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In a well-designed mouse study, where animals breathed air as polluted as the air in New York City, the researchers pinpointed specific mechanisms and showed that air pollution can be particularly damaging when coupled with a high-fat diet, according to new research published in the December 21 issue of JAMA.

“We established a causal link between air pollution and atherosclerosis,” says Lung Chi Chen, Ph.D., Associate Professor of Environmental Medicine at NYU School of Medicine and a lead author of the study. Atherosclerosis—the hardening, narrowing, and clogging of the arteries—is an important component of cardiovascular disease.

The study, done in collaboration with the Mount Sinai School of Medicine and University of Michigan, looked at the effects of airborne particles measuring less than 2.5 microns, referred to as PM2.5, the size linked most strongly with cardiovascular disease. The emissions arise primarily from power plants and vehicle exhaust. The US Environmental Protection Agency (EPA) has regulated PM2.5 since 1997, limiting each person’s average exposure per year to no more than 15 micrograms per cubic meter. These tiny particles of dust, soot, and smoke lead to an estimated 60,000 premature deaths every year in the United States.

Dr. Chen and his colleagues divided 28 mice, which were genetically prone to developing cardiovascular disease, into two groups eating either normal or high-fat diets. For the next six months, half of the mice in each feeding group breathed doses of either particle-free filtered air or concentrated air containing PM2.5 at levels that averaged out to 15.2 micrograms per cubic meter. This amount is within the range of annual EPA limits and equivalent to air quality in urban areas such as New York City.

The researchers then conducted an array of tests to measure whether the PM2.5 exposure had any impact on the mice’s cardiovascular health. Overall, mice who breathed polluted air fared worse than those inhaling filtered air. But when coupled with a high-fat diet, the impact of PM2.5 exposure was even more dramatic. The results added up to a clear cause and effect relationship between PM2.5 exposure and atherosclerosis, according to the study.

On the whole, mice breathing polluted air had far more plaque than those breathing filtered air. In cross sections taken from the largest artery in the body—the aorta—mice on normal diets and exposed to PM2.5 had arteries 19.2 percent filled with plaque, the fatty deposits that clog arteries. The arteries of those breathing particle-free air were 13.2 percent obstructed. Among high-fat diet mice, those exposed to PM2.5 had arteries that were 41.5 percent obstructed by plaque, whereas the arteries of the pollution-free mice were 26.2 percent clogged. In both normal and high-fat diet mice, PM2.5 exposure increased cholesterol levels, which are thought to exacerbate plaque buildup.

Though findings for increased plaque among mice eating normal diets were not statistically significant, Dr. Chen believes that future research on larger numbers of animals will solidify the trend. “Even with the low-fat diet, there’s still something there. So that is something to think about,” he says. He suspects that PM2.5 exposure could also greatly affect even people who do not eat high-fat diets.

Mice exposed to PM2.5 also appeared prone to developing high blood pressure, another element of cardiovascular disease, because their arteries had become less elastic. To measure tension in the arteries, the researchers tested how the neurotransmitters serotonin and acetylcholine affected the aortic arches of PM2.5-exposed mice differently than those of controls. The arteries taken from exposed mice were less elastic than the control group, constricting more in the presence of serotonin and relaxing less in response to acetylcholine. Once again, the mice fed high-fat diets suffered the most pronounced effects from breathing polluted air.

Finally, the researchers also examined various measures of vascular inflammation, which is involved in atherosclerosis on a number of levels. In the aortas of PM2.5–exposed mice, for example, they found increased levels of macrophages, immune cells that are an important ingredient in plaque deposits and also active participants in a biochemical pathway related to inflammation. The study revealed several signs that this pathway was more active, strengthening the connection between airborne particles and cardiovascular disease.

The authors of the new study are: Morton Lippmann, Lung Chi Chen, and Ximei Jin of the NYU School of Medicine’s Nelson Institute of Environmental Medicine, based in Tuxdeo, New York; Qinghua Sun, Alex Natanzon, Juan-Gilberto S. Aguinaldo, Zahi A. Fayad, Valentin Fuster, and Sayjay Rajagopalan of the Mount Sinai School of Medicine, New York; and Robert D. Brook and Damon Duquaine of University of Michigan, Ann Arbor. The study was funded by the EPA and the National Institute of Environmental Health Sciences.

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