How Air Pollution Can Cause Heart Disease

[Guest guest]

Source: New York University Medical Center and School of Medicine

Date: 2005-12-30

URL: http://www.sciencedaily.com/releases/2005/12/051230085740.htm

Researchers Show How Air Pollution Can Cause Heart Disease

New York University School of Medicine researchers provide 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 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.

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The authors of the new study are: Morton Lippmann, Lung Chi Chen,

and Ximei Jin of the NYU School of Medicine's Institute of

Environmental Medicine, based in Tuxdeo, New York; Qinghua Sun,

Natanzon, -Gilberto S. Aguinaldo, Zahi A. Fayad, Valentin

Fuster, and Sayjay Rajagopalan of the Mount Sinai School of

Medicine, New York; and 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.