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Hydrogen cyanide

From Wikipedia, the free encyclopedia

Hydrogen cyanide
Hydrogen-cyanide-2D.svg
Names
IUPAC name
  • Formonitrile[1] (substitutive)
  • Hydridonitridocarbon[2] (additive)
Other names
  • Formic anammonide
  • Hydrocyanic acid
  • Prussic acid
  • Methanenitrile
Identifiers
3D model (JSmol)
3DMet
ChEBI
ChemSpider
ECHA InfoCard 100.000.747
EC Number
  • 200-821-6
KEGG
MeSH Hydrogen+Cyanide
RTECS number
  • MW6825000
UNII
UN number 1051
Properties
HCN
Molar mass 27.0253 g/mol
Appearance Colorless liquid or gas[3]
Odor Oil of bitter almond
Density 0.6876 g cm−3[3]
Melting point −13.29 °C (8.08 °F; 259.86 K)[3]
Boiling point 26 °C (79 °F; 299 K)[3]
Miscible
Solubility in ethanol Miscible
Vapor pressure 100 kPa (25 °C)[4]
75 μmol Pa−1 kg−1
Acidity (pKa) 9.21[5]
Basicity (pKb) 4.79 (cyanide anion)
Conjugate acid Hydrocyanonium
Conjugate base Cyanide
1.2675 [6]
Viscosity 0.183 mPa·s (25 °C)[7]
Structure
C∞v
Linear
2.98 D
Thermochemistry
35.9 J K−1 mol−1 (gas)[8]
201.8 J K−1 mol−1
135.1 kJ mol−1
Hazards
GHS pictograms
GHS02: Flammable
GHS06: Toxic
GHS08: Health hazard
GHS09: Environmental hazard
GHS Signal word Danger
H225, H300, H310, H319, H330, H336, H370, H400, H410
P210, P261, P305+351+338
NFPA 704 (fire diamond)
Flammability code 4: Will rapidly or completely vaporize at normal atmospheric pressure and temperature, or is readily dispersed in air and will burn readily. Flash point below 23 °C (73 °F). E.g. propaneHealth code 4: Very short exposure could cause death or major residual injury. E.g. VX gasReactivity code 2: Undergoes violent chemical change at elevated temperatures and pressures, reacts violently with water, or may form explosive mixtures with water. E.g. white phosphorusSpecial hazards (white): no codeNFPA 704 four-colored diamond
4
4
2
Flash point −17.8 °C (0.0 °F; 255.3 K)
538 °C (1,000 °F; 811 K)
Explosive limits 5.6% – 40.0%[9]
Lethal dose or concentration (LD, LC):
501 ppm (rat, 5 min)
323 ppm (mouse, 5 min)
275 ppm (rat, 15 min)
170 ppm (rat, 30 min)
160 ppm (rat, 30 min)
323 ppm (rat, 5 min)[10]
200 ppm (mammal, 5 min)
36 ppm (mammal, 2 hr)
107 ppm (human, 10 min)
759 ppm (rabbit, 1 min)
759 ppm (cat, 1 min)
357 ppm (human, 2 min)
179 ppm (human, 1 hr)[10]
NIOSH (US health exposure limits):
PEL (Permissible)
TWA 10 ppm (11 mg/m3) [skin][9]
REL (Recommended)
ST 4.7 ppm (5 mg/m3) [skin][9]
IDLH (Immediate danger)
50 ppm[9]
Related compounds
Related alkanenitriles
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
☒N verify (what is ☑Y☒N ?)
Infobox references

Hydrogen cyanide (HCN), sometimes called prussic acid, is a chemical compound[11] with the chemical formula HCN. It is a colorless, extremely poisonous and flammable liquid that boils slightly above room temperature, at 25.6 °C (78.1 °F).[12] HCN is produced on an industrial scale and is a highly valuable precursor to many chemical compounds ranging from polymers to pharmaceuticals.

YouTube Encyclopedic

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  • ✪ Cyanide Poisoning Diagnosis and Treatment
  • ✪ Chemical Weapons: Cyanide Toxicity
  • ✪ Addition of Hydrogen Cyanide in Carbonyl Compounds
  • ✪ Detecting Hydrogen Cyanide and Carbon Monoxide - A Firefighters Perspective
  • ✪ More on Addition of Hydrogen Cyanide in Carbonyl Compounds

Transcription

in the previous video we have discussed cyanide poisoning today let's talk about how to diagnose and how to treat this evil poison remember the most common cause in the United States are fires so firefighters any person who was involved in the fire and don't forget they tried poisoning Rasputin by giving him cyanide. Music Playing...🎶 And these are just a couple of my previous videos, so make sure to subscribe. As you know from the previous lectures, Cyanide could be gas, liquid or solid. Cyanide poisoning could be due to inhalation, ingestion or skin absorption. Causes of cyanide poisoning; smoke inhalation is the most common cause in United states by far. suicide ingestion so, pharmacists, doctors, nurses. Medication such as: sodium nitroprusside. Industrial exposure and the polyurethane in the famous foam bubble wrap, just the one that you keep like picking with your fingers. I love it, that's why I'm crazy, because of the cyanide. Cyanide loves binding to ferric therefore cyanide will either bind to ferric in the Met hemoglobin, or will bind to the ferric in the cytochrome C oxidase in your mitochondria. In the absence of met hemoglobin, cyanide have no choice, but to bind to the ferric in the cytochrome C oxidase. Now this enzyme is gone: irreversible binding. This is an enzyme inhibition. This complex 4 is now gone. Oxygen cannot act as an electron acceptor therefore we will go to an aerobic glycolysis as a source for our energy because ATP from the electron transport chain is no longer viable and as you know this pathway is not gonna work when you have no met hemoglobin but when you are relatively lucky and you have met hemoglobin it will bind cyanide forming cyano met hemoglobin by the liver Rhodanase, thanks to sodium thiosulfate, we end up with thiocyanate, which contains cyanide, and it's gonna be excreted in the urine. Go to hell, cyanide. Go multiply by yourself. Some people will never get this joke. Cyanide binds ferric in the cytochrome oxidase which will lead to inhibition of complex 4... what is complex 4 ?! -Cytochrome a/a3 ...Now, no ATP formation, mitochondria cannot utilize oxygen, we will shift to anaerobic glycolysis which will lead to lactic acid, lactic acidosis, metabolic acidosis. What type? - High anion gap metabolic acidosis. What's the normal anion gap? -It's less than 12 ...Now when your tissue cannot use oxygen, the concentration gradient between hemoglobin and tissue is different... So, here is the red blood cell which contains the famous hemoglobin and here is your tissue normally your tissue is using lots of oxygen lots of oxygen lots of oxygen which makes the concentration of oxygen on the hemoglobin greater than the concentration of oxygen in the tissue which will lead to a diffusion concentration gradient down the concentration gradient down this concentration gradient but now your tissue is not using oxygen so there is no concentration gradient for oxygen to flow from hemoglobin to the tissue oxygen is gonna stay on the hemoglobin from passing it to the artery then to the vein because there is no oxygen going to the tissue because your mitochondria cannot utilize oxygen which destroys the concentration gradient there is no gradient there is no flow to the tissue the venous oxygen content is high as high as the artery that's why in cyanide poisoning pao2 which is the partial pressure of oxygen in the artery equals the P vo2 which is the partial pressure of oxygen and vein some words of wisdom in cyanide poisoning despite the abundance of oxygen it cannot be utilized by the mitochondria that's how it ends up in the vein eating lots of apricots and almonds is bad for you why they contain amygdalin which is hydrolyzed into hydrogen cyanide one apple a day keep the doctor away lots of almonds a day mitochondria has gone astray eating lots of almond will lead to cyanide poisoning however in cyanide poisoning the patient's breath smells like bitter almond just fascinating so here is our nice firefighter who serves his community I serve and protect and smelt like almond now if your doctor is going to test your ability to answer the question about cyanide poisoning correctly they will use one of these scenarios the firefighter in coma with almond like breaths after a fire patient who was prescribed sodium nitroprusside suddenly collapses he has metabolic acidosis why because of the lactic acidosis the factory worker in the middle industry who comes to the ER comatose after an explosion in the mill a pharmacist who suffer from major depressive disorder presents with confusion seizure and loss of consciousness hatred cyanide clinically we have symptoms and we have signs what is the difference between symptom and sign symptom is what you as a patient complain of signs are what I as a great doctor discover or observe so symptoms weakness why there is no ATP the electron transport chain is gone tissue hypoxia yes the tissue is not getting enough oxygen the mitochondria is not utilizing oxygen so the oxygen is not gonna flow from the hemoglobin to the tissue epidermal pain chest pain neurological problems such as headache very important vertigo dizziness seizure in coma all of them are the same as in carbon monoxide poisoning now signs dilated pupils diaphoresis which is excessive sweating because we don't say sweating like the normal public we are sophisticated we say diaphoresis which just means sweating arrhythmia yep cardiovascular collapse possible decrease heart rate decrease blood pressure increased respiratory rate yep shorts of breath and the important cherry cherry red skin why because the partial pressure of oxygen in the vein is high and what gives your blood the bright color at least the arterial blood is the oxyhemoglobin when you have lots of oxyhemoglobin in the vein the vein is gonna look like the artery bright red that's why your skin will look cherry red in color because your veins are more superficial than your arteries don't waste your time on crap and let's go to the lab arterial blood gases venous blood gases what we're gonna find how about the partial pressure of oxygen in the artery normal partial pressure of vein on the oxygen higher than normal why because oxygen is not going to the tissue because we have destroyed the concentration gradient pao2 now roughly equals P vo2 partial pressure of oxygen the artery partial pressure of oxygen in the vein and partial pressure is not the oxygen that's on the hemoglobin it's the oxygen in the bloodstream AV oxygen difference is decreased it's less than 10% what is AV oxygen difference it's the difference between oxygen concentration in the artery and the vein they are now relatively equalizing high anion gap metabolic acidosis due to the lactic acidosis in high anion gap metabolic acidosis it's a freaking acidosis so pH is low what's the normal pH from 735 to 745 so the pH and patients with cyanide is going to be less than 735 important decrease bicarbonate because it's a freaking metabolic acidosis increased anion gap more than 12 okay what's the anion gap it's the positive ions on one end and the negative ions on the other end and the difference between them is called the anion gap there is no actual gap it's a gap in our knowledge it's a gap in our measurement blood lamps we have increased blood lactate level greater than 10 increased plasma cyanide concentration the EKG nonspecific findings sinus tachycardia being the most common carboxy hemoglobin concentration to rule out CO poisoning because both of them are abundant in fires met hemoglobin level why to monitor therapy because we don't want to give the patient too much methemoglobinemia global is also bad you remember methemoglobinemia pros it can treat cyanide poisoning but we can't go too far because met hemoglobin can kill you please let me remind you of normal physiology then we'll discuss the effect of cyanide on each one those you breathe an air the air has oxygen the percentage of oxygen as compared to the atmospheric air is called fio2 normally 21% oxygen goes to the lungs in the alveoli it's called P big AO - that goes to the arterial blood it's called P small a o2 then jumps on the hemoglobin called si O 2 jumps the tissue the tissue needs oxygen for the electron transport chain and it produces carbon dioxide goes to the hemoglobin this is called oxy hemoglobin this is called carb amino hemoglobin not carboxy carb amino that goes to the venous blood it's P vo2 then back to the lungs you exhale carbon dioxide so what's the effect of cyanide on each one of those how about the fio2 it's perfectly normal okay so I nod has no say on that how about P big a o2 in the alveoli again it's normal how about P small a o2 normal sao to normal but how about the partial pressure of oxygen in the vein it's high oxygen content a called hemoglobin concentration plus PA o2 plus si o - what's the effect of cyanide on hemoglobin concentration normal anemia decreases your hemoglobin concentration but not cyanide poisoning about pao2 same thing normal sao to normal so the oxygen content in cyanide poisoning normal believe it or not and here I'm talking about the arterial oxygen content but how about the venous oxygen content it's increased in cyanide poisoning if io2 is normal P big a o2 is normal P small a o2 is normal it's a Oh - is normal P vo2 is increase don't ever forget that is the cell affected yes indeed it's affected the mitochondria cannot utilize oxygen so oxygen is released from hemoglobin to tissue but it cannot utilize it but didn't you say that oxygen is not released in the beginning it is released but then the mitochondria doesn't use it so the oxygen doesn't flow anymore but the problem is not from oxygen being able to leave the hemoglobin and going to the tissue that's why generally speaking the cyanide poisoning does not shift the oxygen binding curve some words of wisdom from the father of Medicine Hippocrates I will use my power to help the sick to the best of my ability I will abstain from harming or wronging any man by it I have a terrible British accent plus Hippocrates was Greek he was not British what am I doing with my life so let's use our power to help the sick and let's learn how to manage cyanide poisoning first remove the clothes why because cyanide poisoning can occur by absorption through the skin and don't waste your time unbuttoning each button with care because the shirt of the patient was expensive just get them off don't be an SS s what I call a super sophisticatedly stupid then wash the body with soap and water do not wait for the stupid labs if you suspect cyanide treat it how to treat saina 100% oxygen then we try the hyperbaric oxygen then the hyperbaric chamber remember your ABCs first airway breathing circulation establish an IV line and continuous EKG monitoring give the cyanide antidote what is the sign of antidote the famous triad hydroxocobalamin sodium nitride sodium thiosulfate let's talk about sodium thiosulfate sodium thiosulfate helps the Sanomat hemoglobin goes to thiocyanate then become excreted in the urine go to hell cyanide go multiply by yourself sodium nitrite converts the normal hemoglobin into meth hemoglobin so the methemoglobinemia with cyanide forming cyano met hemoglobin then the sodium thiosulfate will kick in converting them to thiocyanate which will be excreted in the urine so here is the famous giant hydroxocobalamin sodium thiosulfate and sodium nitrite sodium nitrite converts the hemoglobin into met hemoglobin the Farrah's into ferric then the methemoglobinemia forming cyano met hemoglobin level rhodanese sodium thiosulfate they'll form thiocyanate excreted in the urine go-to-hell hydroxocobalamin on the other hand combines directly with cyanide forming cyano cobalamin again they are excrete is excreted in the urine and that's how the evil cyanide ends up in the urine magnificent repetition is the mother of pedagogy here we have the hemoglobin phorus thanks to sodium nitrite now we have the met hemoglobin which contains furyk cyanides loves ferric without the met hemoglobin cyanide will be able to bind the complex for the cytochrome a a3 in the electron transport chain destroying your mitochondria destroying your cellular respiration but now net hemoglobin has gone distract cyanide and take it away forming Cyanamid hemoglobin sparing the mitochondria from the grief then cyan homuth hemoglobin thanks to sodium thiosulfate is gonna be converted into FeO cyanide thio cyanide how about the methemoglobinemia hemoglobin we can use methylene blue to return it back to hemoglobin later but now let's get rid of the sanno matimak globin use sodium thiosulfate now we have thiocyanate go to hell so we have mentioned two of the triad sodium nitrite and sodium thiosulfate how about the third one hydroxocobalamin vitamin b12 guys hydroxocobalamin will bind cyanide forming cyano cobalamin go to hell without this amazing triad your cellular respiration will be inhibited you will end up smelling like bitter almond with cherry red skin until you die for a plus students while treating acute cyanide poisoning do not give methylene blue why because methylene blue will confer the methemoglobinemia back into regular hemoglobin okay so don't do this wait until we clear all the sign out from the system then you can give methylene blue to convert the methemoglobinemia great normal hemoglobin do not let me t mclogan level rise too much we don't want to go too far yes Matt hemoglobin is beneficial in treating cyanide poisoning by using too much methemoglobinemia hemoglobin amine which is also a disease so everything has to be balanced sodium nitroprusside leads to cyanide poisoning whereas sodium nitrite and sodium thiosulfate treats this poisoning this is very important and most students confuse these sodium nitroprusside is evil it leads to cyanide poisoning sodium nitrite and sodium thiosulfate they treat the cyanide poison sodium nitroprusside and cyanide and sodium nitrate and sodium nitrite all lead to hypotension that's why men die on viagra when they are using sodium nitrate both viagra and sodium nitrate will drop the blood pressure leading to either death or reflex tachycardia which will also lead to death in cyanide poisoning it's difficult to distinguish between original arteries and retinal veins under Fonda's copic exam which is a brilliant point why because the partial pressure of oxygen in the artery calls the partial pressure of oxygen in the vein and oxygen is what gives the vessel its bright color that's why normally arteries have bright red blood all veins have dark but now we can't differentiate between arteries and veins both of them are bright guys it can't get better than that so please join me on patreon com4 / meta kosis and thank you so much for watching my videos until next time be safe stay happy and study hard I'll see you in the next video we have a crazy mnemonic about cyanide poisoning until next time

Contents

Structure and general properties

Hydrogen cyanide is a linear molecule, with a triple bond between carbon and nitrogen. A minor tautomer of HCN is HNC, hydrogen isocyanide.

Hydrogen cyanide is weakly acidic with a pKa of 9.2. It partially ionizes in water solution to give the cyanide anion, CN. A solution of hydrogen cyanide in water, represented as HCN, is called hydrocyanic acid. The salts of the cyanide anion are known as cyanides.

HCN has a faint bitter almond-like odor that some people are unable to detect owing to a recessive genetic trait.[13] The volatile compound has been used as inhalation rodenticide and human poison, as well as for killing whales.[14] Cyanide ions interfere with iron-containing respiratory enzymes.

History of discovery

The red colored ferricyanide ion, one component of Prussian blue
The red colored ferricyanide ion, one component of Prussian blue

Hydrogen cyanide was first isolated from a blue pigment (Prussian blue) which had been known since 1706, but whose structure was unknown. It is now known to be a coordination polymer with a complex structure and an empirical formula of hydrated ferric ferrocyanide. In 1752, the French chemist Pierre Macquer made the important step of showing that Prussian blue could be converted to an iron oxide plus a volatile component and that these could be used to reconstitute it.[15] The new component was what is now known as hydrogen cyanide. Following Macquer's lead, it was first prepared from Prussian blue by the Swedish chemist Carl Wilhelm Scheele in 1782,[16] and was eventually given the German name Blausäure (lit. "Blue acid") because of its acidic nature in water and its derivation from Prussian blue. In English, it became known popularly as prussic acid.

In 1787, the French chemist Claude Louis Berthollet showed that prussic acid did not contain oxygen,[17] an important contribution to acid theory, which had hitherto postulated that acids must contain oxygen[18] (hence the name of oxygen itself, which is derived from Greek elements that mean "acid-former" and are likewise calqued into German as Sauerstoff). In 1811, Joseph Louis Gay-Lussac prepared pure, liquified hydrogen cyanide.[19] In 1815, Gay-Lussac deduced Prussic acid's chemical formula.[20] The radical cyanide in hydrogen cyanide was given its name from cyan, not only an English word for a shade of blue but the Greek word for blue (Ancient Greek: κυανοῦς), again owing to its derivation from Prussian blue.

Production and synthesis

Hydrogen cyanide forms in at least limited amounts from many combinations of hydrogen, carbon, and ammonia. Hydrogen cyanide is currently produced in great quantities by several processes, as well as being a recovered waste product from the manufacture of acrylonitrile.[11] In 2006 between 500 million and 1 billion pounds were produced in the US.[21]

The most important process is the Andrussow oxidation invented by Leonid Andrussow at IG Farben in which methane and ammonia react in the presence of oxygen at about 1200 °C over a platinum catalyst:[22]

2 CH4 + 2 NH3 + 3 O2 → 2 HCN + 6 H2O

The energy needed for the reaction is provided by the partial oxidation of methane and ammonia.

Of lesser importance is the Degussa process (BMA process) in which no oxygen is added and the energy must be transferred indirectly through the reactor wall:[23]

CH4 + NH3 → HCN + 3H2

This reaction is akin to steam reforming, the reaction of methane and water to give carbon monoxide and hydrogen.

In the Shawinigan Process, hydrocarbons, e.g. propane, are reacted with ammonia. In the laboratory, small amounts of HCN are produced by the addition of acids to cyanide salts of alkali metals:

H+ + NaCN → HCN + Na+

This reaction is sometimes the basis of accidental poisonings because the acid converts a nonvolatile cyanide salt into the gaseous HCN.

Historical methods of production

The large demand for cyanides for mining operations in the 1890s was met by George Thomas Beilby, who patented a method to produce hydrogen cyanide by passing ammonia over glowing coal in 1892. This method was used until Hamilton Castner in 1894 developed a synthesis starting from coal, ammonia, and sodium yielding sodium cyanide, which reacts with acid to form gaseous HCN.

Applications

HCN is the precursor to sodium cyanide and potassium cyanide, which are used mainly in gold and silver mining and for the electroplating of those metals. Via the intermediacy of cyanohydrins, a variety of useful organic compounds are prepared from HCN including the monomer methyl methacrylate, from acetone, the amino acid methionine, via the Strecker synthesis, and the chelating agents EDTA and NTA. Via the hydrocyanation process, HCN is added to butadiene to give adiponitrile, a precursor to Nylon-6,6.[11]

Occurrence

HCN is obtainable from fruits that have a pit, such as cherries, apricots, apples, and bitter almonds, from which almond oil and flavoring are made. Many of these pits contain small amounts of cyanohydrins such as mandelonitrile and amygdalin, which slowly release hydrogen cyanide.[24][25] One hundred grams of crushed apple seeds can yield about 70 mg of HCN.[26] Some millipedes release hydrogen cyanide as a defense mechanism,[27] as do certain insects, such as some burnet moths. Hydrogen cyanide is contained in the exhaust of vehicles, and in smoke from burning nitrogen-containing plastics. So-called "bitter" roots of the cassava plant may contain up to 1 gram of HCN per kilogram.[28][29]

The South Pole Vortex of Saturn's moon Titan is a giant swirling cloud of HCN (November 29, 2012).
The South Pole Vortex of Saturn's moon Titan is a giant swirling cloud of HCN (November 29, 2012).

HCN on Titan

HCN has been measured in Titan's atmosphere by four instruments on the Cassini space probe, one instrument on Voyager, and one instrument on Earth.[30] One of these measurements was in situ, where the Cassini spacecraft dipped between 1000–1100 km above Titan's surface to collect some atmospheric gas for mass spectrometry analysis.[31] HCN likely formed in Titan's atmosphere through the reaction of photochemically produced methane and nitrogen radicals which proceeded through the H2CN intermediate, e.g., (CH3 + N → H2CN + H → HCN + H2).[32]

HCN on the young Earth

It has been postulated that carbon from a cascade of asteroids (known as the Late Heavy Bombardment), resulting from interaction of Jupiter and Saturn, blasted the surface of young Earth and reacted with nitrogen in Earth's atmosphere to form HCN.[33]

HCN in mammals

Some authors have shown that neurons can produce hydrogen cyanide upon activation of their opioid receptors by endogenous or exogenous opioids. They have also shown that neuronal production of HCN activates NMDA receptors and plays a role in signal transduction between neuronal cells (neurotransmission). Moreover, increased endogenous neuronal HCN production under opioids was seemingly needed for adequate opioid analgesia, as analgesic action of opioids was attenuated by HCN scavengers. They considered endogenous HCN to be a neuromodulator.[34]

It has also been shown that, while stimulating muscarinic cholinergic receptors in cultured pheochromocytoma cells increases HCN production, in a living organism (in vivo) muscarinic cholinergic stimulation actually decreases HCN production.[35]

Leukocytes generate HCN during phagocytosis, and can kill bacteria, fungi, and other pathogens by generating several different toxic chemicals, one of which is hydrogen cyanide.[34]

The vasodilatation caused by sodium nitroprusside has been shown to be mediated not only by NO generation, but also by endogenous cyanide generation, which adds not only toxicity, but also some additional antihypertensive efficacy compared to nitroglycerine and other non-cyanogenic nitrates which do not cause blood cyanide levels to rise.[36]

HCN is a constituent of tobacco smoke.[37]

HCN and the origin of life

Hydrogen cyanide has been discussed as a precursor to amino acids and nucleic acids, and is proposed to have played a part in the origin of life.[38] Although the relationship of these chemical reactions to the origin of life theory remains speculative, studies in this area have led to discoveries of new pathways to organic compounds derived from the condensation of HCN.[39]

HCN in space

HCN has been detected in the interstellar medium[40] and in the atmospheres of carbon stars.[41] Since then, extensive studies have probed formation and destruction pathways of HCN in various environments and examined its use as a tracer for a variety of astronomical species and processes. HCN can be observed from ground-based telescopes through a number of atmospheric windows.[42] The J=1→0, J=3→2, J= 4→3, and J=10→9 pure rotational transitions have all been observed.[40][43][44]

HCN is formed in interstellar clouds through one of two major pathways:[45] via a neutral-neutral reaction (CH2 + N → HCN + H) and via dissociative recombination (HCNH+ + e → HCN + H). The dissociative recombination pathway is dominant by 30%; however, the HCNH+ must be in its linear form. Dissociative recombination with its structural isomer, H2NC+, exclusively produces hydrogen isocyanide (HNC).

HCN is destroyed in interstellar clouds through a number of mechanisms depending on the location in the cloud.[45] In photon-dominated regions (PDRs), photodissociation dominates, producing CN (HCN + ν → CN + H). At further depths, photodissociation by cosmic rays dominate, producing CN (HCN + cr → CN + H). In the dark core, two competing mechanisms destroy it, forming HCN+ and HCNH+ (HCN + H+ → HCN+ + H; HCN + HCO+ → HCNH+ + CO). The reaction with HCO+ dominates by a factor of ~3.5. HCN has been used to analyze a variety of species and processes in the interstellar medium. It has been suggested as a tracer for dense molecular gas[46][47] and as a tracer of stellar inflow in high-mass star-forming regions.[48] Further, the HNC/HCN ratio has been shown to be an excellent method for distinguishing between PDRs and X-ray-dominated regions (XDRs).[49]

On 11 August 2014, astronomers released studies, using the Atacama Large Millimeter/Submillimeter Array (ALMA) for the first time, that detailed the distribution of HCN, HNC, H2CO, and dust inside the comae of comets C/2012 F6 (Lemmon) and C/2012 S1 (ISON).[50][51]

In February 2016, it was announced that traces of hydrogen cyanide were found in the atmosphere of the hot Super-Earth 55 Cancri e with NASA's Hubble Space Telescope.[52]

As a poison and chemical weapon

In World War One, hydrogen cyanide was used as a chemical weapon against the Central Powers by the French from 1916, and by the United States and Italy in 1918, but it was not found to be effective enough due to weather conditions.[53][54] The gas is lighter than air and rapidly disperses up into the atmosphere; this is in contrast to denser agents such as phosgene or chlorine which tend to remain at ground level. Compared to such agents it must also be present in higher concentrations in order to be fatal. These properties combine to make its use in the field impractical. A hydrogen cyanide concentration in the range of 100–200 ppm in air will kill a human within 10 to 60 minutes.[55] A hydrogen cyanide concentration of 2000 ppm (about 2380 mg/m3) will kill a human in about one minute.[55] The toxicity is caused by the cyanide ion, which halts cellular respiration by acting as a non-competitive inhibitor for an enzyme in mitochondria called cytochrome c oxidase. As such hydrogen cyanide is commonly listed among chemical weapons as a blood agent.[56] It is listed under Schedule 3 of the Chemical Weapons Convention as a potential weapon which has large-scale industrial uses, manufacturing plants in signatory countries which produce more than 30 metric tons per year must be declared to, and can be inspected by, the Organisation for the Prohibition of Chemical Weapons.

Hydrogen cyanide has been absorbed into a carrier for use as a pesticide. Perhaps the most infamous of these is Zyklon B (German: Cyclone B, with the B standing for Blausäure – prussic acid; also, to distinguish it from an earlier product later known as Zyklon A),[57] it was used in Nazi German extermination camps during World War II to kill en masse as part of their Final Solution genocide program. Hydrogen cyanide was also used in the camps for delousing clothing in attempts to eradicate diseases carried by lice and other parasites. The same product is currently made in the Czech Republic under the trademark "BLUE FUME".[58] Hydrogen cyanide was also the agent employed in judicial execution in some U.S. states, where it was produced during the execution by the action of sulfuric acid on potassium cyanide.

Under the name prussic acid, HCN has been used as a killing agent in whaling harpoons, although it proved quite dangerous to the crew deploying it, and thus it was quickly abandoned.[14] From the middle of the 18th century it was used in a number of poisoning murders and suicides.[59]

Hydrogen cyanide gas in air is explosive at concentrations over 5.6%.[60] This is far above its toxicity level.

References

  1. ^ "Hydrogen Cyanide – Compound Summary". PubChem Compound. United States: National Center for Biotechnology Information. 16 September 2004. Identification. Retrieved 2012-06-04.
  2. ^ "hydrogen cyanide (CHEBI:18407)". Chemical Entities of Biological Interest. UK: European Bioinformatics Institute. 18 October 2009. Main. Retrieved 2012-06-04.
  3. ^ a b c d Haynes, 4.67
  4. ^ Haynes, 6.94
  5. ^ Haynes, 5.92
  6. ^ Patnaik, P. (2002). Handbook of Inorganic Chemicals. McGraw-Hill. ISBN 978-0-07-049439-8.
  7. ^ Haynes, 6.231
  8. ^ Haynes, 5.19
  9. ^ a b c d NIOSH Pocket Guide to Chemical Hazards. "#0333". National Institute for Occupational Safety and Health (NIOSH).
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