Cohort studies suggest that long-term exposure to higher levels of outdoor air pollution increases risk of developing cardiovascular disease. One suggested mechanism is that air pollution, especially particulate matter, induces systemic inflammation, thereby increasing the risk of developing long-term pathologic changes in the cardiovascular system, We aimed to examine the association between long-term exposure to higher levels of air pollution and chronic systemic inflammation.Methods:
We examined the relationship between 2 markers of systemic inflammation (fibrinogen and C-reactive protein) and measures of outdoor air pollution estimated for each postcode sector of residence, using models incorporating information on pollutant emissions from multiple sources, and atmospheric dispersion and processing, in 3 representative cross-sectional studies of the English population in 1994, 1998, and 2003. These included about 25,000 adults with fibrinogen measurements and 17,000 adults with C-reactive protein measurements. We used multilevel linear regression modeling and pooled the results from the 3 surveys using meta-analysis.Results:
We found no associations between concentrations of fibrinogen or C-reactive protein and measures of outdoor air pollution (particulate matter <10 μm in diameter (PM10), nitrogen dioxide, sulfur dioxide, and ozone). Specifically, we found, for each 1-μg/m3 increase in PM10 concentration, a change in fibrinogen concentrations of −0.08% (95% confidence interval = 0.25–0.10) and in C-reactive protein concentrations of 0.14% (95% confidence interval = 1.00–1.30).Conclusions:
Our findings do not support the hypothesis that the association between outdoor air pollution exposure and later cardiovascular disease is mediated by chronic systemic inflammation.