Key result
Higher PM2.5, PM10, and black carbon exposure linked to increased right coronary fat attenuation index.
Why the study?
Particulate matter accelerates atherosclerosis through systemic inflammation, but its specific impact on local coronary inflammation remains poorly understood.
Does long-term exposure to particulate matter increase coronary inflammation assessed by pericoronary fat attenuation index in patients with suspected coronary artery disease?
Cohort (n=5,528)
Does long-term exposure to particulate matter increase coronary inflammation assessed by pericoronary fat attenuation index in patients with suspected coronary artery disease?
Effect estimate: Increase of 7.57, 8.72, and 2.35 HU in the right coronary artery per IQR increase in PM2.5, PM10, and BC
Long-term exposure to ambient particulate matter is associated with increased localized coronary inflammation, providing a toxicological link between air pollution and coronary pathophysiology.
PM exposure was associated with higher FAI; leaves open whether pollution reduction mitigates coronary inflammation.
Particulate matter (PM) is known to accelerate atherosclerosis through systemic inflammation, yet its specific impact on local coronary inflammation remains poorly understood. This large-scale retrospective cohort study investigated the long-term effects of PM exposure on coronary inflammation as assessed by the pericoronary fat attenuation index (FAI). We analyzed 5,528 participants undergoing coronary computed tomography angiography (CCTA), including a longitudinal subcohort of 656 individuals with serial scans. FAI values for the left anterior descending, left circumflex, and right coronary arteries were extracted using a deep-learning-based pipeline. Individual-level exposures to fine particulate with an aerodynamic diameter <2.5μm (PM 2.5 ), particulate matter with an aerodynamic diameter of less than 10μm (PM 10 ), and black carbon (BC) were estimated using a validated 1-km resolution spatiotemporal model. Results from generalized additive and linear mixed-effects models indicated that each interquartile range (IQR) increase in 1-year PM 2.5 , PM 10 , and BC exposure was associated with significant elevations in FAI across all vessels, such as increases of 7.57, 8.72, and 2.35 HU in the right coronary artery, respectively. Furthermore, longitudinal analysis revealed that IQR increases in pollutants corresponded to accelerated annual FAI progression. These associations were notably stronger among participants with hypertension, diabetes, or a history of smoking. In conclusion, among patients with suspected coronary artery disease, long-term exposure to PM is intrinsically linked to localized and progressive coronary inflammation. These findings provide a proximal toxicological link between ambient pollution and coronary pathophysiology, underscoring the urgency of integrating environmental determinants into cardiovascular risk assessment and prevention strategies for vulnerable populations.
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Xu et al. (2026) conducted a cohort in Suspected coronary artery disease (n=5,528). Long-term particulate matter and black carbon exposure vs. Lower exposure levels was evaluated on Coronary inflammation assessed by pericoronary fat attenuation index (FAI) (Increase of 7.57, 8.72, and 2.35 HU in the right coronary artery per IQR increase in PM2.5, PM10, and BC). Each interquartile range increase in 1-year PM2.5, PM10, and black carbon exposure significantly increased right coronary artery fat attenuation index by 7.57, 8.72, and 2.35 HU, respectively.
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