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28-09-2011 | Cardiology | Article

High air pollution brings forward time of heart attack

Abstract

Free abstract

MedWire News: High levels of air pollution may cause an impending myocardial infarction (MI) to occur sooner than it would have otherwise, suggest UK researchers.

Krishnan Bhaskaran and colleagues from the London School of Hygiene and Tropical Medicine found that increasing levels of air pollution were associated with a transient increase in risk for MI between 1 and 6 hours after the onset of exposure; after this time, the risk decreased despite continued exposure.

This means that the well-established effect of air pollution on cardiac mortality may not be mediated through directly increasing the risk for MI as previously thought, but through another mechanism, the researchers speculate in the BMJ.

The case-crossover analysis linked time-stratified data on 79,288 cases of ST-segment- elevation myocardial infarction (STEMI) from the Myocardial Ischemia National Audit Project to particulate matter less than 10 (PM10), ozone, carbon monoxide (CO), nitrogen dioxide (NO2), and sulfur dioxide (SO2) data from the UK National Air Quality Archive. All STEMI cases took place across 15 conurbations in England and Wales from 2003 to 2006.

Bhaskaran and team investigated the effects of pollution on the time of STEMI according to delays (lags) of 1-6, 7-12, 13-18, 19-24, and 25-72 hours in single-pollutant and multipollutant models. Both models were adjusted for ambient temperature, humidity, levels of influenza and respiratory syncytial virus, day of the week, holidays, and seasonality.

The main outcome measure was the excess risk for MI per 10 µg/m3 increase in pollutant level.

When each of the five pollutants were modeled separately, exposure to increasing levels of PM10 and NO2 (the primary markers of traffic-related pollution) was associated with a higher risk for MI 1-6 hours later. Indeed, a 10-µg/m3 increase in PM10 level was associated with a significant 1.2% increased risk for MI and a 10-µg/m3 increase in NO2 level was associated with a 1.1% increased risk for MI.

This effect persisted in multipollutant models, albeit with only weak significance.

After 1-6 hours, there was no overall risk increase with higher levels of air pollution, with the cumulative change in risk associated with increased PM10 levels declining by 0.8%, and that associated with increased NO2 declining by 0.4%.

By contrast, there was little evidence of any detrimental effect of CO, ozone, or SO2 on MI risk.

In a related commentary, editorialists Simon Hales and Richard Edwards (University of Otago, Wellington, New Zealand) said: "Given other evidence that exposure to air pollution increases overall mortality and morbidity, the case for stringent controls on pollutant levels remains strong."

By Piriya Mahendra

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