Bing Zhao1, Fay H Johnston1, Farhad Salimi2, Masahiko Kurabayashi3, Kazuaki Negishi4. 1. Menzies Institute for Medical Research, University of Tasmania, Hobart, TAS, Australia. 2. Department of Epidemiology and Preventive Medicine, School of Public Health and Preventive Medicine, Monash University, Melbourne, VIC, Australia; University Centre for Rural Health-North Coast, School of Public Health, University of Sydney, Lismore, NSW, Australia. 3. Department of Cardiology, Graduate School of Medicine, Gunma University, Maebashi, Japan. 4. Menzies Institute for Medical Research, University of Tasmania, Hobart, TAS, Australia; Department of Cardiology, Graduate School of Medicine, Gunma University, Maebashi, Japan; Department of Cardiology, Sydney Medical School Nepean, Faculty of Medicine and Health, Charles Perkins Centre Nepean, The University of Sydney, Kingswood, NSW, Australia. Electronic address: kazuaki.negishi@sydney.edu.au.
Abstract
BACKGROUND: PM2·5 is an important but modifiable environmental risk factor, not only for pulmonary diseases and cancers, but for cardiovascular health. However, the evidence regarding the association between air pollution and acute cardiac events, such as out-of-hospital cardiac arrest (OHCA), is inconsistent, especially at concentrations lower than the WHO daily guideline (25 μg/m3). This study aimed to determine the associations between exposure to ambient air pollution and the incidence of OHCA. METHODS: In this nationwide case-crossover study, we linked prospectively collected population-based registry data for OHCA in Japan from Jan 1, 2014, to Dec 31, 2015, with daily PM2·5, carbon monoxide (CO), nitrogen dioxide (NO2), photochemical oxidants (Ox), and sulphur dioxide (SO2) exposure on the day of the arrest (lag 0) or 1-3 days before the arrest (lags 1-3), as well as the moving average across days 0-1 and days 0-3. Daily exposure was calculated by averaging the measurements from all PM2·5 monitoring stations in the same prefecture. The effect of PM2·5 on risk of all-cause or cardiac OHCA was estimated using a time-stratified case-crossover design coupled with conditional logistic regression analysis, adjusted for daily temperature and relative humidity. Single-pollutant models were also investigated for the individual gaseous pollutants (CO, NO2, Ox, and SO2), as well as two-pollutant models for PM2·5 with these gaseous pollutants. Subgroup analyses were done by sex and age. FINDINGS: Over the 2 years, 249 372 OHCAs were identified, with 149 838 (60·1%) presumed of cardiac origin. The median daily PM2·5 was 11·98 μg/m3 (IQR 8·13-17·44). Each 10 μg/m3 increase in PM2·5 was associated with increased risk of all-cause OHCA on the same day (odds ratio [OR] 1·016, 95% CI 1·009-1·023) and at lags of up to 3 days, ranging from OR 1·015 (1·008-1·022) at lag 1 to 1·033 (1·023-1·043) at lag 0-3. Results for cardiac OHCA were similar (ORs ranging from 1·016 [1·007-1·025] at lags 1 and 2 to 1·034 [1·021-1·047] at lag 0-3). Patients older than 65 years were more susceptible to PM2·5 exposure than younger age groups but no sex differences were identified. CO, Ox, and SO2 were also positively associated with OHCA while NO2 was not. However, in two-pollutant models of PM2·5 and gaseous pollutants, only PM2·5 (positive association) and NO2 (negative association) were independently associated with increased risk of OHCA. INTERPRETATION: Short-term exposure to PM2·5 was associated with an increased risk of OHCA even at relatively low concentrations. Regulatory standards and targets need to incorporate the potential health gains from continual air quality improvement even in locations already meeting WHO standards. FUNDING: None.
BACKGROUND: PM2·5 is an important but modifiable environmental risk factor, not only for pulmonary diseases and cancers, but for cardiovascular health. However, the evidence regarding the association between air pollution and acute cardiac events, such as out-of-hospital cardiac arrest (OHCA), is inconsistent, especially at concentrations lower than the WHO daily guideline (25 μg/m3). This study aimed to determine the associations between exposure to ambient air pollution and the incidence of OHCA. METHODS: In this nationwide case-crossover study, we linked prospectively collected population-based registry data for OHCA in Japan from Jan 1, 2014, to Dec 31, 2015, with daily PM2·5, carbon monoxide (CO), nitrogen dioxide (NO2), photochemical oxidants (Ox), and sulphur dioxide (SO2) exposure on the day of the arrest (lag 0) or 1-3 days before the arrest (lags 1-3), as well as the moving average across days 0-1 and days 0-3. Daily exposure was calculated by averaging the measurements from all PM2·5 monitoring stations in the same prefecture. The effect of PM2·5 on risk of all-cause or cardiac OHCA was estimated using a time-stratified case-crossover design coupled with conditional logistic regression analysis, adjusted for daily temperature and relative humidity. Single-pollutant models were also investigated for the individual gaseous pollutants (CO, NO2, Ox, and SO2), as well as two-pollutant models for PM2·5 with these gaseous pollutants. Subgroup analyses were done by sex and age. FINDINGS: Over the 2 years, 249 372 OHCAs were identified, with 149 838 (60·1%) presumed of cardiac origin. The median daily PM2·5 was 11·98 μg/m3 (IQR 8·13-17·44). Each 10 μg/m3 increase in PM2·5 was associated with increased risk of all-cause OHCA on the same day (odds ratio [OR] 1·016, 95% CI 1·009-1·023) and at lags of up to 3 days, ranging from OR 1·015 (1·008-1·022) at lag 1 to 1·033 (1·023-1·043) at lag 0-3. Results for cardiac OHCA were similar (ORs ranging from 1·016 [1·007-1·025] at lags 1 and 2 to 1·034 [1·021-1·047] at lag 0-3). Patients older than 65 years were more susceptible to PM2·5 exposure than younger age groups but no sex differences were identified. CO, Ox, and SO2 were also positively associated with OHCA while NO2 was not. However, in two-pollutant models of PM2·5 and gaseous pollutants, only PM2·5 (positive association) and NO2 (negative association) were independently associated with increased risk of OHCA. INTERPRETATION: Short-term exposure to PM2·5 was associated with an increased risk of OHCA even at relatively low concentrations. Regulatory standards and targets need to incorporate the potential health gains from continual air quality improvement even in locations already meeting WHO standards. FUNDING: None.
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