Toxicity carbon monoxide

High levels of sulfur not only form dangerous oxides, but they also tend to poison the catalyst in the catalytic converter. As it flows over the catalyst in the exliaust system, the sulfur decreases conversion efficiency and limits the catalyst s oxygen storage capacity. With the converter working at less than maximum efficiency, the exhaust entering the atmosphere contains increased concentrations, not only of the sulfur oxides but also, of hydrocarbons, nitrogen oxides, carbon monoxides, toxic metals, and particulate matter. 

Casida JE, Toia RF. Organophosphorus pesticides their target diversity and bioactivation. In Dekant W, Neumann HG, eds. Tissue Specific Toxicity Biochemical Mechanisms. London Academic Press, 1992. Coburn RF, Forman HJ. Carbon monoxide toxicity. In Fahri LE, Tenney SM, eds. Flandbook of Physiology, The Respiratory System, Section 3, Vol. IV, Bethesda, MD American Physiology Society, 1987. Ellenhorn MJ, Barceloux DG. Medical Toxicology, New York Elsevier, 1988. 

Carbon monoxide toxicity has been studied well in humans. If sufficiently prolonged, exposure at concentrations of 200-1,200 ppm can result in a progression of such hypoxic symptoms as headache, decreased night vision, abnormal visual evoked response, nausea, abnormal fine manual dexterity, vomiting,... 

Numerous studies have been conducted to test carbon monoxide toxicity in experimental animals. Several are reviewed in this section and summarized in Table 3-3. 

The model of carbon monoxide toxicity proposed by Kao and Nanagas (2006) combines the cascade of changes resulting from three primary events - binding to HB, direct cellular injury, and increased NO activity. CO is not a radical but many of the injuries produced by it are those that are caused by oxidative stress, which is secondary to hypoxia. In the model of Kao and Nanagas (2006), the oxidant is NO, which contributes to oxidative damage to the brain and produces the clinical syndrome of delayed neurologic sequelae (Thom et al, 1997). 

Chen, Q., Wang, L. (2000). Carbon monoxide air pollution and its health impact on the major cities of China. In Carbon Monoxide Toxicity (D.G. Penny, ed.), pp. 345-61. CRC Press, Washington, DC. 

Cobum, R.F. (1979). Mechanism of carbon monoxide toxicity. Prev. Med. 8 310-22. 

Goldbaum, L.R., Ramirez, R.G., Absalon, K.B. (1975). What is the mechanism of carbon monoxide toxicity Aviat. Space Environ. Med. 46 1289-91. 

Omaye, S.T. (2002). Metabolic modulation of carbon monoxide toxicity. Toxicology 180 139-50. 

Penny, D.G. (2000). Carbon Monoxide Toxicity. CRC Press, Washington, DC. 

Sangalli, B.C., Bidanset, J.H. (1990). A review of carbox-ymyoglobin formation a major mechanism of carbon monoxide toxicity. Vet. Hum. Toxicol. 32 449-53. 

Prockop LD, Naidu KA Brain CT and MRI findings after carbon monoxide toxicity. J Neuroimaging 9 175-181, 1999... 

Mankind encountered the effects of carbon monoxide as far back as prehistoric times. It is the most common poison with a suffocation action. It is second to carbon dioxide with respect to the amounts of industrial emissions. Carbon monoxide toxicity is due to its affinity to haemoglobin. This affinity is higher by a factor of 200 than that of oxygen. Haemoglobin... 

Despite the results presented above, there has been reluctance to consider carbon monoxide for microbiological control. This may result from fears regarding its inherent toxicity as well as from the public perception of the use of toxic compounds to treat wine. Indeed, carbon monoxide is a toxic, colorless, and odorless gas whose detection requires specialized equipment. However, in terms of potential health risks, SO2 is considerably more toxic than carbon monoxide. Toxicity data for the two show that the IDLH (Immediately Dangerous to Life and Health) level for CO is 1500 mg/L, whereas for SO2, it is only 100 mg/L (Sigma-Aldrich Library of Chemical Safety Data, 1988). 

The second hazard is toxicity. The toxic materials may have direct effects. An example is pulmonary paralysis from hydrogen sulfide. Toxic materials can be asphyxiants that intermpt oxygen transport. An example is carbon monoxide. Toxic materials may be irritants at very low concentrations and lethal at higher levels, such as eye irritants that reduce vision. 

Carbon monoxide toxicity. It is well known that CO can induce negative symptoms in humans. These effects start to occur at levels above 70 ppm. At these levels, the concentration of CO-Hb in the blood can reach 10-15%. When the CO-Hb concentration is much higher than this, more severe symptoms are observed. 

The Chemical Elements of Life Radioactive Bone 265 The Power of Radicals 298 Why Is Carbon Monoxide Toxic ... 

The model of carbon monoxide toxicity proposed by Kao and Nanagas (2006) combines the cascade of... 

Chance, B., Erecinska, M., Wagner, M., 1970. Mitochondrial responses to carbon monoxide toxicity. Ann. NY Acad. Sci. 174, 193-204. 

Godish, T, 2003. Air Quality, fourth ed. Lewis Books, Boca Raton, FL. Goldbaum, L.R., Ramirez, R.G., Absalon, K.B., 1975. What is the mechanism of carbon monoxide toxicity Aviat. Space Environ. Med. 46, 1289-1291. Goldbaum, L.R., Orellano, T, Dergal, E., 1976. Mechanism of the toxic action of carbon monoxide. Ann. Clin. Lab. Sci. 6, 372-376. 

Hamilton-Farrel, M.R., Henry, J., 2000. Treatment of carbon monoxide poisoning in the United Kingdom. In Penny, D.G. (Ed.), Carbon Monoxide Toxicity CRC Press, Washington, DC, pp. 331-343. 

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