When inhaled, carbon monoxide reduces the ability of blood to carry oxygen.
The best understood biological effect of CO is its combination with haemoglobin to form carboxyhaemoglobin (COHb). Carbon monoxide competes with oxygen for the binding sites of the haemoglobin molecules. The affinity of human haemoglobin for CO is about 240 times that of its affinity for oxygen. The formation of COHb has two undesirable effects: it blocks oxygen carriage by inactivating haemoglobin, and its presence in the blood shifts the dissociation curve of oxyhaemoglobin to the left so that the release of remaining oxygen to tissues is impaired. Because of this latter effect, the presence of any percentage level of COHb in the blood interferes with tissue oxygenation considerably more than an equivalent reduction of haemoglobin concentration, [eg] through bleeding. The toxicity of carbon monoxide can be increased considerably by the presence of other pollutants. Among the substances that exert a synergistic action with carbon monoxide are nitrogen oxides, hydrocarbons, and hydrogen sulphide - a highly significant fact because all of these pollutants are present in the urban atmosphere.
Small quantities of CO are produced within the human body from the catabolism of haemoglobin and other haemo-containing pigments leading to an endogenous COHb saturation of about 0.3-0.8% in the blood. Endogenous COHb concentration is increased in haemolytic anaemias and after bruises or haematomas which result in increased haemoglobin catabolism. CO is easily absorbed through the lungs into the blood.
Carbon monoxide is thought to be the most common single cause of poisoning in industry. Occupational exposure occurs in mines after explosions, in the iron and steel industry, where carbon monoxide is used to reduce the iron oxide to iron, and in gas plants. Automobile emissions expose garage workers, traffic police, and street vendors to appreciable amounts of carbon monoxide. Poisoning can be fatal, or if not, it may cause permanent damage to the central nervous system. Immediate symptoms are headache, dizziness and nausea, followed by unconsciousness in the case of exposure of longer than 10 to 45 minutes to carbon monoxide concentrations between 1,000 and 10,000 ppm; higher concentrations lead to death within a few minutes.
A sizeable proportion of the workforce in any country has a significant occupational CO exposure. CO is an ever-present hazard in the automobile industry, garages and service stations. Road transport drivers may be endangered if there is a leak of engine exhaust gas into the driving cab. Occupations with potential exposure to CO are numerous, [eg] garage mechanics, charcoal burners, coke oven workers, cupola workers, blast furnace workers, blacksmiths, miners, tunnel workers, Mond process workers, gas workers, boiler workers, pottery kiln workers, wood distillers, cooks, bakers, firemen, formaldehyde workers, and many others. Welding in vats, tanks or other enclosures may result in production of dangerous amounts of CO if ventilation is not efficient. The explosions of methane and coal dust in coal mines produce 'afterdamp' which contains considerable amounts of CO and carbon dioxide. If ventilation is decreased or CO emission increases owing to leaks or disturbances in process, unexpected CO poisonings may occur in industrial operations that usually do not create CO problems.
Automobiles produce the largest amount of carbon monoxide. Reduction of CO emissions from recent-model automobiles has been offset by a 34% increase since 1970 in the number of vehicles on the road and by an increase in the number of miles driven. Without pollution controls, the total carbon monoxide emitted would have increased significantly. Overall, CO emissions have changed little since 1970.