Record Information
Version1.0
Creation Date2009-06-19 21:58:41 UTC
Update Date2026-04-05 17:54:39 UTC
Accession NumberCHEM001185
Identification
Common NameCadmium cyanide
ClassSmall Molecule
DescriptionCadmium cyanide is a chemical compound of cadmium and cyanide prepared by treating a concentrated aqueous solution of cadmium chloride or cadmium nitrate with potassium cyanide or sodium cyanide. It is used as an electrolyte for electrodeposition of thin metallic cadmium coatings on metal to protect against corrosion. Cadmium is a transition metal and chemical element with the symbol Cd and atomic number 48. It is found naturally in the earth's crust, though rarely on it's own. (4, 12)
Contaminant Sources
  • IARC Carcinogens Group 1
  • T3DB toxins
Contaminant Type
  • Cadmium Compound
  • Cyanide Compound
  • Industrial/Workplace Toxin
  • Inorganic Compound
  • Nitrile
  • Organic Compound
  • Pollutant
  • Synthetic Compound
Chemical Structure
Thumb
SynonymsNot Available
Chemical FormulaC2CdN2
Average Molecular Mass164.446 g/mol
Monoisotopic Mass165.910 g/mol
CAS Registry Number542-83-6
IUPAC Namecadmiumdicarbonitrile
Traditional Namecadmium cyanide
SMILESN#C[Cd]C#N
InChI IdentifierInChI=1S/2CN.Cd/c2*1-2;
InChI KeyRFTZXIHJPQONBE-UHFFFAOYSA-N
Chemical Taxonomy
Description belongs to the class of organic compounds known as organic transition metal salts. These are organic salt compounds containing a transition metal atom in its ionic form.
KingdomOrganic compounds
Super ClassOrganic salts
ClassOrganic metal salts
Sub ClassOrganic transition metal salts
Direct ParentOrganic transition metal salts
Alternative Parents
Substituents
  • Organic transition metal salt
  • Organic nitrogen compound
  • Organopnictogen compound
  • Hydrocarbon derivative
  • Organic cadmium salt
  • Organonitrogen compound
  • Aliphatic acyclic compound
Molecular FrameworkNot Available
External DescriptorsNot Available
Biological Properties
StatusDetected and Not Quantified
OriginExogenous
Cellular Locations
  • Cytoplasm
  • Extracellular
Biofluid LocationsNot Available
Tissue LocationsNot Available
PathwaysNot Available
ApplicationsNot Available
Biological RolesNot Available
Chemical RolesNot Available
Physical Properties
StateSolid
AppearanceWhite crystals.
Experimental Properties
PropertyValue
Melting PointNot Available
Boiling PointNot Available
Solubility17.1 mg/mL at 15°C [MERCK INDEX (1996)]
Predicted Properties
PropertyValueSource
Water Solubility35.5 g/LALOGPS
logP-0.55ALOGPS
logP0.38ChemAxon
logS-0.67ALOGPS
Physiological Charge0ChemAxon
Hydrogen Acceptor Count2ChemAxon
Hydrogen Donor Count0ChemAxon
Polar Surface Area47.58 ŲChemAxon
Rotatable Bond Count0ChemAxon
Refractivity13.31 m³·mol⁻¹ChemAxon
Polarizability7.4 ųChemAxon
Number of Rings0ChemAxon
Bioavailability1ChemAxon
Rule of FiveYesChemAxon
Ghose FilterNoChemAxon
Veber's RuleNoChemAxon
MDDR-like RuleNoChemAxon
Spectra
Spectra
Spectrum TypeDescriptionSplash KeyView
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 10V, Positivesplash10-014i-0900000000-d133962ef785f859dc0cSpectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 20V, Positivesplash10-014i-0900000000-d133962ef785f859dc0cSpectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 40V, Positivesplash10-014i-0900000000-d133962ef785f859dc0cSpectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 10V, Negativesplash10-03di-0900000000-c8a1b220db7a60fc44d7Spectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 20V, Negativesplash10-03di-0900000000-c8a1b220db7a60fc44d7Spectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 40V, Negativesplash10-03di-0900000000-c8a1b220db7a60fc44d7Spectrum
Toxicity Profile
Route of ExposureOral (4) ; inhalation (4) ; dermal (4)
Mechanism of ToxicityCadmium initially binds to metallothionein and is transported to the kidney. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Accumulation of cadmium in the kidney results in increased excretion of vital low and high weight molecular proteins. Cadmium is a high affinity zinc analog and can interfere in its biological processes. It also binds to and activates the estrogen receptor, likely stimulating the growth of certain types of cancer cells and causing other estrogenic effects, such as reproductive dysfunction. Cadmium causes cell apoptosis by activating mitogen-activated protein kinases. 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. (5, 1, 2, 3, 8)
MetabolismCadmium and cyanide are absorbed from oral, inhalation, and dermal routes. Cadmium initially binds to metallothionein and albumin and is transported mainly to the kidney and liver. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Cadmium is not known to undergo any direct metabolic conversion and is excreted unchanged, mainly in the urine. 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. (4, 7)
Toxicity ValuesNot Available
Lethal Dose200 to 300 milligrams for an adult human (cyanide salts). (13)
Carcinogenicity (IARC Classification)1, carcinogenic to humans. (10)
Uses/SourcesCadmium cyanide is used as an electrolyte for electrodeposition of thin metallic cadmium coatings on metal to protect against corrosion. (12)
Minimum Risk LevelAcute Inhalation: 0.00003 mg/m3 (Cadmium) (9) Chronic Inhalation: 0.00001 mg/m3 (Cadmium) (9) Intermediate Oral: 0.0005 mg/kg/day (Cadmium) (9) Chronic Oral: 0.0001 mg/kg/day (Cadmium) (9)
Health EffectsChronic exposure to cadmium fumes can cause chemical pneumonitis, pulmonary edema, and lung diseases such as bronchitis and emphysema. Cadmium also accumulates in the kidneys, causing permanent damage. Loss of bone density also occurs. 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. (4, 7, 8)
SymptomsAcute inhalation of cadmium fumes results in metal fume fever, which is characterized by chills, fever, headache, weakness, dryness of the nose and throat, chest pain, and coughing. Ingestion of cadmium causes vomiting and diarrhea. 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. (4, 7, 8)
TreatmentCadmium poisoning is treated by removal from exposure and supportive care. If ingested, induced vomiting or gastric lavage may be performed. 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. (8, 11)
Concentrations
Not Available
DrugBank IDNot Available
HMDB IDNot Available
FooDB IDNot Available
Phenol Explorer IDNot Available
KNApSAcK IDNot Available
BiGG IDNot Available
BioCyc IDNot Available
METLIN IDNot Available
PDB IDNot Available
Wikipedia LinkCadmium cyanide
Chemspider IDNot Available
ChEBI IDNot Available
PubChem Compound ID101611484
Kegg Compound IDNot Available
YMDB IDNot Available
ECMDB IDNot Available
References
Synthesis ReferenceNot Available
MSDSNot Available
General ReferencesNot Available