Acetonitrile is used mainly as a solvent in the purification of butadiene in refineries. Specifically, acetonitrile is fed into the top of a distillation column filled with hydrocarbons including butadiene, and as the acetonitrile falls down through the column, it absorbs the butadiene which is then sent from the bottom of the tower to a second separating tower. Heat is then employed in the separating tower to separate the butadiene.
In the laboratory, it is used as a medium-polarity non-protic solvent that is miscible with water and a range of organic solvents, but not saturated hydrocarbons. It has a convenient range of temperatures at which it is a liquid, and a high dielectric constant of 38.8. With a dipole moment of 3.92 D,[8] acetonitrile dissolves a wide range of ionic and nonpolar compounds and is useful as a mobile phase in HPLC and LC–MS.
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.
Acetonitrile is a byproduct from the manufacture of acrylonitrile. Most is combusted to support the intended process but an estimated several thousand tons are retained for the above-mentioned applications.[15] 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.[16] In 1992[update], 14,700 tonnes (16,200 short tons) of acetonitrile were produced in the US.
Acetonitrile shortage in 2008–2009
Starting in October 2008, the worldwide supply of acetonitrile was low because Chinese production was shut down for the Olympics. Furthermore, a U.S. factory was damaged in Texas during Hurricane Ike.[17] Due to the global economic slowdown, the production of acrylonitrile used in acrylic fibers and acrylonitrile butadiene styrene (ABS) resins decreased. Acetonitrile is a byproduct in the production of acrylonitrile and its production also decreased, further compounding the acetonitrile shortage.[18] The global shortage of acetonitrile continued through early 2009.[needs update]
Safety
Toxicity
Acetonitrile has only modest toxicity in small doses.[11][19] It can be metabolised to produce hydrogen cyanide, which is the source of the observed toxic effects.[9][20][21] 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).[11]
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.[20] 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 emergency treatments.[20]
It has been used in formulations for nail polish remover, despite its toxicity. At least two cases have been reported of accidental poisoning of young children by acetonitrile-based nail polish remover, one of which was fatal.[22]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.[23]
Ionic cyanide concentrations measured in the brains of Sprague-Dawley rats one hour after oral administration of an LD50 of various nitriles.[24]
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.[25] The first step in this pathway is the oxidation of acetonitrile to glycolonitrile by an NADPH-dependent cytochrome P450monooxygenase. The glycolonitrile then undergoes a spontaneous decomposition to give hydrogen cyanide and formaldehyde.[19][20] Formaldehyde, a toxin and a carcinogen on its own, 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 1⁄20 that for a propionitrile dose 60 times lower (see table).[24]
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.[19][20][21]
^ ab"Archived copy"(PDF). Ashford's Dictionary of Industrial Chemicals, Third edition. p. 76. Archived from the original(PDF) on 2011-05-16. Retrieved 2011-03-31.{{cite web}}: CS1 maint: archived copy as title (link)
^ abcPhilip Wexler, ed. (2005), Encyclopedia of Toxicology, vol. 1 (2nd ed.), Elsevier, pp. 28–30, ISBN0-12-745354-7
^Jürgen-Hinrich., Fuhrhop (2003). Organic synthesis : concepts and methods. Li, Guangtao, Dr. (3rd, completely rev. and enl. ed.). Weinheim: Wiley-VCH. p. 26. ISBN9783527302727. OCLC51068223.
^B. Swanson, D. F. Shriver, J. A. Ibers, "Nature of the donor-acceptor bond in acetonitrile-boron trihalides. The structures of the boron trifluoride and boron trichloride complexes of acetonitrile", Inorg. Chem., 2969., volume 8, pp. 2182-2189, {{doi:10.1021/ic50080a032}}
^Haiges, Ralf; Baxter, Amanda F.; Goetz, Nadine R.; Axhausen, Joachim A.; Soltner, Theresa; Kornath, Andreas; Christe, Kalr O. (2016). "Protonation of nitriles: isolation and characterization of alkyl- and arylnitrilium ions". Dalton Transactions. 45 (20): 8494–8499. doi:10.1039/C6DT01301E. PMID27116374.
^Pozzani, U. C.; Carpenter, C. P.; Palm, P. E.; Weil, C. S.; Nair, J. H. (1959), "An investigation of the mammalian toxicity of acetonitrile", J. Occup. Med., 1 (12): 634–642, doi:10.1097/00043764-195912000-00003, PMID14434606
