Carbon Monoxide

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Research Report 87
Assieh A Melikian
Min Meng
Ray O’Connor
Peifeng Hu
Seth M Thompson
June 1999

Dr. Melikian and colleagues at the American Health Foundation developed and validated a novel, practical method for assaying metabolites of benzene in humans methods using a technique known as Liquid Chromatography–Electrospray Ionization–Tandem Mass Spectrometry (LC-ESI-MS/MS) to measure benzene metabolites in human urine.

Research Report 80
Stephen R Thom
Harry Ischiropoulos
December 1997

Dr. Thom and Dr. Ischiropoulos at the University of Pennsylvania Medical Center examined the effects of low concentrations of carbon monoxide on platelets and cells isolated from blood vessels. The investigators exposed blood platelets (taken from rats) and endothelial cells (isolated from bovine blood vessels) to varying concentrations of carbon monoxide and measured how much nitric oxide was released. To determine if exposure to carbon monoxide causes endothelial cells to produce peroxynitrite, the investigators looked for markers of its presence in the culture medium and in the cells.

Research Report 62
Beatrice A Wittenberg
Jonathan B Wittenberg
December 1993

Human exposure to carbon monoxide can occur from automobile emissions, industrial processes, sidestream or mainstream cigarette smoke, and poorly ventilated appliances such as space heaters and gas stoves. Most researchers consider the major mechanism for the toxicity of carbon monoxide to be its ability to compete with oxygen for binding to hemoglobin, the protein that transports oxygen through the bloodstream and releases it to cells and tissues.

Research Report 57
Arthur Penn
May 1993

Carbon monoxide is a ubiquitous air pollutant. It is found in cigarette smoke and emissions from motor vehicles, industrial processes, and poorly ventilated combustion sources. Dr. Penn and his colleagues at New York University Medical Center sought to determine whether chronic exposure to ambient levels of carbon monoxide is also a risk factor for developing atherosclerosis because this disease is the leading contributor to deaths by heart attack and stroke in the United States.

Research Report 52
Bernard R Chaitman
Thomas E Dahms
Sheila Byers
Lisa W Carroll
Liwa T Younis
Robert D Wiens
September 1992

Drs. Chaitman and coworkers at the St. Louis University School of Medicine examined whether there is a link between carbon monoxide exposure and arrhythmias in subjects with coronary artery disease. Carbon monoxide is a ubiquitous air pollutant. It is found in cigarette smoke and emissions from motor vehicles, industrial processes, and poorly ventilated combustion sources. The investigators studied 25 men and 5 women, aged 45 to 77 years, all of whom were nonsmokers with stable coronary artery disease and who had moderate levels of ventricular arrhythmias.

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
May 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 36
Jay P Farber
Peter J Schwartz
Emilio Vanoli
Marco Stramba-Badiale
Gaetano M De Ferrari
December 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 35
Richard L Verrier
Alex K Mills
William A Skornik
October 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 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
November 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 27
James J McGrath
July 1989

This report describes a study by Dr. McGrath to investigate the effect of chronic exposure of rats to CO at high altitude. Male rats were exposed for 6 weeks to CO ranging from 0 to 500 ppm at simulated altitudes ranging from 3,300 to 18,000 feet. The following weekly measurements were taken throughout the exposure period: weight, hematocrit, hemoglobin, and carboxyhemoglobin concentrations. Arterial pH, partial pressure of CO in the blood (PCO2) and PO2 were measured, as were blood pressure and ECG.