Ozone & Oxidants

Dr. Koutrakis and his colleagues assessed the correlations between personal exposure to PM_2.5 and gaseous copollutants and compare these measurements with those taken at central-site monitors. Three groups of possibly susceptible individuals (children, seniors, and individuals with chronic obstructive pulmonary disease) were recruited in two cities (Boston and Baltimore) in two seasons (summer and winter).

Dr. Schlesinger and colleagues at the New York University School of Medicine used a well-established animal model of airway hyperresponsiveness (a heightened tendency of the bronchial airways to constrict) and allergic asthma to determine whether ozone can induce airway hyperresponsiveness or exacerbate existing airway hyperresponsiveness. Male and female guinea pigs were exposed to ozone concentrations comparable to levels to which humans are exposed during periods of ozone pollution.

Dr. Pryor and colleagues at Louisiana State University developed methods for measuring ozone reaction products in in vitro models of lung lining fluids exposed to ozone and in lung fluids from rats exposed to ozone. During the study, Dr. Mark Frampton of the University of Rochester provided Pryor with lung fluids from humans exposed to air or ozone under controlled conditions. Frampton and colleagues exposed exercising smokers and nonsmokers to filtered air or to 0.22 parts per million (ppm) ozone for four hours.

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.