Air pollution may cause heart attacks

New research has found that as little as two hours after being inhaled, tiny, invisible air pollutants can penetrate the lungs’ natural defences and may trigger a heart attack.


The revelation is reported in the 12 June edition of Circulation: Journal of the American Heart Association. According to its author, Dr. Murray A. Mittleman, director of cardiovascular epidemiology at Boston’s Beth Israel Deaconess Medical Center, although studies have previously linked exposure to particulate air pollution with increased risk of cardiovascular diseases, this is the first research to examine short-term transient effects of air pollution on the risk of heart attack.

In the study, researchers interviewed 772 Boston area heart attack patients about four days after the attack to establish when their symptoms began and compared the findings with daily air pollution measurements collected during the study period. Special attention was paid to levels of the smaller pollutants, known as PM2.5, which are so small that they can get past the normal defence mechanisms in the lungs and penetrate deeply into the air exchange regions, or alveoli.

It was discovered that the risk of heart attack was 48% higher among those with elevated PM2.5 in the two hours before the onset of symptoms. In addition, researchers also observed a 48% higher heart attack risk when 24-hour average exposure to PM2.5 was considered, indicating a delayed response to the particles. The particles blamed are those produced primarily by combustion processes in vehicle engines, power plants, refineries, smelters and other industry, while larger particles of airborne dust and debris from farming, construction work and mining are far less likely to trigger heart attack.

Perhaps more worryingly, numerous other major metropolitan areas have higher average levels of PM2.5 pollution than Boston, the researchers note, meaning a possibly higher risk of pollution-related heart attacks. The average PM2.5 concentration at the monitoring site during the study period was 12.1 micrograms per cubic metre (µg/m3), far below the US Environmental Protection Agency’s current acceptable of 65µg/m3.

“If the Boston exposure data can be generalised to other communities, we would expect proportionately higher effects in more heavily polluted cities,” said co-author Douglas W. Dockery, Sc.D., professor of environmental epidemiology at the Harvard School of Public Health. “But despite the widespread assumption that particulate air pollutants are primarily an urban problem, they can also affect large regions located downwind from the cities. Some of the highest PM2.5 concentrations are often found far from major urban areas, in places where we would expect the air to be cleaner.”

The researchers believe that one piece of encouraging news is that PM2.5 levels have largely decreased in most urban areas over the past few years. Fine-particle pollution is also largely a summer phenomenon, Dockery points out. “Because of their size, these particles readily penetrate indoor spaces, but air conditioning helps somewhat, reducing indoor concentrations by 30% to 50%. The best advice is to avoid outdoor activity on hot, hazy days. If a person exercises outside, the increased respiratory activity also increases the dose of PM2.5.”

The study team also said that it was too early to predict what types of medical intervention might be effective in preventing the cardiovascular consequences of fine-particle exposure and that more research was needed to determine the exact mechanisms by which inhaling fine particles can set off heart attacks.

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