Exposure to carbon monoxide compromises function of the cardiovascular system primarily by decreasing oxygen-carrying capacity in the blood and decreasing venous and tissue oxygen tension. In normal individuals, with concentrations of approximately 18-20% COHb, there is a reduction in the oxygen consumption during high levels of exercise, a higher than predicted cardiac output, and abnormally high concentrations of lactic acid. However, in patients with coronary artery atherosclerosis, concentrations of COHb of 3-5% significantly curtailed exercise tolerance before the onset of angina. In addition, there is suggestive evidence in animals that the hypoxia induced by increased levels of COHb induces atherosclerosis. The mechanisms underlying increased lipid deposition in arterial wall, during exposure to CO, are unclear, and require further investigation. Also, moderately high levels of COHb in the range of 20% are associated with increases in capillary permeability. The studies of the effects of CO exposure on myocardial irritability suggest that concentrations of COHb of approximately 9% and above can lead to abnormalities in the electrocardiogram and arrhythmias in man and a lower threshold for ventricular tachycardia and ventricular fibrillation in animals. With respect to cerebral function, it seems clear that concentrations of COHb in the range of 3-5% can interfere with visual acuity. On the basis of studies thus far, it is difficult to select a 'safe' level of COHb since in the presence of regional vascular insufficiency, even the lowest levels of COHb may critically interfere with adequate oxygen delivery. The data available thus far do not support a completely safe threshold level of COHb for all parts of the cardiovascular system in all segments of the population, for the prolonged periods of exposure which now exist. On this basis, the safest level of CO exposure is the lowest level which can be achieved.
|State||Published - 1981|