Assessing ambient fine particulate matter exposure and associations with coronary artery calcification

Long-term exposure ambient particulate matter (PM2.5) may be associated with atherosclerosis, increasing the risk of adverse cardiovascular outcomes. Few studies have previously examined this relationship, with most research focusing on two different cohorts: the Multi-Ethnic Study and Atherosclerosis (MESA) and the Heinz-Nixdorf Recall Study (HNRS). While several methods are used to assess the risk of cardiovascular outcomes, this study focuses on coronary artery calcification (CAC) as an indicator of atherosclerosis and, therefore, poor cardiovascular health. This study aimed to find associations between ambient PM2.5 concentrations, inflammatory and cardiovascular-specific biomarkers, and CAC. Utilizing data from the Heart Strategies Concentrating on Risk Evaluation (Heart SCORE) cohort in Allegheny County, PA, CAC scores were collected from 724 participants in cohort from 2003-2008 (aged 45-75 years). A general inflammatory marker, Interleukin-6, the cardiovascular-specific augmentation index normalized to 75 beats per minute (AI75), and the Framingham Index (FRHI) were also collected. PM2.5 exposure concentrations were determined via active sampling and Land Use Regression (LUR). Each participant’s exposure was designated as the PM2.5 concentration from the prior year within 300 meters of their address.\ud All examinations considered potential confounding from age, sex, and race. Statistically significant (p < 0.05) associations were found for PM2.5 and IL-6 (0.092), as well as between AI75 and CAC (-0.009). Pairwise correlations between PM2.5 and IL-6 (0.05) as well AI75 and FRHI (0.16) were also significant. Comparison of the 90th and 10th percentiles of PM2.5 exposure showed a 74.55 HU difference in Agatston score for individuals with presence of CAC. No significant association was found between these exposure percentiles and the whether an individual developed CAC.\ud To date, this is one of the few studies to examine PM2.5 exposure associations to atherosclerotic risk using CAC as opposed to CIMT outside of MESA and HNRS. While the analysis found suggestive evidence of a direct link between CAC and ambient PM2.5, the results were not statistically significant. Pairwise correlations between components of the hypothesized pathway were statistically significant, albeit weak. Understanding the association between PM2.5 and CAC can impact primary and secondary public health prevention efforts for cardiovascular disease