Carbon monoxide exposure and

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. 

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. 

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). 

For any pollutant, air quality criteria may refer to different types of effects. For example. Tables 22-1 through 22-6 list effects on humans, animals, vegetation, materials, and the atmosphere caused by various exposures to sulfur dioxide, particulate matter, nitrogen dioxide, carbon monoxide, ozone, and lead. These data are from fhe Air Quality Criteria for these pollutants published by the U.S. Environmental Protection Agency. 

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 Prenatal exposure to carbon monoxide Learning and memory deficits. Science 223 409-411, 1984... 

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

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). 

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). 

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. 

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. 

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. 

Smoking kills because of the smoker s chronic exposure to carbon monoxide, tar, and nicotine in tobacco smoke. 

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. 

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. 

Fig. 4.18. Catalytic behavior and structural changes of glassy Cu7oZr30 alloy during exposure to CO2 hydrogenation conditions [4.23], A) Change of C02 hydrogenation activity and product distribution as a function of time-on-stream. Dashed line indicates the calculated equilibrium conversion. Symbols C02 conversion selectivities to methanol O, carbon monoxide V, and ethanol A. Hydrogenation conditions 1.2 g of sample, feed rates of reactants C02,2.3 mmol/s H2, 7.6 mmol/s total pressure 15 bar. B) X-ray diffraction patterns of active sample after steady-state conversion was reached (Cu K,)...

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