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Chapter: Biology of Disease: Toxicology

Carbon Monoxide - Toxicology Poisons

Carbon monoxide (CO) is a poisonous gas. However it is not an irritant and is odorless. Hence it is insidious and concentrations can build up with the victim being unaware of any danger.

CARBON MONOXIDE

Carbon monoxide (CO) is a poisonous gas. However it is not an irritant and is odorless. Hence it is insidious and concentrations can build up with the victim being unaware of any danger. Carbon monoxide is no longer present in domestic gas in the UK but is still a major cause of poisoning, both accidental and intentional and results in the deaths of several hundred people in the UK each year. Sources of CO include domestic fires, ovens and boilers, coal gas, furnace gas, cigarette smoke, burning plastic and car exhausts, although catalytic converters have reduced the CO output from car petrol engines. Thus traffic policemen, firemen, those trapped in fires and some factory workers are all potentially at a greater risk. In the UK, the major cause of poisoning results from exposure to inefficient oxidation in engines and poorly maintained gas fires, ovens and boilers, especially where ventilation is inadequate.

The mechanism of CO poisoning is well understood at the biochemical level. The gas is absorbed rapidly through the lungs and binds to the iron atom of hemoglobin at same site as dioxygen, but about 240 times more strongly. This prevents the efficient distribution of oxygen to the tissues. The product of CO binding is carboxyhemoglobin. Carbon monoxide is potentially extremely poisonous at low concentrations. Given that air contains 21% O2, approximately 0.1% CO will saturate 50% of the hemoglobin. Concentrations of 60% carboxyhemoglobin in the blood are usually fatal, even if maintained for only a few minutes. A concentration of 20% carboxyhemoglobin may not present obvious symptoms but the ability to perform tasks can be impaired. At 20–30%, the victim may have a headache, with raised pulse, dulling of the senses and feelings of weariness. Concentrations of 30–40% accentuate these symptoms and decrease the blood pressure so that exertions may lead to faintness. At 40–60% and above, the victim becomes unconscious and will suffer convulsions. Other clinical features include pink skin, nausea, vomiting, loss of hearing, hyperpyrexia, hyperventilation, a decrease in light sensitivity, renal failure and acidosis.

The main target organs of CO poisoning are the heart and brain. These organs extensively utilize aerobic metabolic pathways and so their abilities to sustain an oxygen debt are relatively poor. Death is due to brain tissue hypoxia although cardiac arrythmias and heart and respiratory failures may also occur. The duration of exposure is also a factor since hypoxic cell death is not instantaneous. Also, some individuals, for example those with anemia , are more sensitive to CO poisoning than healthy people.

The treatment of CO poisoning involves removing its source and supplying the victim with fresh air or oxygen. The use of 100% oxygen at 2.5 s 105 Pa pressure, that is hyperbaric oxygen, increases the rate of dissociation ofcarboxyhemoglobin and reduces its plasma half-life from 250 min in a patient breathing air to 23 min. Adding carbon dioxide can be useful as this reduces the half-life to 12 min at normal pressure.

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