14 DAY TRIAL // Exposure to ground-level ozone for several weeks increases tumor necrosis factor-alpha (TNF α) in the heart, a study carried out on rats concluded. The results were presented at the American Heart Association's Basic Cardiovascular Sciences 2010 Scientific Sessions - Technological and Conceptual Advances in Cardiovascular Disease, according to ScienceDaily.
Ozone (O3) is a reactive gas made of three oxygen molecules. The ozone layer is normally found in the upper atmosphere and it protects the Earth from the Sun's radiations. Unfortunately, smog also forms at ground-level because of the reactions between sunlight, nitrogen oxides and hydrocarbons from fossil fuel and industrial pollution.
Rajat Sethi, Ph.D., an assistant professor in the Department of Pharmaceutical Sciences at the Texas A&M Health Science Center Irma Lerma Rangel College of Pharmacy in Kingsville, Texas, involved in the study, said that “Several epidemiological studies have linked air pollution to the development of cardiovascular disease, but air pollution contains hundreds of chemicals and those studies were unable to separate out the effects of individual components. Our study looked for direct evidence of the role of ozone alone in cardiac dysfunction by creating a controlled environment.”
The experiment consisted in testing four groups of 10 rats inside clear plastic-glass boxes. Two groups were exposed to 0.8 parts per million of O3, for eight hours a day, 28 or 56 days in a row. The other two groups were exposed to clean, filtered air, for eight hours a day, over the same periods of time. After daily testing, the rats breathed clean air for the remaining 16 hours.
The study concluded that rats who had been exposed to O3 had high levels of tumor necrosis factor-alpha (TNF α) in their hearts. These increased levels have been related to drops in Caveolin-1 (Cav1) level, a protein that protects the heart. Sethi said that Cav1 protects the heart by being linked to a cell death signaling chemical called p38MAPK alpha (p38MAPK α).
Rats that breathed filtered air had normal levels of Cav1. Sethi added that “the decreased levels of Cav1 make more unbound p38MAPK α available for telling the heart cells to die. That link between Cav1 and O3 has never been shown in the heart," he said.