Key result
Long-term PM2.5 exposure shows no independent association with coronary disease severity or calcium score.
Why the study?
Does long-term PM2.5 exposure increase coronary artery disease severity and calcification in individuals undergoing CCTA?
Cohort (n=1,107)
Does long-term PM2.5 exposure increase coronary artery disease severity and calcification in individuals undergoing CCTA?
p-value: p=>0.05
Traditional cardiovascular risk factors and age have a more substantial influence on coronary disease severity and calcification than long-term PM2.5 exposure in this highly polluted urban cohort.
Background Air pollution, particularly fine particulate matter (PM2.5), has been implicated in the development of cardiovascular disease. Coronary Artery Disease Reporting and Data System (CAD-RADS) scoring provides a standardized measure of coronary atherosclerosis severity. Whether chronic exposure to PM2.5 correlates with higher CAD-RADS categories and coronary artery calcification (CAC) remains unclear. Purpose To evaluate the relationship between PM2.5 long-term exposure and the severity of coronary artery disease, as classified by CAD-RADS, in a cohort undergoing coronary computed tomography angiography (CCTA). Methods A total of 1,107 individuals of a highly polluted city underwent CCTA between 2020-2021 and were stratified by CAD-RADS categories. Mean 11-year exposure to PM2.5 was estimated by spatial analysis of data from Tehran air pollution monitoring stations based on their home addresses, and participants were also grouped by quartiles (Q1–Q4) of PM2.5 levels. Differences across groups were assessed using appropriate statistical tests. Linear, multinomial, and binary logistic regression models evaluated the predictive value of PM2.5 for increasing CAD-RADS categories, calcification, and involved segments. Results In this cohort of 1,107 participants, higher CAD-RADS categories were significantly associated with older age (p<0.001), greater lesion burden (number, volume, and mass; all p<0.001), and higher calcium scores (p<0.001), with participants in CAD-RADS 3 and 4 also showing higher rates of diabetes, hypertension, and dyslipidemia. Mean PM2.5 levels did not differ across CAD-RADS categories (p=0.137) and showed no clear pattern when stratifying individuals by quartiles of exposure. Intriguingly, those in the lowest PM2.5 quartile (Q1) were older (51.79±10.44 years) and displayed higher lesion volumes and calcium scores compared to those in the highest quartile (Q4) (p<0.01), suggesting that traditional risk factors closely tied to age may outweigh any discernible effect of PM2.5 in this population. Indeed, in both multinomial/binary and linear regression analyses, adjusting for age, sex, diabetes, hypertension, dyslipidemia, and exercise intensity, mean PM2.5 exposure did not independently predict CAD-RADS severity, lesion characteristics, or calcium score (all p>0.05). Conclusion In this study of 1,107 participants, higher CAD-RADS categories, lesion burden and calcium scores were consistently associated with older age and traditional cardiovascular risk factors (diabetes, hypertension, dyslipidemia). These findings indicate that traditional risk factors have a more substantial influence on coronary disease severity than PM2.5 exposure within this population, though longitudinal studies remain necessary to determine whether chronic air pollution contributes to disease progression over time
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Houshmand et al. (2025) conducted a cohort in Coronary artery disease (n=1,107). PM2.5 long-term exposure vs. Lower PM2.5 exposure was evaluated on CAD-RADS severity, lesion characteristics, and calcium score (p=>0.05). Long-term PM2.5 exposure did not independently predict CAD-RADS severity, lesion characteristics, or calcium score after adjusting for traditional cardiovascular risk factors (all p>0.05).
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