OBJECTIVES:
To investigate associations between air pollution levels and myocardial infarction (MI) on short timescales, with data at an hourly temporal resolution.
DESIGN:
Time stratified case crossover study linking clinical data from the Myocardial Ischaemia National Audit Project (MINAP) with PM(10), ozone, CO, NO(2), and SO(2) data from the UK National Air Quality Archive. Pollution effects were investigated with delays (lags) of 1-6, 7-12, 13-18, 19-24, and 25-72 hours in both single and multi-pollutant models, adjusted for ambient temperature, relative humidity, circulating levels of influenza and respiratory syncytial virus, day of week, holidays, and residual seasonality within calendar month strata.
SETTING:
Population based study in 15 conurbations in England and Wales.
SUBJECTS:
79,288 diagnoses of myocardial infarction recorded over the period 2003-6.
MAIN OUTCOME MEASURES:
Excess risk of myocardial infarction per 10 µg/m(3) increase in pollutant level.
RESULTS:
In single pollutant models, PM(10) and NO(2) levels were associated with a very short term increase in risk of myocardial infarction 1-6 hours later (excess risks 1.2% (95% confidence interval 0.3 to 2.1) and 1.1% (0.3 to 1.8) respectively per 10 μg/m(3) increase); the effects persisted in multi-pollutant models, though with only weak evidence of an independent PM(10) effect (P = 0.05). The immediate risk increases were followed by reductions in risk at longer lags: we found no evidence of any net excess risk associated with the five pollutants studied over a 72 hour period after exposure.
CONCLUSIONS:
Higher levels of PM(10) and NO(2), which are typically markers of traffic related pollution, seem to be associated with transiently increased risk of myocardial infarction 1-6 hours after exposure, but later reductions in risk suggest that air pollution may be associated with bringing events forward in time ("short-term displacement") rather than increasing overall risk. The well established effect of air pollution on cardiorespiratory mortality may not be mediated through increasing the acute risk of myocardial infarction, but through another mechanism.