Abstract
BACKGROUND AND AIMS: While exposure to fine particulate matter (PM2.5) is linked to cardiovascular diseases (CVDs), the specific roles of individual constituents remain unclear. This study assessed differential associations of major PM2.5 constituents with 12 CVD outcomes.
METHODS: We included 477,853 CVDs-free individuals at baseline from the UK Biobank and followed them prospectively for incident CVDs. Exposure levels to total PM2.5 mass and its major constituents, including elemental carbon, organic matter, ammonium, nitrate, and sulfate. Time-varying Cox models evaluated associations with incident CVDs. We used quantile g-computation to assess the relative contribution of each constituent and conducted counterfactual analyses to estimate preventable disease burdens.
RESULTS: During a median follow-up of 12.3 years, 68,806 participants (14.4%) developed incident CVDs. PM2.5 was associated with higher risks across most CVDs, with hazard ratios (HRs) ranging from 1.14 to 1.22. Among individual constituents, sulfate demonstrated the strongest associations overall, particularly with peripheral vascular disease (HR = 1.55; 1.47-1.62) and thoracic aortic aneurysm (HR = 1.54; 1.40-1.68). Ammonium was most associated with intracerebral hemorrhage (HR = 1.27; 1.16-1.38) and abdominal aortic aneurysm (HR = 1.23; 1.14-1.32). Sulfate contributed the largest share to the overall PM2.5-CVD burden (84.6%-91.3% of joint effect). Counterfactual reductions of constituents to the 5th percentile suggested potential decreases in PM2.5-related CVD burden, with the largest proportional reductions observed for sulfate and ammonium.
CONCLUSIONS: Long-term exposure to PM2.5 constituents, especially sulfate and ammonium, substantially raises CVDs risk. These findings support targeted emission controls focusing on specific PM2.5 fractions to maximize cardiovascular health benefits.