Carbon monoxide , exposure

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). 

Strasser AA, Herman C, Sanborn PM, Pickworth WB, Feldman EA (2007) New lower nicotine cigarettes can produce compensatory smoking and increased carbon monoxide exposure. Drug Alcohol Depend 86 294-300... 

Mactutus CF, Fechter LD Moderate prenatal carbon monoxide exposure produces persistent, and apparently permanent, memory deficits in rats. Teratology 31 1-12, 1985... 

Loder RT, Hernandez MJ, Lemer AL, et al The induction of congenital spinal deformities in mice by maternal carbon monoxide exposure. J Pediatr Orthop 20(5) 662-666, 2000... 

The primary health effect of nitric oxide results from its tendency to react with hemoglobin in red blood cells, in much the same way as carbon monoxide does. The concentration of nitric oxide is normally so low, however, that this effect is relatively minor, especially compared with the effects of carbon monoxide exposure. 

Ott, W., P. Switzer, and N. Willits, Carbon Monoxide Exposures inside an Automobile Traveling on an Urban Arterial Highway, J. Air Waste Manage. Assoc., 44, 1010-1018 (1994). 

Gold particulate films have been formed under thiol monolayers spread on aqueous HAuC14 solutions by exposure to carbon monoxide exposure [110]. 

Monoxide for Carboxyhemoglobin Determination in Evaluating Carbon Monoxide Exposures Resulting from the Operation of Gasoline Fork Lift Trucks in Holds of Ships, Am. Ind. Hyg. Assoc. J., 1979, 30, 477-483. 

Whether the toxic effects are mainly due to anemic hypoxia or to the histotoxic effects of carbon monoxide on tissue metabolism is a source of controversy. Carbon monoxide will certainly bind to myoglobin and cytochromes such as cytochrome oxidase in the mitochondria and cytochrome P-450 in the endoplasmic reticulum, and the activity of both of these enzymes is decreased by carbon monoxide exposure. However, the general tissue hypoxia will also decrease the activity of these enzymes. 

This chapter reviews physical and chemical properties and toxicokinetic, toxicologic, and epidemiologic data on carbon monoxide. The Subcommittee on Submarine Escape Action Levels used this information to assess the health risk to Navy personnel aboard a disabled submarine from exposure to carbon monoxide and to evaluate the Navy s proposed submarine escape action levels (SEALs), proposed to avert serious health effects and substantial degradation in crew performance from short-term exposures (up to 10 d). The subcommittee also identifies data gaps and recommends research relevant for determining the health risk attributable to carbon monoxide exposure. 

Cardiac function in healthy persons could be affected by low to moderate carbon monoxide exposures (Davies and Smith 1980). Six matched groups of young healthy subjects lived in a closed environmental chamber for 18 d and were exposed continuously to carbon monoxide at concentrations of 15 or 50 ppm in air during the middle 8 d. Unequivocal P-wave electrocardiogram (ECG) changes were observed during exposure in 3 of the 15 subjects exposed at 15 ppm (2.4% COHb) and in 6 of 15 subjects exposed at 50 ppm (7.1% COHb), compared with none of the 14 exposed at 0 ppm (0.5% COHb). 

Two studies that used subjects with COHb concentrations of up to 15% reported no changes in the ability to do tasks involving coordination (Stewart et al. 1970 Wright et al. 1973). Stewart et al. (1970) used several tests of manual dexterity. In one, subjects had to pick up small pins, place them in small holes, and then put collars over the pins. No effects attributable to carbon monoxide exposure were found at COHb up to 15%. Wright et al. (1973) also observed no effects on a number of coordination tasks at COHb of 5% and 7%. One study did report a decrement in a hand-eye coordination task (5% COHb) (Putz et al. 1976). 

Annau, Z. 1987. Complex maze performance during carbon monoxide exposure in rats. Neurotoxicol. Teratol. 9(2) 151-155. 

Bing, R.J., J.S.Sarma, R.Weishaar, A.Rackl, and G.Pawlik. 1980. Biochemical and histological effects of intermittent carbon monoxide exposure in cynomolgus monkeys (Macaca fascicularis) in relation to atherosclerosis. J. Clin. Pharmacol. 20(8- 9) 487-499. 

Davies, D.M., and D.J.Smith. 1980. Electrocardiographic changes in healthy men during continuous low-level carbon monoxide exposure. Environ. Res. 21(1 ) 197— 206. 

Hudnell, H.K., and V.A.Benignus. 1989. Carbon monoxide exposure and human visual detection thresholds. Neurotoxicol. Teratol. 11 (4) 363—371. 

Mihevic, P.M., J.A.Gliner. and S.M.Horvath. 1983. Carbon monoxide exposure and information processing during perceptual-motor performance. Int. Arch. Occup. Environ. Health 51 (4) 355—363. 

O Donnell, R.D., P.Mikulka, P.Heinig, and J.Theodore. 1971. Low level carbon monoxide exposure and human psychomotor performance. Toxicol. Appl. Pharmacol. 18(3) 583—589. 

Parving, H-H. 1972. The effect of hypoxia and carbon monoxide exposure on plasma volume and capillary permeability to albumin. Scand. J. Clin. Lab. Invest. 30(1) 49- 56. 

Graph 1 gives the symptoms from various low-level carbon monoxide exposures as a function of duration of exposure. The highest CO concentration discussed is 600 ppm (parts per million). 600 ppm is another way of saying 0.06%/vol. The chart shows that after one hour of exposure to an average concentration of 600 ppm of CO, one would experience a headache, but not a throbbing one. Even after 100 hours of exposure, the worst that one would experience would be unconsciousness, but not death. However, after only half an hour of exposure to 600 ppm, no symptoms are indicated at all -not even a mild headache. We should keep 0.06% in mind as another benchmark number to which we will refer later in this chapter. 

Anderson, E.W., Andelman, R.J., Strauch, J.M., Fortuin, N.H., Knelson, J.H. (1973). Effect of low-level carbon monoxide exposure on onset and duration of angina pectoris. A study in ten patients with ischemic heart disease. Ann. Intern. Med. 79 46-50. 

Atkins, E.H., Baker, E.L. (1985). Exacerbation of coronary artery disease by occupational carbon monoxide exposure a report of two fatalities and a review of literature. Am. J. Ind. Med. 7 73-9. 

Meyer-Witting, M., Helps, S., Gorman, D.F. (1991). Acute carbon monoxide exposure and cerebral blood flow in rabbits. Anaesth. Intensive Care 19 373-7. 

Morandi, M., Eisenbud, M. (1980). Carbon monoxide exposure in New York City a historical overview. Bull. NY Acad. Med. 56 817-28. 

Fetcher, L.D., Liu, Y., Pearce, T.A. (1997).Cochlear protection from carbon monoxide exposure by free radical blockers in the guinea pig. Toxicol. Appl. Pharmacol. 142 47-55. 

Chronic, low-level carbon monoxide exposures produce decreased birth weights, cardiomegaly, EKG changes, and disruptions of cognitive function in several animal models. Rabbits exposed to carbon monoxide for 11 weeks demonstrated plaque formation in cardiac vessels indistinguishable from those seen from atherosclerotic heart disease. 

Fechter LD, Annau Z. Toxicity of mild prenatal carbon monoxide exposure. Science 1977 197(4304) 680-2. 

Penney, D. G., Helfman, C. C., Dunbar, J. C., McCoy, L. E. (1991). Acute severe carbon monoxide exposure in the rat Effects of hyperglycemia and hypoglycemia on mortality, recovery, and neurological deficit. Canadian Journal of Physiology, 69, 1168-1177. 

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