Increases in Particulate Matter Trigger Heart Attacks

Douglas W. Dockery, Sc.D.
Harvard School of Publih Health
P30ES00002

Background: NIEHS has supported much of the research on the health effects of particulate matter air pollution. This research has linked exposure to particulate matter with increased risk of cardiovascular diseases. Fine particles are produced by combustion processes in car engines, power plants, refineries, smelters, and other industries. Small particles can penetrate deeply into the air exchange regions of the lung bypassing the normal defense mechanisms of the lung. The current study is the first to link short-term transient effects of particulate matter less than 2.5 microns (PM2.5) in size to the risk of heart attack.

Advance: Regional air pollution measurements taken at the time study participants in the Boston area said their heart attack symptoms began were compared to measurements taken during control periods. The risk of heart attack was about 1.5 times higher among those exposed to elevated PM2.5 in the two hours prior to the development of symptoms. The risk was even greater (about 1.7 times higher) when PM2.5 levels were increased for 24 hours prior to symptoms. The PM2.5 levels were high, but at levels that occur frequently in many parts of the United States. Other recent data suggest that exposure to high PM2.5 levels may cause increased systemic inflammation, increased blood thickness, and an increase in C-reactive protein which causes the formation of blood clots.

Implication: This study provides strong evidence that short-term exposure to PM2.5 causes increased risk of heart attack. Knowing the time between exposure and heart attack is crucial to determining the biological mechanisms responsible for the associations. This study is also very important in establishing proper standards for PM2.5 to reduce the risk for the population especially susceptible sub-populations.

Publication: Peters A, Dockery DW, Muller JE, Mittleman MA. Increased particulate air pollution and the triggering of myocardial infarction. Circulation. 2001 Jun 12;103(23):2810-5.