Publications

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.

This report describes a study by Dr. Verrier and colleagues to explore the effects of acute carbon monoxide (CO) exposure on cardiac electrical stability through a number of biological models. Experiments involved cardiac electrical testing of conscious and anesthetized dogs with normal and ischemic hearts who were exposed to CO for 2 or 24 hours. The experimental plan explored both the direct effects of CO exposure on the myocardium and possible indirect effects through alterations in the ability of platelets to aggregate or changes in nervous system activity.

This report describes a study by Dr. Moon and colleagues to investigate the carcinogenic potential of 1-nitropyrene, a mutagenic constituent of diesel exhaust particles, using a hamster respiratory-carcinogenesis model. Male hamsters were exposed to 1 or 2 mg of 1-nitropyrene via intratracheal administration either once or twice a week for 92 weeks. In order to study activity as a cocarcinogen, 1 or 2 mg of 1-nitropyrene was administered in combination with 0.25 mg of the known environmental carcinogen benzo[α]pyrene once per week for 92 weeks.

This report from the HEI Multicenter CO Study examined the effect of carbon monoxide (CO) exposure of male human participants with coronary artery disease, with a particular focus on myocardial ischemia onset during exercise. The participants were exposed to air or to CO concentrations sufficient to elevate blood carboxyhemoglobin (COHb) levels to 2% or 4% during exercise. The primary health endpoints examined were the time to onset of exercise-induced angina, and the time to a predefined ST-segment change.