|Air Pollution, High-Fat Diet Cause Atherosclerosis in Laboratory
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
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
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
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.
NIEHS, a component of the National Institutes of Health, supports research
to understand the effects of the environment on human health. For more information
on fine particle air pollution and other environmental health topics, please
visit the NIEHS website at http://www.niehs.nih.gov/home.htm.
The National Institutes of Health (NIH) — The Nation's Medical Research
Agency — includes 27 Institutes and Centers and is a component of
the U. S. Department of Health and Human Services. It is the primary Federal
agency for conducting and supporting basic, clinical, and translational medical
research, and it investigates the causes, treatments, and cures for both common
and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov.