PROVO, UTAH—Although the link between acute exposure to fine particulates and cardiopulmonary mortality has been established, the health risks of chronic exposure to particulate pollution have been less well defined. A recent study demonstrates that long-term exposure to fine particulate air pollution elevates both cardiopulmonary and lung cancer mortality.[1]

The powerful new study combines extensive information on personal predisposing variables with the results of expanded environmental monitoring. “It’s really the first study that … can adequately control for individual risk factors (such as smoking, body mass index, diet, etc) and still be large enough that it can realistically evaluate the association of air pollution with lung cancer,” remarked study author C. Arden Pope III, PhD, Professor of Economics at Brigham Young University in Provo, Utah. Furthermore, he emphasized, the quantity of data and advanced statistical approach also allowed the researchers to evaluate the association of particulates with diameter less than 2.5 microns (PM2.5) with nonmalignant cardiopulmonary disease.

Earlier research had shown that “day-to-day changes in particle air pollution, especially the fine particulates, were correlated with day-to-day changes in mortality,” Dr. Pope told RESPIRATORY REVIEWS. “Basically, for every 10-mg/m3 increase in PM10 or PM2.5, we were seeing an increase in mortality of about 1%, … suggesting that maybe as much as 3% to 5% of mortality was related to the pollution” in some regions, said Dr. Pope. This earlier work laid the foundations for the current analysis.

Based, in part, on two previous studies published by Dr. Pope and colleagues demonstrating pollution’s long-term impact on mortality, the US Environmental Protection Agency established new standards for fine particulates. Although these standards were promptly challenged by industry, a recent Supreme Court ruling has upheld the guidelines.

To more conclusively evaluate long-term mortality risk, Dr. Pope and colleagues built on one of the earlier studies: The researchers combined previously collected individual data from 500,000 adults with more detailed statistics on air pollution levels; they also doubled the follow-up period to 16 years. By examining the impact of chronic exposure, the researchers were able to assess its effects on the development of lung cancer and cardiopulmonary disease, Dr. Pope explained.

This study examined a variety of pollutants: total suspended particles, both fine and coarse particulate fractions, sulfate particles, sulfur dioxide, nitrogen dioxide, ozone, and carbon monoxide. Taking individual risk factors into account (age, sex, race, smoking history, education, weight, height, marital status, diet, alcohol consumption, and occupational exposure), the researchers calculated the relative rates of all-cause, cardiopulmonary, and lung cancer mortality among subjects from metropolitan areas monitored for air pollution.

Levels of both fine particulates and sulfur oxide (sulfate particles and/or sulfur dioxide), but not coarse particulates, had a near-linear association with mortality. For example, each 10-µg/m3 increase in fine particulate pollution elevated all-cause, cardiopulmonary, and lung cancer mortality by 4%, 6%, and 8%, respectively. Sulfur oxide pollution was associated with similar increases in those types of mortality and in mortality from other causes as well. These health effects were noted even as air pollution in the United States largely declined, the authors point out. However, coarse particulate pollution did not appear to affect mortality rates.

MIGHT MORTALITY BE REDUCED?

“The association is almost entirely with combustion-related particles, basically particles less than 2.5 microns in diameter, including sulfate particles,” said Dr. Pope. These pollutants predominate “especially in the eastern part of the United States, where, in many communities, as much as half the fine particles is actually sulfate,” noted Dr. Pope. “Most of the sulfur oxides we get are from burning coal,” he explained. However, largely due to environmental controls, such sources have been declining, Dr. Pope pointed out: “There still is a lot of coal burning, but there have been increased attempts to go to low-sulfur coal, as well as to scrubbers and other technology that reduces the emissions of sulfur oxides.”

It is difficult to establish a “safe” threshold for particulate pollution, said Dr. Pope. However, he added, “The current standard of PM2.5 of 15 µg/m3, while it does not eliminate all risk from the air pollution, is probably a very reasonable goal” for our more polluted cities. Dr. Pope stressed, “What these results do show is that any efforts that we make to improve our air quality will likely have additional benefits in terms of reduced risk of mortality.”

—Mimi Zucker, PhD

Reference
1. Pope CA 3rd, Burnett RT, Thun MJ, et al. Lung cancer, cardiopulmonary mortality, and long-term exposure to fine particulate air pollution. JAMA. 2002;287:1132-1141.

Air Pollution Causes Acute Vasoconstriction

ANN ARBOR, MICH—Epidemiological studies have linked elevated levels of airborne pollutants to an increased incidence of cardiovascular events. Controlled human experiments measuring changes in brachial artery diameter (BAD) with exposure to ozone and particulates less than 2.5 microns in diameter (PM2.5) now suggest a mechanism for the increases in cardiovascular risk with air pollution.[1] Robert D. Brook, MD, of the University of Michigan, Ann Arbor, and colleagues entered 25 healthy, nonsmoking subjects, ages 18 to 50 years, into a randomized, double-blind crossover study to compare the effects of two-hour inhalation of either filtered air or a mixture containing approximately 150 mg/m3 of fine particles and 120 ppb ozone. BAD was measured before and within 10 minutes after exposure. BAD was significantly reduced by inhaling the pollutant mixture (mean, –0.09 mm), but it was unchanged by exposure to filtered air (mean, +0.01 mm). IS POLLUTANT-INDUCED VASOCONSTRICTION IMPORTANT? While it is unclear whether one or both components are responsible for the experimental effects noted by Dr. Brook and coworkers, the levels of ozone and PM2.5 tested in their study were comparable to those encountered during peak ambient elevations in pollutants. Further, reactivity of the brachial artery is known to be strongly correlated with that of the coronary artery, suggesting that the observed changes in arterial diameter could occur within cardiac circulation as well. Although the experimental pollutant-induced changes in diameter with air pollution were modest (less than 0.1 mm), such subtle changes could be important in individuals at risk for cardiovascular events, the authors argue. For instance, small decreases in arterial diameter could contribute to cardiac ischemia in individuals with obstructive lesions, or they might destabilize susceptible plaques. —Mimi Zucker, PhD

Reference 1. Brook RD, Brook JR, Urch B, et al. Inhalation of fine particulate air pollution and ozone causes acute arterial vasoconstriction in healthy adults. Circulation. 2002;105:1534-1536.