Particulate matter--a particular concern. (NIEHS News).
A team led by George Thurston published research in the 6 March 2002 issue of the Journal of the American Medical Association presenting what he calls the strongest evidence to date that long-term exposure to airborne P[M.sub.2.5] and related products of sulfur oxide air pollution is an important environmental risk factor for cardiopulmonary and lung cancer mortality. Thurston is an associate professor of environmental sciences at New York University and director of community outreach and education at the university's NIEHS-funded Nelson Institute of Environmental Medicine. Similarly, David Christiani, a professor of occupational medicine and epidemiology at the Harvard School of Public Health, and colleagues published work in the 28 August 2001 issue of Circulation and the May 2002 issue of Epidemiology showing adverse cardiac effects in young boilermakers exposed to fine particulates at work and at home.
Fossil fuel combustion is the main source of P[M.sub.2.5] and sulfur oxide pollution in U.S. air. Most of those particles come from older coal-fired power plants, which are increasing in use because they can operate more cheaply than newer, cleaner plants. The old plants benefited from a grandfather clause under the 1970 Clean Air Act that allowed them to continue operating without cleaning up. Of his findings, Thurston says, "This study provides further evidence that we need to close that loophole in order to protect public health."
More P[M.sub.2.5], More Disease
Thurston's team looked at American Cancer Society data on risk factors and cause of death taken over a 16-year period for some 500,000 Americans living in metropolitan areas. They correlated those data with air pollution data for the same areas over the same period. After controlling for risk factors such as smoking, diet, occupational exposure, and geographic variations, they determined that each 10 [micro]g/[m.sup.3] elevation in P[M.sub.2.5] was associated with a 4%, 6%, and 8% increased risk of death from all causes, cardiopulmonary disease, and lung cancer, respectively.
Those startling numbers garnered the most attention when the study was published, but because they are averaged over all the municipalities studied, they don't completely put the risk in perspective. In the more polluted (and typically more populated) areas of the country, the relative risk is even higher. According to Thurston, the risk associated with living in a large U.S. city translates to about a 20% increased risk of a nonsmoker dying of lung cancer--roughly analogous to the risk faced by a nonsmoker living with a smoker.
With this type of evidence showing that a pollutant to which Americans are exposed on a daily basis is associated with increased risk of cardiopulmonary and lung cancer death, the call to action is clear, says Thurston. "I think this is further confirmation that when we're regulating P[M.sub.2.5] we're on the right track--this is the right area for focus--and that the Environmental Protection Agency was right to promulgate the [more stringent] P[M.sub.2.5] standards."
Of course, the questions at hand are much more complex than when and how to dean up air pollution. As Thurston says, "Energy policy is also health and environment policy ... and right now we're trying to decide on our energy policy. And making this connection between the power plants and pollution makes clear that those are the choices we're making right now. Are we going to build two thousand more coal-fired power plants over the next twenty years? What we do for energy over the next twenty years is going to have a big influence on environment and health, and I think this paper brings this fact home."
The Long and Short of P[M.sub.2.5] Effects
Exposure research conducted by Christiani and colleagues adds a different type of evidence to the P[M.sub.2.5] picture. Their studies focused on the short-term effects on heart rate variability (HRV) in a cohort of young, otherwise healthy workers facing occupational exposure to P[M.sub.2.5] in addition to ambient exposure. HRV is a standard measurement of alteration in cardiac autonomic function; a decrease is cause for concern. Reduced HRV has been associated with increased mortality among heart attack survivors as well as the general population.
In their studies of 40 Boston boilermakers, they found significant HRV reductions when subjects were exposed to typically high levels of P[M.sub.2.5] at work and to ambient levels at home. Their study design let the researchers gather data over longer periods of time and examine the effects of the P[M.sub.2.5] exposure over those time periods, which in turn helped identify the short- and long-acting components of the adverse cardiac effects. They discovered a dose-response relationship between exposure levels and reduction in HRV, and observed that there appear to be both long-acting (several hours) and short-acting (several minutes) components to the mechanisms involved.
The long-acting component may be related to the production of cytokines, an inflammatory response in the lungs. The short-acting component may be related to a sympathetic stress response from inhaled particles affecting the autonomic nervous system directly. Although the two components appear to work independently of each other, the researchers found that the association between the length of P[M.sub.2.5] exposure and the effect on HRV increase~ as the total duration increased. This suggests either the existence of the longer-term component or a cumulative effect that begins shortly after exposure begins.
Although the long-term clinical significance of this association is unclear, the discovery that even short-term exposure to airborne particulate matter has adverse effects on cardiac autonomic control in young, healthy people is disturbing and warrants further investigation. Christiani hopes to expand his research to include measurements of particles smaller than 1.0 [micro]m and assessment of other physiologic responses to exposure, such as acute-phase reactants in serum, gene expression of inflammatory mediators, and pulmonary effects.
"We're really zeroing in on the earliest stages of the disease process with some of these [effects]," says Christiani, "and I think it's a good place to be, because we're not just going to count deaths or severe disease cases. We're looking at basically the earliest responses we can detect in otherwise healthy people to these particles.... The implications are that, in the future, some of the standards we're going to set for environmental exposures may be revised based not just on evidence of mortality, but also on the presence of early markers that predispose people to heart and lung diseases and cancer as a result of particulate exposure."
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|Publication:||Environmental Health Perspectives|
|Date:||Aug 1, 2002|
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