Studies are homing in on which particles polluting the air are most sickening — and why
Tasteless. Invisible to the eye. Air contaminants less than a tenth the size of a pollen grain are nevertheless dangerous.
Even on a clear, sunny day, many tens of thousands — and potentially millions — of tiny particles cloud every breath you take. Some are nearly pure carbon. But reactive metals, acids, oily hydrocarbons and other organic chemicals jacket most of these motes.
Epidemiologists have been calculating human tolls by comparing how many people die when particle numbers in the air are high against mortality figures on cleaner days. Over the past couple of decades, those data have been implicating tiny airborne particles in the deaths of huge numbers of people each year — even where concentrations of these microscopic contaminants never exceed levels permitted by U.S. law.
Based on extrapolations from such data, in China alone an estimated 1 million people die prematurely each year from the toxic inhalation of tiny airborne specks, according to Staci Simonich of Oregon State University in Corvallis and her colleagues in an upcoming Environmental Science & Technology.
Formally referred to as particulate matter, or just PM, these tiny particles from mostly outdoor sources and indoor smoke together “rival ‘overweight and obesity’ as causes of premature death,” Armistead Russell of the Georgia Institute of Technology in Atlanta and Bert Brunekreef of Utrecht University in the Netherlands report in the July 1 issue of the same journal.
Airborne particles range from windblown dust and grit to nanoscale specks that won’t darken the skies, even when 100,000 particles cloud each cubic centimeter of air. The potential impacts of these little particles also vary widely. Particles big enough to taste and feel can be an uncomfortable nuisance but don’t tend to pose big health risks. Fine particles, especially those 2.5 micrometers in diameter or smaller, are another story.
Studies reported over the past few months indict such specks in contributing to or aggravating a host of conditions, from asthma and stroke to heart disease and premature aging of chromosomes.
Industrial smokestacks aren’t the only villains. Several new studies finger vehicular traffic as a major driver of particulate-triggered illness.
Trafficking in heart disease
No surprise, combustion from cars and trucks is a major source of PM-2.5, also known as “fine” particles — ones 2.5 micrometers and smaller — and especially of “ultrafines,” particles no more than 0.1 micrometers (100 nanometers) in diameter, notes Peter Adams of Carnegie Mellon University in Pittsburgh.
The U.S. Environmental Protection Agency regulates concentrations of PM-2.5 in the air. But by number — not mass — the vast majority of airborne particles are ultrafines. They’re as yet unregulated, but not because anyone thinks they are unimportant. Studies have confirmed that they’re the particles inhaled most deeply into the lungs, from which some pass directly into the blood.
The problem, notes Russell, is that ultrafines are devilishly hard to measure, which has impeded the collection of health data linking such Lilliputian specks to disease. But that’s beginning to change. For instance, researchers at the University of California, Irvine and the University of Southern California in Los Angeles have just published data linking the small particles to heart disease.
The scientists measured fine particles and took a rough gauge of ultrafine pollution daily outside four California retirement communities throughout two six-week periods — first in summer, when ozone levels were high, and again in winter. Relatively novel: These scientists analyzed the particulates’ composition to gauge what share came from combustion — here, largely from traffic — and from other sources.
Sixty retirement-home residents, all nonsmokers over age 70 with cardiovascular disease, submitted to weekly blood tests. Assays probed for biomarkers of inflammation, of blood platelets that had turned extra sticky and of cellular stress caused by oxidation — all factors that contribute to and aggravate artery-clogging atherosclerosis.
Although the residents spend the vast majority of their time indoors, all had exposure to traffic pollutants, notes Ralph Delfino, a UC Irvine School of Medicine epidemiologist who led the study. His group and others have shown that fine particulates seep inside homes even when doors and windows are closed.
Changes in the levels of traffic-linked particles outside the retirement homes correlated with changes in biomarkers of inflammation and oxidation in most study volunteers, Delfino and his colleagues report online April 29 in Environmental Health Perspectives.
The traffic–particulate matter trend didn’t hold among some residents taking medicines that can reduce inflammation or platelet aggregation. These drugs made residents relatively immune to the particulates’ atherosclerotic impacts.
Findings from the new study are consistent with those from a German study in 2007 that measured coronary artery calcification, a gauge of atherosclerosis, in nearly 4,500 middle-aged to elderly men and women. After controlling for other risk factors, that study showed that the closer people lived to a major road, the worse their atherosclerosis.
The new California study also showed that particle numbers climbed in winter by almost 50 percent, although the overall PM mass in air varied little. This means particles tended to be smaller in winter.
That makes sense, Delfino says, because cool air close to the ground tends to stagnate. So it takes longer for particles to mix, blow away or glom onto others. He concludes, “Air can get quite a bit more toxic [when it’s cool] than at any other time of year.”
Raising blood pressure
Delfino’s group also collected hourly data on blood pressure from the participants. And blood pressure changes correlated better with increases in traffic-related fines and ultrafines than with similarly small particles from other sources.
At the Experimental Biology meeting in New Orleans in April, Robert D. Brook of the University of Michigan Medical School in Ann Arbor also reported that blood pressure spikes as airborne particulates increase. His group recruited 50 nonsmokers from Ann Arbor to come into a lab for two-hour sessions where the participants breathed either pristine air or local air concentrated to contain 150 micrograms of PM-2.5 pollution per cubic meter. That dirtied air was comparable with levels of pollution that sometimes occur in Detroit, Brook explains, and was only about half as bad as what residents of Beijing, Cairo or Delhi regularly encounter.
During this brief exposure, diastolic blood pressure in volunteers inhaling the dirty air climbed an average of 4 to 5 millimeters of mercury. Blood pressure remained at background levels in the recruits who breathed clean air.
Brook also reported on two longer-term studies at the April meeting. One followed 350 people from three Detroit neighborhoods, correlating blood pressure over a five-day span with local readings of outdoor PM-2.5. In contrast with the lab studies, it was systolic blood pressure that altered in lockstep with the pollution.
Variations in particulate levels generally appeared to trigger changes in blood pressure of 4 to 8 millimeters of mercury. But in an area directly downwind of a power plant, some people experienced bigger, and potentially more dangerous, pressure fluxes, Brook reported — “as much as a 30 mm blood pressure increase for every 10 μg/m 3 increase in PM-2.5.”
Stroke of bad luck
Particulate pollution appears to foster other types of vascular disease as well, such as ischemic stroke, the type caused by the blockage of an artery.
Gregory Wellenius of the Harvard School of Public Health in Boston reported at the Experimental Biology meeting on an analysis of 9,000 patients at regional stroke centers in Ontario, Canada. “We didn’t find any association between ambient air pollution — specifically the PM-2.5 — and risk of ischemic stroke,” he said. Until, that is, his team separated out patients with diabetes, one-quarter of the total group.
“When we looked just at the diabetics,” he said, “there was a very strong effect — a 10 percent increase in risk of being hospitalized for ischemic stroke for every 10 μg/m 3 increase [in PM-2.5].” Overall, the data showed, particulate pollution “tended to be about 10 percent higher on the two days before the diabetics were hospitalized” than earlier or after their symptoms set in.
These findings fit with data that his colleagues published four years ago showing that particulate matter pollution impairs the ability of diabetics’ blood vessels to relax appropriately — a sign of cardiovascular disease. Wellenius says the new diabetes-PM correlation may also explain why earlier studies, which looked at largely healthy people, missed stroke’s link to particulate pollution.
Traffic’s choke hold
Another reason why reports inconsistently link particulates with some ills may stem from the fact that monitoring stations report PM data on the basis of mass and size, not composition. Yet there is considerable variability in what these tiny specks are made of, which tends to reflect their source and whether they’ve morphed during their travels.
To investigate whether PM pollution aggravates childhood asthma, Yale University epidemiologist Janneane Gent and colleagues analyzed PM-2.5 data collected in New Haven, Conn. Then they calculated the likely share of the tiny motes that came from particular sources, based on the ratio of metals and other elements that serve as characteristic markers of the most likely contributors: tailpipe exhaust, road dust, biomass burning, sea spray and power plant (and home heating) emissions.
Mothers of the 149 children recruited for the study kept a yearlong daily log of the kids’ symptoms and any need for asthma medicines. When the researchers correlated the daily particle pollution against these logs, “we didn’t find any association between overall PM-2.5 and health,” Gent notes. But when the team stratified these fines by apparent source, she says, “we found that for every additional 5 μg/m3 mass from motor vehicles or road dust, you see an increase in the [risk] of respiratory symptoms or inhaler use.”
Pollution aggravated some symptoms more than others, they report in an upcoming Environmental Health Perspectives. For each 5 μg/m 3 increase in mass, Gent says, “we see that a child typically had a 10 percent increased risk of wheezing” — in addition to a 3 percent increased risk of persistent cough and a 12 percent increased risk of shortness of breath.
Flipping genetic switches
Some researchers are probing for pollution-induced genetic changes that may underlie symptoms of particulate-linked disease.
At the Experimental Biology meeting, Jesus Araujo described his team’s research into how airborne particulates promote atherosclerosis. Previously, Araujo, who directs environmental cardiology at the University of California, Los Angeles’ Geffen School of Medicine, and his colleagues showed that constituents of certain tiny particles “can synergize” with plaque-fostering elements of low-density lipoprotein cholesterol, or “bad cholesterol.” The combination turned on genes that foster vascular inflammation, a driver of atherosclerosis.
In test tube studies, tiny particulates dramatically boosted the activity of some 1,600 of the 9,000 genes surveyed. Follow-up work showed mice “exposed to ultrafine particles had an up-regulation of those same genes,” Araujo said.
More recently, Araujo’s team exposed genetically engineered mice for 75 hours to clean air or to air enriched with Los Angeles particulates. The animals’ engineered predisposition to atherosclerosis serves to model early stages of this disease in people. Animals getting the dirty air were exposed over five weeks to either fines or to ultrafine particles.
“Those exposed to the fine particles exhibited about a 25 percent increase in lesions — aortic atherosclerotic plaque — over mice breathing clean air,” Araujo says. Mice getting only the ultrafines, a size fraction that tends to contain at least twice the amount of polycyclic aromatic hydrocarbons present in PM-2.5 particles, developed a 50 percent increase in plaques.
Moreover, Araujo observes, “animals exposed to the ultrafine particles developed evidence that their plasma high-density lipoprotein cholesterol, or ‘good cholesterol,’ lost its ability to protect against oxidation and inflammation.” His group recently showed that the inability of this HDL cholesterol to protect correlates strongly with buildup of arterial plaque. So this HDL, which appears to become pro-inflammatory, is no longer “good cholesterol,” he concludes.
Since ultrafine particles constitute the majority of fines, much of the plaque-fostering impact of fine particulates may trace back to the ultrafines, Araujo says. In his region, traffic is a major source of those ultrafines.
Traffic also appears to prematurely age the body’s genetic material. Andrea Baccarelli of the University of Milan and his colleagues compared DNA in white blood cells from 77 people who regularly stand in the roads directing traffic with that from 57 office workers. Outdoor workers assigned to high-traffic streets had significantly shorter protective caps on the tips of their chromosomes than did any of the other recruits.
These caps, known as telomeres, tend to shorten each time cells divide. As such, telomere length serves as a rough gauge of biological aging. After accounting for the individuals’ ages, Baccarelli says, blood cells of workers who regularly had high daily exposures to combustion exhaust “looked 10 years older” than the cells should. Eventually, when telo-meres become too short, a chromosome’s genetic material can start to degrade. Baccarelli’s team reported its findings in San Diego in May at the American Thoracic Society annual meeting.
On the job exposure
At the same meeting, the team also reported a link between exposure to fine particles and epigenetic changes to DNA — either the addition or removal of methyl groups (a carbon bonded to three hydrogen atoms). Such changes inactivated two cancer-suppressor genes and altered the activity of other genes throughout the body in ways that Baccarelli notes have been linked with “higher incidence and mortality from cardiovascular disease.”
Among foundry workers at a steel plant in northern Italy, an increasing incidence of switched-off tumor suppressor genes accumulated during the week, when PM exposures were high, then fell over the weekend, presumably as repair mechanisms caught up. “This signifies,” Baccarelli says, “that after only three days of work, these men experience changes in the regulation of their genes.”
Although such changes appeared reversible, his group witnessed a similarly inappropriate methylation of inflammation-provoking genes that didn’t recover over a weekend, suggesting cardiovascular impacts could be longer lasting.
Another persistent change that didn’t recover after a weekend away from work: The blood cells of foundry workers with high workplace PM exposures had mitochondria with extra copies of their genomes. In these energy powerhouses, the development of additional copies of DNA tends to reflect genetic damage, Baccarelli says, as the mitochondria attempt to compensate for oxidative stress.
It was hard to tease out which size particles were most toxic, he says, because as the number of small particulates rises or falls in the foundry air, so too does the number of even smaller particles. But particulates enriched with metals, especially cadmium and chromium, did correlate with high levels of epigenetic damage in the workers, Baccarelli reported.
When it comes to particulate toxicity, “there’s no question: Size and chemistry are both important,” Russell says. And studies do suggest “that traffic probably has a greater health impact on a per-mass basis than do other [PM] sources.”
That said, Russell argues that science hasn’t presented a clear enough picture to help policy makers know how best to improve regulations. At issue: Should the emphasis remain on regulating solely by size and quantity of particles — perhaps finally tackling ultrafines? Or by size and chemistry? Or maybe even by pollution sources, such as traffic?
“To settle this,” Russell says, “we’re going to need far more of these epidemiology and toxicity studies.”
Araujo. J.A., et al. 2008. Ambient particulate pollutants in the ultrafine range promote early atherosclerosis and systemic oxidative stress. Circulation /research 102(March 14):589.
Delfino, R.J., et al. In press. Air pollution exposures and circulating biomarkers of effect in a susceptible population: Clues to potential casual component mixtures and mechanisms. Environmental Health Perspectives.
Dioni, L. . . . and A. Baccarelli. 2009. Telomere length and particulate matter exposure in steel workers (Abstract F47). American Thoracic Society meeting. May 18. San Diego.
Gent, J.F., et al. In press. Symptoms and medication use in children with asthma and traffic-related sources of fine particle pollution. Environmental Health Perspectives.
Hoffman, B., et al. 2007. Residential exposure to traffic is associated with coronary atheroschlerosis. Circulation 11:489-496.
Hou, L.H. . . . and A. Baccarelli. 2009. Mitochondrial DNA copy number and occupational exposure to particulate matters (Abstract A54). American Thoracic Society meeting. May 20. San Diego.
Hoxha, M. . . . anf A. Baccarelli. 2009. Accelerated telomere shortening in response to air pollution from traffic emissions. American Thoracic Society meeting. May. San Diego.
O'Neill, M.S., et al. 2005. Diabetes enhances vulnerability to particulate air pollution-associated impairment in vascular reactivity and endothelial function. Circulation 111(June 7):2913.
Pegoraro, V. . . . and A. Baccarelli. 2009. Effects of particulate matter exposure on p16, p53, APC and RASSF1A promoter methylation (Abstract C51). American Thoracic Society meeting. May 17. San Diego.
Russell, A.G., and B. Brunekreef. In press. A focus on particulate matter and health. Environmental Science & Technology.
Tarantini, L. . . . and A. Baccarelli. 2009. Effects of exposure to metal-rich air particles on DNA methylation of inflammatory-genes (Abstract F21). American Thoracic Society meeting. May 18. San Diego.
Visit the U.S. Environmental Protection Agency’s particulate matter home page, [Go to]
Baccarelli, A., et al. 2009. Rapid DNA methylation changes after exposure to traffic particles. American Journal of Respiratory & Critical Care Medicine 179:572-578.
Baccarelli, A., et al. 2008. Cardiac autonomic dysfunction: Effects from particulate air pollution and protection by dietary methyl nutrients and metabolic polymorphisms. Circulation.
Clean air Research Program, USEPA. Particulate Matter (PM) Basics. [Go to]
Ehrenberg, R. 2009. Life expectancy up when cities clean the air. Science News Online (Jan. 21). [Go to]
Harder, B. 2005. Pollution ups blood pressure: Inhaled particles linked to transient effect. Science News 168(July 16):37. [Go to]
Harder, B. 2005. An ounce of pollution: Particles' harm varies by person, region, season. Science News 167(March 26):196. [Go to]
Harder, B. 2004. Conduit to the brain: Particles enter the nervous system via the nose. Science News 165(Jan. 24):54. [Go to]
National Center for Environmental Assessment-RTP Division. 2009. Intregrated Science Assessment for Particulate Matter, First External Review Draft. Feb. 19. [Go to]
Polidori, A. . . . R.J. Delfino, et al. Indoor/outdoor relarionships, trends, and carbonaceous content of fine particulate matter in retirement homes of the Los Angeles Basin. Air & Waste Management Association online journal.
Raloff, J. 2003. Air sickness. Science News 164(Aug. 2):72. [Go to]
Raloff, J. 2001. Blood points to pollution's heart risks. Science News 160(July 7):9. [Go to]
Tarantini, L. . . . and A. Baccarelli. 2009. Effects of particulate matter on genomic DNA methylation content and iNOS promoter methylation. Environmental Health Perspectives 117(February):217-222.
Wellenius, G.A., J. Schwartz, and M.A. Mittleman. 2005. Air pollution and hospital admissions for ischemic and hemorrhagic stroke among medicare beneficiaries. Stroke 36(December):2549.