Nitrogen Oxides

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Research Report 60
Hanspeter Witschi
Michael A Breider
Hildegard M Schuller
September 1993

Ozone and nitrogen dioxide are highly reactive oxidant gases that are derived from the combustion of fossil fuels and the atmospheric transformation of these combustion products. A major unanswered question is whether or not exposure to oxidant air pollutants contributes to lung cancer. Dr. Witschi and colleagues at the University of California at Davis examined whether exposure to ozone or nitrogen dioxide enhances the development of tumors induced by the chemical carcinogen diethylnitrosamine (DEN), particularly neuroendocrine tumors, in the respiratory tract of hamsters.

Research Report 58-I & II
Jonathan M Samet
William E Lambert
June 1993

This publications contains two reports by Drs. Jonathan M. Samet, John D. Spengler, and colleagues, who conducted a prospective investigation of 1,205 healthy infants living in homes with gas or electric stoves in Albuquerque, NM. Nitrogen dioxide exposures were carefully estimated from repeated measurements in multiple locations in the subjects' homes throughout the entire 18-month observation period. Respiratory illnesses were monitored prospectively using a surveillance system based on daily parental diaries of respiratory signs and symptoms. Parental reports of illness episodes were validated in a subset of the population by comparison with clinical diagnoses and microbiological testing. Potential confounding factors that influence respiratory infections were reduced by selecting subjects whose parents did not smoke or intend to use day-care services outside the home.

Research Report 47
Jerry K Davis
Maureen Davidson
Trenton R Schoeb
December 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
October 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
August 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
December 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
October 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
September 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
September 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
May 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.