Renjie Chen1, Yixuan Jiang1, Jialu Hu2, Honglei Chen3, Huichu Li4, Xia Meng1, John S Ji5, Ya Gao1, Weidong Wang1, Cong Liu1, Weiyi Fang6, Hongbing Yan7,8, Jiyan Chen9, Weimin Wang10, Dingcheng Xiang11, Xi Su12, Bo Yu13,14, Yan Wang15, Yawei Xu16, Lefeng Wang17, Chunjie Li18, Yundai Chen19, Michelle L Bell20, Aaron J Cohen21,22, Junbo Ge2, Yong Huo23, Haidong Kan1,24. 1. School of Public Health, Key Lab of Public Health Safety of the Ministry of Education and National Health Commission Key Lab of Health Technology Assessment, Fudan University' Shanghai' China (R.C., Y.J., X.M., Y.G., Weidong Wang, C. Liu, H.K.). 2. Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China (J.H., J.G.). 3. Department of Epidemiology and Biostatistics, College of Human Medicine, Michigan State University, East Lansing, MI (H.C.). 4. Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA (H.L.). 5. Vanke School of Public Health, Tsinghua University, Beijing, China (J.S.J.). 6. Department of Cardiology, Huadong Hospital Affiliated to Fudan University, Shanghai, China (W.F.). 7. Center for Coronary Artery Diseases, Chinese Academy of Medical Sciences in Shenzhen, Shenzhen, China (H.Y.). 8. Center for Coronary Artery Diseases, Chinese Academy of Medical Sciences, Beijing, China (H.Y.). 9. Department of Cardiology, Guangdong Provincial People's Hospital, Guangzhou, China (J.C.). 10. Department of Cardiology, Peking University People's Hospital, Beijing, China (Weimin Wang). 11. Department of Cardiology, General Hospital of Southern Theater Command, Guangzhou, China (D.X.). 12. Department of Cardiology, Wuhan ASIA General Hospital, Wuhan, China (X.S.). 13. Department of Cardiology, The 2nd Affiliated Hospital of Harbin Medical University, Harbin, China (B.Y.). 14. The Key Laboratory of Myocardial Ischemia, Chinese Ministry of Education, Harbin, China (B.Y.). 15. Department of Cardiology, Xiamen Cardiovascular Hospital Xiamen University, Xiamen' China (Y.W.). 16. Department of Cardiology, Shanghai Tenth People's Hospital, Shanghai, China (Y.X.). 17. Heart Center and Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China (L.W.). 18. Department of Emergency, Tianjin Chest Hospital, Tianjin' China (C. Li). 19. Department of Cardiology, Chinese PLA General Hospital, Beijing, China (Y.C.). 20. School of Forestry and Environmental Studies, Yale University, New Haven, CT (M.L.B.). 21. Health Effects Institute, Boston, MA (A.J.C.). 22. Institute for Health Metrics and Evaluation, University of Washington, Seattle' WA (A.J.C.). 23. Department of Cardiology, Peking University First Hospital, Beijing, China (Y.H.). 24. Children's Hospital of Fudan University, National Center for Children's Health, Shanghai, China (H.K.).
Abstract
BACKGROUND: Short-term exposure to ambient air pollution has been linked with daily hospitalization and mortality from acute coronary syndrome (ACS); however, the associations of subdaily (hourly) levels of criteria air pollutants with the onset of ACS and its subtypes have rarely been evaluated. METHODS: We conducted a time-stratified case-crossover study among 1 292 880 patients with ACS from 2239 hospitals in 318 Chinese cities between January 1, 2015, and September 30, 2020. Hourly concentrations of fine particulate matter (PM2.5), coarse particulate matter (PM2.5-10), nitrogen dioxide (NO2), sulfur dioxide (SO2), carbon monoxide (CO), and ozone (O3) were collected. Hourly onset data of ACS and its subtypes, including ST-segment-elevation myocardial infarction, non-ST-segment-elevation myocardial infarction, and unstable angina, were also obtained. Conditional logistic regressions combined with polynomial distributed lag models were applied. RESULTS: Acute exposures to PM2.5, NO2, SO2, and CO were each associated with the onset of ACS and its subtypes. These associations were strongest in the concurrent hour of exposure and were attenuated thereafter, with the weakest effects observed after 15 to 29 hours. There were no apparent thresholds in the concentration-response curves. An interquartile range increase in concentrations of PM2.5 (36.0 μg/m3), NO2 (29.0 µg/m3), SO2 (9.0 µg/m3), and CO (0.6 mg/m3) over the 0 to 24 hours before onset was significantly associated with 1.32%, 3.89%, 0.67%, and 1.55% higher risks of ACS onset, respectively. For a given pollutant, the associations were comparable in magnitude across different subtypes of ACS. NO2 showed the strongest associations with all 3 subtypes, followed by PM2.5, CO, and SO2. Greater magnitude of associations was observed among patients older than 65 years and in the cold season. Null associations of exposure to either PM2.5-10 or O3 with ACS onset were observed. CONCLUSIONS: The results suggest that transient exposure to the air pollutants PM2.5, NO2, SO2, or CO, but not PM2.5-10 or O3, may trigger the onset of ACS, even at concentrations below the World Health Organization air quality guidelines.
BACKGROUND: Short-term exposure to ambient air pollution has been linked with daily hospitalization and mortality from acute coronary syndrome (ACS); however, the associations of subdaily (hourly) levels of criteria air pollutants with the onset of ACS and its subtypes have rarely been evaluated. METHODS: We conducted a time-stratified case-crossover study among 1 292 880 patients with ACS from 2239 hospitals in 318 Chinese cities between January 1, 2015, and September 30, 2020. Hourly concentrations of fine particulate matter (PM2.5), coarse particulate matter (PM2.5-10), nitrogen dioxide (NO2), sulfur dioxide (SO2), carbon monoxide (CO), and ozone (O3) were collected. Hourly onset data of ACS and its subtypes, including ST-segment-elevation myocardial infarction, non-ST-segment-elevation myocardial infarction, and unstable angina, were also obtained. Conditional logistic regressions combined with polynomial distributed lag models were applied. RESULTS: Acute exposures to PM2.5, NO2, SO2, and CO were each associated with the onset of ACS and its subtypes. These associations were strongest in the concurrent hour of exposure and were attenuated thereafter, with the weakest effects observed after 15 to 29 hours. There were no apparent thresholds in the concentration-response curves. An interquartile range increase in concentrations of PM2.5 (36.0 μg/m3), NO2 (29.0 µg/m3), SO2 (9.0 µg/m3), and CO (0.6 mg/m3) over the 0 to 24 hours before onset was significantly associated with 1.32%, 3.89%, 0.67%, and 1.55% higher risks of ACS onset, respectively. For a given pollutant, the associations were comparable in magnitude across different subtypes of ACS. NO2 showed the strongest associations with all 3 subtypes, followed by PM2.5, CO, and SO2. Greater magnitude of associations was observed among patients older than 65 years and in the cold season. Null associations of exposure to either PM2.5-10 or O3 with ACS onset were observed. CONCLUSIONS: The results suggest that transient exposure to the air pollutants PM2.5, NO2, SO2, or CO, but not PM2.5-10 or O3, may trigger the onset of ACS, even at concentrations below the World Health Organization air quality guidelines.
Entities:
Keywords:
acute coronary syndrome; air pollution; particulate matter