When paired with consuming a diet high in fat, breathing polluted air on a regular basis accelerates the accumulation of dangerous plaques in arteries, researchers studying mice have found. The research sheds light on how chronic exposure to air pollution contributes to heart attacks and strokes.
“High fat by itself has a strong negative impact” on blood vessel health, notes Nino Künzli of the University of Southern California in Los Angeles, who didn’t participate in the new work. “Air pollution causes additional problems. If you unfortunately have both, you are really badly off.”
“Obese people in dirty cities presumably form a high-risk group,” Künzli adds, but he cautions that the study’s findings need to be confirmed.
Past research had indicated that exposure to air pollution inflames and thickens people’s artery walls (SN: 12/11/04, p. 372: Smog Clogs Arteries: Pollution does lasting harm to blood vessels) and that people living near major roads have elevated rates of cardiovascular disease (SN: 11/9/02, p. 302: Available to subscribers at Is a faster commute worth it?).
In the new study, Lung Chi Chen of New York University School of Medicine in Tuxedo and his collaborators experimented on mice that have a genetic mutation that makes them susceptible to developing plaques of cholesterol in their arteries. The team fed some animals a standard lab diet and others a diet higher in fat and cholesterol.
For 6 months, the researchers also exposed some of the animals to polluted air for 30 hours per week. The other mice breathed only filtered air.
To generate the polluted air, the experimenters took air from outside their rural facility and concentrated all particles smaller than 2.5 micrometers in diameter.
The resulting pollution concentrations were about eight times that in the local air but comparable to concentrations in some cities, Chen notes. “These levels can occur very easily in Los Angeles,” he says.
Mice fed a high-fat diet and exposed to polluted air developed plaque on 42 percent of their major arteries’ surfaces, Chen and his collaborators report in the Dec. 21 Journal of the American Medical Association.
By contrast, plaques covered 26 percent of the arteries in mice fed a fatty diet but given clean air. A normal diet and clean air produced plaques on just 13 percent of the arteries’ internal surfaces.
Since the overall exposure to small particles by the pollution-breathing mice is only slightly above that acceptable to the Environmental Protection Agency, “the standard is not quite adequate in terms of protecting the public health,” Chen says.
“Exposure to relatively low levels of contaminants accelerated the process of depositing plaques,” comments Michael T. Kleinman of the University of California, Irvine. He says that the study also hints that air pollution may accelerate plaque formation in the absence of a high-fat diet.
Michael E. Rosenfeld of the University of Washington in Seattle is surprised that air pollution had a statistically convincing effect in the mice only in conjunction with a bad diet. That suggests a synergistic effect between the two exposures beyond either one’s individual capacity to trigger rapid atherosclerosis, he says.