What is the Lewis structure of CO

Carbon monoxide

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Carbon monoxide (also Carbon monoxide, common: Carbon monoxide, earlier too Carbon dioxide) is a chemical compound of carbon and oxygen with the empirical formula CO. Carbon monoxide is a colorless, odorless, tasteless and poisonous gas. It arises, among other things, from the incomplete combustion of carbon-containing substances.

Carbon monoxide is flammable and burns to carbon dioxide with a blue flame. As a component of town gas, it was used in Germany as a fuel and illuminating gas until the second half of the 20th century. Together with hydrogen, carbon monoxide is required in the chemical industry to produce methanol and other basic chemicals.

Carbon monoxide is produced when formic acid is dehydrated with concentrated sulfuric acid. It burns with a blue flame.


The smelting of metal ores used the reducing effect of carbon monoxide in so-called racing furnaces as early as 1000 BC, but without knowing the nature of the gas. The Greeks and Romans used it for executions.[4] In 1776, the French chemist Joseph de Lassone produced carbon monoxide by heating zinc oxide with coke. He mistakenly assumed that it was hydrogen. Joseph Priestley made carbon monoxide in 1799 by passing carbon dioxide over hot iron.[5] William Cruikshank used the same procedure in 1800. He suggested the correct composition of CO.[6] The toxic properties on dogs were studied by Claude Bernard around 1846.


Satellite measurement of the global carbon monoxide distribution

Carbon monoxide occurs in natural and man-made environments. Typical concentrations in the atmosphere are 0.1 ppm[7] In residential buildings, the normal concentration is 0.5 to 5 ppm, with concentrations of up to 15 ppm in the vicinity of gas burners. Wood fires in chimneys can release up to 5 ‰ carbon monoxide.[8] Other sources of carbon monoxide are charcoal grills operated in living spaces[9] and the use of internal combustion engine ventilation equipment[10]. In urban environments, untreated car exhaust fumes can result in values ​​between 100 and 200 ppm.[11] The concentration in the undiluted exhaust gas of an automobile without a catalytic converter is approx. 7000 ppm[12]. Tobacco smoke contains significant levels of carbon monoxide.[13]

Carbon monoxide enters the atmosphere mainly from volcanic activity and as a combustion product from forest and bush fires. Incomplete combustion of carbonaceous fuels always leads to carbon monoxide emissions. In the atmosphere, carbon monoxide is oxidized to carbon dioxide.


Carbon monoxide can be obtained from numerous raw materials such as B. natural gas, biogas, light gasoline, heavy oils, coal and biomass can be produced, whereby synthesis gas, a mixture of carbon monoxide with hydrogen, is generated first, which is then cleaned and processed (synthesis gas, Fischer-Tropsch synthesis).

On a large scale, carbon monoxide can be produced by combustion as follows:

$ \ mathrm {2 \ C + O_2 \ longrightarrow 2 \ CO \; \ quad \ Delta H = -222 \ \ frac {kJ} {mol}} $[14]

The formation of carbon monoxide is favored by high temperatures or a deficit of oxygen. According to the Boudouard equilibrium, the resulting carbon dioxide also reacts with carbon to form carbon monoxide:

$ \ mathrm {CO_2 + C \ \ rightleftharpoons \ 2 \ CO \; \ quad \ Delta H = +172.45 \ \ frac {kJ} {mol}} $[15]

At temperatures of around 1000 ° C, the equilibrium concentration of carbon dioxide is only around 1%. Pure CO can be obtained from it as a compound stable at room temperature by rapid cooling.

In the laboratory, CO can be produced by decomposing formic acid:

$ \ mathrm {HCOOH \ longrightarrow H_2O + CO} $

The disintegration is caused by the dehydrating effect of concentrated sulfuric acid, which is added dropwise to the formic acid.

Since carbon monoxide is very poisonous, excess quantities must be collected with special absorbers or flamed with a flame device. Particular caution applies to CO-air mixtures, as they can react very explosively. It is also possible to catalytically convert carbon monoxide with copper (II) oxide or hopcalite to carbon dioxide.


Monsanto process for the production of acetic acid from methanol and carbon monoxide

Pure carbon monoxide is mainly used for the production of formic acid via methyl formate. Sodium formate is obtained with sodium hydroxide. Acetic acid is obtained in the Monsanto process by reacting carbon monoxide with methanol.

Phosgene is produced from carbon monoxide and chlorine under the catalytic influence of activated carbon:

$ \ mathrm {CO \ + \ Cl_2 \ longrightarrow \ COCl_2} $

Together with hydrogen, it is used for the hydroformylation of olefins and for carbonylation reactions in organic synthesis.

In the blast furnace it is used as a reducing agent for iron ore.

Carbon monoxide is used to bind carbon fibers in a pure carbon matrix for the production of CFRP.

The moon process uses carbon monoxide to purify the metal nickel through chemical transport reactions.

In fur farms, carbon monoxide and dioxide are used to suffocate the mink so that the fur is damaged as little as possible.[16]


Physical Properties

The ignition temperature is 605 ° C[1]. The critical temperature is −140.2 ° C[1], the critical pressure is 35.0 bar[1] The ΔfH0G is −110.53 kJ / mol.

The dissociation energy is slightly higher than that of the very inert, isoelectronic dinitrogen molecule, namely 1070.3 kJ / mol (N2 946 kJ / mol).[17] Despite the high electronegativity difference of 1, carbon monoxide is almost non-polar: it can only be liquefied under pressure below −140 ° C, and its dipole moment is only 0.12 Debye. Carbon monoxide rises extremely slowly in air; its density is 0.968 times the density of air. (Note: This applies if there is no temperature difference between air and carbon monoxide. Since carbon monoxide is mainly formed when carbon is not completely burned, it is very likely that the exhaust gases are warmer than the surrounding air and therefore rise quickly. When these exhaust gases cool down Carbon monoxide, on the other hand, will not sink, as gases that are heavier than air would and therefore tend to concentrate in the upper areas. Convection ensures thorough mixing. If this is missing, the gas exchange only takes place via diffusion.)

Molecular Properties

The bond length between the carbon and oxygen atoms is 106 pm in the solid phase and 112.8 pm in the gas phase.[17]

The molecular structure can best be described using molecular orbital theory. The C – O bond, which is about 10 pm shorter than that of organic carbonyl compounds, indicates a partial triple bond.[18]

Chemical properties

The formation of carbon monoxide from the elements is exothermic, but carbon monoxide is in a disproportionation equilibrium with carbon and carbon dioxide. Because this equilibrium is almost immeasurably slow at room temperature, CO can be isolated despite the unfavorable equilibrium position - CO is metastable. At higher temperatures, the equilibrium shifts in favor of carbon monoxide (LeChatelier's principle). This is used, for example, in iron production (blast furnace process), where the gaseous carbon monoxide is a much more effective reducing agent than the solid coke. The half-life of carbon monoxide in the atmosphere is about one to four months, depending on the air temperature and the presence of other gases.[19]

Carbon monoxide is a good and inexpensive reducing agent and is used in this function in a variety of ways. The oxidizing power of CO, on the other hand, is only weak.

Carbon monoxide is a widely used ligand in organometallic chemistry, so the chemistry of metal carbonyls has been well researched. Carbon monoxide is one of the strong-field ligands and is isoelectronic with dinitrogen (N.2) and the ions cyanide (CN) and nitrosyl (NO+). A strong metal-ligand bond is created through the development of synergetically strengthening back and forth bonds. CO is a strong σ donor and π acceptor.

In carbon monoxide, carbon and oxygen are very tightly bound to one another. 1073 kJ / mol are required for splitting into two atoms (homolytic splitting). This binding energy is particularly large for N2 only 946 kJ / mol are required,[20]


Carbon monoxide is a dangerous breath poison. When it has entered the bloodstream via the lungs, it binds to the central iron atom of hemoglobin, thereby impeding the transport of oxygen in the blood, which can lead to death from asphyxiation. Symptoms of mild poisoning include headache, dizziness, and flu-like symptoms. Higher doses are significantly toxic to the central nervous system and the heart. In addition to acute poisoning, there are consequential damages. Carbon monoxide has serious negative effects on fetal development. Chronic exposure to low levels of carbon monoxide can lead to depression. Carbon monoxide is easily absorbed through the lungs. Since carbon monoxide is colorless, odorless, tasteless and non-irritating, it is hardly noticed. The individual tolerance level varies.[21] On average, exposures of more than 100 ppm are considered to be hazardous to health. The occupational exposure limit (OEL - previously: MAK value) is 30 ppm.[22] Carbon monoxide can lead to reduced life expectancy due to heart damage.[23]

The percentage of hemoglobin in the blood that is covered with carbon monoxide is also called COHb abbreviated (Carbon monoxide hemoglobin). According to older studies, there is no danger for healthy adults even with continuous exposure of eight hours a day at concentrations of up to 115 ppm; there are only concentrations of 4% COHb in non-smokers and 7.6% in smokers. However, recent studies show that in risk groups with cardiovascular diseases, stress levels of 2.7% or more can increase the symptoms of the disease.[1] With higher chronic exposure above 150 to 300 ppm, dizziness, drowsiness, nausea and vomiting occur. Acutely lethal quantities of the gas (LD50)[1]: see info box (above). Hearing impairment is increased by up to 50% when exposed to CO.[24][25]

The individual carbon monoxide tolerance is influenced by various factors, such as the activity carried out, the breathing rate, previous damage or diseases such as cardiovascular diseases, anemia or sickle cell anemia. Other factors are atmospheric pressure or basal metabolic rate.[26][27][28]

Carbon monoxide binds about 325 times more strongly to the red blood pigment hemoglobin than oxygen, so with a carbon monoxide content of 0.1 percent in the breath, about half of the red blood cells are deactivated. The poisonous effect of CO is reduced by the protein environment of the heme in the hemoglobin, so CO binds to an unhindered heme about 26,000 times more strongly than oxygen. It is assumed that the cause is that there is not enough space in the enzyme pocket to allow the linear Fe-C-O geometry preferred by CO, while the angled coordination preferred by dioxygen is not hindered.[29] If the proportion of air breathed is over one percent, death occurs within one to two minutes.[30][31] The elimination half-life of carbon monoxide from the blood is 2 to 6.5 hours,[1] depending on the amount of CO absorbed and the ventilation rate of the person affected.

7-wavelength pulse oximeter that can detect CO intoxication

By binding the CO to hemoglobin, conventional pulse oximeters are fooled and incorrectly indicate high oxygen saturation rates. With newer 7-wavelength pulse oximeters, however, the CO-saturated fraction of hemoglobin can also be detected.[32] The outward signs of carbon monoxide poisoning are cherry-red mucous membranes. According to more recent studies with a high number of cases (231 patients), this clinical sign is rarely encountered, especially in milder forms of intoxication.[33]

The color is a result of the deep red hemoglobin carbon monoxide charge transfer complexes. Furthermore, the death spots (livores) that appear on the corpse after death can typically also be colored bright red by this mechanism and thus provide an indication of carbon monoxide poisoning. Carbon monoxide is a photosynthetic poison and also damages the chlorophyll in plants.

Patients with severe carbon monoxide poisoning are generally intubated and ventilated with positive end-expiratory pressure (PEEP) and 100% oxygen. Due to the significantly increased oxygen supply, the carbon monoxide is displaced by the hemoglobin. Hyperbaric oxygenation can also be considered.[34][35]

Biological importance

In humans, the percentage of hemoglobin in the blood that is covered with carbon monoxide is COHb in the venous blood between 0.7 to 1.1%, of which about 0.5% is produced endogenously. An increased CO level in the cells leads to an up to 1000-fold increased release of the glycoprotein erythropoietin (EPO).[36]

The enzyme heme oxygenase breaks down heme compounds, which are primarily derived from hemoglobin, releasing carbon monoxide. This enzyme and a guanylate cyclase, which is regulated by CO, could be detected in the olfactory center of the human brain and in the olfactory bulb. According to this, carbon monoxide could serve as a gaseous messenger substance (see gasotransmitter) for the sense of smell. The activated guanylate cyclase then releases the secondary messenger substance cGMP.[37] In addition to carbon monoxide, cGMP and cAMP, nitric oxide is also called Second Messenger considered.[38] Both nitrogen and carbon monoxide, as extremely low molecular weight, water-soluble gases, can penetrate biomembranes very quickly and relatively unhindered and therefore serve as neurotransmitters in the transmission of information from the primary or sensory in the secondary or Long-term memory through the limbic system.[39][40]

Carbon monoxide has an anti-inflammatory effect in chronic intestinal inflammation, which also explains the previously puzzling fact that smokers are much less likely to use it Ulcerative colitis fall ill as a non-smoker.[41][42] Even after lung transplants, low-dose inhalation of carbon monoxide prevented damage from ischemia or reperfusion.[36] If kidneys that are intended for transplantation are kept in a solution containing carbon monoxide in low concentrations, the otherwise observed increase in free heme and decrease in cytochrome P450 is inhibited, and cell-damaging lipid peroxidation is thus reduced.[43] Favorable effects of carbon monoxide have also been described in animal models of septic shock, intestinal obstruction (ileus) and arteriosclerosis.[44] In women with gestational hypertension and pregnancy poisoning (preeclampsia), the carbon monoxide concentration in the exhaled air is reduced.[45] Women who smoke have a reduced risk of developing preeclampsia.[46] Drugs that can transport and release controlled amounts of carbon monoxide are under development.[47]


CO monitor in an underground car park

Today there are portable and stationary electronic sensors (gas warning devices) on the market which allow the detection of carbon monoxide in the range of 20-2000 ppm in the room air[48]. In the case of electronic sensors, however, no hydrogen gas should be present at the same time, as otherwise the detection accuracy is significantly affected. Diiodopentoxide I is also used as a precise detection reagent2O5, which is quantitatively converted into elemental iodine I in a U-tube at higher temperatures (approx. 80–160 ° C) in the presence of carbon monoxide2 is reduced, with simultaneous formation of carbon dioxide CO2. By back-titrating the iodine with thiosulphate S2O32− The CO content of the gas can then be determined (iodometry). Ditte researched this process with diiodine pentoxide as early as 1870. Hydrogen - even in higher concentrations - only minimally disturbs the detection accuracy of this method. The simultaneous quantitative determination of the converted carbon dioxide (determination by conductivity or by precipitation of a barium hydroxide solution) makes the determination very precise.


In the withdrawn German standard DIN 32640 "Chemical elements and simple inorganic compounds - names and symbols" from December 1986, only the spellings "carbon monoxide" and "carbon monoxide" are recommended with "oo", because according to the IUPAC rules for the nomenclature of inorganic ones Chemistry End vowels of prefixed Greek numerals cannot be omitted.

In contrast, the 1990 edition of the IUPAC nomenclature only mentions the spellings “carbon monoxide” and “carbon monoxide”; when using the multiplicative prefixes, it says: “The final vowels of the multiplicative prefixes are not omitted unless there are compelling linguistic ones Reasons before. Monoxide is one such exception ”.[49]

Individual evidence

  1. 1,001,011,021,031,041,051,061,071,081,091,101,111,121,131,141,151,161,171,18Entry to CAS no. 630-08-0 in the GESTIS substance database of the IFA, accessed on December 12, 2007 (JavaScript required).
  2. 2,02,1Entry from the CLP regulation too CAS no. 630-08-0 in the GESTIS substance database of the IFA (JavaScript required)
  3. ↑ Since December 1, 2012, only GHS hazardous substance labeling has been permitted for substances. The R-phrases of this substance may still be used to classify preparations until June 1, 2015, after which the EU hazardous substance labeling is of purely historical interest.
  4. ↑ Ivan Blumenthal: Carbon monoxide poisoning, Journal of the Royal Society of Medicine 2001 June; 94 (6): pp. 270-272; PMC 1281520.
  5. ↑ R. E. Schofield: The enlightened Joseph Priestley: a study of his life and work from 1773 to 1804, p. 103, Pennsylvania State University Press (2004).
  6. ^ William Cruickshank (FRS - 1802): Clinical chemist, by Guy H. Neild.
  7. Committee on Medical and Biological Effects of Environmental Pollutants: Carbon monoxide, P. 29, Washington, D.C .: National Academy of Sciences 1977, ISBN 0-309-02631-8
  8. ↑ Green W: An Introduction to Indoor Air Quality: Carbon Monoxide (CO). United States Environmental Protection Agency. Retrieved December 16, 2008.
  9. ↑ A. Hahn, K. Begemann, R. Burger, M. Friedemann, J. Hillebrand, H. Meyer, R. Kolbusa, M. Gessner, Press Office of the Federal Institute for Risk Assessment (Eds.): Medical reports in the event of poisoning in 2008. Berlin 2010, ISBN 3-938163-54-2, ISSN 1435-4047.
  10. ↑ Sabine Sickinger, Stefan Sellmeier, Oliver Meisenberg, Sebastian Schöttner: Carbon Monoxide Poisoning From Ventilation Equipment? In: Fire protection. No. 7, 2011, pp. 538-540.
  11. Siegfried Fred Singer: The Changing Global Environment, P. 90, Dordrecht: D. Reidel Publishing Company, ISBN 90 277 0385 X
  12. ↑ Tom Gosink (January 28, 1983): What do carbon monoxide levels mean?. In: Alaska Science Forum. Geophysical Institute, University of Alaska Fairbanks. Retrieved December 1, 2007.
  13. Queensland Health Smoking Management Policy. QH. Retrieved March 2010.
  14. ↑ o.A .: Student boys chemistry, Bibliographical Institute & F.A. Brockhaus AG, Mannheim 2007, ISBN 978-3-411-05386-5, p. 378.
  15. ↑ Atkins: Physikalische Chemie, VCH, 2nd edition 1996
  16. §6 killing in the Ordinance on the keeping of fur animals, Retrieved April 25, 2012.
  17. 17,017,1Holleman, Wiberg: Inorganic Chemistry Textbook, 102nd edition, de Gruyter; ISBN 978-3-11-017770-1; P. 898.
  18. ↑ J.E. Huheey, E.A. Keiter, R.L. Keiter: Inorganic chemistry: principles of structure and reactivity, de Gruyter, 2003, ISBN 3-11-017903-2.
  19. ↑ Dr. Peter Bützer: Car catalytic converter
  20. Paperback of Chemistry, VEB Fachbuchverlag, Germany.
  21. Raub JA, Mathieu-Nolf M, Hampson NB, Thom SR: Carbon monoxide poisoning - a public health perspective. In: Toxicology. 145, No. 1, April 2000, pp. 1-14. doi: 10.1016 / S0300-483X (99) 00217-6. PMID 10771127.
  22. ↑ Information about harmful substances carbon monoxide
  23. Henry CR, Satran D, Lindgren B, Adkinson C, Nicholson CI, Henry TD: Myocardial Injury and Long-term Mortality Following Moderate to Severe Carbon Monoxide Poisoning. (Free full text) In: JAMA. 295, No. 4, January 2006, pp. 398-402. doi: 10.1001 / jama.295.4.398. PMID 16434630.
  24. ↑ carbon monoxide
  25. ↑ Markus Fritz: Clear and clear, 100 times the environment. Bibliographisches Institut AG, Mannheim 1977, ISBN 3-411-01706-6, page 18.
  26. Carbon monoxide. American Lung Association. Retrieved September 14, 2009.
  27. Lipman GS: Carbon monoxide toxicity at high altitude. In: Wilderness & Environmental Medicine. 17, No. 2, 2006, pp. 144-145. PMID 16805152.
  28. first draft prepared by Mr J. Raub .: Environmental Health Criteria 213 (Carbon Monoxide). Geneva: International Program on Chemical Safety, World Health Organization 1999, ISBN 9241572132.
  29. ↑ James Collman et al: Nature of O2 and CO Binding to Metalloporphyrins and Heme Proteins, 1976.
  30. ↑ Oxides of carbon-carbon monoxide.
  31. ^ Hu & Speizer: Environmental and occupational hazards. Carbon monoxide. In: Harrison's Principles of Internal Medicine, McGraw-Hill, New York City, 14th edition, page 2533.
  32. ↑ Coulange M, Barthelemy A, Hug F, Thierry AL, De Haro L. Reliability of new pulse CO-oximeter in victims of carbon monoxide poisoning. Undersea Hyperb Med. 2008 Mar-Apr; 35 (2): pp. 107-111; PMID 18500075.
  33. ↑ Cevik AA et al. Interrelation between the PSS, CO-Hb levels and in-hospital clinical course of CO poisoning. Int J Clin Pract 2006; 60: pp. 1558-1564; PMID 16918999.
  34. ↑ Weaver et al .: Carbon monoxide poisoning: risk factors for cognitive sequelae and the role of hyperbaric oxygen. Am J Respir Crit Care Med. 2007; 176 (5): pp. 491-497; PMID 17496229.
  35. ↑ Weaver et al. Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med. 2002 Oct 3; 347 (14): pp. 1057-1067; PMID 12362006.
  36. 36,036,1C.S. Gebhard: Studies on the regulation of the carbon monoxide-induced stimulation of erythropoietin secretion in the rat, Dissertation 2007, Eberhard Karls University of Tübingen.
  37. ↑ Science online encyclopedias: Entry to Carbon monoxide in the lexicon of neurology.
  38. ↑ P. Weydt: Receptor-mediated calcium signals in cultured human glioma cells, 2000, Tectum Verlag, ISBN 3-8288-8137-8.
  39. ↑ R.F. Schmidt, F. Lang: Human Physiology: Learning and Memory, Springer-Verlag, ISBN 978-3-540-32908-4.
  40. ↑ P. A. Berg: Chronic fatigue and fibromyalgia syndrome, 2003, Springer-Verlag, ISBN 3-540-44194-8.
  41. The "good" thing about carbon monoxide - immunology: anti-inflammatory effect in the intestine, Evening paper of December 24, 2005
  42. ^ "Journal of Experimental Medicine". 2005, Vol. 202, pp. 1703-17139.
  43. ↑ Atsunori Nakao, Gaetano Faleo, Hiroko Shimizu, Kiichi Nakahira, Junichi Kohmoto, Ryujiro Sugimoto, Augustine M. K. Choi, Kenneth R. McCurry, Toru Takahashi, Noriko Murase: Ex vivo carbon monoxide prevents cytochrome P450 degradation and ischemia // reperfusion injury of kidney grafts. In: Kidney Int. 74, No. 8, June 16, 2008, pp. 1009-1016, PMID 11035334.
  44. ↑ Atsunori Nakao, Augustine M. K Choi, Noriko Murase: Protective effect of carbon monoxide in transplantation. In: Journal of Cellular and Molecular Medicine. 10, No. 3, June 1, 2006, pp. 650-671, doi: 10.1111 / j.1582-4934.2006.tb00426.x, PMID 16989726.
  45. ↑ M tree: End-tidal carbon monoxide measurements in women with pregnancy-induced hypertension and preeclampsia. In: American Journal of Obstetrics and Gynecology. 183, No. 4, 2000, pp. 900-903, doi: 10.1067 / mob.2000.109047, PMID 11035334.
  46. ^ S. Bainbridge, E. Sidle, G. Smith: Direct placental effects of cigarette smoke protect women from pre-eclampsia: the specific roles of carbon monoxide and antioxidant systems in the placenta. In: Medical hypotheses. 64, No. 1, 2005, pp. 17-27, doi: 10.1016 / j.mehy.2004.06.019, PMID 15533604.
  47. ↑ Roberta Foresti, Mohamed G. Bani-Hani, Roberto Motterlini: Use of carbon monoxide as a therapeutic agent: promises and challenges. In: Intensive Care Medicine. 34, No. 4, 2008, pp. 649-658, doi: 10.1007 / s00134-008-1011-1, PMID 18286265.
  48. ↑ http: //www.sparkfun.com/datasheets/Sensors/Biometric/MQ-7.pdf
  49. ↑ IUPAC: