Effects of Air Pollution on Cardiovascular Events in England
Effects of Air Pollution on Cardiovascular Events in England
Objective To inform potential pathophysiological mechanisms of air pollution effects on cardiovascular disease (CVD), we investigated short-term associations between ambient air pollution and a range of cardiovascular events from three national databases in England and Wales.
Methods Using a time-stratified case-crossover design, over 400 000 myocardial infarction (MI) events from the Myocardial Ischaemia National Audit Project (MINAP) database, over 2 million CVD emergency hospital admissions and over 600 000 CVD deaths were linked with daily mean concentrations of carbon monoxide (CO), nitrogen dioxide (NO2), particulate matter less than 10 μm in aerodynamic diameter (PM10), particulate matter less than 2.5 μm in aerodynamic diameter (PM2.5) and sulfur dioxide (SO2), and daily maximum of 8-hourly running mean of O3 measured at the nearest air pollution monitoring site to the place of residence. Pollutant effects were modelled using lags up to 4 days and adjusted for ambient temperature and day of week.
Results For mortality, no CVD outcome analysed was clearly associated with any pollutant, except for PM2.5 with arrhythmias, atrial fibrillation and pulmonary embolism. With hospital admissions, only NO2 was associated with a raised risk: CVD 1.7% (95% CI 0.9 to 2.6), non-MI CVD 2.0% (1.1 to 2.9), arrhythmias 2.9% (0.6 to 5.2), atrial fibrillation 2.8% (0.3 to 5.4) and heart failure 4.4% (2.0 to 6.8) for a 10th–90th centile increase. With MINAP, only NO2 was associated with an increased risk of MI, which was specific to non-ST-elevation myocardial infarction (non-STEMIs): 3.6% (95% CI 0.4 to 6.9).
Conclusions This study found no clear evidence for pollution effects on STEMIs and stroke, which ultimately represent thrombogenic processes, though it did for pulmonary embolism. The strongest associations with air pollution were observed with selected non-MI outcomes.
Experimental and epidemiological studies have provided evidence of associations between air pollution and cardiovascular health. More pollution-related deaths occur from heart disease than from any other cause. A comparative risk assessment concluded that 7.4% of all cases of myocardial infarction (MI) is attributable to traffic-related air pollution, and a recent systematic literature review found associations with MI to be significant with all pollutants except O3.
Uncertainties remain, however, about the likely mechanisms of pollution-related cardiovascular disease (CVD). For example, hypotheses for particulate pollution include disturbance of the autonomic nervous system, changes in blood coagulability consequent to alveolar inflammation and the translocation of particles and/or their constituents into the blood.
This study aims to further current understanding of pathophysiological mechanisms by examining the strength and specificity of acute relationships between ambient air pollution and a range of CVD events. The key mechanistic question addressed is whether events of clear thrombotic origin, namely, acute MI, stroke and related outcomes, have a stronger association with air pollution than non-thrombotic outcomes.
Abstract and Introduction
Abstract
Objective To inform potential pathophysiological mechanisms of air pollution effects on cardiovascular disease (CVD), we investigated short-term associations between ambient air pollution and a range of cardiovascular events from three national databases in England and Wales.
Methods Using a time-stratified case-crossover design, over 400 000 myocardial infarction (MI) events from the Myocardial Ischaemia National Audit Project (MINAP) database, over 2 million CVD emergency hospital admissions and over 600 000 CVD deaths were linked with daily mean concentrations of carbon monoxide (CO), nitrogen dioxide (NO2), particulate matter less than 10 μm in aerodynamic diameter (PM10), particulate matter less than 2.5 μm in aerodynamic diameter (PM2.5) and sulfur dioxide (SO2), and daily maximum of 8-hourly running mean of O3 measured at the nearest air pollution monitoring site to the place of residence. Pollutant effects were modelled using lags up to 4 days and adjusted for ambient temperature and day of week.
Results For mortality, no CVD outcome analysed was clearly associated with any pollutant, except for PM2.5 with arrhythmias, atrial fibrillation and pulmonary embolism. With hospital admissions, only NO2 was associated with a raised risk: CVD 1.7% (95% CI 0.9 to 2.6), non-MI CVD 2.0% (1.1 to 2.9), arrhythmias 2.9% (0.6 to 5.2), atrial fibrillation 2.8% (0.3 to 5.4) and heart failure 4.4% (2.0 to 6.8) for a 10th–90th centile increase. With MINAP, only NO2 was associated with an increased risk of MI, which was specific to non-ST-elevation myocardial infarction (non-STEMIs): 3.6% (95% CI 0.4 to 6.9).
Conclusions This study found no clear evidence for pollution effects on STEMIs and stroke, which ultimately represent thrombogenic processes, though it did for pulmonary embolism. The strongest associations with air pollution were observed with selected non-MI outcomes.
Introduction
Experimental and epidemiological studies have provided evidence of associations between air pollution and cardiovascular health. More pollution-related deaths occur from heart disease than from any other cause. A comparative risk assessment concluded that 7.4% of all cases of myocardial infarction (MI) is attributable to traffic-related air pollution, and a recent systematic literature review found associations with MI to be significant with all pollutants except O3.
Uncertainties remain, however, about the likely mechanisms of pollution-related cardiovascular disease (CVD). For example, hypotheses for particulate pollution include disturbance of the autonomic nervous system, changes in blood coagulability consequent to alveolar inflammation and the translocation of particles and/or their constituents into the blood.
This study aims to further current understanding of pathophysiological mechanisms by examining the strength and specificity of acute relationships between ambient air pollution and a range of CVD events. The key mechanistic question addressed is whether events of clear thrombotic origin, namely, acute MI, stroke and related outcomes, have a stronger association with air pollution than non-thrombotic outcomes.
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