Acetonitrile is the chemical compound with the formula CH3CN. This colourless liquid is the simplest organic nitrile (hydrogen cyanide is a simpler nitrile, but the cyanide anion is not classed as organic). It is produced mainly as a byproduct of acrylonitrile manufacture. It is used as a polar aprotic solvent in organic synthesis and in the purification of butadiene.
In the laboratory, it is used as a medium-polarity solvent that is miscible with water and has a convenient liquid range. With a dipole moment of 3.92 D[citation needed], acetonitrile dissolves a wide range of ionic and nonpolar compounds (e.g. Wohl-Ziegler reaction) and is useful as a mobile phase in HPLC and LCMS.
Acetonitrile was first prepared in 1847 by the French chemist Jean-Baptiste Dumas.
Applications
Acetonitrile is used mainly as a solvent in the purification of butadiene in refineries.
It is widely used in battery applications because of its relatively high dielectric constant and ability to dissolve electrolytes. For similar reasons it is a popular solvent in cyclic voltammetry.
Its low viscosity and low chemical reactivity make it a popular choice for liquid chromatography.
Acetonitrile plays a significant role as the dominant solvent used in the manufacture of DNA oligonucleotides from monomers.
Industrially, it is used as a solvent for the manufacture of pharmaceuticals and photographic film.
Organic synthesis
Acetonitrile is a common two-carbon building block in organic synthesisof many useful chemicals, including acetophene, thiamine, acetamidine, and α-napthaleneacetic acid. Its reaction with cyanogen chloride affords malononitrile.
Ligand in coordination chemistry
In inorganic chemistry, acetonitrile is employed as a solvent and often an easily displaceable ligand. For example, PdCl2(CH3CN)2 is prepared by heating a suspension of (polymeric) palladium chloride in acetonitrile:
PdCl2 + 2 CH3CN → PdCl2(CH3CN)2
The CH3CN groups undergo rapid displacement by many other ligands.
Production
Acetonitrile is a by-product from the manufacture of acrylonitrile. Production trends for acetonitrile thus generally follow those of acrylonitrile. Acetonitrile can also be produced by many other methods, but these are of no commercial importance as of 2002. Illustrative routes are by dehydration of acetamide or by hydrogenation of mixtures of carbon monoxide and ammonia.The main distributors of acetonitrile in the world are: INEOS, Purification Technologies Inc, BioSolve BV, Carlo Erba Reagents, Panreac, J.T. Baker Chemical, VWR, Sigma Aldrich, and Petrolchem Trading Ltd. In 1992[update], 32.3 million pounds (14,700 t) of acetonitrile were produced in the US.
Toxicity
Acetonitrile has only a modest toxicity in small doses. It can be metabolised to produce hydrogen cyanide, which is the source of the observed toxic effects. Generally the onset of toxic effects is delayed, due to the time required for the body to metabolize acetonitrile to cyanide (generally about 2–12 hours).
Cases of acetonitrile poisoning in humans (or, to be more specific, of cyanide poisoning after exposure to acetonitrile) are rare but not unknown, by inhalation, ingestion and (possibly) by skin absorption. The symptoms, which do not usually appear for several hours after the exposure, include breathing difficulties, slow pulse rate, nausea, and vomiting: Convulsions and coma can occur in serious cases, followed by death from respiratory failure. The treatment is as for cyanide poisoning, with oxygen, sodium nitrite, and sodium thiosulfate among the most commonly used remedies.
It has been used in formulations for nail polish remover, despite its low but significant toxicity. Acetone and ethyl acetate are often preferred as safer for domestic use, and acetonitrile has been banned in cosmetic products in the European Economic Area since March 2000.
In common with other nitriles, acetonitrile can be metabolised in microsomes, especially in the liver, to produce hydrogen cyanide, as was first shown by Pozzani et al. in 1959. The first step in this pathway is the oxidation of acetonitrile to glycolonitrile by an NADPH-dependent cytochrome P450 monooxygenase. The glycolonitrile then undergoes a spontaneous decomposition to give hydrogen cyanide and formaldehyde. Formaldehyde is further oxidized to formic acid which is another source of toxicity.
The metabolism of acetonitrile is much slower than that of other nitriles, which accounts for its relatively low toxicity. Hence, one hour after administration of a potentially lethal dose, the concentration of cyanide in the rat brain was one-twentieth that for a propionitrile dose 60 times lower (see table).
The relatively slow metabolism of acetonitrile to hydrogen cyanide allows more of the cyanide produced to be detoxified within the body to thiocyanate (the rhodanese pathway). It also allows more of the acetonitrile to be excreted unchanged before it is metabolised. The main pathways of excretion are by exhalation and in the urine.
Skype1
