Carbon monoxide (CO) is a colorless, odorless, tasteless gas that is the by-product of incomplete combustion of organic material. It is a chemical asphyxiant, and its toxicity involves the interaction of the gas with cellular component macromolecules such as hemoglobin and myoglobin. Carbon monoxide binds to hemoglobin more avidly than oxygen, producing carboxyhemoglobin (COHb) and thus decreasing the oxygen-carrying capacity of the blood and oxygen release, which can result in tissue hypoxia. In addition, carbon monoxide can bind to cytochrome oxidase, interfering with mitochondrial respiration.

Small amounts of carbon monoxide are produced endogenously, resulting in COHb levels of 0.5% in healthy individuals, but this normal level may vary. For example, cigarette smokers can have COHb levels of 5% to 10% depending on how much they smoke, while urban dwellers may have COHb levels of 1% to 2%. People such as firefighters, construction and garage workers, indoor propane forklift operators, welders, cooks, underground parking attendants, and outdoor workers in urban areas with heavy traffic can be exposed to carbon monoxide at work. Carbon monoxide exposure can also occur unexpectedly in nonindustrial workplaces such as hospitals, schools, office buildings, and shopping centres, typically from fugitive emissions such as idling vehicles near ventilation-system air intakes. WorkSafeBC typically receives 20 claims per year for carbon monoxide intoxication.

The uptake of carbon monoxide is by inhalation, and it depends on many factors, including the ambient concentration of the gas, duration of exposure, and alveolar ventilation. Eighty percent to 90% of absorbed carbon monoxide is bound to hemoglobin. The equilibration of COHb concentration in the blood is not immediate and may take several hours to reach steady state at constant-exposure concentration. The elimination of carbon monoxide is by exhalation and depends on several factors, including blood concentration, pulmonary ventilation, alveolar blood flow, and diffusion capacity. The half-life of COHb in room air is about 5 hours, but if 100% oxygen is administered, the half-life can be decreased to about 1 to 1.5 hours. Hyperbaric oxygen treatment can markedly reduce the half-life to less than 30 minutes.

The severity of symptoms associated with carbon monoxide toxicity varies proportionately with the COHb concentration. Generally, the following symptoms are exhibited at the associated concentration levels:

• Less than 10%: most individuals are asymptomatic.
• 10% to 20%: headaches and dyspnea.
• 20% to 30%: more severe headaches with nausea, vomiting, dizziness, and difficulty concentrating.
• 30% to 40%: lethargy, syncope, visual and auditory disturbance, dizziness, and chest pain.
• 40% to 50%: tachycardia, syncope, seizures, and cardiac ischemic injury.
• 50% to 60%: coma, cardiac arrest, and brain damage.
• 70% or more: potentially fatal.

Following serious carbon monoxide toxicity, the individual may develop parkinsonism or delayed neuropsychiatric and behavioral sequelae. Some individuals, including pregnant women and those with pre-existing cardiopulmonary disease, may be more susceptible to the toxic effects of carbon monoxide.

If you suspect your patient has occupational carbon monoxide toxicity, measure COHb as soon as possible, and then start treatment with high-flow oxygen. More severe intoxications are medical emergencies and should be evaluated in hospital. COHb may be measured in venous or arterial blood, or by exhaled-air carbon monoxide, or by CO-oximetry. Obtaining accurate information on the exposure events is important, with detailed chronology including the use of oxygen. Any suspected case of workplace carbon monoxide toxicity should be reported to WorkSafeBC and should include a detailed medical report. For assistance, contact Peggy Tunks, WorkSafeBC client services manager of occupational disease services, at 604 231-8842.
—Sami Youakim, MD, MSc, FRCP
WorkSafeBC Occupational Disease Services

Suggested reading
Ernst A, Zibrak JD. Carbon monoxide poisoning. N Engl J Med 1998;339:1603-1608.
Struttmann T, Scheerer A, Prince TS, Goldstein LA. Unintentional carbon monoxide poisoning from an unlikely source. J Am Board Fam Pract 1998;11:481-484.

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This article is the opinion of WorkSafeBC and has not been peer reviewed by the BCMJ Editorial Board.