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Body Synthesis Essay

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Introduction
Carbon monoxide (CO) is a tasteless, odorless, and colorless toxic gas that is produced primarily as a result of incomplete combustion of carbon material. Due to humans inability to perceive this gas CO it is commonly referred to as ‘silent killer.’ Inhalation of CO is the leading cause of accidental deaths in the United States. Excluding deaths caused by fires, there are around 2,700 deaths as a result of carbon monoxide poisoning annually. The Center for Disease Control and Prevention (CDC) reports that around 450 deaths are caused by accidental CO toxicity every year. While the total number of deaths seems low, an estimated 50,000 people in America visit the emergency hospital departments showing signs of CO poisoning. Exposure to CO results
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It causes death by the CO binding rapidly to the haemoglobin (Hb) resulting in the carboxyhemoglobin (COHb) formation. As a result, the blood’s oxygen carrying capacity is reduced leading to tissue hypoxia (Chand-Meena, 2014). The presence of COHb changes the Hb’s oxygen affinity by altering oxyhemoglobin dissociation reducing the oxygen delivered to the tissues, leading to tissue hypoxia. More importantly, other oxygen-carrying hemeproteins such as cytochrome P-450, myoglobin, and cytochrome c oxidase also compete with oxygen for binding sites (Caughey, 1970). It has been demonstrated that cytochrome oxidase oxygen affinity causes impairment of mitochondrial respiration. Even though the level of COHb is a vital clinical measure of carbon monoxide exposure, the most crucial mechanism by which carbon monoxide causes toxicity is its combination with cytochrome oxidase. In addition, carbon monoxide may produce toxicity by binding to myoglobin causing impairment of the cardiac output and leading to cerebral ischemia. The dissociation of carboxymyoglobin is slower compared to COHb because of CO’s increased affinity for myoglobin (Myers, Linberg, & Cowley,
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