Role of CO (Carbon Monoxide) on human health & its Impact

CO (Carbon monoxide) is known as the silent killer and its negative side has been investigated for many years. It is one of the most common and widely distributed air pollutants. It is known that CO is the diatomic oxide of carbon which is a colorless and odorless gas. This invisible and chemically inert gas can be fatal and can induce both acute and chronic health hazards with prolonged exposure and eventually death. The chief source of CO is the incomplete combustion of carbon-based fuels from motor vehicles, various appliances, fireplaces at home, gas-powered engines, and paints containing methylene chloride, etc. Human bodies too generate CO after hemoglobin decomposition since Heme Oxygenase (HO) is the enzymatic source of CO. This chemically stable gas occurs in nature as a result of oxidation or combustion of organic materials (Ryter et al., 2004). CO is one of the most common sources of exposure in industrial regions and can cause poisoning to more than half of the population in many industrial countries. CO in the gaseous form is freely diffusible and traverses all membranes, bypassing archetypical receptors and transporters, and hence is capable of mediating functional changes in the cell fastly.

Human Health Impact

The CO can bind to hemoglobin and reduce the oxygen-carrying capacity of the blood giving rise to tissue hypoxia. The inhalation of CO is responsible for pulmonary ischemia damage (Wu and Wang, 2005). This gas plays an important role in regulating ejaculation and has a role in penile erection control (Burnett et al., 1998). Some solvents that are used in paint strippers or the degreasing machinery contain methylene chloride. This methylene chloride is dangerous for the lung and liver as in the vapor form it is easily absorbed by the lungs and after reaching the liver is converted to CO.

  • Pregnant women and their fetuses are more vulnerable to the exposure of CO.
  • Pregnant women exposed to CO have reduced blood hemoglobin concentrations and an increase ventilation rate.

The fetal blood has a greater affinity for CO and the CO forms a complex with hemoglobin called carboxyhemoglobin which can be 10-15% higher in fetus as compared with the mother (Farrow and Davis, 1990).

The non-smokers exposed to environmental tobacco smoke can have 1% higher carboxyhemoglobin levels than the non-exposed normal persons.

In a response to chronic smoking, regular smokers can have higher red cell volumes and reduced plasma volumes to increased carboxyhemoglobin levels (Omaye, 2002).

Short-term poisoning of CO affects Central Nervous System (CNS), depending on the wide range and severity of exposure causing headaches, dizziness, weakness, nausea, vomiting, disorientation, confusion, collapse, and coma (Raub and Beningnus, 2002).  The hemoglobin affinity for CO is 240 times higher than that of oxygen. CO competitively binds to the oxygen-carrying heme moiety of hemoglobin formed of an organic protoporphyrin ring and a central iron ion in the ferrous state (Fe2+), detaching oxygen and isolating tissue from their oxygen supply. The binding of two CO molecules to hemoglobin also causes a change in the allosteric conformation of the hemoglobin molecule, preventing oxygen at the other two binding sites from being easily released. This results in a leftward shift of the hemoglobin dissociation curve and further exacerbates tissue hypoxia (Morse and Sethi, 2002).  In the year 1998, it was calculated that every year, 1000 to 2000 accidental deaths resulted from CO exposure (Hampson, 1998). Today, there is enough proof of serious neurological sequelae i.e prolonged loss of consciousness and elevated S100B (a calcium-binding peptide and is used as a parameter of glial activation and/or death in many disorders of the central nervous system), and reduced life expectancy due to CO exposure.

CO affects the physiological and pathophysiological processes in the eye, in general, and in glaucoma, in particular.

This gas harms both oxidative stress and the inflammatory process that causes a period of hypoxia and cellular damage. CO directly hinders the aerobic metabolism that has a similar effect to cyanide by binding and suppressing the mitochondrial cytochrome oxidase (Zhang and Piantadosi, 1992). In the brain, CO binds to cytochrome c oxidase, which results in impairment of ATP synthesis and increased production of reactive oxygen species (Brown and Piantadosi, 1992). Neurological sequelae are most commonly subjective and affect mood, short-term memory, attention, and concentration. The most common problem experienced is depressed mood and short-term memory and difficulty in concentration (Chiew and Buckley, 2014).

  • Sudden chest pain may occur in people with angina. Other than tightness in the chest, headache, fatigue, dizziness, drowsiness or nausea are some of the initial symptoms.
  • Exposure in high concentration or for a longer period of time may cause vomiting, confusion, and collapse along with unconsciousness and muscle.

CO is a very intriguing molecule, and that is why we need a better understanding of its regulation and interactions with other gases in order to extend our knowledge of its epidemiological effects.

 

References

  • Brown, S. D., & Piantadosi, C. A. (1992). Recovery of energy metabolism in rat brain after carbon monoxide hypoxia. The Journal of clinical investigation89(2), 666-672.
  • Burnett, A. L., Johns, D. G., Kriegsfeld, L. J., Klein, S. L., Calvin, D. C., Demas, G. E., … & Poss, K. D. (1998). Ejaculatory abnormalities in mice with targeted disruption of the gene for heme oxygenase-2. Nature medicine4(1), 84-87.
  • Chiew, A. L., & Buckley, N. A. (2014). Carbon monoxide poisoning in the 21st century. Critical Care18(2), 1-8.
  • Farrow, J., Davis, G., 1990. Fetal death due to nonlethal maternal carbon monoxide poisoning. J. Forensic 35, 1448/ 1452
  • Morse, D., & Sethi, J. (2002). Carbon monoxide and human disease. Antioxidants and Redox Signaling4(2), 331-338.
  • Omaye, S. T. (2002). Metabolic modulation of carbon monoxide toxicity. Toxicology180(2), 139-150.
  • https://www.osha.gov/sites/default/files/publications/carbonmonoxide-factsheet.pdf. Accessed on 11-03-2022
  • Raub, J. A., & Benignus, V. A. (2002). Carbon monoxide and the nervous system. Neuroscience & Biobehavioral Reviews26(8), 925-940.
  • Ryter, S. W., Morse, D., & Choi, A. M. (2004). Carbon monoxide: to boldly go where NO has gone before. Science’s STKE2004(230), re6-re6.
  • Wu, L., & Wang, R. (2005). Carbon monoxide: endogenous production, physiological functions, and pharmacological applications. Pharmacological reviews57(4), 585-630.
  • Zhang, J., & Piantadosi, C. A. (1992). Mitochondrial oxidative stress after carbon monoxide hypoxia in the rat brain. The Journal of clinical investigation90(4), 1193-1199.

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