Blood carbon monoxide, effects

Molecular diffusion ( ) has been used in various ways in micro analysis. In Figure 27, is seen the Conway diffusion dish, in which the substance to be tested is placed on the outside, and the reagent is placed in the central cup. The cup is covered, and after a time, the substance being analyzed diffuses into the central cup where it produces an effect which can then be interpreted in various ways. In the Figure, carbon monoxide is being determined. This same method is very useful for alcohol determination, where dichromate oxidizes the alcohol after it diffuses into the dichromate from the blood. 

Adult male volunteers were exposed to purified air,2 -2 - to ozone alone, or to ozone in combination with nitrogen dioxide and carbon monoxide. No additional effects were detected when nitrogen dioxide at 0.3 ppm was added to ozone. The addition of carbon monoxide at 30 ppm to the ozone-nitrogen dioxide mixture produced no additional effects, other than a slight increase in blood carboxyhemoglobin content and small decreases in psychomotor performance, which were not consistent in different subject groups. 

Metabolic studies of inhaled chlorobromomethane in rats have shown production of carbon monoxide, halide ions, and other reactive intermediates. It has been noted that some central nervous system effects may be a consequence of elevated carbon monoxide in the blood, which can result from chlorobromomethane metabolism. ... 

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. 

However, the mathematics describes an idealized situation, and the real situation in vivo may not be so straightforward. For example, with carbon monoxide, as already indicated, the toxicity involves a reversible interaction with a receptor, the protein molecule hemoglobin (see chap. 7 for further details of this example). This interaction will certainly be proportional to the concentration of carbon monoxide in the red blood cell. However, in vivo about 50% occupancy or 50% carboxyhemoglobin may be sufficient for the final toxic effect, which is cellular hypoxia and lethality. Duration of exposure is also a factor here because hypoxic cell death is not an instantaneous response. This time-exposure index is also very important in considerations of chemical carcinogenesis. 

Figure 7.67 The dissociation of carboxyhemoglobin in the blood of a patient poisoned with carbon monoxide. The graph shows the effects of (A) breathing air (B), oxygen, or (C) oxygen at increased pressure (2.5 atmospheres) on the rate of dissociation. Source From Ref. 19.

Fig 5 Effects of carbon monoxide on human beings This chad can be considered only as a general guide because the percent of CO blood saturation will vary with exertion, excitement, fear, depth of respiration, anemia, and general physical condition of the individual... 

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