Sodium cyanide is a compound with the formula NaCN and the structure Na+ −C≡N. It is a white, water-soluble solid. Cyanide has a high affinity for metals, which leads to the high toxicity of this salt. Its main application, in gold mining, also exploits its high reactivity toward metals. It is a moderately strong base.
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ECHA InfoCard | 100.005.091 |
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UNII |
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UN number | 1689 |
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Properties | |
NaCN | |
Molar mass | 49.0072 g/mol |
Appearance | white solid |
Odor | faint bitter almond-like |
Density | 1.5955 g/cm3 |
Melting point | 563.7 °C (1,046.7 °F; 836.9 K) |
Boiling point | 1,496 °C (2,725 °F; 1,769 K) |
48.15 g/100 mL (10 °C) 63.7 g/100 mL (25 °C) | |
Solubility | soluble in ammonia, methanol, ethanol very slightly soluble in dimethylformamide, SO2 insoluble in dimethyl sulfoxide |
Refractive index (nD)
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1.452 |
Thermochemistry[1] | |
Heat capacity (C)
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70.4 J·mol−1·K−1 |
Std molar
entropy (S⦵298) |
115.6 J·mol−1·K−1 |
Std enthalpy of
formation (ΔfH⦵298) |
−87.5 kJ·mol−1 |
Gibbs free energy (ΔfG⦵)
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−76.4 kJ·mol−1 |
Enthalpy of fusion (ΔfH⦵fus)
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8.79 kJ·mol−1 |
Hazards | |
GHS labelling: | |
NFPA 704 (fire diamond) | |
Flash point | Non-flammable |
Lethal dose or concentration (LD, LC): | |
LD50 (median dose)
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6.44 mg/kg (rat, oral) 4 mg/kg (sheep, oral) 15 mg/kg (mammal, oral) 8 mg/kg (rat, oral)[3] |
NIOSH (US health exposure limits): | |
PEL (Permissible)
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TWA 5 mg/m3[2] |
REL (Recommended)
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C 5 mg/m3 (4.7 ppm) [10-minute][2] |
IDLH (Immediate danger)
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25 mg/m3 (as CN)[2] |
Safety data sheet (SDS) | ICSC 1118 |
Related compounds | |
Other cations
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Potassium cyanide |
Related compounds
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Hydrogen cyanide |
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
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Infobox references
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Sodium cyanide is produced by treating hydrogen cyanide with sodium hydroxide:[4]
Worldwide production was estimated at 500,000 tons in the year 2006. Formerly it was prepared by the Castner process involving the reaction of sodium amide with carbon at elevated temperatures.
The structure of solid NaCN is related to that of sodium chloride.[5] The anions and cations are each six-coordinate. Potassium cyanide (KCN) adopts a similar structure. [6]
When treated with acid, it forms the toxic gas hydrogen cyanide:
Because the salt is derived from a weak acid, sodium cyanide readily reverts to HCN by hydrolysis; the moist solid emits small amounts of hydrogen cyanide, which is thought to smell like bitter almonds (not everyone can smell it—the ability thereof is due to a genetic trait[7]). Sodium cyanide reacts rapidly with strong acids to release hydrogen cyanide. This dangerous process represents a significant risk associated with cyanide salts. It is detoxified most efficiently with hydrogen peroxide (H2O2) to produce sodium cyanate (NaOCN) and water:[4]
Gold cyanidation (also known as the cyanide process) is the dominant technique for extracting gold, much of which is obtained from low-grade ore. More than 70% of cyanide consumption globally is used for this purpose. The application exploits the high affinity of gold(I) for cyanide, which induces gold metal to oxidize and dissolve in the presence of air (oxygen) and water, producing the salt sodium dicyanoaurate (or sodium gold cyanide) (NaAu(CN)2):[4]
A similar process uses potassium cyanide (KCN, a close relative of sodium cyanide) to produce potassium dicyanoaurate (KAu(CN)2).
Several commercially significant chemical compounds are derived from cyanide, including cyanuric chloride, cyanogen chloride, and many nitriles. In organic synthesis, cyanide, which is classified as a strong nucleophile, is used to prepare nitriles, which occur widely in many chemicals, including pharmaceuticals. Illustrative is the synthesis of benzyl cyanide by the reaction of benzyl chloride and sodium cyanide.[8]
Being highly toxic, sodium cyanide is used to kill or stun rapidly such as in collecting jars used by entomologists and in widely illegal cyanide fishing.
Sodium cyanide, like other soluble cyanide salts, is among the most rapidly acting of all known poisons. NaCN is a potent inhibitor of respiration, acting on mitochondrial cytochrome oxidase and hence blocking electron transport. This results in decreased oxidative metabolism and oxygen utilization. Lactic acidosis then occurs as a consequence of anaerobic metabolism. An oral dosage as small as 200–300 mg can be fatal.
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