Nitrogen Oxides

Nitrogen dioxide is an ubiquitous air pollutant that can react with and damages lung cells when inhaled at high levels. Although outdoor and indoor levels of nitrogen dioxide are usually below the annual standard of 0.053 ppm, peaks can occur that reach up to 10 times this standard. Dr. Mark Utell and coworkers at the University of Rochester examined the human health impacts of higher (peak) levels of nitrogen dioxide that exceed the annual standard. The investigators exposed healthy, nonasthmatic, human volunteers to either nitrogen dioxide or filtered air for three hours.

This report describes a study by Dr. Mauderly and colleagues to examine the influence of preexisting pulmonary emphysema on adverse health effects induced by chronic exposure of rats to diesel engine exhaust (DEE) or NO₂. Rats were exposed 7 hours/day, 5 days/week for 24 months to 9.5 ppm NO₂ or 3.5 mg soot/m³ DEE. Prior to exposure, a subset of rats was instilled with the proteolytic enzyme elastase to induce pulmonary emphysema.

This report describes a study by Dr. Evans and colleagues to develop an early marker of lung injury that changes in response to exposure to NO₂, which is an important component of mobile source emissions. Rats were exposed to NO₂ in concentrations ranging from 0.5 to 30 ppm for 6 hours per day for periods ranging from 2 days to 4 weeks. Urine and bronchoalveloar lavage samples were collected and analyzed for the presence of the lung injury markers hydroxylysin, angiotensin-converting enzyme, and desmosine.

This report examined the effect of nitrogen dioxide exposure on the sensitivity of the lower respiratory tract to viral infection and reinfection. Dr. Rose and colleagues exposed mice to concentrations of nitrogen dioxide ranging from 1-10 ppm or to air prior to and after inoculation with varying doses of murine cytomegalovirus. A subset of mice was reinfected 30 days later. Infection status, macrophage phagocytic uptake, lymphocyte function, and virus-specific antibody levels were measured, and the results were compared by exposure condition.

This report investigated the influence of acute exposure to nitrogen dioxide on susceptibility to and severity of viral and bacterial infection in mice. Dr. Jakab exposed normal and immunosuppressed mice to concentrations of nitrogen dioxide ranging from 1 to 30 ppm before or after bacterial or viral challenge and measured host resistance to infection by physiologic parameters.

This report investigated whether asthmatic and healthy adolescents differ in their sensitivity to near-ambient concentrations of ozone and nitrogen dioxide. Dr. Koenig and colleagues exposed healthy and asthmatic participants to concentrations of 0.12 and 0.18 ppm ozone or 0.12 and 0.18 ppm nitrogen dioxide during rest or rest followed by moderate exercise.

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).