Carbon Monoxide

Carbon monoxide (CO) is a colorless, tasteless, and odorless gas. It is produced by the incomplete oxidation of carbon during the combustion of fuels such as gasoline, wood, propane, or charcoal. Sources of CO include:

• Unvented kerosene and gas space heaters.
• Leaking chimneys and furnaces.
• Back-drafting from furnaces, gas water heaters, wood stoves, and fireplaces.
• Gas stoves.
• Generators and other gasoline-powered equipment.
• Automobile exhaust from attached garages.
• Tobacco smoke. 
• Incomplete oxidation during combustion in gas ranges and unvented gas or kerosene heaters may cause high concentrations of CO in indoor air. 
• Worn or poorly adjusted and maintained combustion devices (e.g., boilers, furnaces) can be significant sources, or if the flue is improperly sized, blocked, disconnected, or is leaking. 
• Auto, truck, or bus exhaust from attached garages, nearby roads, or parking areas can also be a source.

CO poisoning is the most common form of unintentional poisoning.  Exposure to CO accounts for more than 100,000 emergency department visits, 14,000 hospitalizations, and 400 deaths annually in the United States. 

CO binds to hemoglobin 220 times more tightly than oxygen. CO induces toxic effects by tightly binding to hemoglobin to form carboxyhemoglobin (COHb) and reducing the oxygen carrying capacity of red blood cells. It also interferes with cellular respiration by binding to mitochondrial cytochrome oxidase. 

Low concentrations of CO between 2 and 6% can cause fatigue in healthy people and angina in people with known coronary artery disease. 

CO poisoning may be misdiagnosed as an acute self-limited illness because its early symptoms are nonspecific (headache, dizziness, weakness, confusion, shortness of breath, and sleepiness). The diagnosis is confirmed by detecting increased COHb % saturation in either venous or arterial blood. 

Endogenous heme catabolism in the absence of environmental exposure results in COHb levels below 1%. Most nonsmoking urban dwellers have COHb saturations of <3%, whereas most smokers have chronic saturations of 3 to 8%. COHb levels >3% in a nonsmoker suggest exogenous CO exposure or cryptic smoking. COHb levels >10% in urban smokers should be investigated for other potential sources of CO exposure.  

The clinical severity of CO poisoning correlates poorly with CO saturation and is determined by four factors: concentration of CO in the environment, duration of exposure, activity level of the exposed, and interval between exposure and clinical assessment. A brief intense exposure may give COHb levels >50% with minimal symptoms, while other patients may become comatose with COHb levels of 20%.

In general, exposure to CO concentrations of 105 to 205 ppm for 1 to 2 hours produces COHb levels of 10 to 20%. The elimination half-life of COHb is approximately 4 hours when breathing room air and decreases to 1 hour after giving 100% oxygen.

CoHb levels are measured by a blood gas analysis with co-oximetry. The reference range for carboxyhemoglobin (CoHb) is  0– 2%. 

Specimen requirement is one green top (lithium heparin), lavender top (EDTA) tube of blood or a heparinized blood gas syringe.  Venous or arterial blood is acceptable.

References

United States Environmental Protection Agency, What is carbon monoxide? Updated on December 4, 2024.

Reumuth G, et al. Carbon monoxide intoxication: What we know. Burns. 2019 May;45(3):526-530.

Hampson NB. Carboxyhemoglobin: a primer for clinicians. Undersea Hyperb Med. 2018 Mar-Apr;45(2):165-171.

McMahon K, Launico MV. Carbon Monoxide Toxicity. [Updated 2025 Apr 19]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 

Marshall MD et al. Are Reference Intervals for Carboxyhemoglobin Appropriate? A Survey of Boston Area Laboratories, Clin Chem 1995;41(10):1434-1438.