ORLANDO, Fla. Duke University Medical Center pulmonologists have linked a gene to the lung irritation commonly suffered following chronic exposure to ozone, a major component of urban air pollution. Should the new finding in mice be corroborated in human studies, drugs that block the function of the gene might serve as useful treatments for patients with asthma, the researchers said.

The new study adds to earlier work highlighting the importance of genetic factors in determining the lung's response to environmental toxins by pinpointing a key player in the process, said Duke pulmonologist John Hollingsworth II, M.D., lead author of the study.

"The lung is constantly exposed to a broad spectrum of environmental toxins, which can impact the severity of asthma," said Hollingsworth. "While the body's response to environmental exposures can facilitate the clearance of pathogens, it can also lead to injury and compromised lung function. By understanding the molecular mechanisms that initiate inflammation and injury, we may advance on new treatments to prevent the damage."

Hollingsworth presented the research at the 100th International Conference of the American Thoracic Society on May 25, 2004. The study will also appear in a forthcoming issue of the American Journal of Respiratory and Critical Care Medicine. The work was supported by the Department of Veterans' Affairs, the National Institute of Environmental Health Sciences, the National Heart Lung and Blood Institute and GlaxoSmithKline.

Ozone is an unstable molecule comprising three oxygen atoms. Natural ozone in the upper atmosphere plays an important role in filtering out ultraviolet rays from the sun. In the lower atmosphere, however, man-made ozone pollution results from a chemical reaction with nitrous oxide compounds released in automobile exhaust and industrial emissions, particularly under warm, sunny conditions. Such ozone is toxic in small concentrations and can exacerbate as
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Contact: Kendall Morgan
kendall.morgan@duke.edu
919-684-4148
Duke University Medical Center
25-May-2004

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