Nitrogen Oxides

This report describes a study by Dr. Heinrich and colleagues to investigate the effects of exposure to NO₂ and SO₂ or diesel engine exhaust on tumor formation in hamsters. Hamsters were exposed for 6, 10.5, 15, or 18 months to whole diesel exhaust, diesel exhaust without particles, or a mixture of NO₂ and SO₂. Additional groups of animals exposed to each test atmosphere were also injected with 3 or 6 mg of diethylnitrosamine/kg body weight to evaluate any enhancing effect of diethylnitrosamine on exposure-related changes.

This report investigated changes in pulmonary function, as well as the occurrence of symptoms, in potentially susceptible human subpopulations exposed to nitrogen dioxide. Drs. Morrow and Utell exposed healthy individuals and individuals with asthma, chronic obstructive pulmonary disease, and acute respiratory infection to air or 0.3 ppm nitrogen dioxide. The exposure period (four hours per day for five consecutive days) included defined periods of moderate exercise and pulmonary function measurements including spirometry, airway conductance, airway reactivity, and symptoms.

This report investigated the association of occupational exposure to nitrogen oxides with respiratory infections in British coal miners. Dr. Jacobsen and colleagues leveraged data from the Pneumoconiosis Field Research Study, a long-term epidemiological study of British coal miners with information for the years 1953-1978.

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.

Addressing the need for better assessment of human exposure to mobile source emissions, this report investigates proteinase inhibitor activity as a potential biomarker of oxidant exposure. In this study by Dr. Johnson, human participants were exposed to 0.5 ppm ozone for four hours on consecutive days and to concentrations ranging from 0.6-2 ppm nitrogen dioxide for three hours. Blood samples were obtained and the functional activity of the proteinase inhibitors, alpha-1-proteinase, and bronchial leukocyte proteinase was assessed.

Previous research has reported that the lung development of animals exposed to oxidant gases early in life might be impaired, or that developing lungs might be more susceptible than adult lungs to inhaled toxicants. Dr. Mauderly and colleagues at the Lovelace Biomedical and Environmental Research Institute examined the age-related differences in the physiological responses of rats to inhaled automotive emissions. The younger group was exposed during gestation and through the age of six months, while the older group was exposed between the age of six and twelve months.

Acute hemolytic anemia is associated with a deficiency in glucose 6-phosphate dehydrogenase (G6PD), an X-linked inheritable characteristic. Hemolytic anemia is thought to be caused by a depletion of glutathione and other reducing compounds in red blood cells. Dr. Amoruso and colleagues sought to experimentally test the Calabrese hypothesis, which suggests that G6PD-deficient individuals may be at an increased risk of hemolysis during exposure to low levels of oxidants such as ozone.