Abstract P243: Long-Term Exposure to Air Pollution and Markers of Inflammation, Coagulation and Endothelial Activation: A Repeat Measures Analysis in the Multi-Ethnic Study of Atherosclerosis

Abstract

Air pollution is associated with CVD and systemic inflammation is posited to mediate this effect. Animal, experimental and epidemiologic studies suggest that increases in short-term air pollution cause an inflammatory response. Few studies, however, have assessed the contribution of long-term exposure to pollutants even though chronic inflammation may be more relevant to the observed risk of atherosclerotic disease. We assessed the hypothesis that long-term exposure to pollutants is associated with markers of inflammation, coagulation and endothelial activation. We studied participants from the Multi-Ethnic Study of Atherosclerosis (MESA) cohort with repeat measures of serum C-reactive protein (CRP), fibrinogen, D-dimer, soluble E-selectin and soluble Intercellular Adhesion Molecule-1 (sICAM-1). We estimated associations of these markers with outdoor PM2.5, individual-level ambient PM2.5 (integrating indoor concentrations and time-location data) and oxides of nitrogen (NOX). Pollutant concentrations were predicted from likelihood based models from cohort-specific monitoring and were averaged over the year prior to blood draw. CRP and D-Dimer were log-transformed for analysis. A random effects model controlling for relevant covariates was used to account for within person clustering. Participants with a recent history of acute infection were excluded from analysis. A total of 713 participants contributed 1736 observations (mean 1.8 observations per person over 3 visits). After excluding those with a recent infection we were left with 1233 observations among 491 participants. In multivariable models, both D-dimer and E-selectin were associated with pollutants, specifically PM2.5 and NOx (see table). There was no association between pollutants and CRP, fibrinogen or sICAM-1. In conclusion, these data are consistent with the hypothesis that associations between long-term exposure to particulate and traffic-related air pollution and CVD may be related to endothelial activation and fibrinolysis.