THURSDAY, July 22 (HealthDay News) -- A new animal study offers the first direct bit of evidence that ozone, a major component of smog, may trigger the death of heart cells.
In small early tests with rats, U.S. researchers found that exposure to ground-level ozone over several weeks boosted the activity of tumor necrosis factor-alpha (TNF-A), an indication of inflammation. Increased TNF-A levels have been linked to a drop in levels of a heart-protective protein called Caveolin-1 (Cav1). This protein is believed to protect the heart by binding to a chemical called p38MAPK alpha, which is a known cell death signaling chemical.
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Levels of the heart-protective Cav1 protein decreased in the hearts of rats exposed to ozone compared to the hearts of rats who breathed filtered air.
"We believe the decreased levels of Cav1 make more unbound p38MAPK alpha available for telling the heart cells to die. That link between Cav1 and (ozone) has never been shown in the heart," Rajat Sethi, an assistant professor in the pharmaceutical sciences department at Texas A&M Health Science Center's college of pharmacy, said in an American Heart Association news release.
The study was to be presented Wednesday at an American Heart Association meeting in California.
"Several studies have already shown that air pollution increases the risk of coronary arteriosclerosis and heart attack. Post-menopausal women have been shown to have an increased risk of stroke as well from fine particulate matter in air pollution," Dr. Len Horovitz, a pulmonary specialist at Lenox Hill Hospital in New York City, said in a news release.
"Now there is evidence (in rats) that ozone, a key component among others in smog, can trigger a direct effect on cardiac tissue through a cascade of inflammatory mediators. The endpoint in this domino effect can result in death of heart cells -- a heart attack, in essence," he said.
The researchers cautioned, however, that more evidence was needed before human studies can begin.
-- Robert Preidt
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SOURCE: American Heart Association, news release, July 21, 2010
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