European journal of preventive cardiology · 2026
Long-term ambient air pollution exposure and coronary calcium score in men: insights from the DANCAVAS study.
СтатьяМногоцентровое исследованиеНазвание и аннотация: Перевод в очереди
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Mohamed Roda Abdulkadir, Peronard Mayntz Stephan, Møller Jens-Jakob Kjer, Mejldal Anna, Schultz Overgaard Katrine, Rueskov Andersen Thomas, Madsen Freja Sønder, Frohn Lise Marie, Brandt Jørgen, Ketzel Matthias, Khan Jibran, Egstrup Kenneth, Diederichsen Axel, Lindholt Jes Sanddal, Lambrechtsen Jess
Аннотация
AIMS: This study assessed the relationship between air pollution exposure, fine particulate matter ≤2.5 µm (PM2.5) and nitrogen dioxide (NO2), and coronary calcium score (CCS) in a cohort of 60-75-year-old men from the Danish Cardiovascular Screening Trials (DANCAVAS).
METHODS AND RESULTS: A total of 12 301 participants were included. Residential and novel workplace address spanning up to 40 years was geocoded. Air pollution exposure was modelled using the Danish Eulerian Hemisphere model (DEHM)/Urban Background Model (UBM)/AirGIS system. Median PM2.5 exposure was 13.7 µg/m3 (interquartile range [IQR]: 13.2-14.1). The median NO2 exposure was 16.3 µg/m3 (IQR: 14.7-18.4). The median CCS was 99 (IQR: 8-410). The primary outcome was CCS ≥ 100, secondary outcomes included CCS ≥ 400 and ordinal-scaled CCS (0, 1-99, 100-399, 400-999, and >999). Binary logistic regression analyses revealed no significant associations; however, generalized ordinal logistic regression analysis of CCS indicated that PM2.5 exposure was associated with coronary artery calcification (CAC) presence (CCS = 0 vs. CCS ≥ 1) with an adjusted odds ratio = 1.11 (95% confidence interval: 1.04-1.18) per 1 µg/m3 increase in PM2.5. No associations were observed for higher CAC categories. The findings for NO2 were non-significant. Addition of workplace exposure showed only moderate changes in effect estimates.
CONCLUSION: Exposure to PM2.5 was modestly associated with the presence of CAC, particularly when combining residential and workplace exposures. No consistent associations were observed with NO2 or advanced stages of calcification. Findings suggest that long-term ambient PM2.5 exposure may contribute to early subclinical atherosclerotic changes; however, modest effect sizes and lack of association with CAC severity call for cautious interpretation.
METHODS AND RESULTS: A total of 12 301 participants were included. Residential and novel workplace address spanning up to 40 years was geocoded. Air pollution exposure was modelled using the Danish Eulerian Hemisphere model (DEHM)/Urban Background Model (UBM)/AirGIS system. Median PM2.5 exposure was 13.7 µg/m3 (interquartile range [IQR]: 13.2-14.1). The median NO2 exposure was 16.3 µg/m3 (IQR: 14.7-18.4). The median CCS was 99 (IQR: 8-410). The primary outcome was CCS ≥ 100, secondary outcomes included CCS ≥ 400 and ordinal-scaled CCS (0, 1-99, 100-399, 400-999, and >999). Binary logistic regression analyses revealed no significant associations; however, generalized ordinal logistic regression analysis of CCS indicated that PM2.5 exposure was associated with coronary artery calcification (CAC) presence (CCS = 0 vs. CCS ≥ 1) with an adjusted odds ratio = 1.11 (95% confidence interval: 1.04-1.18) per 1 µg/m3 increase in PM2.5. No associations were observed for higher CAC categories. The findings for NO2 were non-significant. Addition of workplace exposure showed only moderate changes in effect estimates.
CONCLUSION: Exposure to PM2.5 was modestly associated with the presence of CAC, particularly when combining residential and workplace exposures. No consistent associations were observed with NO2 or advanced stages of calcification. Findings suggest that long-term ambient PM2.5 exposure may contribute to early subclinical atherosclerotic changes; however, modest effect sizes and lack of association with CAC severity call for cautious interpretation.