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A nationwide case-crossover study uncovers the link between traffic-related PM2.5 and acute coronary syndrome incidence, suggesting urgent emission reduction measures.
The transportation sector powered by fossil fuels is a significant contributor to PM2.5 pollution. Systematic evaluation of traffic-related PM2.5 on acute coronary syndrome (ACS) onset is not yet characterized, and the health benefits of reduced traffic-related PM2.5 and evidence-based mitigation strategies are currently absent. We investigated the association of ACS onset with short-term traffic-related PM2.5 exposure in a nationwide time-stratified case-crossover study, using 627,828 ACS cases extracted from the China Cardiovascular Association. We evaluated the risks of ACS onset associated with traffic-related PM2.5, calculated the attributable onsets, and then conducted cluster analysis using the K-means algorithm to identify priority cities for emission reduction. We found a robust association between traffic-related PM2.5 and ACS onset, i.e., an increased risk of 2.39% (95% CI: 1.79–3.00%) for same-day (lag 0) PM2.5 per 10 μg/m3 increase. The greatest health benefits due to a 1 μg/m3 PM2.5 reduction were achieved by traffic-related PM2.5, reaching 10,267 (95%CI: 4503–16,063) onsets per year. In addition, three obvious categories were clustered, and traffic-polluted cities were highlighted (cluster 2, not belonging to megacities), with high emissions and concentrations of traffic-related PM2.5. Therefore, intensified efforts to mitigate traffic-related PM2.5 emissions should be promoted, and the prioritization of emission reduction strategies in these traffic-polluted cities is imperative for safeguarding public health.
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Du et al. (2026) studied this question.
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