In Reply: Carboxyhemoglobin Levels in Banked Blood

Abstract

Currently, the most important mechanism of carbon monoxide toxicity at low-level carbon monoxide exposures is still considered to be carboxyhemoglobin hypoxia. As the affinity of hemoglobin for carbon monoxide is approximately 245 times greater than its affinity for oxygen, carbon monoxide displaces oxygen from hemoglobin, reducing the amount of oxygen available for delivery to the tissues. The carbon monoxide bound to hemoglobin also causes a leftward shift of the oxyhemoglobin dissociation curve. Tighter binding of oxygen to hemoglobin in the presence of carboxyhemoglobin further decreases oxygen delivery to the tissues. Other alternative mechanisms of carbon monoxide toxicity include carbon monoxide binding to hemoproteins such as myoglobin, cytochrome oxidase, tryptophan deoxygenase, and tryptophan catalase. Regardless of the mechanism of carbon monoxide toxicity, carboxyhemoglobin levels provide the best marker currently available for carbon monoxide toxicity. Numerous studies, including references 1-12 cited in our article, have demonstrated that exposure to carbon monoxide from smoking or heavy atmospheric carbon monoxide pollution causes adverse health effects in susceptible patients. The US Environmental Protection Agency has stated that ambient carbon monoxide levels exceeding 9 ppm for an eight-hour average exceed air quality standards. According to the Coburn equation, a constant 9 ppm carbon monoxide exposure for eight hours in the presence of light or moderate physical activity would produce a carboxyhemoglobin level of 1.4 percent. On the basis of currently available data, as stated in our article in Chest, “It would appear to be inadvisable to transfuse susceptible patients with blood containing high levels of carboxyhemoglobin, particularly when multiple transfusions are required.”