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Carbon Monoxide Toxicity

  • Author: Guy N Shochat, MD; Chief Editor: Asim Tarabar, MD  more...
 
Updated: May 06, 2016
 

Background

Carbon monoxide (CO) is a colorless, odorless gas produced by incomplete combustion of carbonaceous material. Commonly overlooked or misdiagnosed, CO intoxication often presents a significant challenge, as treatment protocols, especially for hyperbaric oxygen therapy (see the image below), remain controversial because of a paucity of definitive clinical studies.

Monoplace hyperbaric chamber. Courtesy JG Benitez, Monoplace hyperbaric chamber. Courtesy JG Benitez, MD, MPH.

See Clues on the Skin: Acute Poisonings, a Critical Images slideshow, to help diagnose patients based on their dermatologic presentations.

CO is formed as a by-product of burning organic compounds. Many cases of CO exposure occur in private residences.[1] CO toxicity is especially common during power outages due to storms, as a result of the improper use of gasoline-powered portable generators to provide electricity and indoor use of charcoal briquettes for cooking and heating.[2, 3] Exhaust from generators and propulsion engines on houseboats has also been linked to CO poisoning.[4]

Most fatalities from CO toxicity result from fires, but stoves, portable heaters, and automobile exhaust cause approximately one third of deaths. These often are associated with malfunctioning or obstructed exhaust systems and suicide attempts. Cigarette smoke is a significant source of CO. Natural gas contains no CO, but improperly vented gas water heaters, kerosene space heaters, charcoal grills, hibachis, and Sterno stoves all emit CO. Other sources of CO exposure include the following[5, 6] :

  • Propane-fueled forklifts
  • Gas-powered concrete saws
  • Inhaling spray paint
  • Indoor tractor pulls
  • Swimming behind a motorboat

CO intoxication also occurs by inhalation of methylene chloride vapors, a volatile liquid found in degreasers, solvents, and paint removers. Dermal methylene chloride exposure may not result in significant systemic effects but can cause significant dermal burns. Rarely, methylene chloride is ingested, and can result in delayed CO toxicity. The liver metabolizes as much as one third of inhaled methylene chloride to CO. A significant percentage of methylene chloride is stored in the tissues, and continued release results in elevated CO levels for at least twice as long as with direct CO inhalation.

Children riding in the back of enclosed pickup trucks seem to be at particularly high risk. Industrial workers at pulp mills, steel foundries, and plants producing formaldehyde or coke are at risk for exposure, as are personnel at fire scenes and individuals working indoors with combustion engines or combustible gases.

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Pathophysiology

CO toxicity causes impaired oxygen delivery and utilization at the cellular level. CO affects several different sites within the body but has its most profound impact on the organs (eg, brain, heart) with the highest oxygen requirement.

Cellular hypoxia from CO toxicity is caused by impedance of oxygen delivery. CO reversibly binds hemoglobin, resulting in relative functional anemia. Because it binds hemoglobin 230-270 times more avidly than oxygen, even small concentrations can result in significant levels of carboxyhemoglobin (HbCO).

An ambient CO level of 100 ppm produces an HbCO of 16% at equilibration, which is enough to produce clinical symptoms. Binding of CO to hemoglobin causes an increased binding of oxygen molecules at the three other oxygen-binding sites, resulting in a leftward shift in the oxyhemoglobin dissociation curve and decreasing the availability of oxygen to the already hypoxic tissues.

CO binds to cardiac myoglobin with an even greater affinity than to hemoglobin; the resulting myocardial depression and hypotension exacerbates the tissue hypoxia. Decrease in oxygen delivery is insufficient, however, to explain the extent of the CO toxicity. Clinical status often does not correlate well with HbCO level, leading some to postulate an additional impairment of cellular respiration.

CO can produce direct cellular changes involving immunological or inflammatory damage by a variety of mechanisms, including the following[2] :

  • Binding to intracellular proteins (myoglobin, cytochrome a,a 3)
  • Nitric oxide generation leading to peroxynitrite production
  • Lipid peroxidation by neutrophils
  • Mitochondrial oxidative stress
  • Apoptosis
  • Immune-mediated injury
  • Delayed inflammation

Studies have indicated that CO may cause brain lipid peroxidation and leukocyte-mediated inflammatory changes in the brain, a process that may be inhibited by hyperbaric oxygen therapy. Following severe intoxication, patients display central nervous system (CNS) pathology, including white matter demyelination. This leads to edema and focal areas of necrosis, typically of the bilateral globus pallidus. Interestingly, the pallidus lesions, as well as the other lesions, are watershed area tissues with relatively low oxygen demand, suggesting elements of hypoperfusion and hypoxia.[7]

Studies have demonstrated release of nitric oxide free radicals (implicated in the pathophysiology of atherosclerosis) from platelet and vascular endothelium, following exposure to CO concentrations of 100 ppm. One study suggests a direct toxicity of CO on myocardium that is separate from the effect of hypoxia.[8]

HbCO levels often do not reflect the clinical picture, yet symptoms typically begin with headaches at levels around 10%. Levels of 50-70% may result in seizure, coma, and fatality.

CO is eliminated through the lungs. Half-life of CO at room air temperature is 3-4 hours. One hundred percent oxygen reduces the half-life to 30-90 minutes; hyperbaric oxygen at 2.5 atm with 100% oxygen reduces it to 15-23 minutes.

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Epidemiology

Frequency

United States

Unintentional, non–fire-related CO poisoning is responsible for approximately 15,000 emergency department visits annually in the United States. In 2000-2009 the exposure site was reported as residence in 77.6% of cases and workplace in 12%.[9] The most common source of CO exposure in the home is furnaces (18.5%), followed by motor vehicles, stoves, gas lines, water heaters, and generators.[10] During 1999–2012, deaths from unintentional non–fire-related CO poisoning in the US totaled 6136, an average of 438 deaths per year.[11]

In 2014, the American Association of Poison Control Centers reported 12,478 single exposures to CO, 302 of which were intentional. Major outcomes occurred in 154 cases, and 46 deaths were reported.[12]

International

Quantifying the global incidence of CO poisoning is impossible because of the transient duration of symptoms in mild intoxication, the ubiquitous and occult nature of exposure, and the tendency of misdiagnosis. In contrast to findings in the United States, one Australian study of suicidal poisonings indicated no decrease following significantly lowered CO emissions from 1970-1996 and revealed no difference between the HbCO levels of occupants in cars with and without catalytic converters.[13]

Race

All ages, ethnic populations, and social groups are affected, yet particular groups may be at higher risk.

  • Earlier data stated that, for unintentional fatalities, race-specific death rates were 20% higher for blacks. More recent data reveal non-Hispanic whites and non-Hispanic blacks to have equally high death rates, significantly above that of Hispanic and those classified as Other. [14]
  • Conversely, intentional fatalities demonstrate that race-specific rates for blacks and other minority racial groups are 87% lower than for whites, revealing a cultural partiality to this form of suicide.

Two North American studies, from the 1990s and 2005, examined the incidence of CO toxicity from indoor heating devices used during severe winter storms. Both studies identified a strong association between CO toxicity and US immigrants who were non-English speaking.[15] However, a study of acute, severe CO poisoning from portable electric generators in the US from August 1, 2008 to July 31, 2011 found that 96% of patients spoke English.[3]

Sex

During 1999–2010, the average annual death rate from unintentional non–fire-related CO poisoning was more than three times higher for males than for females (0.22 versus 0.07 per 100,000 population, respectively). Males represented an overwhelming 74% of unintentional non–fire-related deaths.[14]

Age

Age-specific fatality rates increase with age and are highest in those older than 65 years. However, nonfatal exposures are more common in older teens and young adults (aged 15-34 y) than in older adults and are most common in young children (aged 0-4 y).[14, 10]

Individuals with pulmonary and cardiovascular disease tolerate CO intoxication poorly; this is particularly evident in those with chronic obstructive pulmonary disease (COPD) who have the additional concern of ventilation-perfusion abnormalities and possible respiratory depressive response to 100% oxygen therapy.

Neonates and the in utero fetus are more vulnerable to CO toxicity because of the natural leftward shift of the dissociation curve of fetal hemoglobin, a lower baseline PaO2, and levels of HbCO at equilibration that are 10-15% higher than maternal levels.

Climate and weather

Age-adjusted fatality rates are higher in cold and mountainous Midwestern and Western states and peak in the winter months. However, multiple incidents of CO poisoning were reported in Southern states following the Katrina and Rita hurricanes of 2005, and in Northeastern states following Hurricane Sandy in 2012.[16, 17]

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Contributor Information and Disclosures
Author

Guy N Shochat, MD Associate Clinical Professor of Emergency Medicine, University of California, San Francisco, School of Medicine

Guy N Shochat, MD is a member of the following medical societies: Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Michael Lucchesi, MD Chair, Associate Professor, Department of Emergency Medicine, State University of New York Downstate Medical Center

Michael Lucchesi, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

John T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

John G Benitez, MD, MPH Associate Professor, Department of Medicine, Medical Toxicology, Vanderbilt University Medical Center; Managing Director, Tennessee Poison Center

John G Benitez, MD, MPH is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, American College of Preventive Medicine, Undersea and Hyperbaric Medical Society, Wilderness Medical Society, American College of Occupational and Environmental Medicine

Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

Additional Contributors

Peter MC DeBlieux, MD Professor of Clinical Medicine and Pediatrics, Section of Pulmonary and Critical Care Medicine, Program Director, Department of Emergency Medicine, Louisiana State University School of Medicine in New Orleans

Peter MC DeBlieux, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Radiological Society of North America, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

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Monoplace hyperbaric chamber. Courtesy JG Benitez, MD, MPH.
 
 
 
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