57-12-5[C-]#NXFXPMWWXUTWYJX-UHFFFAOYSA-NAqueous solutions with a faint odor of bitter almonds. Toxic by skin absorption, by ingestion, and inhalation of the hydrogen cyanide from the decomposition of the material. Toxic oxides of nitrogen are produced in fires involving this material. Obtain the technical name of the material from the shipping papers and contact CHEMTREC, 800-424-9300 for specific response information.
57-12-5DTXSID6023991CHEMBL183419CHEBI:17514Hazardous Air Pollutants (HAPs)
Toxic Gases & Vapors -> Cyanides
Toxic Gases & Vapors -> Chemical Asphyxiants
Major ion
Aqueous solutions with a faint odor of bitter almonds. Toxic by skin absorption, by ingestion, and inhalation of the hydrogen cyanide from the decomposition of the material. Toxic oxides of nitrogen are produced in fires involving this material. Obtain the technical name of the material from the shipping papers and contact CHEMTREC, 800-424-9300 for specific response information.
Generally white crystals or powders but possibly colored Toxic by skin absorption through open wounds, by ingestion, and inhalation of the hydrogen cyanide from the decomposition of the material. Toxic oxides of nitrogen are produced in fires. Obtain the technical name of the material form the shipping papers and contact CHEMTREC, 800-424-9300 for specific response information.
Varies; See specific cyanide salt;
Safety information is for reference only and does not replace the supplier’s Safety Data Sheet (SDS), applicable regulations, or professional assessment.
Regulation (EC) No 178/2002 (amended)
Cyanide: Does not have an individual approval but may be used as a component in a product covered by a group standard. It is not approved for use as a chemical in its own right.
The New Jersey Worker and Community Right to Know Act requires public and private employers to provide information about hazardous substances at their workplaces. (N.J.S.A. 34:5A-1 et. seq.)
Poison
Poison
Excerpt from ERG Guide 157 [Substances - Toxic and/or Corrosive (Non-Combustible / Water-Sensitive)]:
Excerpt from ERG Guide 157 [Substances - Toxic and/or Corrosive (Non-Combustible / Water-Sensitive)]:
Excerpt from ERG Guide 157 [Substances - Toxic and/or Corrosive (Non-Combustible / Water-Sensitive)]:
Excerpt from ERG Guide 157 [Substances - Toxic and/or Corrosive (Non-Combustible / Water-Sensitive)]:
Cyanide is used in a number of industries and is found at low levels in air from car exhaust. Cyanide is extremely toxic to humans. Chronic (long-term) inhalation exposure of humans to cyanide results primarily in effects on the central nervous system (CNS). Other effects in humans include cardiovascular and respiratory effects, an enlarged thyroid gland, and irritation to the eyes and skin. No data are available on the carcinogenic effects of cyanide in humans via inhalation. Animal studies have suggested that oral exposure to cassava (a cyanide-containing vegetable) may be associated with malformations in the fetus and low fetal body weights. EPA has classified cyanide as a Group D, not classifiable as to human carcinogenicity.
A fatal inhalation dose of hydrogen cyanide is 600 to 700 ppm for 5 minutes or 200 ppm for 30 minutes. In victims overcome by smoke inhalation, hypoxia from carbon monoxide is initially indistinguishable from that caused by cyanide. Smokers have elevated whole blood cyanide levels up to 0.4 ug/ml. In poisoning cases, victims are agitated at levels above 1.0 ug/ml and comatose at levels above 2.5 ug/ml. Acrylonitrile, acetonitrile, and other aliphatic nitriles can cause cyanide poisoning after absorption and hepatic transformation. [ATSDR Case Studies # 15] Symptoms of cyanide toxicity can occur within seconds of inhalation of hydrogen cyanide or within minutes of ingestion of cyanide salts. Onset may be delayed up to 12 h after ingestion of cyanogenic glycosides, nitriles, or thiocyanates. [INCHEM: CICAD 61] Cyanide is detoxified in the body when it is combined with sulfur to form thiocyanate. [Ford, p. 705] Urine thiocyanate levels are <0.11 mg/24h without occupational exposure. The no-adverse-effect-level is 6.5 mg/24h. Smokers have higher levels. [LaDou, 4th edition, p. 633] In nitroprusside poisoning cases, the half-life of thiocyanate is 2.7 days (normal renal function). [Ford, p. 410] Thiocyanate levels correlate with thiocyanate toxicity, not with degree of cyanide poisoning. Thiocyanate toxicity occurs when thiocyanate levels exceed 100 mg/L. [Haddad, p. 985] Chronic exposure to cyanide causes tobacco amblyopia (from cigarette smoking) and tropical ataxic neuropathy (from eating improperly processed cassava). Both conditions are associated with low B12 levels. Thiocyanate can competitively inhibit the entry of iodide into the thyroid gland and cause hypothyroidism and goiters. [Goldfrank, p. 1680] Handle all cyanide compounds with care. HCN may be released from relatively stable compounds like ferro- and ferricyanides in the presence of strong acids. Even weak acids can cause a slow release of cyanide. [Ullmann] Workers exposed to HCN for seven years at 4.2 to 12.4 ppm in breathing zone air had increased headache, weakness, and thyroid gland enlargement. [ACGIH: HCN] See Hydrogen cyanide. See NITRILES.
Organic nitriles are converted into cyanide ions through the action of cytochrome P450 enzymes in the liver. Cyanide is rapidly absorbed and distributed throughout the body. Cyanide is mainly metabolized into thiocyanate by either rhodanese or 3-mercaptopyruvate sulfur transferase. Cyanide metabolites are excreted in the urine. (L96)
Organic nitriles are converted into cyanide ions through the action of cytochrome P450 enzymes in the liver. Cyanide is rapidly absorbed and distributed throughout the body. Cyanide is mainly metabolized into thiocyanate by either rhodanese or 3-mercaptopyruvate sulfur transferase. Cyanide metabolites are excreted in the urine. (L96)
The major uses of hydrogen cyanide are as an intermediate in the production of a number of chemicals and as an insecticide for fumigating enclosed spaces. Hydrogen cyanide has also been used in gas chamber executions.
Used in electroplating, silver and gold extraction, metal cleaning, metal nitriding, ship fumigating, mining processes, cement stabilizing, photo developing, and organic synthesis; Used in the past to fumigate fruit trees, railroad cars, ships, warehouses, rabbit and rat burrows, and termite nests; In tropical countries where the potato-like tubers of the cassava plant are grown, cyanide poisonings due to ingestion of the cassava root have been reported. [ATSDR ToxProfiles] In the past, occupational cyanide poisoning was most common in metal extraction, electroplating, metal hardening, and fumigation; [Sullivan, p. 706] The cyanides of mercury, lead, cobalt, and nickel do not have any major industrial importance. [Ullmann]
Steel Producing [Category: Industry]
Sculpturing plastics [Category: Hobbies]
Cyanide compounds are used in electroplating, metallurgy, organic chemicals production, photographic developing, manufacture of plastics, fumigation of ships, and some mining processes. (L96)
Hydrogen cyanide is a precursor to many chemical compounds, ranging from polymers to pharmaceuticals. (L101)
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Causes tremor, convulsions, and dyspnea in intraperitoneal lethal-dose studies of mice (LD50 = 3 mg/kg); [RTECS] Aqueous solutions slowly evolve hydrogen cyanide; [CAMEO] Free cyanide (as HCN or CN-) is the most toxic form of cyanide; [EPA: Exposure Risk Assessment] See CYANIDES.
Cyanides, Inorganic
Cyanides, Inorganic
CYANIDE SOLUTIONS slowly evolve hydrogen cyanide, a flammable and poisonous gas. Acids cause the rapid evolution of HCN. Carbon dioxide from the air is sufficiently acidic to liberate HCN from solutions of cyanides. Incompatible with isocyanates, nitrides, and peroxides. Mayinitiate polymerization reactions of epoxides. May react exothermically with metal salts to produce explosive products or evolve gaseous hydrogen.
CYANIDES, INORGANIC, SOLID, N.O.S. react slowly with water to evolve gaseous hydrogen cyanide (HCN). Acids cause the rapid evolution of HCN; carbon dioxide from the air is sufficiently acidic to liberate HCN from solutions of inorganic cyanides. Incompatible with isocyanates, nitrides, and peroxides. May initiate polymerization reactions of epoxides. Form compounds with metal salt in exothermic reactions that may produce flammable hydrogen. Some inorganic cyanides can detonate when shocked, heated or rubbed.
Water soluble. Inorganic cyanides react slowly with water to evolve gaseous hydrogen cyanide (HCN).
Water soluble. Slowly decomposed by water to give off hydrogen cyanide, a flammable poison gas.
Excerpt from ERG Guide 157 [Substances - Toxic and/or Corrosive (Non-Combustible / Water-Sensitive)]:
Excerpt from ERG Guide 157 [Substances - Toxic and/or Corrosive (Non-Combustible / Water-Sensitive)]:
Excerpt from ERG Guide 157 [Substances - Toxic and/or Corrosive (Non-Combustible / Water-Sensitive)]:
Excerpt from ERG Guide 157 [Substances - Toxic and/or Corrosive (Non-Combustible / Water-Sensitive)]:
Excerpt from ERG Guide 157 [Substances - Toxic and/or Corrosive (Non-Combustible / Water-Sensitive)]:
Excerpt from ERG Guide 157 [Substances - Toxic and/or Corrosive (Non-Combustible / Water-Sensitive)]:
Excerpt from ERG Guide 157 [Substances - Toxic and/or Corrosive (Non-Combustible / Water-Sensitive)]:
Excerpt from ERG Guide 157 [Substances - Toxic and/or Corrosive (Non-Combustible / Water-Sensitive)]:
0.45 [mg/m3]
5.0 [mg/m3]
25 [mg/m3]
Excerpt from ERG Guide 157 [Substances - Toxic and/or Corrosive (Non-Combustible / Water-Sensitive)]:
Excerpt from ERG Guide 157 [Substances - Toxic and/or Corrosive (Non-Combustible / Water-Sensitive)]:
Antidotes to cyanide poisoning include hydroxocobalamin and sodium nitrite, which release the cyanide from the cytochrome system, and rhodanase, which is an enzyme occurring naturally in mammals that combines serum cyanide with thiosulfate, producing comparatively harmless thiocyanate. Oxygen therapy can also be administered. (L97)
Antidotes to cyanide poisoning include hydroxocobalamin and sodium nitrite, which release the cyanide from the cytochrome system, and rhodanase, which is an enzyme occurring naturally in mammals that combines serum cyanide with thiosulfate, producing comparatively harmless thiocyanate. Oxygen therapy can also be administered. (L97)
Exposure to high levels of cyanide for a short time harms the brain and heart and can even cause coma, seizures, apnea, cardiac arrest and death. Chronic inhalation of cyanide causes breathing difficulties, chest pain, vomiting, blood changes, headaches, and enlargement of the thyroid gland. Skin contact with cyanide salts can irritate and produce sores. (L96, L97)
Exposure to high levels of cyanide for a short time harms the brain and heart and can even cause coma, seizures, apnea, cardiac arrest and death. Chronic inhalation of cyanide causes breathing difficulties, chest pain, vomiting, blood changes, headaches, and enlargement of the thyroid gland. Skin contact with cyanide salts can irritate and produce sores. (L96, L97)
Other Poison - Chemical Asphyxiant
Other Poison - Chemical Asphyxiant
Oral (L96) ; inhalation (L96) ; dermal (L96)
Oral (L96) ; inhalation (L96) ; dermal (L96)
Organic nitriles decompose into cyanide ions both in vivo and in vitro. Consequently the primary mechanism of toxicity for organic nitriles is their production of toxic cyanide ions or hydrogen cyanide. Cyanide is an inhibitor of cytochrome c oxidase in the fourth complex of the electron transport chain (found in the membrane of the mitochondria of eukaryotic cells). It complexes with the ferric iron atom in this enzyme. The binding of cyanide to this cytochrome prevents transport of electrons from cytochrome c oxidase to oxygen. As a result, the electron transport chain is disrupted and the cell can no longer aerobically produce ATP for energy. Tissues that mainly depend on aerobic respiration, such as the central nervous system and the heart, are particularly affected. Cyanide is also known produce some of its toxic effects by binding to catalase, glutathione peroxidase, methemoglobin, hydroxocobalamin, phosphatase, tyrosinase, ascorbic acid oxidase, xanthine oxidase, succinic dehydrogenase, and Cu/Zn superoxide dismutase. Cyanide binds to the ferric ion of methemoglobin to form inactive cyanmethemoglobin. (L97)
Organic nitriles decompose into cyanide ions both in vivo and in vitro. Consequently the primary mechanism of toxicity for organic nitriles is their production of toxic cyanide ions or hydrogen cyanide. Cyanide is an inhibitor of cytochrome c oxidase in the fourth complex of the electron transport chain (found in the membrane of the mitochondria of eukaryotic cells). It complexes with the ferric iron atom in this enzyme. The binding of cyanide to this cytochrome prevents transport of electrons from cytochrome c oxidase to oxygen. As a result, the electron transport chain is disrupted and the cell can no longer aerobically produce ATP for energy. Tissues that mainly depend on aerobic respiration, such as the central nervous system and the heart, are particularly affected. Cyanide is also known produce some of its toxic effects by binding to catalase, glutathione peroxidase, methemoglobin, hydroxocobalamin, phosphatase, tyrosinase, ascorbic acid oxidase, xanthine oxidase, succinic dehydrogenase, and Cu/Zn superoxide dismutase. Cyanide binds to the ferric ion of methemoglobin to form inactive cyanmethemoglobin. (L97)
Cyanide poisoning is identified by rapid, deep breathing and shortness of breath, general weakness, giddiness, headaches, vertigo, confusion, convulsions/seizures and eventually loss of consciousness. (L96, L97)
Cyanide poisoning is identified by rapid, deep breathing and shortness of breath, general weakness, giddiness, headaches, vertigo, confusion, convulsions/seizures and eventually loss of consciousness. (L96, L97)
Cyanide, free
Reproductive
6.3 x 10 ^-4 mg/kg-day
No indication of carcinogenicity to humans (not listed by IARC).
No indication of carcinogenicity to humans (not listed by IARC).
0.0008
SURROGATE. See Hydrogen Cyanide
0.0006
IRIS Current
0.02
HEAST Current
DescriptionKCN and NaCN are white crystalline solids with a faint almond odor. Sodium cyanide also has a slight odor of hydrocyanic acid when damp. KCN: Boilingpoint=1625℃; Freezing/Melting point=634℃. NaCN:Boiling point=1496℃; Freezing/Melting point=564℃.NFPA 704 M Hazard Identification (KCN and NaCN):Health 3, Flammability 0 [(4) gas], Reactivity 1 [(2) gas].Soluble in water.
UsesCyanide, standard solution is used to dissolve metals and their ores. It is also used in clinical chemistry and in waste water treatment facilities to determine the concentration of dissolved and particulate materials.
UsesFumigants, soil sterilizers, fertilizers, rodenticides.
General DescriptionAqueous solutions with a faint odor of bitter almonds. Toxic by skin absorption, by ingestion, and inhalation of the hydrogen cyanide from the decomposition of the material. Toxic oxides of nitrogen are produced in fires involving Methyl4-(cyanomethyl)benzoate. Obtain the technical name of the material from the shipping papers and contact CHEMTREC, 800-424-9300 for specific response information.
Definitioncyanide: 1. An inorganic salt containingthe cyanide ion CN–. Cyanidesare extremely poisonousbecause of the ability of the CN– ionto coordinate with the iron inhaemoglobin, thereby blocking theuptake of oxygen by the blood. 2. Ametal coordination complex formedwith cyanide ions.
DefinitionChEBI: A pseudohalide anion that is the conjugate base of hydrogen cyanide.