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Research Reports

HEI’s mission is to provide credible science to support environmental regulations and other policy decisions. The results of each HEI-funded project undergo peer-review by outside scientists and the Health Review Committee. The HEI Research Reports contain the Investigator’s Report and the Review Committee’s evaluation of the study, summarized in a Commentary or short Critique.

ISSN 1041-5505 (print)        ISSN 2688-6855 (online) 

Research Report 49
George D Leikauf
1992
Topics: 

Dr. George Leikauf and coworkers at the University of Cincinnati Medical Center examined the mechanism by which aldehyde inhalation can alter breathing patterns and damage cells lining the airways. Emissions from motor vehicles using gasoline and diesel fuels add to the outdoor levels of aldehydes, including formaldehyde and acrolein, which are known irritants of the respiratory tract. The investigators prposed to examine whether airway constriction due to exposure to aldehydes is caused by damage to airway cells, by the entry of white blood cells into the lungs, or both.

Research Report 46
Frederick A Beland
1991

Nitropyrenes are a class of chemicals found in diesel engine exhaust that can form DNA adducts and are suspected animal carcinogens. Dr. Beland at the University of Arkansas for Medical Sciences examined the relationship between DNA adducts and cancer in laboratory animals treated with 1-nitropyrene, the major nitropyrene present in diesel engine exhaust. The investigator used state-of-the-art techniques to study DNA adducts formed from 1-nitropyrene under different conditions of exposure, with an emphasis on identifying unique adducts that had not been recognized before.

Research Report 48
Philip A Bromberg
Venkatachalam Ranga
M Jackson Stutts
1991

Ozone is a highly reactive gas that is a pervasive air pollutant at ground level. It is a major component of urban smog, forming when emissions from mobile and industrial sources interact with sunlight. When inhaled, ozone can cause cough, shortness of breath, and transient changes in breathing patterns; however the health significance of these effects is unknown. Dr. Philip Bromberg and coworkers at the University of North Carolina, Chapel Hill examined whether exposure to ozone alters properties of the airway epithelium.

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 44
Kenneth Donaldson
Geraldine M Brown
David M Brown
Joan Slight
William M Maclaren
John MG Davis
1991

Ozone is a highly reactive gas that is a pervasive air pollutant at ground level. It is a major component of urban smog, forming when emissions from mobile and industrial sources interact with sunlight. When inhaled, ozone can cause cough, shortness of breath, and transient changes in breathing patterns; however the health significance of these effects is unknown. Drs. Kenneth Donaldson and coworkers at the Institute of Occupational Medicine examined whether exposure to ozone activates white blood cells to release substances that can damage lung tissue.

Research Report 42
Mary R Cook
Fred J Bergman
Harvey D Cohen
Mary M Gerkovich
Charles Graham
Roger K Harris
Linda G Siemann
1991

In this pilot study, Dr. Mary Cook and colleagues at the Midwest Research Institute explored how exposure to methanol vapor might affect the human nervous system. Methanol could be used as an alternative fuel, but it may lead to increased levels of methanol and formaldehyde in the atmosphere. The investigators exposed 12 young male volunteers to either filtered air or methanol vapor and assessed their response using 20 commonly used tests of sensory, behavioral, and reasoning performance before, during, and after each exposure.

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 41
David S Sheps
Margaret C Herbst
Alan L Hinderliter
Kirkwood F Adams
Lars G Ekelund
John J O'Neil
George M Goldstein
Philip A Bromberg
Martha Ballanger
Sonia M Davis
Gary Koch
1991

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.

Research Report 40
CP Yu
KJ Yoon
1991

This report describes a study by Drs. Yu and Yoon to mathematically predict the lung burden in rats and humans of diesel exhaust particles (DEP) from automobile emissions. Building on a previously constructed model describing DEP deposition, the present work focused on clearance and retention of DEPs deposited in the lung. The transport rates of each component of DEPs were derived using experimental data and mathematical approximations. The complete model was first developed for rats and then extrapolated to humans of different age groups.

Research Report 39
James S Ultman
Abdellaziz Ben-Jebria
1991

This report describes a study by Drs. Ultman and Ben-Jebria to develop a chemiluminescent ozone analyzer and constructed an ozone bolus generator with the goal of using bolus concentration-response methods to noninvasively measure the longitudinal distribution of ozone absorption in human lungs. The analyzer was based on the chemiluminescent reaction between 2-methyl-2-butene and ozone. Validation of the system was performed in excised pig and sheep tracheas, and the resulting absorption coefficient was computed.

Research Report 38
Jerold A Last
1991

This report describes a study by Dr. Last to investigate possible synergistic effects of multiple air pollutants on pulmonary measures in rats. Rats were exposed for 1-9 days to mixtures of O3 or NO2 and aerosols of sulfuric acid, ammonium sulfate, or sodium chloride, and to each pollutant individually. Responses were evaluated by various biochemical and morphometric analyses of lung tissue and lavage fluid. An additional preliminary experiment treated exposed rats in vivo with various free-radical scavengers to elucidate possible protective properties.

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 36
Jay P Farber
Peter J Schwartz
Emilio Vanoli
Marco Stramba-Badiale
Gaetano M De Ferrari
1990

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%.

Research Report 33
Marc B Schenker
Steven J Samuels
Norman Y Kado
S Katharine Hammond
Thomas J Smith
Susan R Woskie
1990

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.

Research Report 35
Richard L Verrier
Alex K Mills
William A Skornik
1990

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.

Research Report 34
Alan M Jeffrey
Regina M Santella
Diana Wong
Ling-Ling Hsieh
Volker Heisig
George Doskocil
Soraya Ghayourmanesh
1990

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.

Research Report 32
Richard C Moon
Kandala VN Rao
Carol J Detrisac
1990

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.

Research Report 31
Frederick A Beland
1989

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.

Research Report 25
Elizabeth N Allred
Eugene R Bleecker
Bernard R Chaitman
Thomas E Dahms
Sidney O Gottlieb
Jack D Hackney
Denise Hayes
Marcello Pagano
Ronald H Selvester
Sandra M Walden
Jane Warren
1989

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.