Research Reports

This report assessed in rats the carcinogenicity of inhaled 1-nitropyrene, a compound frequently adsorbed to diesel particulate matter, and whether this effect is modified when 1-nitropyrene is associated with particles or irritant gases. Dr. Wolff and colleagues exposed rats to atmospheres containing 14C radiolabeled 1-nitropyrene alone or in combination with gallium oxide, sulfur dioxide, or both. After exposure, tissue samples were analyzed for radiolabel content to determine the tissue distribution of 1-nitropyrene and its metabolites.

This report describes a study by Dr. Maher and colleagues to investigate the biological effects of nitropyrene compounds, found in diesel emission particulate, on diploid human fibroblasts in culture in order to better evaluate potential health effects. Diploid human fibroblasts from normal individuals and individuals with a genetic predisposition to cancer were studied and compared through a series of experiments.

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.

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.

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.

Research Report 7 describes a study that attempted to produce monoclonal antibodies to DNA adducts of nitropyrene that could be used to study the mechanism of nitropyrene-induced carcinogenesis or develop analytical techniques for monitoring exposed populations. Dr. Groopman immunized mice against nitropolycyclic aromatic hydrocarbons conjugated with a carrier protein to study the progression of immune response. Dr. Groopman injected four antigens into groups of BALB/c, AJ, and NZB mice. Two of the antigens failed to produce any immune response.

Dr. Bagley and colleagues at Michigan Technical University examined the chemical mutagenic effects of a ceramic particle trap on a medium-duty diesel engine. Diesel exhaust particles and vapor phase samples were collected from diluted (15:1) exhaust of a 10.4L displacement Caterpillar 3208 engine. The investigators compared uncontrolled (baseline) emissions with exhaust that had been modified by the use of an uncatalyzed monolithic ceramic trap.

The pulmonary epithelium is a cellular, avascular layer of tissue that is the first point of contact between the lung and inhaled pollutants. Previous research has indicated that altered epithelial permeability may be an early marker of subsequent lung damage. Dr. Crocker and colleagues at the University of California, Irvine sought to study the study the sites of epithelial injury in rat airways following inhalation of formaldehyde, ozone, and nitrogen dioxide.