Air pollution affects non-MI outcomes, but not STEMI

Short-term effects of air pollution on a range of cardiovascular events in England and Wales: case-crossover analysis of the MINAP database, hospital admissions and mortality

Literature - Milojevic A et al., Heart 2014 - Heart 4 June 2014

Milojevic A, Wilkinson P, Armstrong B, et al.,
Heart 4 June 2014doi:10.1136/heartjnl-2013-304963


Experimental and epidemiological studies have pointed towards associations between air pollution and heart disease [1-3]. It is estimated that 7.4% of all cases of myocardial infarction (MI) are attributable to traffic-related air pollution [4].
Mechanisms via which pollution may cause cardiovascular disease (CVD) remain unclear. This study aimed to contribute to the current understanding of pathophysiological mechanisms by examining the strength and specificity of acute relationships between ambient air pollution and a range of CVD events. Specifically, the question was addressed whether events of clear thrombotic origin (acute MI, stroke and related outcomes) have a stronger association with air pollution than non-thrombotic outcomes. Data from three databases on hospital admissions in England and Wales were used, encompassing 452343 geographically coded MI events. Short-term associations between air pollution and CVD events were assessed using a case-crossover approach, in which the day of health events were considered cases, and all other days in the same month as controls.

Main results

  • Percent changes in MI risk for 10th-90th centile increases in different pollutants were calculated for all MI events and separately for STEMI and non-STEMI. There was very little evidence of a pollution effect on MI risk. The strongest evidence for any adverse effect was with NO2, where a 10th-90th centile increase was associated with a 2.4% increase (95%CI: 0.3-4.5%). The association appeared stronger for non-STEMI than for STEMI events.
  • Only a 10th-90th centile increase of NO2 was associated with higher risk of emergency hospital admission  of 1.7% (95%CI: 0.9-2.6%) for CVD, 2.0% (95%CI: 1.1-2.9%) non-MI CVD, 2.9% (95%CI: 0.6-5.2%) arrhythmias, 2.8% (95%CI: 0.3-5.4%) atrial fibrillation and 4.4% (95%CI: 2.0-6.8%) heart failure. The NO2 associations were greater in females and those aged 70 and older for non-MI admissions, and in females for arrhythmia.
  • Mortality outcomes were generally not associated with pollutant exposure, except for an increased risk of arrhythmia (21%, 95%CI: 3.9-40.8%), atrial fibrillation (21%, 95%CI: 3.9-41%) and pulmonary embolism (20.5%, 95%CI: 3.5-39.7%), with a 10th-90th centile increase of PM2.5. For all deaths due to CVD and IHD, PM2.5 and O3 risk was significantly higher in women and in those of 70 years and older.


Little acute effect of ambient air pollution on STEMIs or stroke was seen. Increased hospital admissions for CVD overall, non-MI CVD and arrhythmias were associated with NO2, while PM2.5 had adverse effect on CVD deaths, arrhythmias and pulmonary embolism. Some of these effects may be more frequent in those over 70 years old and in females, although the sex differences may also reflect differences in age distribution.
The stronger associations with selected non-MI outcomes in this study suggest that pollution effects on CV health may partly be mediated by non-thrombotic pathways. Thrombogenic pathways may, however, also be at play, and be the most likely explanation for the observed association with pulmonary embolism.

Editorial comment [5]

“The authors argue that thrombotic pathways may be less important given the lack of association of gaseous and particulate pollution with stroke and STEMI. However, they report a positive association with pulmonary embolism and also with non-STEMI: both thrombotic conditions affecting the venous and arterial circulations, respectively. Patients with non- STEMI are generally 10 years older than those suffering from STEMI. The stronger association seen with non- STEMI may therefore reflect prothrombotic effects of ambient air pollution in the elderly: an at-risk and potentially more susceptible population.
 It is important to note that in this study within the UK, the median PM2.5 concentration was 10 mg/m3 within a relatively narrow range (IQR, 7–15 mg/m3). This contrasts with levels that are more than 10–20 times higher in many of the megacities across the world. Some have suggested that associations with adverse cardiovascular events persist even at low pollutant concentrations, but as air quality continues to improve, the adverse impact on health will decline. This may explain the current lack of consistent associations with contemporary UK data.”

Find this articleonline


1 Ayres JG. Cardiovascular disease and air pollution: a report by the Committee on the Medical Effects of Air Pollution. Department of Health, 2006.
2 Brook RD, Franklin B, Cascio W, et al. Air pollution and cardiovascular disease: a statement for healthcare professionals from the expert panel on population and prevention science of the American Heart Association. Circulation 2004;109:2655–71.
3 Brook RD, Rajagopalan S, Pope CA 3rd, et al. Particulate matter air pollution and cardiovascular disease: an update to the scientific statement from the American Heart Association. Circulation 2010;121:2331–78.
4 Nawrot TS, Perez L, Kunzli N, et al. Public health importance of triggers of myocardial infarction: a comparative risk assessment. Lancet 2011;377:732–40.
5 Shah ASV, Newby DE. Less clarity as the fog begins to lift. Heart doi:10.1136/heartjnl-2014-305877

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