Abstract 4366892: Air Pollution, Social Vulnerability, and Cardiovascular Outcomes in Individuals With Coronary Artery Disease

Abstract

Background: Ambient air pollutants such as fine particulate matter (PM 2.5 ), nitrogen oxides (NO x ), and carbon monoxide (CO) contribute to cardiovascular (CV) morbidity. However, the role of social vulnerability in modifying pollution-related CV risk remains underexplored, especially in high-risk populations with coronary artery disease (CAD). We evaluated the associations between air pollutant exposures, the Social Vulnerability Index (SVI), and CV outcomes, hypothesizing that higher exposures would be associated with worse outcomes, particularly among socially vulnerable individuals. Methods: The study consisted of 1,602 participants (mean age of 62, 63% men, 62% White race, 31% Black race) undergoing coronary angiography enrolled in the Emory Cardiovascular Biobank. Participants were stratified into high vs. low pollutant exposure groups based on pollutant medians (PM 2.5 : 10.6 μg/m 3 ; NO x : 39.4 ppb; CO: 635 ppb) estimated at residential address using a 250m-resolution model. Clinical characteristics and SVI domains (socioeconomic status, household characteristics, racial/ethnic minority status, housing and transportation, and overall SVI ranking) were compared between high vs. low pollutant groups. SVI domain scores were obtained from the CDC/ATSDR Social Vulnerability Index linked by residential census tract. Cox models assessed associations between pollutants and CV outcomes (CV death, myocardial infarction [MI], stroke, heart failure [HF], and their composite [MACE]), and tested for effect modification by SVI domains. Results: Participants with hypertension, female sex, and higher SVI were more likely to fall in the high PM 2.5 group (all p<0.05). Similar gradients were observed across NO x and CO strata. In adjusted models, PM 2.5 and CO were significantly associated with increased MACE (PM 2.5 : HR 1.73, p=0.002; CO: HR 1.001, p=0.005), and PM 2.5 was associated with HF (HR 1.16, p=0.003). SVI significantly modified the relationship between air pollution and CV events with stronger pollutant-outcome associations among those with higher SVI—particularly for NO x and risk of HF (p=0.033) and stroke (p=0.025), and for CO and HF (p=0.046). Conclusion: In patients with CAD, PM 2.5 and CO exposure were associated with increased risk of MACE. Social vulnerability amplified the adverse effects of NO x and CO exposures on CV events highlighting the need to consider neighborhood-level social determinants of health in pollution-related CV disease prevention efforts.