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Air Pollution Causes Healthy Blood Vessels To Constrict

March 12, 2002
American Heart Association
For the first time researchers have shown that air pollution negatively affects the blood vessels of healthy humans, according to a study in Circulation: Journal of the American Heart Association.

DALLAS, March 12 – For the first time researchers have shown that air pollution negatively affects the blood vessels of healthy humans, according to a study in today’s rapid access issue of Circulation: Journal of the American Heart Association.

In the study, 25 healthy people inhaled elevated concentrations of fine particles plus ozone for two hours. After exposure, volunteers’ blood vessels constricted between 2 percent and 4 percent on average. Their vessels did not constrict when they were exposed to ozone-free and particle-free air.

“We have a wealth of epidemiological data saying that air pollution is associated with adverse respiratory and cardiovascular outcomes, but there is still a lack of understanding as to how the association occurs physiologically. These findings suggest a possible reason why the rate of heart attacks and other cardiovascular events increases with exposure to air pollution for people with known heart and blood vessel disease,” says Robert D. Brook, M.D., study co-author and assistant professor of internal medicine in the division of hypertension and vascular medicine program at the University of Michigan, Ann Arbor.

“There have been some suggestions in previous studies that people with atherosclerosis tend to respond with greater-than-normal constriction, or narrowing of blood vessels, in response to certain hormones in the body. Could it be that their blood vessels also have enhanced constriction in response to air pollution? Future studies will be needed to answer that question,” Brook says.

The researchers focused on ozone and fine particulate matter. Fine particles are those with a diameter of less than 2.5 micrometers. Fine particles are emitted from burning fossil fuels, mostly from car engine exhaust, power generation and many industrial processes. Ozone and additional particulate materials are created when the sun shines on these emissions.

“In other research, exposure to fine particles has been implicated in coronary events such as heart attacks,” Brook explains. “In contrast to larger particles, which are trapped in the upper airways when inhaled, the fine particles travel down to the alveoli, tiny air sacs at the base of the lungs, where they can affect the rest of the cardiovascular system by adversely impacting circulating blood. It is possible that the particles may even directly enter the blood.”

The University of Toronto has one of only a few facilities in the world currently using human volunteers that is capable of concentrating outdoor urban air particles to a desired pollution level, then piping them into a special air chamber for experiments such as this one, he says.

In this study, the researchers used ultrasound to measure the diameter of the volunteers’ brachial artery – which runs from the shoulder to the elbow – before and after two hours of exposure to a concentrated mixture of ozone and fine particles. The level of concentration (150 micrograms per cubic meter) was about twice the EPA-suggested level for 24 hours of exposure (65 micrograms per cubic meter). Brook described that exposure as similar to those found in urban areas during peak air pollution times such as rush-hour traffic.

At least two days before or after the pollutant exposure, subjects underwent the same measurements after being exposed to air that was filtered to remove the pollutants.

The volunteers’ arteries showed no change in response to breathing filtered air, but constricted from 2 percent to 4 percent in response to the polluted air.

Researchers measured the width, or dilation, of the brachial artery. Before exposure to fine particles, brachial artery dilation was 3.92mm; after exposure to pollution it was 3.82mm. For the filtered air, dilation was virtually unchanged (3.89mm vs. 3.90mm).

“Although the degree of constriction in and of itself is unlikely to produce significant problems in healthy individuals, such a constriction could conceivably trigger cardiac events in those individuals who have or are at risk for heart disease,” says Brook.

These are the first findings to show such an effect in people. Because the 25 subjects in this study were all healthy and relatively young (average age 35), these results call attention to the need for further research on the air pollution problems that plague most of the world’s major cities, Brook says.

“Our results are a clear demonstration that environmentally relevant concentrations of common air pollutants that can occur in urban settings adversely affect the blood vessels of healthy people,” Brook says. Brook adds that more research is needed to fully understand why air pollution has negative effects on blood vessels and to clarify the public health implications of the findings of these initial studies.

The study was conducted at the University of Toronto and funded by the Toxic Substance Research Initiative, a joint program of the Canadian Federal Ministries of Health and Environment, known as Health Canada and Environment Canada.

In the United States, the Environmental Protection Agency estimates that air pollution contributed to 60,000 heart-related deaths in 1996, according to figures in the federal register.

Co-authors include: Jeffrey R. Brook, Ph.D.; Bruce Urch, M.Sc.; Renaud Vincent, Ph.D.; Sanjay Rajagopalan, M.D.; and Frances Silverman, Ph.D.

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Materials provided by American Heart Association. Note: Content may be edited for style and length.

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American Heart Association. "Air Pollution Causes Healthy Blood Vessels To Constrict." ScienceDaily. ScienceDaily, 12 March 2002. <>.
American Heart Association. (2002, March 12). Air Pollution Causes Healthy Blood Vessels To Constrict. ScienceDaily. Retrieved December 5, 2023 from
American Heart Association. "Air Pollution Causes Healthy Blood Vessels To Constrict." ScienceDaily. (accessed December 5, 2023).

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