A colourless, odourless, tasteless, non-irritating gas formed by incomplete combustion of organic fuels. Exposure to CO is frequently due to defective gas, oil or solid-fuel heating appliances. CO is a component of car exhaust fumes and deliberate exposure to these is a method of suicide. Victims of fires often suffer from CO poisoning. CO combines reversibly with oxygen-carrying sites of HAEMOGLOBIN (Hb) molecules with an affinity 200 to 300 times greater than oxygen itself. The carboxyhaemoglobin (COHb) formed becomes unavailable for oxygen transportation. In addition, the partial saturation of the Hb molecule results in tighter oxygen binding, impairing delivery to the tissues. CO also binds to MYOGLOBIN and respiratory cytochrome ENZYMES. Exposure to CO at levels of 500 parts per million (ppm) would be expected to cause mild symptoms only and exposure to levels of 4,000 ppm would be rapidly fatal.

Each year around 400 people are admitted to UK hospitals with carbon monoxide poisoning and there are 40 to 50 deaths. Experts have suggested that as many as 25,000 people a year are exposed to its effects within the home, although most are unrecognised, unreported and untreated, even though victims may suffer from long-term effects. This is regrettable, given that Napoleon's surgeon, Larrey, recognised in the 18th century that soldiers were being poisoned by carbon monoxide when billeted in huts heated by wood burning stoves. Clinical effects of acute exposure resemble those of atmospheric HYPOXIA. Tissues and organs with high oxygen consumption are affected to a greater extent. Common effects include headaches, weakness, fatigue, flushing, nausea, vomiting, irritability, dizziness, drowsiness, disorientation, incoordination, visual disturbances, TACHYCARDIA and HYPERVENTILATION. In severe cases drowsiness may progress rapidly to COMA. There may also be metabolic ACIDOSIS, HYPOKALAEMIA, CONVULSIONS, HYPOTENSION, respiratory depression, ECG changes and cardiovascular collapse. Cerebral OEDEMA is common and may lead to severe brain damage and focal neurological signs. Significant abnormalities on physical examination include impaired short-term memory, and unsteadiness of gait including heel-toe walking. Any one of these signs would classify the episode as severe. Victims’ skin may be coloured pink, though this is very rarely seen even in severe incidents. The venous blood may look ‘arterial’. Patients recovering from acute CO poisoning may suffer neurological sequelae including TREMORS, personality changes, memory impairment, visual loss, inability to concentrate and PARKINSONISM. Chronic low-level exposures may result in nausea, fatigue, headache, confusion, VOMITING, DIARRHOEA, abdominal pain and general malaise. It may be misdiagnosed initially as influenza or food poisoning.

First-aid treatment is to remove the patient from the source of exposure, ensure an effective airway and give 100-per-cent oxygen by tight-fitting mask. In hospital, management is largely supportive, with oxygen administration. Oxygen therapy is given until the COHb level falls below 5 per cent. Patients with any history of unconsciousness, a COHb level greater than 20 per cent on arrival, any neurological signs, any cardiac arrhythmias or anyone who is pregnant should be referred for an expert opinion about possible treatment with HYPERBARIC oxygen, though this remains a controversial therapy. Hyperbaric oxygen therapy shortens the half-life of COHb, increases plasma oxygen transport and reverses the clinical effects resulting from acute exposures. Carbon monoxide is also an environmental poison and a component of cigarette smoke. Normal body COHb levels due to ENDOGENOUS CO production are 0.4 to 0.7 per cent. Non-smokers in urban areas may have level of 1–2 per cent as a result of environmental exposure. Smokers may have a COHb level of 5 to 6 per cent.