Air Sickness

How microscopic dust particles cause subtle but serious harm

On Oct. 26, 1948, a temperature inversion laid a blanket of cold, stagnant air over Donora, Pa., a tiny mill town on the Monongahela River. Over the next 5 days, the buildup of pollution cloaked the sun, sometimes restricting vision to just a few feet. Twenty people died outright and 50 more perished within a month from lingering health damage, says consulting epidemiologist Devra Davis, a former Donora resident whose own family survived the tragedy.

LOOK HARD. Fine, metal-laden particles from industrial sources in Hettstedt, Germany, are too diffuse to make the air hazy. When Environmental Protection Agency scientists collected and applied these particles to lung tissue from mice, however, they aggravated symptoms of asthma. Similar amounts of relatively metalfree dust had no such effect. Heinrich/ GSF Inst. of Epidemiology
SOOTY RESIDUES. This chain of ultrafine particles came from mucus lining an airway of a nonsmoking, lifetime resident of Mexico City. The sooty, submicron-scale spheres appear to be diesel-exhaust particles. Churg/Univ. of British Columbia

As bad as her hometown’s pollution had been, its impact would pale against a 5-day killer smog that settled on London in December 1952. It killed some 12,000 people within 3 months, according to calculations in a June 2001 report by Davis and Michelle L. Bell of Johns Hopkins University in Baltimore. “With a death rate more than three times the norm for this period, the London fog of 1952 is widely regarded as a catalyst for the study of air pollution epidemiology,” the pair noted.

That science would eventually show that even the diffuse dust wafting in seemingly clear air could kill. Its victims are just harder to identify than those in the London and Donora catastrophes because most who succumb are elderly or already in ill health. Indeed, a trailblazing 1991 analysis by Joel Schwartz, then at the Environmental Protection Agency, concluded that some 60,000 U.S. residents die from heart attacks and respiratory problems each year because of the effects of airborne dust at concentrations within federal pollution limits (SN: 4/6/91, p. 212).

Stunning as those numbers were at first, they’re now accepted by most researchers. In that 1991 study and subsequent ones, Schwartz, now at the Harvard School of Public Health in Boston, has shown that community death rates rise and fall nearly in lock-step with local changes in concentrations of tiny dust particles—even when concentrations of those particulates are just one-quarter of the federal limit for outdoor air.

Yet more than a decade later, nagging questions remain: What makes dust and smoke particles, especially small ones, toxic? Is particulate matter, as scientists call it, inherently poisonous, regardless of its composition? Or does a large surface area per unit mass make those particles robust vehicles for ferrying toxicants such as metal atoms deep into the lungs?

In the past 2 years, a flurry of new data has finally begun answering these questions. The research links the greatest harm to the tiniest dust: particulate matter no more than 2.5 micrometers in diameter, called the PM-2.5 fraction. Some studies suggest that the most dangerous of all may be ultrafines, particles less than 0.1 micrometer across—a class of dust that environmental studies and regulations have generally ignored.

Remodeled airways

Although most people who die from particulate pollution had heart disease or respiratory problems, the new data are showing that even young and healthy people aren’t immune to the violence that dust can perpetrate on lung tissue.

In Fresno, Calif., for instance, outwardly robust people routinely harbor damage in their lungs’ small airways, setting the stage for respiratory and cardiovascular disease. These lung effects appear to trace to Fresno’s high level of PM-2.5 pollution, which is as bad as that in Los Angeles and worse than that in nearly any other U.S. city, according to Kent E. Pinkerton of the University of California, Davis and his colleagues. They surveyed the airways of more than 80 men who had been longtime residents of Fresno—many of them in their 20s to 40s—who died from auto accidents and other events unrelated to pollution.

Pinkerton’s team found that PM-2.5 has little effect on the lungs’ larger passages but injures the deeper, smaller, thin-walled bronchioles that mark where the body begins to extract oxygen from air. The damage was apparently caused by the ravages of molecular fragments called free radicals. The affected tissue exhibited a kind of scarring called fibrosis and an abnormal thickening, two features that make breathing more difficult.

To confirm the role of particulate pollution in these subtle changes to the lung, Pinkerton’s colleague Kevin R. Smith exposed young-adult rats for 4 hours on 3 consecutive days to air deliberately concentrated with the particulates in Fresno’s atmosphere. The amount of PM-2.5 in the test air, Pinkerton notes, reflected “what can exist in Fresno on bad-air days.”

After the exposures, Smith examined areas of the rats’ lungs and extracted unusually large numbers of inflammatory cells, called neutrophils, as well as hosts of dead cells.

“It’s not unusual to see an occasional dead cell” in the lungs of rats that had breathed only clean air, Pinkerton notes, but the dust-exposed rats showed many dead lung cells, including macrophages—the organ’s housekeeping cells. Because macrophages normally gobble up cellular trash such as pollutant particles, their loss could prove important, the Davis team notes in the June Environmental Health Perspectives.

In the May issue of that journal, Andrew Churg of the University of British Columbia in Vancouver and his colleagues report similar findings in the autopsied lungs of 11 nonsmoking women from Mexico City, but not in an equal number from Vancouver. Though the Canadian city’s air is relatively clear of particulates, Mexico City’s air carries a dense haze of fine dust much of the year.

The scientists focused on the lungs’ smallest, oxygen-absorbing airways. Compared with those from the Canadian women, the tiny airways from residents of Mexico City “were very abnormal,” Churg says. They were twisted and exhibited significantly more fibrosis and thickness than normal lung tissue. “A heavy smoker could have airways that look very much the same,” he told Science News.

Churg’s colleague David Bates plans to test whether the effects the team documented translate into breathing problems in healthy Mexico City adults.

Lilian Calderón-Garcidue±as of the University of North Carolina at Chapel Hill says she knows what Bates will find. At the Experimental Biology meeting in San Diego last April, she documented mildly obstructed breathing in 10 percent of the 174 ostensibly healthy Mexico City children she examined. All the children came from middle- to upper-class nonsmoking families living where the air wasn’t the city’s dustiest.

Heart of the matter

Despite the natural expectation that lungs should be especially vulnerable to dust, “the worst effects, it turns out, are on the cardiovascular system,” observes particle toxicologist Ken Donaldson of the University of Edinburgh.

Some of the most intriguing clues to what underlies these effects are emerging from studies on endothelin. This small protein, produced in healthy lungs, ordinarily prompts blood vessels to constrict to maintain proper blood pressure.

Renaud Vincent of Health Canada in Ottawa, Ont., and his colleagues had been wondering what makes some people particularly vulnerable to an increase in pollution, even in a relatively unpolluted Canadian city. To find out, the researchers exposed healthy volunteers to high concentrations of PM-2.5. They found that endothelin concentrations doubled in healthy people’s blood when their exposures tripled from 50 micrograms per cubic meter (µg/m3) to 150 µg/m3, a range typical for the world’s most polluted cities.

Although the endothelin jolt didn’t hurt these healthy volunteers, previous studies have shown that people with artery-clogging atherosclerosis have a higher risk of dying after a heart attack if they had endothelin concentrations comparable to the spikes observed in the volunteers’ blood.

Interestingly, Vincent notes, his team could trigger increases of endothelin only with the kind of dirty dust usually encountered outside—particles that carry some chemical hitchhikers, including metals and hydrocarbons. When the researchers washed the particles to remove those hitchhikers, the PM-2.5 exposures had no impact on blood concentrations of endothelin.

Harvard School of Public Health scientists also have begun exploring dust’s cardiovascular effects. Gregory A. Wellenius and his colleagues exposed dogs to either clean filtered air or air seeded with 30 times the concentration of particulates that local outdoor air carried that day. The exposures lasted 6 hours on 3 or 4 consecutive days.

Right after each exposure, the researchers simulated a heart attack in the dogs by constricting a surgically implanted balloon that temporarily shut off a coronary artery. During this blockage, the researchers measured the heart’s growing oxygen debt.

The debt was significantly larger in animals that had been exposed to fine airborne dust, the scientists reported in the April Environmental Health Perspectives. A dog’s other coronary arteries couldn’t dilate as well and couldn’t compensate for the blocked vessel if the animal was inhaling particulates, Wellenius speculates. Such a reaction is “entirely consistent” with an endothelin boost from exposure to particulate pollution, he says.

A nose for clues

The collective message from the 200-or-so Mexico City mongrels that Calderón-Garcidue±as and her colleagues studied is also alarming.

A neuropathologist, she was concerned that if dust could damage lung tissue, it might also break down the capacity of nasal passages to block substances from entering the brain. She now reports tracing metals associated with fossil fuel combustion—chiefly vanadium and nickel—from the dogs’ nasal tissue, through the olfactory bulb, and into the frontal lobe and hippocampus of the animals’ brains.

Because such metals can foster damage by generating free radicals, Calderón-Garcidue±as looked for signs of brain changes in dogs living in areas with heavy particulate pollution.

Dogs often serve as a model for human age-related cognitive impairments. Some dogs at age 10 and older develop the waxy brain plaques characteristic of Alzheimer’s disease (SN: 11/3/01, p. 286: Available to subscribers at Attacking Alzheimer’s). “In Mexico City,” Calderón-Garcidue±as told Science News, “we are seeing [plaque] pathology in 11-month-old pups”—a dramatic acceleration in the development of the signature of Alzheimer’s disease.

These data are “definitely worrisome,” she says, especially in light of her preliminary findings of a similar breakdown in the nasal tissue of many people living in Mexico City.

Another new study in mice, this one by EPA scientists, suggests that particulates do their harm via the metals they sometimes carry. They found signs that exposure to metal-laden PM-2.5 aggravates asthma much more than does relatively metalfree dust.

Stephen H. Gavett of the agency’s Research Triangle Park, N.C., laboratory and his colleagues used dust collected in two eastern German towns—one an industrial community polluted with metals and other combustion products and the other a farm village with relatively clean air. The metal-rich dust, gathered by Joachim Heinrich of the GSF Institute of Epidemiology in Neuherberg, Germany, proved far more potent in aggravating asthmatic constrictions of an animal’s airways, the researchers will report in the September Environmental Health Perspectives.

Ultrafines, ultrabad?

If such studies suggest that the composition of inhaled particles affects their toxicity, other findings indicate that particle size can greatly exacerbate the problem.

In studies with isolated lung cells, for example, ultrafine particles proved to be between 10 and 50 times as potent as PM-2.5 or PM-10 particles in inducing free-radical damage, such as inflammation. Andre Nel of the University of California, Los Angeles and his team reported their findings in the April Environmental Health Perspectives.

Nel’s team also found that ultrafine particles from urban air carry far more toxic combustion hydrocarbons on their surface, per unit mass, than larger particles do. Further probing showed that the smaller motes tend to lodge in cells’ mitochondria, the organelles that generate power. The particles turn the mitochondria into “functionless bags,” says Nel. And when these powerhouses die, he says, so do the cells they power.

Donaldson has tested “particles that are completely naked”—motes of pure carbon or titanium dioxide, for instance—and shown they cause no damage when delivered to rat lungs as 10-micrometer-wide particles. But crush them into submicron pieces, he says, and “they become highly inflammogenic to the lungs.”

Why? Lung-defending macrophages can easily catch and discard the occasional big particle that gets lobbed their way. Exposing the lungs to large numbers of the smallest particles, however, “may completely overwhelm their defenses,” Donaldson says. His team’s data support that scenario.

After decades of research, says Donaldson, toxicologists are still discovering ways that fine dust particles can kill. And as the dust particles in their sights get ever smaller, the challenge of controlling their release gets ever larger.


Dust Rules

A finer standard governing particulate pollution is on the horizon

Environmental agencies around the world today regulate dusty pollutants on the basis of mass—not chemistry—and most governments focus on the particles easiest to catch and quantify: those that are 10 micrometers across (the PM-10 fraction), rather than 2.5-micrometer particles (PM-2.5) and smaller ones.

Seven years ago, the U.S. Environmental Protection Agency announced it would soon require states to regulate airborne concentrations of PM-2.5 pollution in recognition of the smaller particles’ significantly greater toxicity than larger

particles and ability to move far deeper into the lungs, (SN: 12/21/96, p. 410). Almost immediately, the agency was sued by several industries that would be affected.

It took a Supreme Court ruling 2 years ago to get the regulations back on track (SN: 3/10/01, p. 159: Available to subscribers at High court gives EPA a partial victory). Yet “we’re definitely several years away” from enforcement of any regulation limiting PM-2.5 pollution, says EPA spokesman Dave Deegan in Washington, D.C.

So, for now, federal law prohibits PM-10 concentrations in air from exceeding an average of 150 micrograms per cubic meter (µg/m3) over any 24-hour period or a 50 µg/m3 daily average over an entire year. When PM-2.5 rules do go into effect, they’ll restrict the 24-hour average air concentration of those small particles in any city to 65 µg/m3 and the annual average concentration to just 15 µg/m3.

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Janet Raloff

Janet Raloff is the editor of Science News for Students, a daily online magazine for middle school students. She started at Science News in 1977 as the environment and policy writer.

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