Researchers Prove Air Pollution Causes Heart Disease

By Caitlin E. Cox

NYU School of Medicine researchers are providing some of the most compelling evidence yet that long-term exposure to air pollution—even at levels within federal standards—causes heart disease. Previous studies have linked air pollution to cardiovascular disease but until now it was poorly understood how pollution damaged the body’s blood vessels.

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 research recently published in the Journal of the American Medical Association (JAMA).

“We established a causal link between air pollution and atherosclerosis,” says Lung Chi Chen, associate professor of environmental medicine at the 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 U.S. Environmental Protection Agency (EPA) has regulated PM2.5 since 1997, currently setting the ambient air quality standard at an annual average of 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.

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, 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. Chen suspects that PM2.5 exposure could also affect even people who do not eat high-fat diets.