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 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 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.

Research Report 30
Joe L Mauderly
David E Bice
Yung S Cheng
Nancy A Gillett
Rogene F Henderson
John A Pickrell
Ronald K Wolff
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
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
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.