Publications

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.

Dr. Sheps and colleagues assessed the effect of exposure to carbon monoxide (CO) on ventricular arrhythmias in 41 nonsmoking human volunteers with coronary artery disease. On 3 consecutive days, volunteers were exposed in random order to air, 100 ppm CO (target 4% carboxyhemoglobin), and 200 ppm CO (target 6% carboxyhemoglobin), followed by a bicycle exercise test. Radionuclide cardiac ventriculography and ambulatory electrocardiogram were performed at rest and during exercise.

The Special Report Asbestos in Public and Commercial Buildings: A Literature Review and Synthesis of Current Knowledge (1991) describes the findings of the Asbestos Literature Review Panel, which was charged to determine what was known, not known, and uncertain about the risks of exposure to asbestos in public buildings.

This report describes a study by Dr. Farber and colleagues to investigate the effect of carbon monoxide (CO) exposure on cardiac parameters in dogs. They tested dogs that developed ventricular fibrillation during a test of exercise and acute myocardial ischemia (i.e. that were susceptible) and dogs that survived the test without fatal arrhythmias (i.e that were resistant). Susceptible and resistant dogs were exposed to a concentration of CO sufficient to raise carboxyhemoglobin levels to 5 – 15%.

This report describes a study by Dr. Schenker and colleagues to investigate the usefulness of urinary mutagenicity as a biological marker of occupational diesel exhaust exposure. Personal exposure to diesel exhaust over 2 consecutive work shifts was monitored via personal air samplers in 87 railroad workers, with adjustment for first-hand and environmental tobacco smoke exposure. Urine samples collected at the end of shifts were evaluated for mutagenicity and analyzed for any correlation with diesel exhaust exposure.

This report describes a study by Dr. Jeffrey and colleagues to investigate the potential genotoxicity of components of diesel engine emissions using a variety of biological systems. In the first set of in vitro experiments, radiolabeled nitropyrenes were administered to DNA isolated from human bronchial tissue, mouse embryo fibroblasts, and rabbit tracheal tissue, and elution times were compared by high-pressure liquid chromatography. Antisera antibodies were also prepared against DNA modified by 1-nitrosopyrene to test for the presence of DNA adducts.

This report describes a study by Dr. Beland to investigate the extents to which 1-nitropyrene and 1,6-dinitropyrene, two PAHs found in diesel exhaust, bind DNA in order to better understand the higher relative mutagenicity of 1,6-Dinitropyrene. DNA binding was determined in rats by assay of tissue isolated from a variety of organs. A subset of rats was pretreated with 1-nitropyrene to determine any effect on induction of nitroreductases and subsequent DNA binding by both nitropyrenes.

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 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 addressed the hypothesis that hypertrophy of the lung after oxidant injury with ozone or oxygen is due to local generation of lung-specific growth factors. Dr. Tanswell exposed rats to either 85% oxygen, 1 ppm ozone, or air for up to two weeks while samples of plasma, lung washings, and lung tissue were periodically collected. These samples were tested for their effect on the DNA synthesis of purified populations of three major lung cell types (pneumocyte, fibroblast, and endothelial cell) in culture.

This report examined the interactive effects induced by exposure to altitude and carbon monoxide. Dr. Horvath and colleagues exposed 23 healthy young human volunteers living at sea level to concentrations of 0, 50, 100, or 150 ppm carbon monoxide in a hyperbaric chamber simulating altitudes of 55, 1,524, 2,134, or 3, 048 meters above sea level. Maximal aerobic capacity tests were performed under each exposure condition while respiratory and cardiac variables and blood levels of carboxyhemoglobin, hemoglobin, and lactate were monitored.