Air pollution in relation to very short-term risk of ST-segment elevation myocardial infarction : Case-crossover analysis of SWEDEHEART
(2019) In International Journal of Cardiology 275. p.26-30- Abstract
Objective: Studies 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. Methods: We 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... (More)
Objective: Studies 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. Methods: We 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. Results: Risk 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. Conclusion: Risk 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.
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- author
- Sahlén, Anders ; Ljungman, Petter ; Erlinge, David LU ; Chan, Mark Y. ; Yap, Jonathan ; Hausenloy, Derek J. ; Yeo, Khung Keong and Jernberg, Tomas
- organization
- publishing date
- 2019-01-15
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Air pollution, ST-elevation myocardial infarction, Weather
- in
- International Journal of Cardiology
- volume
- 275
- pages
- 26 - 30
- publisher
- Elsevier
- external identifiers
-
- scopus:85055648315
- pmid:30509372
- ISSN
- 0167-5273
- DOI
- 10.1016/j.ijcard.2018.10.069
- language
- English
- LU publication?
- yes
- id
- 7f0c7ff6-9f4c-4b22-a96b-826862557458
- date added to LUP
- 2018-12-14 15:45:42
- date last changed
- 2024-04-01 15:41:43
@article{7f0c7ff6-9f4c-4b22-a96b-826862557458, abstract = {{<p>Objective: Studies 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. Methods: We 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 (SO<sub>2</sub>), nitrogen dioxide (NO<sub>2</sub>), ozone and particulate pollutants (PM<sub>2.5</sub>, PM<sub>10</sub>) were studied in conditional logistic regression models for interquartile range increments. Results: Risk of STEMI (n = 14,601) was associated with NO<sub>2</sub> (strongest at 15-h lag) and with PM<sub>2.5</sub> (strongest at 20-h lag), in single-pollutant models adjusting for air temperature and humidity (NO<sub>2</sub>: odds ratio (OR; 95% confidence interval) 1.065 (1.031–1.101); PM<sub>2.5</sub>: 1.026 (1.001–1.054)). After adjusting models for atmospheric pressure (significantly associated with STEMI risk at 14–24-h lags), NO<sub>2</sub> remained highly statistically significant (1.057 (1.022–1.094)) but not PM<sub>2.5</sub> (1.024 (0.997–1.052)). No associations were seen for SO<sub>2</sub>, ozone or PM<sub>10</sub>. Conclusion: Risk of STEMI rises within hours of exposure to air pollutants, with strongest impact of NO<sub>2</sub>. These findings are complementary to earlier reports which have not acknowledged widely the importance of very short-term fluctuations in air pollution.</p>}}, author = {{Sahlén, Anders and Ljungman, Petter and Erlinge, David and Chan, Mark Y. and Yap, Jonathan and Hausenloy, Derek J. and Yeo, Khung Keong and Jernberg, Tomas}}, issn = {{0167-5273}}, keywords = {{Air pollution; ST-elevation myocardial infarction; Weather}}, language = {{eng}}, month = {{01}}, pages = {{26--30}}, publisher = {{Elsevier}}, series = {{International Journal of Cardiology}}, title = {{Air pollution in relation to very short-term risk of ST-segment elevation myocardial infarction : Case-crossover analysis of SWEDEHEART}}, url = {{http://dx.doi.org/10.1016/j.ijcard.2018.10.069}}, doi = {{10.1016/j.ijcard.2018.10.069}}, volume = {{275}}, year = {{2019}}, }