Hourly Air Pollutants and Acute Coronary Syndrome Onset in 1.29 Million Patients

Circulation. 2022 Jun 14;145(24):1749-1760. doi: 10.1161/CIRCULATIONAHA.121.057179. Epub 2022 Apr 22.


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.

Keywords: acute coronary syndrome; air pollution; particulate matter.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Coronary Syndrome* / epidemiology
  • Air Pollutants* / analysis
  • Air Pollutants* / toxicity
  • Air Pollution* / adverse effects
  • Air Pollution* / analysis
  • Carbon Monoxide / analysis
  • Carbon Monoxide / toxicity
  • China / epidemiology
  • Cities / epidemiology
  • Cross-Over Studies
  • Environmental Exposure* / adverse effects
  • Environmental Exposure* / analysis
  • Humans
  • Nitrogen Dioxide / analysis
  • Nitrogen Dioxide / toxicity
  • Ozone / analysis
  • Ozone / toxicity
  • Particulate Matter / analysis
  • Particulate Matter / toxicity
  • Sulfur Dioxide / analysis
  • Sulfur Dioxide / toxicity
  • Time Factors


  • Air Pollutants
  • Particulate Matter
  • Sulfur Dioxide
  • Ozone
  • Carbon Monoxide
  • Nitrogen Dioxide