Heart attack

Diesel exhaust linked to higher heart attack, stroke risk in men

Increased amount of roadway pollution is leading to a cascade of conditions that might result in heart attack or stroke in men, says a new study.

Washington, Nov 7 : Increased amount of roadway pollution is leading to a cascade of conditions that might result in heart attack or stroke in men, says a new study.

The study, led by Andrew Lucking, M.D., a cardiology fellow at the University of Edinburgh in the United Kingdom, found that diesel exhaust increased clot formation and blood platelet activity in healthy volunteers, which could lead to heart attack and stroke.

"The study results are closely tied with previous observational and epidemiological studies showing that shortly after exposure to traffic air pollution, individuals are more likely to suffer a heart attack," Lucking said.

"This study shows that when a person is exposed to relatively high levels of diesel exhaust for a short time, the blood is more likely to clot. This could lead to a blocked vessel resulting in heart attack or stroke," he said.

In the double blind, randomised, crossover study 20 healthy men, in the age group of 21 to 44 years old were examined.

The participants were separately exposed to filtered air (serving as a control) and to diluted diesel exhaust at 300 micrograms per meter cubed (mcg/m3), a level comparable to curb side exposure on a busy street.

For the study, the researchers performed the exposures in a specially built diesel exposure chamber.

At two hours and at six hours after exposure, researchers allowed a small amount of participants' blood to flow through a perfusion chamber. They measured clot formation, coagulation, platelet activation and inflammatory markers after each exposure.

In order to measure clot formation, researchers used low and high shear rates, recreating flow conditions inside the body's blood vessels.

Compared to filtered air, breathing air with diluted diesel exhaust increased clot formation in the low shear chamber by 24.2 percent and the high shear chamber by 19.1 percent. This was seen at both two and six hours after diesel exposure.

The analysis also found an increase in platelet activation, assessed by measuring the number of platelets associated with white blood cells.

Lucking said that platelets play a central role in blood clotting, and when they are activated, they associate with white blood cells such as neutrophils and monocytes.

Diluted diesel exhaust inhalation increased platelet-neutrophil aggregates from 6.5 percent to 9.2 percent and platelet-monocyte aggregates from 21 percent to 25 percent at two hours after exposure.

At six hours, a trend toward platelet activation was found, but it was not statistically significant.

"After exposure to diesel exhaust, the participants had increased levels of activated platelets that became attached to white blood cells. When activated, the platelets can stick together and form a clot.

"High levels of traffic pollution are known to increase the risk of heart attack in the immediate hours or days after exposure. These findings provide a potential mechanism that could link exposure to traffic-derived air pollution with acute heart attack," Lucking said.

"Diesel engines are becoming very popular because of increased fuel economy.

"While diesel engines burn more efficiently, they also put more fine particulate matter into the air," Lucking said.

Lucking encouraged physical activity but suggested that people with existing cardiovascular disease should try to exercise away from traffic congestion.

ANI