Web edition: June 26, 2012
As reported this week, breathing elevated ozone levels can mess with the cardiovascular system, potentially putting vulnerable populations — such as the elderly and persons with diabetes or heart disease — at heightened risk of heart attack, stroke and sudden death from arrhythmias. Is this really new?
Turns out it is, says Robert Devlin, the Environmental Protection Agency toxicologist who led the new study. Among the chief priority air pollutants affecting human health that his agency regulates are ozone and near-nano-scale particles called PM (for particulate matter). Although air pollution can affect the heart, there has been a longstanding question about which constituents deserve the blame.
In urban areas especially, many different pollutants are produced by the same or similar processes, so they tend to show up as a mix. Teasing out the role of any individual element can prove challenging.
A little more than 20 years (SN: 4/6/91, p. 212), studies emerged showing that airborne PM levels below the federal limit were killing people in many U.S. cities. An ambitious hunt immediately commenced to find out how and why. Data on the why are still emerging and a bit equivocal. But clearly, this pollution can damage the lungs, heart and brain.
Ozone, by contrast, had for years appeared fairly wimpy. Sure, it could aggravate asthma. But for decades there were no data indicating this pollutant would kill people without pre-existing lung disease. And to this day, Devlin notes, data on non-lung impacts from ozone tend to be quite thin.
So until ozone mortality data started to come out around 2004 (SN: 12/11/04, p. 372), his team had little motivation to probe for cardiovascular impacts. But it’s probed them now — and found plenty of potentially adverse changes in a trial involving 23 healthy young men and women. Some of the more compelling observations involve markers of inflammation, the scientists report in a paper published ahead of print June 25 in Circulation.
Tracy Stevens finds them compelling, anyway. The reason: “The big theory about cardiovascular disease centers around inflammation,” notes this cardiologist at St. Luke’s Mid America Heart Institute in Kansas City, Mo.
“I think of plaque in the arteries like pimples,” she says. Yes — she’s talking about zitz.
As pimples become inflamed, they fill with pus, eventually rupturing and then scabbing over. “And that’s essentially what happens in a sudden heart attack or sudden stroke,” she argues.
Beginning in childhood, fatty plaque deposits can begin to accumulate along the interior walls of arteries. Various agents of the body’s immune system (such as the interleukins and tumor necrosis factor elevated in the new study) can inflame this plaque. And when they do, the fatty deposits can engorge with immunity-driven materials, eventually to the point of bursting.
The body will interpret a rupture as the equivalent of a cut — something that needs immediate repair, Stevens explains. In an attempt to seal the breach, a clot forms — “and it’s the clot that obstructs the blood flow and triggers the sudden crisis.” This, in fact, explains why some people survive a stress test in the doctor’s office only to drop dead a day later from a heart attack. It’s not that the stress test failed to find a problem, she says, but that “the patient, for whatever reason, had a spontaneous plaque rupture the next day.”
The elderly may be especially vulnerable to ozone’s inflammatory impacts, she worries, because they tend to have the most plaque and the longest exposure to this pollutant.
In addition, Stevens points out that some of the inflammatory chemicals that rose in the new study following ozone inhalation “can trigger inappropriate artery constriction and cause spasms.”
Cardiologist Wayne Cascio, who heads a division on environmental public health at EPA’s National Health and Environmental Effects Laboratory, noted that his scientists’ new study also identified provocative signs of an elevated risk of clotting after the volunteers had breathed in ozone-enriched air.
The pollutant altered levels of several clot-related proteins, including plasminogen, tissue plasminogen activator and plasminogen activator inhibitor. Concentrations of some went up, others down. Based on the pattern of changes, notes Cascio, “one might predict that [high ozone] would slow the dissolving of clots.” That suggests clots might propagate or enlarge, he says — “or potentially block up a vessel, causing a heart attack or stroke.”
Keep in mind, Devlin notes, many different conditions spawn clots. But once they form, he says, his group's data are now “suggesting that exposure to ozone might inhibit the body’s ability to dissolve them.”
When EPA is charged with imposing or revising health-related pollution standards, it’s not enough to have good epidemiology — observations and survey data suggesting associations between events (like disease) and possible predisposing factors, explains air pollution epidemiologist Douglas Dockery of the Harvard School of Public Health. Although epidemiology can point to associations, he explains, it can’t establish causes. Yet to set federal health-protecting pollutant limits, “you really need to know that there is a true causal link between this pollutant and a health effect.”
“And that’s what makes the new study so remarkable,” he says. The EPA scientists carried out controlled exposures in people and then conducted electrocardiograms and blood sampling over a prolonged followup period. Through this intensive probing, he maintains, those researchers have at last demonstrated that ozone “is causally linked” to adverse cardiovascular changes.
R.B. Devlin et al. Controlled exposure of healthy young volunteers to ozone causes cardiovascular effects. Circulation. Published online June 25, 2012. doi: 10.1161/CIRCULATIONAHA.112.094359. [Go to]
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