Research Reports

Ozone, a common outdoor air pollutant, is a highly reactive gas and a major component of smog. A public health concern is that prolonged exposure to ozone might damage the airways and contribute to the development of noncancerous respiratory diseases. To examine this issue, the Health Effects Institute collaborated with the NTP to provide HEI-funded investigators access to animals that underwent the same rigorously controlled ozone exposure and quality assurance processes along with the animals used for NTP studies. One of the NTP/HEI investigator groups, Dr.

Dr. Ira Tager and colleagues at the University of California at Berkeley (UCB), and Dr. Patrick Kinney and colleagues at the School of Public Health, Columbia University objectives were to develop new methods for estimating an individual's past exposure to ozone.

Dr. Ultman and his colleagues at Pennsylvania State University redesigned their first-generation analyzer that measures the dose of inhaled ozone to reduce electronic noise (interference) and improve the signal's stability. To do so, they adjusted each parameter that influenced the analyzer's performance: the flow of the air sample into the instrument, the pressure in the chamber where the air sample and the reactant gas mixed, the relative amounts of the reactant gas and air sample, and electronic variables (frequency and voltage).

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?