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Seven years ago, an
Environmental Protection Agency statistician stunned researchers studying the
effects of air pollution on health when he reported analyses indicating that as
many as 60, 000 U. S. residents die each year from breathing federally allowed
concentrations of airborne dust. This and subsequent studies figured prominently
in EPA's decision last year to ratchet down the permitted concentration of
breathable particles in urban air -- and in human airways.
At
the time, many industrialists argued that they shouldn't have to pay for better
pollution control because science had yet to suggest a plausible biological
mechanism by which breathing low concentrations of urban dust might sicken or
kill people.
Now, scientists at the University of Texas Houston
Health Science Center describe how they uncovered what they think may be one of
the basic elements of that toxicity.
On the alert for foreign
debris, a community of white blood cells known as alveolar macrophages patrols
small airways of the lung. When these cells encounter suspicious material, they
identify it and send out a chemical clarion call to rally the immune system
cells best suited to disabling and disposing of such matter.
The
trick is to recruit only as many troops as are needed. If they call in too many,
the lung can sustain inflammatory damage from friendly fire. Alongside the small
troop of macrophages that stimulates defense measures, a larger squadron of
macrophages halts immune activity when it threatens the host.
Andrij Holian and his coworkers in Houston have found that people with
healthy lungs normally have 10 times as many suppressor macrophages as
stimulatory ones. In people with asthma and other chronic lung diseases -- who
face an increased risk of respiratory disease from inhaling urban dust -- that
ratio may be only 3 to 1. The reason for the difference is not known.
In a report to be published in the March Environmental Health
Perspectives, Holian's team describes test-tube studies of human alveolar
macrophages. The macrophages showed no response to ask collected from the Mount
St. Helen's eruption. However, when exposed to airborne dust from St. Louis and
Washington, D. C. , most of the suppresser macrophages underwent apoptosis, or
cellular suicide, while the stimulatory ones survived unaffected. Ash from
burned residual oil, a viscous boiler fuel, proved even more potent at
triggering suppressor cell suicides.
It this test-tube system
models what's actually happening in the human lung, Holian told Science News,
the different responses of the two classes of lung macrophages could result in
an overly aggressive immune response to normal triggering events. Indeed, he
says, it would be the first step in a cascade that can end in inflammatory lung
injury. "We may one day be able to target this up stream event and prevent that
injury."
"This is, I think, an important contribution to the
overall story," says Daniel L. Costa of EPA's pulmonary toxicology branch in
Research Triangle Park, N.C.
Studies by EPA suggest that certain
metals -- especially iron, vanadium, nickel, and copper -- in smoke from
combustion of fossil fuels trigger particularly aggressive inflammatory
responses by lung cells. Costa says these metals play a "preminent" role in the
toxicity of airborne particulates. When EPA researchers removed the metals, they
also removed the toxicity, he says. Moreover, he notes, these metals tend to
reside on the smallest water-soluble particles in urban air --the fraction
targeted for more aggressive controls under the new rules.
John
Vandenberg, assistant director of EPA's National Health and Environmental
Effects Research Laboratory in Research Triangle Park, says Holian's results are
"a nice complement to our studies."