Carbon Monoxide Poisoning



Carbon monoxide (CO) is an odorless, tasteless, colorless gas produced during the incomplete combustion of carbon-based compounds. If inhaled, CO may cause nonspecific symptoms and is potentially fatal (1).

  • CO inhalation leads to displacement of oxygen (O2) from binding sites on hemoglobin to form carboxyhemoglobin (COHb). The formation of COHb leads to tissue hypoxia from decreased O2 carrying capacity and a left shift of the oxyhemoglobin dissociation curve (resulting in less O2 delivery to a tissue at a given arterial O2 pressure). CO binds to mitochondrial cytochrome oxidase, impairing adenosine triphosphate (ATP) production. It also binds to myoglobin, resulting in decreased contractility and vascular smooth muscle relaxation.

Pregnancy Considerations
Tissue hypoxia, due to CO poisoning, may cause significant fetal abnormalities because CO has a stronger affinity and a longer half-life when bound to fetal hemoglobin. The fetus is, therefore, susceptible to adverse outcomes even if the mother is unaffected.



  • CO poisoning is the third leading cause of poisoning death in the United States. There were 481 deaths in 2020, a decrease of 8% from 2019.
  • Accounts for 50,000 ER visits annually (16 cases per 100,000 population); 1–3% are fatal.
  • Approximately 15,000 intentional poisoning occur per year, accounting for 2/3 reported deaths (10-fold higher than unintentional poisonings); results in approximately 1,200 to 1,600 deaths a year in the United States due to fire and non–fire-related poisoning.
  • Vague symptoms may cause patients to not seek care, leading to underdiagnosis.
  • May have concurrent co-exposures such as cyanide poisoning or intoxicants.


  • More prevalent during the winter months in areas with colder climate.
  • Occupational exposure to methylene chloride, found in industrial solvents such as paint remover, is metabolized to CO in the liver and can result in exposure and toxicity.

Etiology and Pathophysiology

  • CO is rapidly absorbed through the lungs, binding hemoglobin with 210 to 240 times the affinity of O2. This stabilizes hemoglobin in the relaxed high affinity state (R state), reducing O2-carrying capacity and delivery, leading to left shift of the oxyhemoglobin dissociation curve. CO inactivates cytochrome oxidase. This leads to decreased ATP production, especially in tissues with high metabolic demands (brain, heart). The electron transport chain continues, generating superoxide radicals, leading to further damage.
  • CO displaces nitric oxide (NO) from platelets, leading to platelet activation and aggregation. Oxidative stress, lipid peroxidation, and apoptosis are additional effects. NO also causes vasodilation and profound hypotension.
  • Mitochondrial dysfunction and hypoxia leads to myocardial stunning and injury. Proteases released from neutrophil degranulation interact with xanthine hydrogenase forming xanthine oxidase. This inhibits endogenous defense against oxidative stress.
  • CO also initiates an inflammatory cascade that can lead to oxidative degradation of nervous system lipids and delayed neurologic damage.

Risk Factors

  • Alcohol and tobacco use
  • Patients with severe COPD regardless of current tobacco smoke exposure; closed or improperly ventilated spaces
  • Fires and fire-related injuries; high-risk vocations: coal miners, auto mechanics, paint stripping, work in the solvent industry; exposure to exhaust from motor vehicles, faulty furnaces, stoves, generator use (power outages and storms), and other fuel burning devices

General Prevention

  • Appropriate ventilation around fuel-burning devices; installation of in-home CO monitors or alarms
  • Postexposure determination of CO source to limit future exposures, eliminate source, and initiate treatment
  • Public policy to ensure building code safety; limiting occupational exposures for those who work with automobiles, paint, solvents, or mines

Commonly Associated Conditions

  • CO and cyanide poisoning often occur simultaneously after smoke inhalation and have synergistic effects.
  • Intentional poisoning often occurs in the context of coingestion of other substances (~40%).
  • Up to 50–75% of fire-related injuries have a component of CO poisoning.

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