Editing Cyanide (section)

==Toxicity==
{{Main|Cyanide poisoning}}
Among the most toxic cyanides are [[hydrogen cyanide]] (HCN), [[sodium cyanide]] (NaCN), [[potassium cyanide]] (KCN), and [[calcium cyanide]] ({{chem2|Ca(CN)2}}). The cyanide anion is an [[enzyme inhibitor|inhibitor]] of the [[enzyme]] [[cytochrome c oxidase]] (also known as aa<sub>3</sub>), the fourth complex of the [[electron transport chain]] found in the [[Inner mitochondrial membrane|inner membrane]] of the [[mitochondria]] of [[Eukaryote|eukaryotic]] cells. It attaches to the iron within this protein. The binding of cyanide to this enzyme prevents transport of electrons from [[cytochrome c]] to oxygen. As a result, the electron transport chain is disrupted, meaning that the cell can no longer aerobically produce [[adenosine triphosphate|ATP]] for energy.<ref>{{cite book|last1=Nelson|first1=David L.|last2=Cox|first2=Michael M.|title=Lehniger Principles of Biochemistry|publisher=[[Worth Publishers]]|year=2000|location=New York|edition=3rd|isbn=978-1-57259-153-0|pages=[https://archive.org/details/lehningerprincip01lehn/page/668 668,670–71,676]|url=https://archive.org/details/lehningerprincip01lehn/page/668}}</ref> Tissues that depend highly on [[aerobic respiration]], such as the [[central nervous system]] and the [[heart]], are particularly affected. This is an example of [[histotoxic hypoxia]].<ref name=Biller>{{cite book
|title=Interface of neurology and internal medicine
|edition=illustrated
|first1=José
|last1=Biller
|publisher=Lippincott Williams & Wilkins
|year=2007
|isbn=978-0-7817-7906-7
|chapter=163
|page=939
|chapter-url=https://books.google.com/books?id=SRIvmTVcYBwC&pg=PA939}}
</ref>

Hydrogen cyanide, which is a gas, kills by inhalation. For this reason, working with hydrogen cyanide requires wearing an air respirator supplied by an external oxygen source.<ref name="CDC">{{Cite web|url=https://emergency.cdc.gov/agent/cyanide/basics/facts.asp|title=Facts about cyanide:Where cyanide is found and how it is used|last=Anon|date=June 27, 2013|work=CDC Emergency preparedness and response|publisher=Centers for Disease Control and Prevention|access-date=10 December 2016}}</ref> Hydrogen cyanide can be produced by adding acid to a solution containing a cyanide salt. Alkaline solutions of cyanide are safer to use because they do not evolve hydrogen cyanide gas. Oral ingestion of a small quantity of solid cyanide or a cyanide solution of as little as 200&nbsp;mg, or exposure to airborne cyanide of 270 [[parts per million|ppm]], is sufficient to cause death within minutes.<ref name=Biller/>

Organic [[nitrile]]s do not readily release cyanide ions, and so have low toxicities. 

===Disposal===
Due to toxicity considerations, the disposal of cyanide is subject to stringent regulations. Industrial cyanide effluent is typically destroyed by oxidation using [[Peroxysulfuric acid (disambiguation)|peroxysulfuric acid]], [[hydrogen peroxide]], [[sulfur dioxide]]/copper salts ("Inco process") or all three ("Combiox Process").  Use of [[sodium hypochlorite]], traditional for laboratory-scale wastes, is impractical on a commercial scale.  Hydrolysis at higher temperatures is highly effective, but requires specialized equipment.  Lastly, cyanide wastes can be acidified for recovery of [[hydrogen cyanide]].<ref name=Ullmann>{{cite book|doi=10.1002/14356007.a08_159.pub3 |chapter=Cyano Compounds, Inorganic |title=Ullmann's Encyclopedia of Industrial Chemistry |date=2011 |last1=Gail |first1=Ernst |last2=Gos |first2=Stephen |last3=Kulzer |first3=Rupprecht |last4=Lorösch |first4=Jürgen |last5=Rubo |first5=Andreas |last6=Sauer |first6=Manfred |last7=Kellens |first7=Raf |last8=Reddy |first8=Jay |last9=Steier |first9=Norbert |last10=Hasenpusch |first10=Wolfgang |isbn=978-3-527-30385-4 }}</ref>

===Antidote===
[[Hydroxocobalamin]] reacts with cyanide to form [[cyanocobalamin]], which can be safely eliminated by the kidneys. This method has the advantage of avoiding the formation of methemoglobin (see below). This antidote kit is sold under the brand name Cyanokit and was approved by the U.S. FDA in 2006.<ref>{{EMedicine|article|814287|Cyanide Toxicity|treatment}}</ref>

An older cyanide antidote kit included administration of three substances: [[amyl nitrite]] pearls (administered by inhalation), [[sodium nitrite]], and [[sodium thiosulfate]]. The goal of the antidote was to generate a large pool of [[ferric]] iron ({{chem2|Fe(3+)}}) to compete for cyanide with cytochrome a<sub>3</sub> (so that cyanide will bind to the antidote rather than the enzyme). The [[nitrite]]s [[oxidize]] [[hemoglobin]] to [[methemoglobin]], which competes with cytochrome oxidase for the cyanide ion. Cyanmethemoglobin is formed and the [[cytochrome oxidase]] enzyme is restored. The major mechanism to remove the cyanide from the body is by enzymatic conversion to [[thiocyanate]] by the [[mitochondrial]] enzyme [[rhodanese]]. Thiocyanate is a relatively non-toxic molecule and is excreted by the kidneys. To accelerate this detoxification, sodium thiosulfate is administered to provide a sulfur donor for [[rhodanese]], needed in order to produce thiocyanate.<ref>{{cite journal | last1 = Chaudhary | first1 = M. | last2 = Gupta | first2 = R. | year = 2012 | title = Cyanide Detoxifying Enzyme: Rhodanese | journal = Current Biotechnology | volume = 1 | issue = 4 | pages = 327–335 | doi = 10.2174/2211550111201040327}}</ref>

===Sensitivity===
Minimum risk levels (MRLs) may not protect for delayed health effects or health effects acquired following repeated sublethal exposure, such as hypersensitivity, [[asthma]], or [[bronchitis]]. MRLs may be revised after sufficient data accumulates.<ref>{{cite report|title=Toxicological Profile for Cyanide |publisher=U.S. Department of Health and Human Services |date=2006 |url=https://www.atsdr.cdc.gov/toxprofiles/tp8.pdf |archive-url=https://web.archive.org/web/20040331014808/http://www.atsdr.cdc.gov/toxprofiles/tp8.pdf |archive-date=2004-03-31 |url-status=live |pages=18–19}}</ref>