Hongjing Shi, Si Cheng, D J Y Sun, Yuting Han, Canqing Yu, D J Y Sun, P Pei, Ling Yang, Yuehua Chen, H D Du, Lingli Chen, Dan Schmidt, J S Chen, Z M Chen, Liming Li, J N Wei, Jun Lv, Robert Clarke, Rory Collins, Richard Peto, Robin Walters, Jun Lv, Yuanjie Pang, Can Hou, Qingmei Xia, Chao Liu, Lang Pan, Xiao Han, Honglu Bian, Xinxin Chen, Daniel Avery, Maxim Barnard, Derrick Bennett, Ruth Boxall, Jonathan Clarke, Ahmed Edris Mohamed, Hannah Fry, Prapthi Harish, Pek Kei Im, Andri Iona, Christiana Kartsonaki, Kshitij Kolhe, Hubert Lam, Kuang Lin, James Liu, Iona Millwood, Sam Morris, Qunhua Nie, Alfred Pozarickij, Maryam Rahmati, Paul Ryder, Maruf Sarder, Becky Stevens, Iain Turnbull, Baihan Wang, Lin Wang, Neil Wright, Xiaoming Yang, Pang Yao, Zengchang Pang, Ruqin Gao, Kunzheng Lv, Shanpeng Li, Haiping Duan, Shaojie Wang, Yongmei Liu, Ranran Du, Liang Cheng, Xiaocao Tian, Hua Zhang, Dan Hu, Xiaoyan Zheng, Yujie Wang, Wei Sun, Shichun Yan, Yong Zhou, Chi Wang, Zhenyuan Wu, Lishun Zhai, Zhaoxi Pang, Shiwen Dong, Li Liu, Dapeng Yin, Bin He, Ying Liu, Xingren Wang, Ou Ty, Xiangyang Zheng, Dewei Zheng, Shuai Yang, Lihui Li, Xingjiao Chen, Yan Xu, Jinyi Zhou, R C Tao, Jian Su, Xikang Fan, Xuejia Chen, Yuxiao Huang, Yan Lu
BackgroundEvidence linking components of particulate matter with diameters ≤2.5 μm (PM2.5) to the incidence of cardiovascular disease (CVD) remains scarce and inconsistent. ObjectivesThe aim of this study was to investigate the associations of long-term exposure to PM2.5 components with incident CVD risk, considering both absolute concentrations and relative proportions. MethodsThis study included 487,037 participants from the China Kadoorie Biobank who were free of CVD or cancer at baseline. Three-year moving average concentrations of PM2.5 and its components (black carbon [BC], organic matter, chloride [Cl−], nitrate [NO3−], sulfate [SO42−], and ammonium [NH4+]) were geocoded to participants at 1 × 1 km resolution according to their community recruitment clinic locations. Time-varying Cox proportional hazards models were used to evaluate the associations between PM2.5 components and incident CVD risk. Substitution models were used to estimate the effects of reallocating PM2.5 component proportions while keeping total PM2.5 mass constant, thereby evaluating changes in CVD risk associated with shifts in component composition. ResultsOver a median 15.1-year follow-up, a total of 196,224 CVD cases, including 72,747 of ischemic heart disease, 74,594 of ischemic stroke, 17,553 of hemorrhagic stroke, and 54,306 of other cerebrovascular diseases, were documented. Long-term exposure to PM2.5 components was associated with increased risk for CVD and its major subtypes. For total CVD, the HRs per IQR increase were 1.15 (95% CI: 1.13-1.17) for BC, 1.17 (95% CI: 1.15-1.18) for organic matter, 1.28 (95% CI: 1.25-1.32) for Cl−, 1.29 (95% CI: 1.24-1.33) for NO3−, and 1.23 (95% CI: 1.20-1.25) for SO42−. Higher proportions of Cl−, SO42−, and BC were associated with an increased risk for ischemic stroke, and the aforementioned inorganic ions were also positively associated with ischemic heart disease. Substituting 1% of any other PM2.5 component with Cl− was associated with a 3% to 8% higher risk for total CVD, whereas substitutions with BC were associated with a 1% to 8% higher risk for ischemic stroke, and substitution with SO42− was associated with a 2% to 5% higher risk for ischemic heart disease. ConclusionsLong-term exposure to PM2.5 chemical components was positively associated with CVD risk. Critically, CVD risk was influence by compositional shifts, with a particularly hazardous profile characterized by higher proportions of Cl−, BC, or SO42−. These findings underscore the importance of implementing targeted, health-oriented control strategies that prioritize specific PM2.5 components.