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Carbon monoxide poisoning effects

C.P. Wang, H.S. Chu, 2006. Transient analysis of multicomponent transport with carbon monoxide poisoning effect of a PEM fuel cell. Journal of Power Sources, 159 1025-1033. [Pg.285]

Wang CP, Chu HS, Yan YY et al (2007) Transient evolution of carbon monoxide poisoning effect of PBI membrane fuel cells. J Power Sources 170 235-241... [Pg.419]

In the past, hyperbaric oxygenation as a medical procedure has received considerable attention. In this treatment the patient is given pure oxygen and may be placed in a pressurized chamber. In effect, the patient may thus receive >400 kPa (>4 atm) of pure oxygen. Beneficial results in cases of carbon monoxide poisoning, gangrene, severe bums, and other difficulties are often achieved as a result of this treatment. [Pg.482]

Occurrence. Carbon monoxide is a product of incomplete combustion and is not likely to result where a flame bums in an abundant air supply, yet may result when a flame touches a cooler surface than the ignition temperature of the gas. Gas or coal heaters in the home and gas space heaters in industry have been frequent sources of carbon monoxide poisoning when not provided with effective vents. Gas heaters, though properly adjusted when installed, may become hazardous sources of carbon monoxide if maintained improperly. Automobile exhaust gas is perhaps the most familiar source of carbon monoxide exposure. The manufacture and use of synthesis gas, calcium carbide manufacture, distillation of coal or wood, combustion operations, heat treatment of metals, fire fighting, mining, and cigarette smoking represent additional sources of carbon monoxide exposure (105—107). [Pg.59]

Describe the effects of carbon dioxide, pH, temperature, 2,3-bispho-sphoglycerate, anemia, and carbon monoxide poisoning on the transport of oxygen... [Pg.240]

The precise technical name of HCN is Hydrocyanic Acid. The cyanides are true protoplasmic poisons, combining in the tissues with the enzymes associated with cellular oxidation. They thereby render the oxygen unavailable to the tissues, and cause death through asphyxia. Inhaling concentrations of more than 180 ppm of HCN will lead to unconsciousness in a matter of minutes, but the fatal effects would normally be caused by carbon monoxide poisoning after HCN has made the victim unconscious. Exposure to HCN concentrations of 100 to 200 ppm for periods of 30 to 60 minutes can also cause death. [Pg.52]

Ernst, A., and J.D.Zibrak. 1998. Carbon monoxide poisoning. N. Engl. J. Med. 339(22) 1603-1608. Ettema, J.H., R.L.Zielhuis, E.Burer, H.A.Meier, L.Kleerekoper, and M.A.de Graaf. 1975. Effects of alcohol, carbon monoxide and trichloroethylene exposure on mental capacity. Int. Arch. Occup. Environ. Health 35(2) 117—132. [Pg.114]

Some of the solvent wiU be metabolized in the liver, and one product of the metabolism is the poisonous gas carbon monoxide. There have been cases of severe carbon monoxide poisoning due to prolonged exposure to methylene chloride. Someone exposed to the solvent for two to three hours may achieve a level of 15 per cent carbon monoxide in the blood, which would cause only mild effects in a healthy individual but possibly more severe problems in someone with heart or lung disease. [Pg.187]

The long-term effects of carbon monoxide poisoning for victims who recover are less clear. Those who recover from exposure to high levels, especially if they have been unconscious, can suffer effects on the memory and the brain and heart which may last some time or even be permanent. Some victims may suffer heart attacks some time after apparent recovery or succumb to pneumonia, especially the elderly. Similarly, despite an apparent full recovery, some weeks after the poisoning the victim may suffer from effects on the brain (for example, encephalopathy) which can cause symptoms similar to Parkinson s disease or personality changes (irritability, for example) which can persist for some time. Loss of short-term memory is common. Muscle damage sometimes occurs, which can lead to renal failure. This is because the breakdown products of the muscle are excreted into the urine and overload the kidneys. These effects are most likely in those who are victims of severe poisoning. [Pg.192]

End, R., Long, C.W. (1942). Oxygen under pressure in carbon monoxide poisoning. I. Effect on dogs and guinea pigs. J. Ind. Hyg. Toxicol. 24 302-6. [Pg.286]

White, S.R., Penny, D.G. (1994). Effects of insulin and glucose treatment on neurologic outcome after carbon monoxide poisoning. Ann. Emerg. Med. 23 606 (Abst.). [Pg.292]

Burney RE, Wu S, and Nemiroff MJ (1982) Mass carbon monoxide poisoning Clinical effects and results of treatment in 184 victims. Annals of Emergency Medicine 11 394-399. [Pg.425]

One of the more insidious effects of carbon monoxide poisoning is the delayed development of neuropsychiatric sequelae, which may include personality changes, motor disturbances, and memory impairment. These manifestations do not correlate either with the length of exposure or the maximum blood carboxyhemoglobin concentration but are more likeiy if patients experienced a deep coma. ... [Pg.1297]

L8. Lawson, D. D., McAllister, R. A., and Smith, G., The effect of high pressure oxygen in experimental acute carbon monoxide poisoning. Scot. Med. J. 4, 327 (1959). [Pg.132]


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See also in sourсe #XX -- [ Pg.306 , Pg.1101 ]




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