CO has two hundred to three hundred times greater affinity for hemoglobin than that of oxygen It displaces oxygen from its combination with hemoglobin and forms a relatively stable compound known as carboxyhaemoglobin. It thus reduces the oxygen content of the blood, and hence that of the tissues. It acts as a chemical asphyxiant and produces death due to anemic anorexia. CO is a potent cellular toxin. It effectively and firmly binds to hemoglobin and myoglobin.
It inhibits the electron transport by blocking cytochrome A3 oxidase and cytochrome P-450, and therefore intracellular respiration. The presence of COHb in the circulation interferes with the release of the oxygen from what little oxyhaemoglobin remains. Normally, after somatic death, the cells near the capillaries continue to function, extract oxygen from oxyhaemoglobin and cause blue staining.
In CO poisoning this cannot occur, because the cells cannot break the COHb compound. Potent cellular poisons, e.g. cyanide, fluoroacetate and freezing, block the metabolism of the cells so fast and completely that they cannot extract oxygen from oxyhaemoglobin. In these cases, the blood under the skin and in the tissues will be cherry-red due to oxyhaemoglobin.
About fifteen percent of CO is present in extracellular tissues combined with myoglobin and haemoproteins. The affinity constant of CO for myoglobin is forty. It is eliminated through lungs. The half-life of COHb at room temperature is four to five hours. It is not metabolized and is not lost through the skin, bile, perspiration, urine or faeces. CO is not absorbed by a body after death.
Sources :
The common sources of CO include coal gas, smoke from fires and the fumes from defective heating appliances, e.g., furnace, stove, water heater, burning oil lamps. It is also found as a component of the fumes of coke kilns, lime kilns, explosion in mines, detonation of explosives, and the exhaust fumes of internal combustion engines. The exhaust gas of motor cars contain one to seven percent of CO, which causes the air of a small garage poisonous in five to ten minutes. Diesel engines produce far less CO than petrol engines.
During hemoglobin catabolism 0.4 to 0.7% COHb is produced in the body endogenously. In hemolytic anemia, COHb levels may reach 8%.
Signs and-Symptoms :
The development of symptoms has a progression, roughly parallel to the rise in the saturation of the blood by CO. Similarly, regression of symptoms corresponds with the clearance of CO from the blood. The effects of CO are simply those of suboxia. Damage to the CNS may produce monoplegia or hemiplegia. Impairment of higher intellectual functions, personality changes, cerebellar damage, and severe Parkinsonism may occur and may be delayed by several weeks after apparent recovery.
The saturation required to cause death varies with the age and health of the person. Death usually occurs when eighty percent of hemoglobin is saturated with CO. Senility, or the co-existence of any respiratory or circulatory deficiency, or of anemia or in association with depressive drugs like barbiturates, and alcohol result in a significant reduction of maximum lethal saturation and death can occur from as little as thirty percent saturation.
CO can pass from the maternal to the fetus blood, and can produce intrauterine death, even though the mother survives. The rate of CO combining with hemoglobin depends on the atmospheric concentration and rate of respiratory exchange. Physical activity during exposure increases rate of saturation of blood. Children saturate their blood more rapidly than adults because of their relatively high rates of respiratory exchange.
Symptoms of CO according to COHb concentration:
* COHb concentration ranging between 0 to 10% : No appreciable symptoms.
* COHb concentration ranging between 10 to 20% : Breathlessness on moderate exertion, mild headache.
* COHb concentration ranging between 20 to 30% : Throbbing headache, irritability, emotional instability, disturbed judgment, defective memory and rapid fatigue.
* COHb concentration ranging between 30 to 40% : Severe headache, nausea, vomiting, dizziness, dimness of vision, confusion.
* COHb concentration ranging between 40 to 50% : Increasing confusion, sometimes hallucinations, severe ataxia, rapid respirations and collapse with attempts at exertion.
* COHb concentration ranging between 50 to 60% : Syncope or coma with intermittent convulsions, rapid respirations, tachycardia with a weak pulse and pink or red discoloration of the skin.
* COHb concentration ranging between 60 to 70% : Increasing depth of coma with incontinence of urine and faeces.
* COHb concentration ranging between 70 to 80% : Profound coma with depressed or absent reflexes, a weak thready pulse, shallow and irregular respirations and death.
* COHb concentration ranging between 70 to 80% : Rapid death from respiratory arrest.
Carbon monoxide poisonings at hotels and motels may not be common, but they're not becoming rarer with time either, according to a new study.
Using databases of news reports and court cases, researchers were able to document 68 incidents of carbon monoxide poisoning at U.S. hotels, motels and resorts between 1989 and 2004.
The incidents sickened 772 people, 27 of whom died, the researchers report in the American Journal of Preventive Medicine.
Based on these figures, the odds of any one person suffering carbon monoxide poisoning at a hotel are quite low, said lead study author Dr. Lindell Weaver of LDS Hospital in Salt Lake City, Utah.
However, he told Reuters Health, "when it happens, it can be serious and lethal."
Carbon monoxide is a colorless, odorless gas found in combustion fumes, such as those from cars, gas ranges and heating systems. Carbon monoxide can build up indoors if a furnace, water heater or other fuel-burning appliance is in poor condition or not properly vented.
Some symptoms of carbon monoxide poisoning include dizziness, nausea, chest pain and confusion. Exposure is particularly dangerous when people are asleep, since the gas may prove fatal before they awake.
In the U.S., federal law requires hotels, motels and resorts to have smoke detectors in every guest room, but there are no national laws regarding carbon monoxide detectors.
In a search of state government Web sites, Weaver and colleague Kayla Deru found that a few states require hotels to have carbon monoxide alarms on the premises. No state, however, requires detectors in all guest rooms.
It "makes sense," according to Weaver, for these businesses to have carbon monoxide detectors, which cost about $25 each. Yet, of the 43 sites the investigators were able to contact after their poisoning incidents, only 12 percent had since installed carbon monoxide detectors.
There was also no sign that carbon monoxide poisoning in hotels has become less common over the 15-year study period.
For frequent travelers who are concerned about carbon monoxide, there is one solution, however. Weaver said he carries his own carbon monoxide detector when he's on the road.
The risk of poisoning may be low, but "why take chances?" he said
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