|Carbon monoxide (CO) is an odourless and colourless gas produced by incomplete
burning of carbon-based fuels. CO is also a constituent of tobacco
smoke. Exposure to CO is common in many occupational areas, including those
associated with vehicle exhaust. CO is an important industrial gas used in the
production of chemical intermediates. CO is formed endogenously and acts as
a signalling substance in the neuronal system.
The main mechanism behind CO-induced toxicity is the binding of CO to haemoglobin
in the blood, resulting in carboxyhaemoglobin (COHb) formation, reduced
oxygen transport capacity of the blood and hypoxia. The relation between CO in
air and COHb is well known and can be calculated using the Coburn-Forster-Kane
(CFK) equation. Endogenous CO formation leads to a background COHb of 0.4–
0.7%. Non-smokers typically have COHb levels up to 2% whereas smokers may
have COHb levels up to 10% immediately after smoking.
The effects seen in acute CO poisoning cover a wide range, from mild symptoms,
like shortness of breath during exercise or occasional headache at COHb 20%, to
more severe ones like headache, dizziness, disturbed judgement, dimness of vision,
confusion, unconsciousness, intermittent convulsion and respiratory failure at
COHb above 30%. COHb levels of 50–60% are often lethal. Even COHb levels
of 20% may be lethal for patients with coronary artery disease. The foetus is at
higher risk than the healthy adult because of higher CO haemoglobin affinity.
From controlled human and animal exposure studies the adverse effects of concern
are impaired exercise performance, i.e. decreased maximal aerobic capacity in
healthy volunteers (lowest observed adverse effect level (LOAEL) COHb 4.3%),
increased myocardial ischaemia in patients with coronary artery disease (LOAEL
COHb 2.4%), and persistent changes in the developing auditory system of the rat
(LOAEL 12 ppm, corresponding to COHb 1.8% and 2.0% assuming 8 hours constant
exposure at rest and heavy work, respectively). It was not possible to identify
any no observed adverse effect levels (NOAELs) in these studies.
No or limited data were found regarding genotoxicity, carcinogenicity, irritation
Combined exposure to CO and dihalomethanes causes increased formation of
COHb. Combined exposure to CO and noise may potentiate noise-induced hearing