Abstract
ObjectivesTo assess the association between traffic-related ambient air pollution and emergency hospital visits for cardiac arrest.DesignCase–crossover design was used with a lag time to 4 days.SettingThe Reykjavik capital area and the study population was the inhabitants 18 years and older identified by encrypted personal identification numbers and zip codes.Participants and exposureCases were those with emergency visits to Landspitali University Hospital during the period 2006–2017 and who were given the primary discharge diagnosis of cardiac arrest according to the International Classification of Diseases 10th edition (ICD-10) code I46. The pollutants were nitrogen dioxide (NO2), particulate matter with aerodynamic diameter less than 10 µm (PM10), particulate matter with aerodynamic diameter less than 2.5 µm (PM2.5) and sulfur dioxide (SO2) with adjustment for hydrogen sulfide (H2S), temperature and relative humidity.Main outcome measureOR and 95% CIs per 10 µg/m3increase in concentration of pollutants.ResultsThe 24-hour mean NO2was 20.7 µg/m3, mean PM10was 20.5 µg/m3, mean PM2.5was 12.5 µg/m3and mean SO2was 2.5 µg/m3. PM10level was positively associated with the number of emergency hospital visits (n=453) for cardiac arrest. Each 10 µg/m3increase in PM10was associated with increased risk of cardiac arrest (ICD-10: I46), OR 1.096 (95% CI 1.033 to 1.162) on lag 2, OR 1.118 (95% CI 1.031 to 1.212) on lag 0–2, OR 1.150 (95% CI 1.050 to 1.261) on lag 0–3 and OR 1.168 (95% CI 1.054 to 1.295) on lag 0–4. Significant associations were shown between exposure to PM10on lag 2 and lag 0–2 and increased risk of cardiac arrest in the age, gender and season strata.ConclusionsA new endpoint was used for the first time in this study: cardiac arrest (ICD-10 code: I46) according to hospital discharge registry. Short-term increase in PM10concentrations was associated with cardiac arrest. Future ecological studies of this type and their related discussions should perhaps concentrate more on precisely defined endpoints.