Effects of Ozone on Normal and Potentially Sensitive Human Subjects

Research Report 78, June 1997

Part I: Airway Inflammation and Responsiveness to Ozone in Normal and Asthmatic Subjects John R Balmes, Robert M Aris, Lisa L Chen, Cornelius Scannell, Ira B Tager, Walter Finkbeiner, Dorothy Christian, Thomas Kelly, Patrick Q Hearne, Ronald Ferrando, and Barbara Welch

Part II: Airway Inflammation and Responsiveness to Ozone in Nonsmokers and Smokers Mark W Frampton, Paul E Morrow, Alfonso Torres, Karen Z Voter, John C Whitin, Christopher Cox, Donna M Speers, Ying Tsai, and Mark J Utell

Part III: Mediators of Inflammation in Bronchoalveolar Lavage Fluid from Nonsmokers, Smokers, and Asthmatic Subjects Exposed to Ozone: A Collaborative Study Mark W Frampton, John R Balmes, Christopher Cox, Peter M Krein, Donna M Speers, Ying Tsai, and Mark J Utell

Dr. John Balmes and colleagues of the University of California, San Francisco, and Dr. Mark Frampton and associates of the University of Rochester characterized ozone-induced responses in two different study populations: normal and asthmatic men and women in the Balmes study (Part I), and male and female nonsmokers and smokers in the Frampton study (Part II). The investigators addressed three issues: (1) Is an individual's reactivity to inhaled methacholine related to changes in lung function after exposure to ozone? (2) What is the relation between ozone-induced airway inflammation and changes in lung function? and (3) Do the changes in lung function and markers of inflammation in response to ozone exposure differ between normal people and people with asthma? In both studies, participants performed moderate exercise during the exposure period. The investigators made a number of pulmonary function measurements and used a procedure called bronchoscopy to collect fluids and tissue samples from the subjects\' airways. They analyzed these samples for indicators of inflammation and lung damage. The two investigator groups collaborated to compare the levels of three markers of airway inflammation among the normal, asthmatic, and smoker groups (described in Part III).