Carbon monoxide (CO) is a gas produced due to the incomplete combustion of organic material (Luchini et al. 2009). It is odorless, colorless, and tasteless that is inspired into the respiratory system and easily enters the bloodstream. Different sources of carbon monoxide can be enumerated, namely: fires, stoves, automobile exhaust, improperly ventilated furnaces, gasoline engines, among others. Cigarette smoke is also a significant source of carbon monoxide.
What makes Carbon monoxide a significant toxic substance?
The gas being implicated is known to be rapidly absorbed in the blood. CO, though binds hemoglobin (Hb – a red blood cell molecule that carries oxygen) slower than oxygen, has an affinity of 200-255 times greater than that of oxygen and its release is 10,000 times slower. The resulting compound formed from CO and Hb binding is known as carboxyhemoglobin (COHb). The formation of such a compound indicates competition between CO and oxygen for binding sites. An increase, therefore, of carbon monoxide concentration in blood could cause a decrease in the oxygen carrying capacity of the blood. This would lead to a decrease of oxygen delivery to various tissues and organs leading to hypoxia. The effects of such a situation is usually significantly seen in organs that rely heavily on oxygen, e.g. the brain and the heart.
The impaired delivery of oxygen and its utilization is causes by the toxicity of carbon monoxide. This gas affects many sites in the body but it has a profound effect on organs which has high oxygen requirement. This results from cellular hypoxia which is mainly caused by the hindrance in oxygen delivery. Relative functional anemia happens when carbon monoxide binds with hemoglobin. An encompassing atmospheric carbon monoxide level of 100 ppm would produce an HbCO of 16% during equilibration.
Since carbon monoxide have a greater affinity to hemoglobin, an increase in carbon monoxide concentration would cause the increased binding of the molecules of oxygen to other oxygen binding sites and would cause a leftward shift in the oxyhemoglobin dissociation curve which means that there is a decreased availability of oxygen to tissues which are hypoxic. Carbon monoxide has a greater affinity to cardiac myoglobin which may result to myocardial depression and hypotension.
Carbon monoxide has a half-life of 3-4 hours at room temperature and this gas is eliminated through the lungs.
What makes it more lethal is that the presence of CO in the environment cannot be readily felt due to its odorless, colorless and tasteless properties, hence, is termed as the silent killer. Manifestations range from shortness of breath and to death due to continued exposure. No pathognomonic sign is known except for a cherry red color of the face which is a strong clue to acute CO poisoning. (McPherson and Pincus, Henry’s Clinical Diagnosis and Management by Laboratory Methods, 22nd edition, 2012, p. 360) It is while the known treatment prescribed is hyperbaric oxygen therapy.
Due to the aforementioned clinical significance of CO, different methods of measuring the substance were employed overtime. The most common ones are: Gas chromatography, spectrophotometry, and the use of specialized spectrophotometric machines known and CO-oximeters. Such tests will be discussed in the succeeding posts.