Nitrogen Oxides

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Research Report 47
Jerry K Davis
Maureen Davidson
Trenton R Schoeb
1991

Nitrogen dioxide is an ubiquitous air pollutant resulting from the combustion of fossil fuels. When inhaled at high levels, it reacts with and damages lung cells, including those cells that fight infection. This damage can affect breathing and may increase the risk of respiratory infections. Dr. J.K. Davis and his colleagues at the University of Alabama, Birmingham examined whether exposure to lower levels of nitrogen dioxide (less than 5 ppm) compromises mouse lung defense.

Research Report 45
Michael T Kleinman
William J Mautz
1991

The human health effects that result from breathing air pollutants depend on the amount of pollutant inhaled from the air (exposure dose) and the amount of inhaled material that stays in the respiratory tract (retained dose). Because the retained dose of a pollutant may damage the respiratory tract and cause disease, it is a key factor for determining appropriate government regulations for air pollutants. Drs.

Research Report 43
Mark J Utell
Mark W Frampton
Norbert J Roberts Jr
Jacob N Finkelstein
Christopher Cox
Paul E Morrow
1991

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.

Research Report 37
David A Johnson
R Steve Winters
Kwan R Lee
Craig E Smith
1990

This report describes a study by Dr. Johnson and colleagues to test the hypothesis that inhaled oxidants can cause lung damage by inactivating the proteinase inhibitors that normally protect the lung from proteolysis. In the first set of experiments, the functional activity of rat alpha-1-proteinase inhibitor (á1-PI) was measured in rat lung lavage fluid from rats exposed acutely or chronically to varying concentrations of NO2, diesel exhaust, O3, and O3 in conjunction with CO2.

Research Report 30
Joe L Mauderly
David E Bice
Yung S Cheng
Nancy A Gillett
Rogene F Henderson
John A Pickrell
Ronald K Wolff
1989

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.

Research Report 28
Jonathan M Samet
John Spengler
1989

This report describes two pilot investigations for a longitudinal study of infants designed to determine if NO2 exposure from cooking stoves increases the incidence or severity of respiratory infections during the first 18 months of life. In the first study, Drs. Samet and Spengler selected 147 households with electric or gas stoves and infants for home indoor monitoring of NO2 concentrations; the infants\' mothers completed a daily calendar-diary on respiratory symptoms and provided illness information every 2 weeks.

Research Report 29
John N Evans
David R Hemenway
Jason Kelley
1989

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.

Research Report 26
Uwe Heinrich
Ulrich Mohr
Rainer Fuhst
Carsten Brockmeyer
1989

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.

Research Report 24
Richard M Rose
Paula Pinkston
William A Skornik
1989

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.

Research Report 23
Paul E Morrow
Mark J Utell
1989

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.