Researchers find marker for ozone-induced cardiac dysfunction

August 14, 2012

(COLLEGE STATION, TEXAS) – Researchers at the Texas A&M Health Science Center (TAMHSC) have identified a protein marker specific to cardiac dysfunction stemming from incidental exposure to ozone, a strong oxidizing agent and major atmospheric pollutant. This finding may enable health care providers to more specifically treat heart disease, especially in the case of patients exposed to chronically high levels of ambient air pollution.

Rajat Sethi

Dr. Rajat Sethi

The study is available online in the journal Molecular and Cellular Biochemistry and will be in an upcoming print edition.

Lead scientist and principal investigator Rajat Sethi, Ph.D., assistant dean for research and evidence-based practice at the TAMHSC-College of Nursing, and a multidisciplinary team of researchers found a potentially invaluable link between membrane bound proteins caveolin-1 and caveolin-3 and cardiac injury due to exposure to high ozone levels. The study revealed changes in cardiac levels of caveolin-3 that are specific to ozone-mediated cardiac injury.

This research is the first to report the significance of caveolin-3 levels and its regulatory role in ozone-induced cardiac dysfunction. The findings now enable clinicians to look at caveolin-3 levels as a potential predictor for cardiac injury specific to ozone exposure, especially in locations infamous for smog.

“Clinical biomarkers for most pathological conditions have been identified to understand the specific disease progression, its diagnosis and management,” Dr. Sethi said. “We wanted to characterize the markers associated with cardiac dysfunction resulting from chronic ozone exposure.”

“What this means to science is that while ozone can and does affect the heart, a specific biomarker, caveolin-3, has the potential to guide treatment of heart disease, specifically in the population chronically exposed to high ozone levels from air pollution,” continued Dr. Sethi, noting more than 60,000 deaths annually are linked to environmental pollutants. “Although more studies are needed, this finding has the potential to save thousands of dollars in heart disease treatment if the treatment can be as simple as reducing the amount of bad ozone.”

Dr. Sethi and a multidisciplinary team of TAMHSC researchers have studied the effects of air pollution on heart function since 2006. Previous scientific contributions from his Cardiovascular and Drug Development Research Laboratory determined ozone to be a major player in myocardial (heart) dysfunction.

In an earlier study in Molecular and Cellular Biochemistry, Dr. Sethi found ozone can trigger cardiac toxicity through a cascade of inflammatory mediators. The endpoint in this domino effect can result in death of heart cells, leading to a heart attack. These findings recently were cited by the U.S. Environmental Protection Agency (EPA) in a study published in the journal Circulation, where they also showed cardiac dysfunction in humans exposed to ozone in a controlled environment.

A long-term objective of this research and this Molecular and Cellular Biochemistry study is to provide relevant data useful in guiding regulatory policies to the EPA regarding air quality standards pertaining to ozone levels, as the federal agency is required to set ozone standards under the Clean Air Act.

Other contributors to the Molecular and Cellular Biochemistry study were David Dostal, Ph.D., TAMHSC-College of Medicine; Srinath Palakurthi, Ph.D., Shubham Manchanda, Rama Surya Prakesh Perepu and Ajay Kumar, all of TAMHSC-Irma Lerma Rangel College of Pharmacy; Carlos Garcia, Ph.D., Texas A&M University-Kingsville; and Richard H. Kennedy, Ph.D., Loyola University Medical Center. Research was supported by the EPA and the Texas A&M Health Science Center.

— Holly Shive