Humans have been poisoned by carbon monoxide since they first discovered hydrocarbon fuels, incomplete combustion of which is the usual cause of poisoning. Napoleon's surgeon, Larrey, saw soldiers with carbon monoxide induced myonecrosis when billeted in huts heated by woodburning stoves. And over 60 years ago American physicians were warned that chronic carbon monoxide exposure could mimic many neurological conditions, such as “cerebral haemorrhage, encephalitis, multiple sclerosis, spastic paraplegia, chorea and tetany.”² Throughout the world people continue to die unnecessarily from carbon monoxide exposure or to survive their encounter with disabling symptoms whose cause is misdiagnosed.

Carbon monoxide famously binds to haemoglobin over 200 times more strongly than oxygen, a strange evolutionary quirk explained by the tiny amounts of carbon monoxide produced naturally in the body by haem oxygenase and the need to have an efficient scavenging system for such a toxic substance.³ Although the carboxyhaemoglobin which results from inhaling the gas is an indicator of exposure, clinical features may persist or begin long after the disappearance of measurable carboxyhaemoglobin, which has a half life of only four to five hours when clean air is breathed. Displacement of oxygen from haemoglobin is merely the best known property of carbon monoxide, which poisons the body in many more subtle and complex ways.

Carbon monoxide interferes with other ferroproteins such as myoglobin and various enzymes including members of the cytochrome family.⁴ Studies suggest that endogenous carbon monoxide may share properties with nitric oxide, such as smooth muscle relaxation and altered platelet aggregation, and be intimately linked with nitric oxide dependent reactions, which if unregulated can lead to cellular death. Oxidative damage to neurovascular epithelium produced by carbon monoxide causes increased leucocyte adherence and subsequent peroxidation of brain lipid.^5,6

The central nervous system is thus especially vulnerable, with areas at arterial “watersheds”—such as the medulla and basal ganglia—at particular risk.¹ The damage can be shown radiologically.⁷ Isolated neurological symptoms such as gesture apraxia and single seizures have been ascribed to carbon monoxide poisoning, as has “winter headache.” A delayed neurological syndrome,⁸ which may mimic almost any neuropsychiatric complaint, though impaired motor control is usually a prominent feature, has been reported up to 80 days after carbon monoxide exposure. Yet this syndrome is both preventable and treatable if the true cause is recognised.⁹

Economics and geography, as much as pathology and biochemistry, determine someone's susceptibility to carbon monoxide poisoning. Korea's population is slightly smaller the United Kingdom's, yet 20 years ago there were around 3000 deaths and a million admissions a year,¹⁰ and by 1982, 300 hospitals were equipped with hyperbaric oxygen facilities. Korean houses are still commonly heated by a large coal brick dropped into a space beneath the living area. Horizontal “chimneys” pass under other rooms in the house to provide heat, and several dwellings often share a final common flue.

In Chesterfield recently a family of four and their elderly neighbour died because the common chimney to their houses—built of porous materials—became blocked, venting fumes from a gas boiler into both homes.¹¹ All five deaths would almost certainly have been prevented by a domestic carbon monoxide alarm. More modern house design brings its own problems, however. In a well insulated home the negative pressure created by a bathroom extractor fan can be enough to cause retrograde flow in an otherwise normal chimney. Most people think of engine exhaust as a means of deliberate self poisoning, but in Quebec it is the commonest cause of unintentional carbon monoxide deaths, when engines are left running in enclosed spaces, for warmth or when being repaired.

Numbers of cases sublethal exposure to carbon monoxide in Britain are traditionally quoted as 200 a year, but up 250000 gas appliances are condemned annually. Even assuming that as few as 10% of these appliances were giving off significant amounts of carbon monoxide, and discounting exposure from other domestic sources, this suggests that as many as 25000 people every year may be exposed to the effects of carbon monoxide within the home. Whatever the actual number, the overwhelming majority of cases go unrecognised, unreported, and untreated. Chronic carbon monoxide exposure is misdiagnosed. A survey carried out by the charity Carbon Monoxide Support showed that in only one case out of 77 was exposure correctly identified on the basis of symptoms alone.¹²

The early symptoms of carbon monoxide poisoning are usually said to be flu like, which, though arguably true, also encourages the wrong diagnosis. As a result a doctor's most likely response when faced with more than one member of a household exhibiting similar symptoms is to think of a vague microbial cause (a diagnosis never tested) when in reality a far more prosaic cause may exist. Symptoms may initially be mild, often include gastrointestinal upset more in children, and usually bear a temporal relation to occupancy of a particular building or room. Classically, several family members (including pets) are affected. Testing for carboxyhaemoglobin is straightforward and will pick up exposure in its early stages. Oximetry on a sample of blood has long been the only useful immediate investigation, but breath meters, originally developed as smoking cessation aids, are now available.¹³ Most of the time no one thinks to do the test.

Perhaps the most tragic consequence of a missed diagnosis is that patients may be discharged to the very environment that is poisoning them. When deaths are investigated it is not uncommon to find that the victim—sometimes even several members of the same family—had visited a doctor with symptoms of carbon monoxide toxicity in the days before death. With a simple, non-invasive testing device the chances of such tragedies could be dramatically lessened. But to achieve this we must also see increased awareness of the problem, among both patients and their doctors.

We acknowledge the help of Debbie Davis at Carbon Monoxide Support.