Nitrogen Oxides

This report addressed the hypothesis that exposure to oxidant air pollutants enhances susceptibility to viral infection. Drs. Kulle and Clements exposed healthy human volunteers who were seronegative to cold-adapted influenza A virus to clean air or nitrogen dioxide concentrations of 1, 2, or 3 ppm for two hours a day for three consecutive days. Live influenza A virus was administered intranasally to all participants after the second day of exposure.

This report describes a study by Dr. Crandall and colleagues to investigate the ability of nitrogen dioxide (NO₂) to adversely alter the barrier and transport properties of mammalian alveolar epithelium and cause pulmonary edema. Rat type II alveolar cell monolayers cultured on non-porous and porous surfaces were used as models of isolated alveolar epithelium for in vitro exposure to NO₂.

Nitrogen dioxide is a ubiquitous air pollutant resulting from the combustion of fossil fuels. Since NO₂ is a reactive free radical, one postulated mechanism on NO₂ pulmonary injury involves peroxidation of membrane lipids. Dr. Patel and colleagues at the University of Florida evaluated the dose- and time-dependent effects of NO₂ exposure by measuring metabolic function, biochemical and biophysical parameters. The porcine pulmonary artery and aortic endothelial cells in monoculture cells were exposed to 3 or 5ppm of NO₂ or air for 3-24 hours.

Dr. Drechsler-Parks and colleagues at the Institute of Environmental Stress sought to examine the effects of nitrogen dioxide, ozone, and peroxyacetyl nitrate on metabolic and pulmonary function. Because it is possible that two or more pollutants could interact in ambient air and cause effects that could not be predicted from the effects observed with the individual pollutants, the investigators examined varying levels of different pollutants in 32 non-smoking men and women (8 men and 8 women 18-26 years of age and 8 men and 8 women 51-76 years of age).