carbon monoxide

A colorless, odorless, highly poisonous gas, CO, formed by the incomplete combustion of carbon or a carbonaceous material, such as gasoline.

A colourless odourless gas, CO, sparingly soluble in water and soluble in ethanol and benzene; d. 1.25 g dm⁻³ (0°C); m.p. –199°C; b.p. –191.5°C. It is flammable and highly toxic. In the laboratory it can be made by the dehydration of methanoic acid (formic acid) using concentrated sulphuric acid. Industrially it is produced by the oxidation of natural gas (methane) or (formerly) by the water-gas reaction. It is formed by the incomplete combustion of carbon and is present in car-exhaust gases.

It is a neutral oxide, which burns in air to give carbon dioxide, and is a good reducing agent, used in a number of metallurgical processes. It has the interesting chemical property of forming a range of transition metal carbonyls, e.g. Ni(CO)₄. Carbon monoxide is able to use vacant p-orbitals in bonding with metals; the stabilization of low oxidation states, including the zero state, is a consequence of this. This also accounts for its toxicity, which is due to the binding of the CO to the iron in haemoglobin, thereby blocking the uptake of oxygen.

Carbon monoxide is a gas which is best known to us as a product of incomplete combustion. As such, mankind must have been aware of its deadly effect since the discovery and use of fire, and increasingly so as the development of the industrial revolution led to more use of combustion as a source of energy. The important producers of carbon monoxide are industrial processes, heating equipment, accidental fire, cigarettes, and the internal combustion engine. Blast furnace gas contains 25% carbon monoxide, and coal gas, which was used as a fuel in Europe up until North Sea (natural) gas became plentiful, contains 16%. Carbon monoxide poisoning is the most common cause of fatal gassing and is the cause of death in about 90% of fire victims. Domestic gas supplies still lead to carbon monoxide poisoning, but now due to leakage of products of combustion from a damaged flue or poorly maintained equipment, rather than the fuel itself, since natural gas is carbon monoxide free. In the mining industry carbon monoxide contaminates the atmosphere during and after fires or explosions. The ‘afterdamp’ occurring in such situations is a mixture of carbon dioxide and carbon monoxide.

Carbon monoxide is a colourless, odourless gas which is tasteless and non-irritant. It is somewhat less dense than air and, although it is a product of imperfect combustion, it is inflammable. The gas was first identified by Joseph Priestley in the eighteenth century, but it was Claude Bernard in 1870 who discovered the affinity between carbon monoxide and haemoglobin which accounts for its deadliness: carboxyhaemoglobin is formed and oxygen transport from the lungs to the tissues disrupted. In 1895 J. S. Haldane demonstrated that the formation of carboxyhaemoglobin is an equilibrium reaction which depends upon the relative partial pressures of carbon monoxide and oxygen in inspired gas. Haldane's interest was stimulated by the problems caused by carbon monoxide in British coal mines. By breathing carbon monoxide gas which was passed through a bottle containing a mouse, he was able to determine that man was very much more resistant to the gas. Small animals such as mice and canaries, who are more vulnerable than man due to their high metabolic rate, were used in mines to give an indication of carbon monoxide contamination. Canaries responded to the gas by falling off their perches before workers noticed any ill effects, and this normally gave ample warning. Occasionally, however, in low concentrations of the order of 0.05% carbon monoxide, the bird adapted to the gas and the workers could collapse while the bird remained well.

Carbon monoxide, like oxygen, has an affinity for iron-containing molecules, but it is about 210 times more effective in binding to iron-containing haemoglobin than oxygen is. Since air contains 21% oxygen this means that only 0.1% carbon monoxide in the air will eventually lead to 50% of the haemoglobin being combined to form carboxyhaemoglobin. Once carboxyhaemoglobin is formed, and after exposure ceases, it takes 4-5 hours for its level in the blood to fall, exponentially, by 50%. The ill effect of the gas can therefore be cumulative, and a person can be poisoned by intermittent exposure during the day.

Because carboxyhaemoglobin does not carry oxygen, a level of 50% means that the oxygen carrying capacity of the blood is reduced by 50% and there is a corresponding reduction in the ability to perform maximum exercise. The body compensates for the blood's reduction in oxygen carrying capacity by increasing cardiac output, and in the early stages of carbon monoxide poisoning the heart beats faster and more strongly. Unfortunately, haemoglobin is not the only molecule affected. Muscle myoglobin also binds carbon monoxide, 60 times more effectively than it binds oxygen. This results in a reduction of heart muscle contractility and a failure of the body's compensatory mechanisms, leading to profound tissue hypoxia, which can be fatal. The presence of carboxyhaemoglobin also diminishes the oxygen held by the normal haemoglobin, which further compounds the hypoxic effect. As tissue oxygen level falls, carbon monoxide is able to bind to other iron-containing molecules: notably cytochrome P450, an important drug-metabolizing enzyme, and cytochrome A₃, an enzyme in the terminal respiratory chain which can also be poisoned by cyanide.

The scientific history of carbon monoxide is not one of uniform gloom, however. The intense affinity of carbon monoxide for haemoglobin has allowed low concentrations to be used as a marker for measurement of the speed of blood through the lungs and the surface area of the lung available for the transfer of oxygen. This latter remains as one of the standard lung function tests. In 1951 Sjöstrand discovered that Haldane's poison gas is a normal product of the body's metabolism. The enzyme haem oxygenase breaks down the haem from senescent red blood cells, and this reaction produces carbon monoxide and bile salts. The bile salts are excreted by the liver and the carbon monoxide released gives the blood a normal carboxyhaemoglobin level of 0.2-1.0%. This endogenous carbon monoxide was thought to be just a waste product, but more recent work by Verma has demonstrated that a type of haem oxygenase is located in specific areas in the brain, and suggested that the carbon monoxide produced acts as a neurotransmitter. The carbon monoxide activates the enzyme guanylyl cyclase, as does nitric oxide, regulating the intracellular levels of the second messenger cyclic GMP, which in turn regulates cellular activity. Other workers have demonstrated the haem oxygenase enzyme system in blood vessel walls and demonstrated that the carbon monoxide released causes vasodilation, as does nitric oxide. So far, endogenous carbon monoxide release has been suggested to have a role in the sense of smell, memory, cerebellar function (and hence the body's balance and co-ordination), control of blood hormone levels from the hypothalamus, and control of smooth muscle tone and vasodilatation.

The symptoms of carbon monoxide poisoning depend on the concentration breathed. The victim may pass out without warning, but often the onset of poisoning is slow. Headache, with or without nausea, is common, and this may relate to carbon monoxide's vasodilating effect. Drowsiness and lethargy then occur, along with breathlessness on exertion. At any stage there may be chest pain; this is angina due to cardiac hypoxia. At the stage of lethargy and drowsiness, cerebral function is affected and the person may not be able to think well enough to make an escape effort. Coma follows, and death. Treatment is by removal to an uncontaminated atmosphere and the administration of 100% oxygen. Hyperbaric oxygen speeds up recovery, and there is increasing evidence that it reduces long-term neurological problems.

Endogenous carbon monoxide function is undoubtedly disrupted during poisoning, but at our present state of knowledge it is difficult to say how this contributes to the toxic action of exogenous carbon monoxide. It may well be that our picture of the mechanisms of carbon monoxide poisoning will change as the function of endogenous carbon monoxide becomes clearer. Patients with carbon monoxide poisoning may have very poor balance and yet have good cerebral function. Short-term memory may also be severely disrupted. It is tempting to link these two features with the functions suggested for endogenous carbon monoxide. No doubt time will tell if there is a relationship.

— John A. S. Ross

Bibliography

• World Health Organisation (1979). Environmental health criteria 13: carbon monoxide. WHO, Geneva.
• Dawson, T. M. and Snyder, S. H. (1994). Gases as biological messengers: nitric oxide and carbon monoxide in the brain. (Review article.) Journal of Neuroscience, 14 (9), 5147-59

A colorless, odorless, poisonous gas produced by the combustion of carbon or organic fuels in a limited oxygen supply. Carbon monoxide combines irreversibly with hemoglobin, preventing the formation of oxyhemoglobin and reducing the oxygen supply to the tissues.

Carbon monoxide (CO) is a clear, colorless, odorless, and insidious poison that is responsible for hundreds of inadvertent and preventable deaths in the United States each year. The major environmental source of CO is incomplete combustion of carbonaceous fossil fuels. The reason for its toxicity is that it combines with the oxygen-carrying site of hemoglobin, the red protein within red blood cells that is responsible for delivering oxygen from the lung to body tissues. CO has a more than two-hundredfold greater affinity for this oxygen-carrying site than does oxygen. This means that, at sea level, exposure to 1,000 parts per million (ppm) CO in 20 percent oxygen (200,000 ppm) would lead, at equilibrium, to about 50 percent of hemoglobin sites being combined with CO rather than oxygen. Fortunately, it requires eight to twelve hours for maximum blood levels to be achieved when the body encounters a new CO concentration, otherwise mainstream cigarette smoke, which contains even higher levels of CO, might be instantaneously lethal. When CO combines with hemoglobin, the resulting chemical is called carboxy hemoglobin (COHb).

The negative effect of CO on the delivery of oxygen to the tissues extends beyond just the simple blockage of oxygen-combining sites. Each hemoglobin molecule contains four oxygen-carrying sites. Once the first oxygen molecule is released at the tissue level the second, third, and fourth come off even more rapidly. Oxygen release is delayed by CO so that there is even less oxygen delivered than would be expected purely on the basis of the amount of oxygen not being carried by hemoglobin. For this reason, overt symptoms due to lack of oxygen can be observed at COHb levels of approximately 15 to 20 percent, or even less, in healthy people. Levels of COHb over 40 percent can be lethal.

The uptake of CO increases as respiratory rates increase. This puts children at greater risk since they breathe more rapidly, in proportion to their body weight, than adults. This explains the unfortunate situation of a family in an automobile stuck in a snowstorm with the motor running being found with the adults unconscious and the children dead. The fetus is also at higher risk due to the greater affinity of CO for fetal, as compared to adult, hemoglobin.

All cases of fatal CO poisoning are readily preventable. In addition to automobile exhaust, other lethal sources of CO are often related to home heating systems. Blockage of flues, or inappropriate repair work on the home heating source or on ducts, is often responsible for CO toxicity. Symptoms of CO toxicity, such as headache, weakness, and listlessness, tend to be worse in the morning and to go away during the day if people leave the home. Many fatal cases are preceded by visits to physicians or emergency departments with only symptomatic treatment. Home CO alarms are relatively cheap and are an effective means of prevention. CO poisoning occurs more rapidly at high altitude due to the relative lack of oxygen to compete for the oxygen-combining site of hemoglobin. Conversely, symptomatic CO poisoning is treated with oxygen.

CO is also made in the human body through the normal catabolism of heme (oxygen-carrying hemoglobin), which leads to a background concentration in the blood of approximately 0.5 percent COHb. Concentrations of 2 to 3 percent COHb have been associated with an increased risk of angina attacks in susceptible individuals with preexisting arteriosclerotic heart disease. Preventing this adverse consequence is the major basis for the current U.S. ambient standard for CO. There has been a significant decline in outdoor CO levels in the United States as a result of decreased automotive emissions of carbon monoxide.

(SEE ALSO: Ambient Air Quality [Air Pollution])

Bibliography

Ernst, A., and Zibrak, J. D. (1998). "Carbon Monoxide Poisoning." New England Journal Medicine 339:1603–1608.

Raub, J. A.; Mathieu-Nof, M.; Hampson, M. B.; and Thom, S. R. (2000). "Carbon Monoxide Poisoning— A Public Health Perspective." Toxicology 145(1):1–14.

Tomaszewski, C. (1999). "Carbon Monoxide Poisoning— Early Awareness and Intervention Can Save Lives." Postgrad Medicine 105(1):39–40.

— BERNARD D. GOLDSTEIN

For more information on carbon monoxide, visit Britannica.com.

A poisonous, odourless gas that occurs in the atmosphere as a result of incomplete combustion of carbon and carbon compounds. It is a common constituent of vehicle exhaust fumes and tobacco smoke. Carbon monoxide enters the blood stream rapidly and combines with haemoglobin to form carboxyhaemoglobin, a relatively stable compound, which reduces the oxygen-carrying capacity of blood. The affinity of haemoglobin for carbon monoxide is about 230 times its affinity for oxygen. High blood carbon monoxide levels reduce the ability to perform aerobic activities and impair attention.

A compound made up of molecules containing one carbon atom and one oxygen atom.

A colorless, odorless, tasteless gas, CO, formed by burning carbon or organic fuels with a scanty supply of oxygen; inhalation causes central nervous system damage and asphyxiation. Carbon monoxide is present in the exhaust of petrol engines, in the smoke of wood and coal fires, in manufactured gas such as that used in the household, and wherever carbon burns without a sufficient supply of oxygen. Used as a euthanizing agent for dogs and laboratory animals.

• c. m. poisoning — poisoning by carbon monoxide; one of the most common types of gas poisoning. When carbon monoxide is inhaled, it comes in contact with the blood and combines with hemoglobin. Since carbon monoxide combines more readily with hemoglobin than does oxygen, it takes the place of oxygen in the erythrocytes, and the tissues are thus deprived of their normal oxygen supply. Death from asphyxia results if a large enough quantity of carbon monoxide is inhaled. Because death is very sudden, carbon monoxide has been used as a euthanatizing agent for dogs in large numbers. It is not widely used because of the danger to human attendants and the difficulty in maintaining a CO generator in good condition for long periods.

This article needs additional citations for verification. Please help improve this article by adding reliable references. Unsourced material may be challenged and removed. (November 2009)

Carbon monoxide
IUPAC name	Carbon monooxide Carbon monoxide Carbon(II) oxide
Other names	Carbonic oxide
Identifiers
CAS number	630-08-0 Y
PubChem	281
EC number	211-128-3
UN number	1016
ChEBI	17245
RTECS number	FG3500000
SMILES	[O+]#[C-]
InChI	1/CO/c1-2
InChI key	UGFAIRIUMAVXCW-UHFFFAOYAT
ChemSpider ID	275
Properties
Molecular formula	CO
Molar mass	28.010 g mol−1
Appearance	Colourless, odorless gas
Density	0.789 g mL−1, liquid 1.250 g L−1 at 0 °C, 1 atm 1.145 g L−1 at 25 °C, 1 atm
Melting point	−205 °C, 68 K, -337 °F
Boiling point	−191.5 °C, 82 K, -313 °F
Solubility in water	0.0026 g/100 mL (20 °C)
Solubility	Soluble in chloroform, acetic acid, ethyl acetate, ethanol, and ammonium hydroxide
Dipole moment	0.112 D
Hazards
MSDS	External MSDS
EU Index	006-001-00-2
EU classification	Highly flammable (F+) Repr. Cat. 1 Very toxic (T+)
R-phrases	R61R12R26R48/23
S-phrases	S53S45
NFPA 704	4 4 0
Flash point	−191 °C
Autoignition temperature	609 °C
Related compounds
Related Carbon oxides	Carbon dioxide Carbon suboxide Oxocarbons
Supplementary data page
Structure and properties	n, εr, etc.
Thermodynamic data	Phase behaviour Solid, liquid, gas
Spectral data	UV, IR, NMR, MS
Y (what is this?)  (verify) Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa)
Infobox references

Carbon monoxide (CO) is a colorless, odorless and tasteless gas, yet very toxic to humans and animals. It consists of one carbon atom and one oxygen atom, connected by a covalent double bond and a dative covalent bond. It is the simplest oxocarbon, and is an anhydride of formic acid.^{[citation needed]}

Carbon monoxide is produced from the partial oxidation of carbon-containing compounds; it forms when there is not enough oxygen to produce carbon dioxide (CO₂), such as when operating a stove or an internal combustion engine in an enclosed space. Carbon monoxide burns with a blue flame, producing carbon dioxide.^[1] Despite its toxicity, coal gas, which was widely used before the 1960s for domestic lighting, cooking and heating, produced carbon monoxide as a byproduct. Some processes in modern technology, such as iron smelting, still produce carbon monoxide as a byproduct.^{[citation needed]}

Contents 1 History 2 Molecular properties 3 Biological and physiological properties 3.1 Toxicity 3.2 Human physiology 3.3 Microbiology 4 Occurrence 4.1 Atmospheric presence 4.2 Urban pollution 4.3 Indoor pollution 5 Production 5.1 Laboratory preparation 5.2 Industrial production 6 Coordination chemistry 7 Organic and main group chemistry 8 Uses 8.1 Chemical industry 8.2 Meat coloring 8.3 Medicine 9 See also 10 References 11 External links

History

This section requires expansion.

Carbon monoxide was used for executions by the Greek and Romans in Classical Antiquity.^[2]

Molecular properties

The bond length between the carbon atom and the oxygen atom is 112.8 pm.^[3] The effects of atomic formal charge and electronegativity result in a small bond dipole moment with its negative end on the carbon atom.^[4] The reason for this, despite oxygen's greater electronegativity, is that the highest occupied molecular orbital has an energy much closer to that of carbon's p orbitals, meaning that greater electron density is found near the carbon atom. In addition, carbon's lower electronegativity creates a much more diffuse electron cloud, enhancing the polarizability. This is also the reason why almost all chemistry involving carbon monoxide occurs through the carbon atom, and not the oxygen.^{[citation needed]}

The bond length of CO is consistent with a partial triple bond, and the molecule can be represented by three resonance structures:

In this model, the leftmost structure contributes the most. Carbon monoxide resembles molecular nitrogen, and it has nearly the same molecular mass. Their physical properties (boiling point, melting point, etc.) are very similar.^{[citation needed]}

Biological and physiological properties

Toxicity

Main article: Carbon monoxide poisoning

Carbon monoxide poisoning is the most common type of fatal air poisoning in many countries.^[5] Carbon monoxide is colorless, odorless and tasteless, but extremely toxic. It combines with hemoglobin to produce carboxyhemoglobin, which is ineffective for delivering oxygen to bodily tissues. This condition is known as anoxemia). Concentrations as low as 667 ppm may cause up to 50% of the body's hemoglobin to convert to carboxyhemoglobin.^{[citation needed]} In the United States, the OSHA limits long-term workplace exposure levels above 50 ppm.^[6]

The most common symptoms of carbon monoxide poisoning may resemble other types of poisonings and infections (such as the flu), including headache, nausea, vomiting, dizziness, lethargy and a feeling of weakness. Infants may be irritable and feed poorly. Neurological signs include confusion, disorientation, visual disturbance, syncope and seizures.^[2]

Some descriptions of carbon monoxide poisoning include retinal hemorrhages, and an abnormal cherry-red blood hue.^[7]. In most clinical diagnoses these signs are seldom seen.^[2]

Carbon monoxide binds to other molecules such as myoglobin and mitochondrial cytochrome oxidase. Exposures to carbon monoxide may cause significant damage to the heart and central nervous system, especially to the globus pallidus,^[8] often with long-term sequelae. Carbon monoxide may have severe adverse effects on the fetus of a pregnant woman.^{[citation needed]}

Human physiology

Carbon monoxide is produced naturally by the human body. This carbon monoxide may have positive physiological roles in the body, such as a neurotransmitter or a blood vessel relaxant.^[9] Because of carbon monoxide's role in the body, abnormalities in its metabolism have been linked to a variety of diseases, including neurodegenerations, hypertension, heart failure, and inflammation.^[9]

Microbiology

Carbon monoxide is a nutrient for methanogenic bacteria,^[10] a building block for acetylcoenzyme A. This the theme for the emerging field of bioorganometallic chemistry. In bacteria, carbon monoxide is produced via the reduction of carbon dioxide by the enzyme carbon monoxide dehydrogenase, an Fe-Ni-S-containing protein.^[11]

CooA is a carbon monoxide sensor protein.^[12] The scope of its biological role is still unknown; it may be part of a signaling pathway in bacteria and archaea. Its occurrence in mammals is not established.

Occurrence

Carbon monoxide occurs in various natural and artificial environments. Typical concentrations in parts per million are as follows:

Concentration	Source
0.1 ppm	Natural atmosphere level (MOPITT)[13]
0.5 to 5 ppm	Average level in homes[14]
5 to 15 ppm	Near properly adjusted gas stoves in homes[15]
100 to 200 ppm	Exhaust from automobiles in the Mexico City central area[16]
5,000 ppm	Exhaust from a home wood fire[17]
7,000 ppm	Undiluted warm car exhaust without a catalytic converter[15]

Atmospheric presence

MOPITT 2000 global carbon monoxide

Carbon monoxide is present in small amounts in the atmosphere, chiefly as a product of volcanic activity but also from natural and man-made fires (such as forest and bushfires, burning of crop residues, and sugarcane fire-cleaning).^{[citation needed]} The burning of fossil fuels also contributes to carbon monoxide production. Carbon monoxide occurs dissolved in molten volcanic rock at high pressures in the Earth's mantle.^{[citation needed]} Because natural sources of carbon monoxide are so variable from year to year, it is extremely difficult to accurately measure natural emissions of the gas.

Carbon monoxide has an indirect radiative forcing effect by elevating concentrations of methane and tropospheric ozone through chemical reactions with other atmospheric constituents (e.g., the hydroxyl radical, OH^.) that would otherwise destroy them.^{[citation needed]} Through natural processes in the atmosphere, it is eventually oxidized to carbon dioxide. Carbon monoxide concentrations are both short-lived in the atmosphere and spatially variable.^{[citation needed]}

Urban pollution

Carbon monoxide is a major atmospheric pollutant in some urban areas, chiefly from the exhaust of internal combustion engines (including vehicles, portable and back-up generators, lawn mowers, power washers, etc.), but also from improper burning of various other fuels (including wood, coal, charcoal, oil, paraffin, propane, natural gas, and trash). Along with aldehydes, it reacts photochemically to produce peroxy radicals. Peroxy radicals react with nitrogen oxide to increase the ratio of NO₂ to NO, which reduces the quantity of NO that is available to react with ozone.^{[citation needed]}

Indoor pollution

In closed environments the concentration of carbon monoxide can easily rise to lethal levels. On average, 170 people in the United States die every year from carbon monoxide produced by non-automotive consumer products.^{[citation needed]} These products include malfunctioning fuel-burning appliances such as furnaces, ranges, water heaters and room heaters; engine-powered equipment such as portable generators; fireplaces; and charcoal that is burned in homes and other enclosed areas. The American Association of Poison Control Centers (AAPCC) reported 15,769 cases of carbon monoxide poisoning resulting in 39 deaths in 2007.^[18] In 2005, the CPSC reported 94 generator-related carbon monoxide poisoning deaths.^{[citation needed]} Forty-seven of these deaths were known to have occurred during power outages due to severe weather, including Hurricane Katrina.^{[citation needed]} Still others die from carbon monoxide produced by non-consumer products, such as cars left running in attached garages. The Centers for Disease Control and Prevention estimates that several thousand people go to hospital emergency rooms every year to be treated for carbon monoxide poisoning.^{[citation needed]}

Carbon monoxide is also a constituent of tobacco smoke.^{[citation needed]}

Production

Many methods have been developed for carbon monoxide's production.^[19]

Laboratory preparation

Carbon monoxide is conveniently produced in the laboratory by the dehydration of formic acid, for example with sulfuric acid. Another method is heating an intimate mixture of powdered zinc metal and calcium carbonate, which releases CO and leaves behind zinc oxide and calcium oxide:

Zn + CaCO₃ → ZnO + CaO + CO

Industrial production

A major industrial source of CO is producer gas, a mixture containing mostly carbon monoxide and nitrogen, formed by combustion of carbon in air at high temperature when there is an excess of carbon. In an oven, air is passed through a bed of coke. The initially produced CO₂ equilibrates with the remaining hot carbon to give CO. The reaction of O₂ with carbon to give CO is described as the Boudouard equilibrium. Above 800 °C, CO is the predominant product:

O₂ + 2 C → 2 CO (ΔH = −221 kJ/mol)

Another source is "water gas", a mixture of hydrogen and carbon monoxide produced via the endothermic reaction of steam and carbon:

H₂O + C → H₂ + CO (ΔH = +131 kJ/mol)

Other similar "synthesis gases" can be obtained from natural gas and other fuels.

Carbon monoxide is also is a byproduct of the reduction of metal oxide ores with carbon, shown in a simplified form as follows:

MO + C → M + CO

Since CO is a gas, the reduction process can be driven by heating, exploiting the positive (favorable) entropy of reaction. The Ellingham diagram shows that CO formation is favored over CO₂ in high temperatures.

Coordination chemistry

Main article: metal carbonyl

The HOMO of CO is a σ MO

The LUMO of CO is a π* antibonding MO

Most metals form coordination complexes containing covalently attached carbon monoxide. Only those in lower oxidation states will complex with carbon monoxide ligands. This is because there must be sufficient electron density to facilitate back donation from the metal d_xz-orbital, to the π* molecular orbital from CO. The lone pair on the carbon atom in CO, also donates electron density to the d_x²−y² on the metal to form a sigma bond. In nickel carbonyl, Ni(CO)₄ forms by the direct combination of carbon monoxide and nickel metal at room temperature. For this reason, nickel in any tubing or part must not come into prolonged contact with carbon monoxide (corrosion). Nickel carbonyl decomposes readily back to Ni and CO upon contact with hot surfaces, and this method was once used for the industrial purification of nickel in the Mond process.^[20]

In nickel carbonyl and other carbonyls, the electron pair on the carbon interacts with the metal; the carbon monoxide donates the electron pair to the metal. In these situations, carbon monoxide is called the carbonyl ligand. One of the most important metal carbonyls is iron pentacarbonyl, Fe(CO)₅:

Many metal-CO complexes are prepared by decarbonylation of organic solvents, not from CO. For instance, iridium trichloride and triphenylphosphine react in boiling 2-methoxyethanol or DMF) to afford IrCl(CO)(PPh₃)₂.

Organic and main group chemistry

In the presence of strong acids and water, carbon monoxide reacts with olefins to form carboxylic acids in a process known as the Koch-Haaf reaction.^[21] In the Gattermann-Koch reaction, arenes are converted to benzaldehyde derivatives in the presence of AlCl₃ and HCl.^[22] Organolithium compounds (e.g. butyl lithium) react with carbon monoxide, but these reactions have little scientific use.

Although CO reacts with carbocations and carbanions, it is relatively nonreactive toward organic compounds without the intervention of metal catalysts.^[23]

With main group reagents, CO undergoes several noteworthy reactions. Chlorination of CO is the industrial route to the important compound phosgene. With borane CO forms an adduct, H₃BCO, which is isoelectronic with the acylium cation [H₃CCO]⁺. CO reacts with sodium to give products resulting from C-C coupling such as Na₂C₂O₂ (sodium acetylenediolate), and potassium to give K₂C₂O₂ (potassium acetylenediolate) and K₂C₆O₆ (potassium rhodizonate).

The compounds cyclohexanehexone or triquinoyl (C₆O₆) and cyclopentanepentone or leuconic acid (C₅O₅), which so far have been obtained only in trace amounts, can be regarded as polymers of carbon monoxide.^{[citation needed]}

At pressures of over 5 gigapascals, carbon monoxide disproportionates into carbon dioxide (CO₂) and is a solid polymer of carbon and oxygen, in 3:2 atomic ratio.^[24][25]

Uses

Chemical industry

Carbon monoxide is an industrial gas that has many applications in bulk chemicals manufacturing.^[26]

Large quantities of aldehydes are produced by the hydroformylation reaction of alkenes, carbon monoxide, and H₂. Hydroformylation is coupled to the Shell Higher Olefin Process to give precursors to detergents. Methanol is produced by the hydrogenation of carbon monoxide. In a related reaction, the hydrogenation of carbon monoxide is coupled to C-C bond formation, as in the Fischer-Tropsch process where carbon monoxide is hydrogenated to liquid hydrocarbon fuels. This technology allows coal or biomass to be converted to diesel.

In the Monsanto process, carbon monoxide and methanol react in the presence of a homogeneous rhodium catalyst and hydroiodic acid to give acetic acid. This process is responsible for most of the industrial production of acetic acid.

An industrial scale use for pure carbon monoxide is purifying nickel in the Mond process.

Meat coloring

Carbon monoxide is used in modified atmosphere packaging systems in the US, mainly with fresh meat products such as beef, pork, and fish to keep them looking fresh. The carbon monoxide combines with myoglobin to form carboxymyoglobin, a bright cherry red pigment. Carboxymyoglobin is more stable than the oxygenated form of myoglobin, oxymyoglobin, which can become oxidized to the brown pigment, metmyoglobin. This stable red color can persist much longer than in normally packaged meat.^[27] Typical levels of carbon monoxide used in the facilities that use this process are between 0.4% to 0.5%.

The technology was first given "generally recognized as safe" (GRAS) status by the U.S. Food and Drug Administration (FDA) in 2002 for use as a secondary packaging system, and does not require labeling. In 2004 the FDA approved CO as primary packaging method, declaring that CO does not mask spoilage odor.^[28] Despite this ruling, the process remains controversial for fears that it masks spoilage.^[29] In 2007 a bill^[30] was introduced to the United States House of Representatives to label modified atmosphere carbon monoxide packaging as a color additive, but the bill died in subcommittee. The process is banned in many other countries, including Canada, Japan, Singapore and the European Union.^[31][32][33]

Medicine

Carbon monoxide is also currently being studied in several research laboratories throughout the world for its anti-inflammatory and cytoprotective properties that can be used therapeutically to prevent the development of a series of pathologic conditions such as ischemia reperfusion injury, transplant rejection, atherosclerosis, sepsis, severe malaria or autoimmunity. Clinical tests on humans have been performed, however, results have not yet been released.^[34].

See also

• Carbon monoxide (data page)
• Carbon monoxide poisoning
• Boudouard reaction
• Criteria air contaminants
• Undersea and Hyperbaric Medical Society Hyperbaric Treatment for CO Poisoning
• Carbon monoxide detector
• Rubicon Foundation research articles on CO Poisoning
• Molecular cloud

References

1. ^ Carbon Monoxide - Molecule of the Month, Dr Mike Thompson, Winchester College, UK
2. ^ ^{a b c} Blumenthal, Ivan (01 June 2001). "Carbon monoxide poisoning". J R Soc Med (The Royal Society of Medicine) 94 (6): 270–272. PMID 11387414. PMC 1281520. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=11387414. Retrieved May 2009. 
3. ^ O. R. Gilliam, C. M. Johnson and W. Gordy (1950). "Microwave Spectroscopy in the Region from Two to Three Millimeters". Physical Review 78 (2): 140. doi:10.1103/PhysRev.78.140. 
4. ^ W. Kutzelnigg (2002). Einführung in die Theoretische Chemie. Wiley-VCH. ISBN 3-527-30609-9. 
5. ^ Omaye ST. (2002). "Metabolic modulation of carbon monoxide toxicity". Toxicology 180 (2): 139–150. doi:10.1016/S0300-483X(02)00387-6. 
6. ^ "OSHA CO guidlines". OSHA. http://www.osha.gov/SLTC/healthguidelines/carbonmonoxide/recognition.html. Retrieved May 2009. 
7. ^ Ganong, William F (2005). "37". Review of medical physiology (22 ed.). McGraw-Hill. p. 684. ISBN 0071440402. http://books.google.com/books?id=OLa8vDBXDD4C&dq=Ganong+WF.+Review+of+Medical+Physiology.+Norwalk+Ct:+Appleton+%26+Lange,+1995&printsec=frontcover&source=bn&hl=en&ei=QU8dSvnhG5OeMoHU0J8P&sa=X&oi=book_result&ct=result&resnum=4#PPA684,M1. Retrieved May 2009. 
8. ^ Prockop LD, Chichkova RI (2007). "Carbon monoxide intoxication: an updated review". J Neurol Sci 262 (1-2): 122–130. doi:10.1016/j.jns.2007.06.037. PMID 17720201. 
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External links

• International Chemical Safety Card 0023
• National Pollutant Inventory - Carbon Monoxide
• NIOSH Pocket Guide to Chemical Hazards
• CID 281 from PubChem
• External MSDS data sheet
• Carbon Monoxide Detector Placement
• Carbon Monoxide Kills Awareness Campaign Site
• Carbon Monoxide Purification Process
• Carbon Monoxide Hazards with Backpacking Stoves
• USFDA IMPORT BULLETIN 16B-95, May 1999
• FDA Agency Response Letter GRAS Notice No. GRN 000083
• Microscale Gas Chemistry Experiments with Carbon Monoxide
• Instant insight outlining the physiology of carbon monoxide from the Royal Society of Chemistry
• Pictures of CO Poisoning Radiology and Pathology Images from MedPix.

v • d • e Oxocarbons Common oxides CO2 · CO Exotic oxides C2O2 · C3O2 · C5O2 · C2O · CO3 Compounds derived from oxides Metal carbonyls · Carbonic acid · Bicarbonates · Carbonates

v • d • e Neurotransmitters Amino Acids 1,4-Butanediol • Alanine • Aspartate • Cycloserine • DMG • GABA • GHB • Glutamate • Glycine • Hypotaurine • Kynurenic Acid (Transtorine) • NAAG (Spaglumic Acid) • NMG (Sarcosine) • Serine • Taurine • TMG (Betaine) Endocannabinoids 2-AG • 2-AGE (Noladin Ether) • AEA (Anandamide) • NADA • OAE (Virodhamine) • Oleamide Gasotransmitters Carbon Monoxide • Hydrogen Sulfide • Nitric Oxide • Nitrous Oxide Monoamines Dopamine • Epinephrine (Adrenaline) • Melatonin • Norepinephrine (Noradrenaline) • Serotonin (5-HT) Neuropeptides See here for more details. Purines Adenosine • ADP • AMP • ATP Trace Amines 3-ITA • 5-MeO-DMT • Bufotenin • DMT • NMT • Octopamine • Phenethylamine • Synephrine • Thyronamine • Tryptamine • Tyramine Others Acetylcholine • Histamine

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