Carbon monoxide, even at fairly low concentrations, causes headache, flu-like symptoms, neurological damage and death. Health effects associated with exposure to carbon monoxide occur at significantly higher concentrations than those found outdoors in the UK
Carbon monoxide is a gas produced when carbon containing fuel burns without an adequate supply of air.Outdoor concentrations of carbon monoxide in the UK are now low and expected to continue to fall in urban areas of the UK
Deaths due to indoor exposure continue to occur: these are often due to malfunctioning gas heating appliances. The department of health reported that were 'approximately 40 accidental deaths per year in England and Wales (range 25-45 between 2006-2011)
The COMEAP report on cardiovascular disease and air pollution in 2006 concluded that there was limited evidence from time-series studies of associations between peak hourly concentrations of carbon monoxide and admissions to hospital for treatment of heart attacks (acute myocardial infarctions).
It is thought that the effects of carbon monoxide acts as a proxy (marker) for other motor-vehicle-generated pollutants including fine particles. However, carbon monoxide remains robust in co-pollutant models, which might suggest a direct effect of short-term ambient exposure to carbon monoxide on cardiovascular disease (see, for example, US EPA, 2010).
There is some evidence that both short- and long-term exposure to high concentrations of carbon monoxide can lead to lasting damage to the central nervous system. This may be due to processes unrelated to the binding of carbon monoxide to haemoglobin (US EPA, 2010).
Formation of carboxyhaemoglobin
Carbon monoxide diffuses from the alveoli of the lung to the blood it combines with haemoglobin, the oxygen-carrying pigment in the red blood cells, to produce carboxyhaemoglobin. This impedes the carriage and release of oxygen by and from the blood.
Carbon monoxide has about 250 times more affinity for haemoglobin than oxygen. The more haemoglobin combines with carbon monoxide the less there is free to carry oxygen to the tissues.
Normally, 0.4-0.7% of haemoglobin in the body exists as carboxyhaemoglobin (COHb). This is the result of carbon monoxide being produced in small amounts as a by-product of metabolism. Exposure to carbon monoxide from, for example, smoking or a blocked gas flue causes this to rise. Typical non-smoking individuals exposed to carbon monoxide have COHb levels of 0.0-1%. Policemen, traffic wardens and tunnel workers, though, may have COHb levels up to 5%.
Table 1 Effects of increasing the concentration of carboxy-haemoglobin (COHb)
Other mechanisms of action
Since 2000, research has focused on other mechanisms of action. High concentrations of carbon monoxide can disrupt cellular signalling and studies have shown evidence for involvement in the inhibition of cytochrome oxidase, disruption of iron homeostasis and modulation of protein kinase pathways. Animal studies have demonstrated oxidative injury and inflammation in response to 50–100 ppm CO (US EPA, 2010).
The toxicology studies generally involve exposure to concentrations of carbon monoxide rather higher than ambient concentrations so whether these mechanisms play a part at ambient concentrations remains unknown.
There is insufficient evidence to attempt to quantify the possible but unproven effects of exposure to ambient concentrations of carbon monoxide on mortality. 2009 report "Long-Term Exposure to Air Pollution: Effect on Mortality1.51 MB
Public Health England (PHE) formerly the Health Protection Agency (HPA) is involved several initiatives to raise CO awareness. Information on PHE's work on CO and CO awareness can be found on the HPA's website [external link]
The United States Environmental Protection Agency's (EPA) report on integrated Science Assessment for carbon monoxide 2010 can be accessed on the EPA's website [external link]