Air pollution, high-fat diet cause atherosclerosis in laboratory mice (press release)

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Test results with laboratory mice show a direct cause-and-effect link between exposure to fine particle air pollution and the development of atherosclerosis, commonly known as hardening of the arteries. Mice that were fed a high-fat diet and exposed to air with fine particles had 1.5 times more plaque production than mice fed the same diet and exposed to clean filtered air.

Plaque, a fatty deposit on the inner lining of the blood vessels, can predispose individuals to conditions such as heart attacks and strokes. The fine particle exposure also led to increased inflammation of the artery walls and reduced function of the artery wall's inner lining.

The National Institute of Environmental Health Sciences, part of the federal National Institutes of Health, and the U.S. Environmental Protection Agency provided funding to researchers at the Mount Sinai School of Medicine and the New York University School of Medicine for the two-year study. The study results are published in the December 21, 2005 issue of the Journal of the American Medical Association.

The study showed that the combination of fine particle pollution and high-fat diet can promote the development of atherosclerosis, and may explain why people who live in highly polluted areas have a higher risk of heart disease. The findings are also important because the fine particle concentrations used in the study were well within the range of concentrations found in the air around major metropolitan areas.

The researchers did not observe significant differences in plaque production and artery wall inflammation in fine particle-exposed mice given the normal diet. However, among mice given clean air, those on the high-fat diet had greater plaque production and artery wall inflammation than those given the normal diet. These results suggest that both diet and fine particle pollution contributed to the development of atherosclerosis in the mice.

"This is one of the first studies to demonstrate measurable changes in plaque production and artery inflammation following exposure to fine particle matter," said NIEHS Director David A. Schwartz, M.D. "These findings have important implications for the long-term impact of fine particle air pollution on urban populations."

Fine particle pollution consists of microscopic particles of dust and soot less than 2.5 microns in diameter – about thirty times smaller than the width of a human hair. These tiny particles primarily come from motor vehicle exhaust, power plant emissions, and other operations that involve the burning of fossil fuels. Fine particles can travel deep into the respiratory tract, reducing lung function and worsening conditions such as asthma and bronchitis.

To evaluate the effects of fine particle exposure on cardiovascular health, the researchers used mice that were genetically programmed to develop atherosclerosis at a higher-than-normal rate. Half of the mice were placed on a regular diet, while the remaining half received chow with a high fat and calorie content. Mice from both groups were then exposed to either concentrated air particles or clean, filtered air for 6 hours per day, 5 days per week, for a total of 6 months.

Following the exposures, the researchers measured plaque concentration in the aorta, the largest artery in the body. They found that among mice fed the high-fat diet, those exposed to fine particles had plaque concentrations more than 1.5 times higher than those exposed to clean air. "These results suggest that the fine particle exposure is actually accelerating the development of atherosclerosis in the high-fat group," said Sanjay Rajagopalan, M.D., a vascular medicine specialist and cardiologist with the Mount Sinai School of Medicine and senior author of the study.

Further comparison of the high-fat groups showed that the artery walls of the mice exposed to fine particle pollution were significantly more inflamed than their clean-air counterparts. "We noted a significant increase in the number of inflammatory cells and enzymes in the arteries of the mice exposed to air particles," said Rajagopalan.

In addition, the fine particles had a measurable effect on the ability of the arteries to dilate, an important indicator of artery wall function. "We found that the constrictive effect of certain stress hormones was increased in the arteries of the particle-exposed mice, while the ability of the arteries to dilate was impaired," said Rajagopalan. "This suggests the artery function had been compromised."

According to Rajagopalan, the effects on plaque production and artery wall inflammation were obtained with relatively low exposure concentrations. "The average particle exposure over the course of the study was 15 micrograms per cubic meter, which is typical of the particle concentrations that urban area residents would be exposed to, and well below the federal air quality standard of 65 micrograms per cubic meter in a 24-hour period," he said.

A number of human population studies have confirmed an association between exposure to airborne particles and an increased risk of cardiovascular disease, particularly among those with underlying risk factors such as hypertension, diabetes, high cholesterol, or prior cardiovascular disease. "These results support the need for additional studies that can identify the underlying mechanisms linking fine particle exposure and atherosclerosis in human populations," said Rajagopalan.

Contact: John Peterson peterso4@niehs.nih.gov 919-541-7860 NIH/National Institute of Environmental Health Sciences

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