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Carbon monoxide - What is it? Sources Fossil fuel and biomass combustion Vehicle transport is the greatest source by far in the UK but combustion of wood and coal can produce high concentrations close to the source. It is difficult to achieve a low emission of carbon monoxide with most solid domestic fuels. The smoke stream from a burning wood log, for example, can contain a carbn monoxide concentration in excess of 10 000 milligrams per cubic metre. It is easy to achieve a very low emission with most gaseous fuels as long as the oxygen supply to the flame is adequate , but if oxygen is inadequate for these rapid burning, pressurised systems then very high CO levels are produced which have resulted in many CO related deaths and injuries. Our main, persistent but relatively low level sources of carbon monoxide are tobacco smoking, environmental tobacco smoke (ETS), vehicle exhausts and the burning of wood, coal and charcoal. The residency time in air is about one month but dispersal and dilution mean that ambient air away from sources is harmless most of the time. Health Effects Short term exposure to high levels of CO in an interior environment causes drastic poisoning to the point of death. This site concerns itself with long term low level CO exposure. After breathing in, carbon monoxide interfers with the cardiovascular system by readily combining with haemoglobin to form carboxyhaemoglobin (COHb). The percentage of COHb in the blood determines the ill health effect to the body mainly by causing and exacerbating cardiovascular disease. There is also evidence that CO even at low levels of concentration is associated with neurological damage especially in young children and also with adverse developmental effects in the unborn child. A 2.5% COHb due to from CO in air is now acknowledged to be definitely harmful to health but it is probable that a 1% COHb due to CO may be as much as the human body can harmlessly take in addition to its endogeneous (internally generated) production. Increased cardiovascular demand produces COHb endogenously such as in exercise and the later stages of pregnancy increases COHb percentage levels significantly. Foetal blood has usually higher levels of COHb than even maternal blood. Birthweight and long term health prospects are affected by too high a level of COHb whilst in the womb Exposure To prevent ambient CO from contributing more than 2.5% COHb, the exposure limits have been set as: 100 mg/m3 (87.1 ppm) for 15 min.60 mg/m3 (52.3 ppm) for 30 min. 30 mg/m3 (26.1 ppm) for 1 h. 10 mg/m3 (8.7 ppm) for 8 h. However, because of evidence from low birthweight and studies on neurological damage being due to low level CO, this site recommends that ambient CO should contribute no more than 1% COHb. Therefore, the exposure limits should be set at: 40 mg/m3 for 15 min. 25 mg/m3 for 30 min. 12 mg/m3 for 1 h. 6 mg/m3 for 8 h. These limits have serious implications for interior smoky environments such as pubs especially for bar staff and waiters but also for customers. Other people as risk are drivers and those living within ten metres of a busy road. Smoking tobacco can contribute up to 10% COHb. Pregnant women should not smoke at all. The alternative of cutting down say from twenty to ten only has a marginal benefit in comparison. Carbon monoxide is an ozone precursor and the substantial emissions from domestic combustion, although small relative to vehicular emissions, contribute to the formation of ground level ozone which is harmful to human health. External links carbonmonoxide kills website lowbirthweight and co COHb uptake plot Another COHb uptake plot UK COHb uptake plot UK dept of health advice (pdf) UK Institute of Environmental Health publication Very good UK govt review on CO health effects (pdf) Dieselnet links page US EPA carbon monoxide main page US EPA review on carbon monoxide (pdf) very large file 1994 UK govt CO review on health effects |