Study tracks damage from air pollution
May 23, 2002

By DELTHIA RICKS
Newsday

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.