Abstract

Air pollution is associated with cardiovascular disease (CVD) and systemic inflammation is posited to mediate this effect. Animal, experimental and epidemiologic studies suggest increases in short-term air pollution cause an inflammatory response. Much of the past literature has focused on the association between short-term air pollution exposure and markers of inflammation and coagulation. We assessed both the association between long- and short-term exposure to air pollution and markers of inflammation, coagulation and endothelial activation. We studied participants from the Multi-Ethnic Study of Atherosclerosis (MESA) with repeat measures of serum C-reactive protein (CRP), interleukin-6 (IL-6), fibrinogen, D-dimer, soluble E-selectin and soluble Intercellular Adhesion Molecule-1 (sICAM-1). We estimated associations of these markers with long-term ambient fine particulate matter (PM2.5), individual-level ambient PM2.5 (integrating indoor concentrations and time-location data), oxides of nitrogen (NOX), nitrogen dioxide (NO) and black carbon averaged over the year prior to blood draw. Short-term concentrations of PM2.5 reflected day of blood draw, prior day, and moving average of prior 2, 3, 4, and 5 day periods. CRP, IL-6 and D-Dimer were log-transformed. A random effects model was used to account for within-person clustering. After controlling for confounders, a 5 µg/m3 increase in long-term ambient PM2.5 was associated with a 5.53% higher IL-6 level (95% CI: 1.83, 9.36) and a 40 ppb increase in long-term NOx was associated with 7.07% higher level in D-dimer (95% CI: 1.62, 12.83). CRP, E-selectin and sICAM-1 showed little association with long-term air pollution and associations between short-term ambient PM2.5 and blood markers was largely null. These data are consistent with the hypothesis that associations between long-term exposure to air pollution are related to inflammation and fibrinolysis.

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