Chronic PM_2.5 Exposure Is Associated With Invasively Assessed Coronary Endothelial Dysfunction.

Abstract (English)

BACKGROUND: Coronary endothelial dysfunction (ED) represents an early stage of coronary artery disease (CAD). Several factors may induce ED. Air pollution, more specifically particulate matter <2.5 &#x3bc;m (PM_2.5), has emerged as a major nontraditional cardiovascular risk factor contributing to early vascular injury, but its impact on coronary ED remains poorly defined. OBJECTIVES: In this study, we sought to identify an association between chronic PM_2.5 exposure and epicardial endothelial dysfunction (EED) determined by means of invasive coronary vasoreactivity testing, the criterion standard technique to assess EED. METHODS: This observational study included prospectively enrolled patients with angina and nonobstructive CAD who underwent coronary reactivity testing at Mayo Clinic from 2000 to 2023. Residential addresses at the time of testing were geocoded to derive monthly PM_2.5 exposure at a 0.01&#xb0; &#xd7; 0.01&#xb0; spatial resolution, averaged over the 2 years preceding testing. EED was defined as percentage change of less than -20% in coronary artery diameter in response to acetylcholine infusion. Associations between continuous PM_2.5 and EED were assessed according to a generalized propensity score with a gamma-distributed model to derive stabilized inverse probability weights, applied in multivariable logistic regression. RESULTS: A total of 1,485 patients with a median age of 51.7 years (Q1-Q3: 42.7-60.1 years) were included in the analysis. Individuals exposed to PM_2.5 above environmental protection agency standards (9 &#x3bc;g/m³) were younger and had less cardiovascular comorbidities, although they had worse lipid profiles. In weighted multivariable logistic regression, each 1 &#x3bc;g/m³ increase in PM_2.5 was associated with increased odds of EED (OR: 1.078; 95% CI: 1.021-1.139; P = 0.007), adjusted for age, sex, body mass index, and cardiovascular comorbidities. CONCLUSIONS: Chronic PM_2.5 exposure is associated with epicardial coronary ED, suggesting a potential biological link between PM_2.5 and CAD.