MetHb is continuously produced under physiological conditions in a limited amount due to auto-oxidation, but it is rapidly converted back to Hb primarily by nicotinamide adenine dinucleotide (NADH)-dependent cytochrome-b5 reductase (also known as MetHb reductase) and to a limited degree also by ascorbate and glutathione [13]. COHb is formed when Hb and carbon monoxide (CO) interact; CO binds to heme molecules 240 times more than O2. The resulting COHb limits the blood’s O2-carrying capacity [14]. In healthy, non-smoking individuals, MetHb is in the range of 0.67 ± 0.33% [15] and COHb in the range of 0.5–1.5% [16].