Air pollution in relation to very short-term risk of ST-segment elevation myocardial infarction: Case-crossover analysis of SWEDEHEART

Abstract

ObjectiveStudies have related air pollution to myocardial infarction (MI) events over days or weeks, with few data on very short-term risks. We studied risk of ST-segment elevation MI (STEMI) within hours of exposure to air pollution while adjusting for weather. MethodsWe performed a case-crossover study of STEMI cases in Stockholm, Sweden (Jan 2000–June 2014) based on SWEDEHEART. Exposures during hazard periods up to 24 h prior to admission were compared to bidirectionally sampled control periods. Risks attributable to sulphur dioxide (SO2), nitrogen dioxide (NO2), ozone and particulate pollutants (PM2.5, PM10) were studied in conditional logistic regression models for interquartile range increments. ResultsRisk of STEMI (n = 14,601) was associated with NO2 (strongest at 15-h lag) and with PM2.5 (strongest at 20-h lag), in single-pollutant models adjusting for air temperature and humidity (NO2: odds ratio (OR; 95% confidence interval) 1.065 (1.031–1.101); PM2.5: 1.026 (1.001–1.054)). After adjusting models for atmospheric pressure (significantly associated with STEMI risk at 14–24-h lags), NO2 remained highly statistically significant (1.057 (1.022–1.094)) but not PM2.5 (1.024 (0.997–1.052)). No associations were seen for SO2, ozone or PM10. ConclusionRisk of STEMI rises within hours of exposure to air pollutants, with strongest impact of NO2. These findings are complementary to earlier reports which have not acknowledged widely the importance of very short-term fluctuations in air pollution.