DALLAS, June 12 – As few as two hours after being inhaled, tiny, invisible air pollutants can penetrate the lungs’ natural defenses and may trigger a heart attack, according to a report in today’s Circulation: Journal of the American Heart Association.
“Studies of hospital admissions and emergency department visits have linked exposure to particulate air pollution with increased risk of cardiovascular diseases,” says study author Murray A. Mittleman, M.D., Dr.PH., director of cardiovascular epidemiology at Boston’s Beth Israel Deaconess Medical Center. “But the current study is the first to examine short-term transient effects of air pollution on the risk of heart attack.”
Between Jan. 1995 and May 1996, researchers interviewed 772 Boston area heart attack patients about four days after their heart attack to establish when their symptoms began. Participants were enrolled in the Determinants of Myocardial Infarction Onset Study, which is aimed at gathering information about factors associated with myocardial infarction, or heart attack. Researchers compared the times heart attack symptoms began with daily air pollution measurements collected in Boston during the study period. They paid special attention to levels of the smaller pollutants.
“These tiny particles are known as PM2.5 because they measure less than 2.5 micrometers in diameter,” explains co-author Douglas W. Dockery, Sc.D., professor of environmental epidemiology at the Harvard School of Public Health. “They are so small that they can get past the normal defense mechanisms in the lungs and penetrate deeply into the air exchange regions, or alveoli.”
Air pollution measurements taken at the time patients said their heart attack symptoms began were compared to measurements taken during “control” periods. Control periods were selected 24 hours apart, starting three days before the date and time heart attack symptoms began.
The risk of heart attack was higher among those with elevated PM2.5 in the two hours before the onset of symptoms. In addition, researchers observed a higher heart attack risk when 24-hour average exposure to PM2.5 was considered, indicating a delayed response to the particles. Data analysis considering both time windows jointly revealed a 48 percent higher risk of heart attack when PM2.5 concentration increased by 25 micrograms per cubic meter of air (µg/m3) in the two-hours before symptoms began. Fine-particulate air pollution is produced primarily by combustion processes in automobile engines, power plants, refineries, smelters and other industry, says Dockery. Larger, more readily
noticed particles of airborne dust and debris from farming, construction work and mining are far less likely to trigger heart attack, he says.
Some recent data suggest that exposure to high levels of PM2.5 may cause increased systemic inflammation, increased plasma viscosity (thicker blood) and an increase in certain proteins in the blood that can cause clots to form, he says.
“It’s too early to predict what types of medical intervention might be effective in preventing the serious cardiovascular consequences of fine-particle exposure,” Mittleman adds. “More research is needed to determine the exact mechanisms by which inhaling fine particles can set off heart attacks.”
Numerous other major metropolitan areas have higher average levels of PM2.5 pollution than Boston, the researchers note, meaning that residents of those cities may face even greater risk of pollution-related heart attacks than Bostonians. The average PM2.5 concentration at the monitoring site during the study period was 12.1 µg/m3.
“If the Boston exposure data can be generalized to other communities, we would expect proportionately higher effects in more heavily polluted cities,” Dockery says. “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.”
Mittleman says one bit of encouraging news is that levels of the tiny pollutants have decreased somewhat in most urban areas over the past few years.
Fine-particle pollution is largely a summer phenomenon, Dockery points out. “Pollution monitors show seasonal variations where hot, hazy days have higher levels of fine particles on average,” he says. Also, he says it is much more difficult for individuals to take protective measures against PM2.5 than against gaseous pollutants, which can be effectively removed from indoor air.
“Because of their size, these particles readily penetrate indoor spaces,” says Dockery, “but air conditioning helps somewhat, reducing indoor concentrations by 30 percent to 50 percent. 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 Environmental Protection Agency’s (EPA) current acceptable standard is 65 micrograms of PM2.5 per cubic meter of air. “Even at PM2.5 concentrations below that standard, our study shows that the risk of a heart attack is increased,” says Mittleman. Co-authors include Annette Peters, Ph.D., and James E. Muller, M.D.
This study was supported by a grant from the National Heart, Lung and Blood Institute.
The above post is reprinted from materials provided by American Heart Association. Note: Materials may be edited for content and length.
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