ABSTRACT
Carbon monoxide (CO) is a colorless, tasteless, odorless, non-irritating and commonly occurring substance. An individual exposed to potentially dangerous levels of CO is unlikely to detect its presence (US Environmental Protection Agency, 2000). CO is known to often be quite toxic, especially to organ systems that require high levels of oxygenization (i.e., the heart and brain) (e.g., Raub, Mathieu-Nolf, Hampson, & Thom, 2000). As CO enters the lungs, it is quickly absorbed into the bloodstream where it readily binds with hemoglobin (Hb) to form carboxyhemoglobin (COHb). Inasmuch as the affinity of CO for Hb is much (200 times) greater than that of oxygen (O2), hypoxia can and often does result from the competitive displacement of life-sustaining levels of oxygen. The resultant disruption of oxygen delivery promotes cell injury and death and can set in motion a cascade of other pathophysiological events that place sensitive organs at risk. Factors that influence the toxicity of CO include length of exposure, concentration of the gas, respiratory processing, cardiac output, hematocrit, oxygen requirements of tissues, metabolic status, and preexisting disease (e.g., Raub & Benignus, 2002; Yudofsky & Hales, 1997).
