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The Dirt on How Pollution Exacerbates Heart Disease

By Delthia Ricks
STAFF WRITER

April 16, 2002

AMID A GROWING catalog of data on disorders that air pollution can trigger, a recent investigation has shown precisely how air pollution leaves its signature on the cardiovascular system.

The study tracks the path of inhaled particles as they travel through nasal passages down the trachea - the windpipe - lodge in the alveoli, the tiny air sacs of the lungs, and possibly enter the bloodstream destined
for parts unknown.

Anecdotal evidence and statistical studies have made a correlation between pollution and a host of diseases, particularly asthma, heart disease, respiratory disorders and cancer. Michigan scientists decided to find out how pollutants cause heart disease.

"We have a wealth of epidemiological data saying that air pollution is associated with adverse respiratory
and cardiovascular outcomes," said Dr. Robert D. Brook, a specialist in hypertension and cardiovascular
diseases at the University of Michigan in Ann Arbor. "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."

Brook and his team undertook an unusual line of study, exposing people to some of the most potent components of air pollution. This was done by enclosing subjects in a special chamber at the University of Toronto, which is equipped to concentrate outdoor, urban air pollutants to a desired, measurable level.

Scientists blew into the chamber fine particulate matter, the microscopic metals and other compounds
produced by combustion in fuel-burning vehicles and power-generating industries. Also blown into the
mix was gaseous ozone. Fine particulate matter, Brook said, are those particles with a diameter less than
2.5 micrometers, a dimension less than that of a human hair. Two days before their exposure, volunteers
were exposed to filtered, pollution-free air to get a sense of what effects, if any, clean air has on blood
vessels.

After signing consent forms, 25 healthy participants entered the chamber one at a time and were
instructed to inhale the pollution for two hours. The concentrated level of pollutants, about 150
micrograms per cubic meter, was roughly twice the Environmental Protection Agency's suggested
exposure level for 24 hours. Brook described this level as similar to that found in urban areas during peak
pollution periods, such as rush-hour traffic.

Brook knew if his robust subjects, people in their 20s and 30s, showed a cardiovascular response to
pollutants, he would have a basis for explaining what happens in smog to those crippled by serious
cardiovascular conditions.

Using ultrasound technology to measure the diameter of each volunteer's brachial artery, which runs from shoulder to elbow, the team found that before exposure to polluted air, the brachial artery dilation was 3.92 millimeters. After breathing polluted air, the participants' brachial arteries were, on average, only 3.82 millimeters in diameter. Their arteries had constricted in response to air pollution.

Even though such constriction is unlikely to pose significant problems for healthy individuals, Brook said
"such constriction could conceivably trigger cardiac events in those individuals who are at risk for heart
disease."

Emerging from the investigation is the first documented evidence of how smog-like conditions affect the
cardiovascular system, even when exposure is short.

Brook and his team have extrapolated the findings into a hypothesis that may explain something that has
mystified doctors for years: why people with cardiovascular diseases, such as atherosclerosis,
hypertension and diabetes get sicker during peak periods of pollution. One hypothesis, Brook said, is that
fine particulate matter may travel directly into the bloodstream.

Brook's research was reported in a recent issue of the journal Circulation, a publication of the American
Heart Association.

The investigation comes on the heels of groundbreaking research reported last month in the Journal of the
American Medical Association. Dr. George Thurston, an epidemiologist at New York University in
Manhattan, and C. Arden Pope, an air quality expert at Brigham Young University in Utah, found air
pollution is a more insidious trigger of disease than most people think. Thurston and Pope concluded that
air pollution is as potent as second-hand cigarette smoke in its ability to cause heart disease and lung
cancer. The project ran for 20 years.

Commenting on Brook's research, Thurston said the study bolsters the body of scientific work - including
his own - that shows pollution is to be a potent cause of human disease.

"The difference between their study and ours is that they tell you what happens in acute exposure. Ours
would be chronic exposure. But their work is consistent with our epidemiology," Thurston said. By
chronic exposure, Thurston means inhaling pollution for many years. He said his study helps account for
lung cancer cases unrelated to smoking.

Brook's work, according to Thurston, also adds dimension to other studies, which have shown an
association between pollution and human illness. At least two recent investigations have found that heart
patients with implanted defibrillators tend to get stronger stimulation from the devices during peak
pollution periods.

If pollutants so adversely affect the cardiovascular system as Brook suggests, then it is likely that the
devices aren't going haywire, scientists say, but that heart rhythms are somehow affected by pollution.
More than 500 studies have been reported in medical journals in recent years reporting various types of
links between human disease and air pollution.

Despite a large body of scientific data, including animal studies, Thurston says that not everyone is
convinced air pollution can be a potent cause of heart disease and cancer.

Thurston summed up the response to his work this way: The project is revered by environmentalists and
health experts but reviled by industries that consume fossil fuels. His research also was criticized by The
Statistical Assessment Service. The Washington, D.C.-based group comments on statistical studies
reported in the media. That organization asserted that Thurston used a statistical measure that inflated the
amount of danger posed by pollution. The real danger is not as large as Thurston found, the group said.

Thurston's study reached its conclusion, the group charged, "by means of what are called confidence
intervals - a range of values within which the researchers are reasonably certain that the true value lies. ...

" ... This begs the question of exactly what sort of level of increased risk one needs, to be able to say the
study has found clear evidence of causation, rather than simple correlation," the group wrote.

In their analysis of 500,000 people, Thurston and Pope found those in the most polluted cities have a 12
percent increased risk of dying from lung cancer.

"When you look at the article, they are trying to account for a number of factors that might influence the
outcome," said Dr. Phil B. Fontanarosa, deputy executive editor of the Journal of the American Medical
Association.

Fontanarosa strongly defended Thurston's and Pope's research, saying that their study was rigorously
reviewed before it was accepted for publication, and that their statistical methodology is sound.

If the study were repeated, Fontanarosa said, "95 times out of a 100, the risk would be in the same
range."

Scientists at the National Institute of Health Sciences, which funded Thurston's research, called it the best
evidence to date linking air pollution to lung cancer.

Copyright © 2002, Newsday, Inc.