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Model-Based Estimate of Carbon Monoxide Uptake by Heart Muscle During Exercise.

PB2012108966

Publication Date	2010
Personal Author	Bruce, E.; Bruce, M. C.; Patwardhan, A.
Page Count	11
Abstract	Exposure to carbon monoxide (CO) concentrations that exceed the Permissible Exposure Level (PEL) (50 ppm averaged over 8 hr) is the most common cause of work-related inhalation fatalities. The morbidity and mortality resulting from these CO exposures are due primarily to the effects of severe hypoxia on the heart and central nervous system. The long-standing practice of focusing on the carboxyhemoglobin (HbCO) level as the primary indicator of the severity of a CO exposure essentially ignores the CO load that accumulates in the extravascular tissues that are most vulnerable to a diminished oxygen supply such as the myocardium and brain. We propose that a predictive measure of the CO burden in these tissues during acute or chronic CO exposures in an occupational setting would provide a more accurate assessment of the risk associated with these exposures. The first aim of this proposal was to use existing data sets from human CO exposure studies to develop and enhance our mathematical model of whole-body CO uptake and distribution. We will use this model to predict CO and oxygen levels in blood and tissues of workers engaged in physical activity who are exposed to CO, both during the poisoning event and during therapy under room air or hyperoxia. All of our findings are based on simulation studies after developing mathematical models of whole-body CO uptake and distribution during CO exposures and therapies. Our modeling studies have shown repeatedly that therapies involving the breathing of 100% oxygen do lead to more rapid removal of CO from blood (than breathing air) but some of that CO diffuses into muscle and combines with myoglobin (Mb), where it may remain for hours. In rest and in situations of moderate physical activity, the myocardium is predicted to be at greater risk for hypoxic injury than skeletal muscle during the course of CO exposure and washout (therapy). The time course and depth of hypoxia in cardiac muscle during CO poisoning and therapy differs greatly from that in skeletal (exercising) muscles.
Keywords	Carbon monoxide Heart Muscles Air pollution effects(Humans) Carbonyls Exposure level Exercise(Physiology) Fatalities Hypoxia Inhalants Morbidity Mortality Nervous system disorders Oxygen Toxicity Mycardium Brain damage Humans Blood cells
Source Agency	National Institute for Occupational Safety and Health
Corporate Authors	Kentucky Univ. Research Foundation, Lexington.; National Inst. for Occupational Safety and Health, Washington, DC.
Supplemental Notes	Sponsored by National Inst. for Occupational Safety and Health, Washington, DC.
Document Type	Technical Report
NTIS Issue Number	201217

Model-Based Estimate of Carbon Monoxide Uptake by Heart Muscle During Exercise.

Model-Based Estimate of Carbon Monoxide Uptake by Heart Muscle During Exercise.
PB2012108966

Publication Date	2010
Personal Author	Bruce, E.; Bruce, M. C.; Patwardhan, A.
Page Count	11
Abstract	Exposure to carbon monoxide (CO) concentrations that exceed the Permissible Exposure Level (PEL) (50 ppm averaged over 8 hr) is the most common cause of work-related inhalation fatalities. The morbidity and mortality resulting from these CO exposures are due primarily to the effects of severe hypoxia on the heart and central nervous system. The long-standing practice of focusing on the carboxyhemoglobin (HbCO) level as the primary indicator of the severity of a CO exposure essentially ignores the CO load that accumulates in the extravascular tissues that are most vulnerable to a diminished oxygen supply such as the myocardium and brain. We propose that a predictive measure of the CO burden in these tissues during acute or chronic CO exposures in an occupational setting would provide a more accurate assessment of the risk associated with these exposures. The first aim of this proposal was to use existing data sets from human CO exposure studies to develop and enhance our mathematical model of whole-body CO uptake and distribution. We will use this model to predict CO and oxygen levels in blood and tissues of workers engaged in physical activity who are exposed to CO, both during the poisoning event and during therapy under room air or hyperoxia. All of our findings are based on simulation studies after developing mathematical models of whole-body CO uptake and distribution during CO exposures and therapies. Our modeling studies have shown repeatedly that therapies involving the breathing of 100% oxygen do lead to more rapid removal of CO from blood (than breathing air) but some of that CO diffuses into muscle and combines with myoglobin (Mb), where it may remain for hours. In rest and in situations of moderate physical activity, the myocardium is predicted to be at greater risk for hypoxic injury than skeletal muscle during the course of CO exposure and washout (therapy). The time course and depth of hypoxia in cardiac muscle during CO poisoning and therapy differs greatly from that in skeletal (exercising) muscles.
Keywords	Carbon monoxide Heart Muscles Air pollution effects(Humans) Carbonyls Exposure level Exercise(Physiology) Fatalities Hypoxia Inhalants Morbidity Mortality Nervous system disorders Oxygen Toxicity Mycardium Brain damage Humans Blood cells
Source Agency	National Institute for Occupational Safety and Health
Corporate Authors	Kentucky Univ. Research Foundation, Lexington.; National Inst. for Occupational Safety and Health, Washington, DC.
Supplemental Notes	Sponsored by National Inst. for Occupational Safety and Health, Washington, DC.
Document Type	Technical Report
NTIS Issue Number	201217