7%) respectively in the crude model and 16.2% (95% CI 3.2-30.8%) and 2.9% (95% CI 0.5-5.4%) respectively in the adjusted model. Associations were strongest in males and smokers. Residential proximity to a major road was not consistently associated with inflammatory markers.

Conclusions: We found epidemiological evidence that long-term exposure to PM may activate inflammatory mechanisms that play a role in atherogenesis.