Short-term exposure to ambient air pollution has been linked with daily hospitalization and mortality of acute coronary syndrome (ACS); however, the associations of sub-daily (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 ACS patients from 2,239 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 subtype. These associations were strongest in the concurrent hour of exposure and were attenuated thereafter, with the weakest effects observed after 15-29 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 0-24 hours preceding 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. Generally, NO2 showed the strongest associations with all three subtypes, followed by PM2.5, CO, and SO2. Greater magnitude of associations was observed among patients older than 65, without a history of smoking or chronic cardiorespiratory diseases, 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 of PM2.5, NO2, SO2, 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