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Related to hydrocyanic acid: prussic acid
hydrocyanic acid(hī'drōsīăn`ĭk): see hydrogen cyanidehydrogen cyanide,
HCN, colorless, volatile, and extremely poisonous chemical compound whose vapors have a bitter almond odor. It melts at −14°C; and boils at 26°C;. It is miscible in all proportions with water or ethanol and is soluble in ether.
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(also hydrogen cyanide, prussic acid, formonitrile), HCN, a colorless, mobile liquid with an odor of bitter almonds. Hydrocyanic acid was discovered in 1782 by K. W. Scheele. In 1811, J. Gay-Lussac obtained anhydrous hydrocyanic acid and determined its quantitative composition.
Hydrocyanic acid has a density of 0.688 g/cm3 at 20°C, a boiling point of 25.7°C, and a freezing point of – 14°C. It burns in air to yield H2O, CO2, and N2; a mixture of hydrocyanic acid vapors and air explodes when ignited. Hydrocyanic acid, a very weak acid, decomposes upon storage, especially in the presence of impurities. Its salts are called cyanides, and its organic derivatives, nitriles. Hydrocyanic acid is formed upon hydrolysis of amygdalin, present in bitter almonds and apricots. An aqueous hydrocyanic acid solution can be obtained by the distillation of potassium ferrocyanide, K4[Fe(CN)6], with dilute sulfuric acid, H2SO4. The commercial method of hydrocyanic acid preparation is based on the interaction of a mixture of ammonia, methane, and air in the presence of a catalyst (Pt or an alloy of Pt and Rh):
2NH3 + 2CH4 + 3O2 = 2HCN + 6H2O
Hydrocyanic acid is highly toxic. It is used in railroad cars, granaries, and ships for disinsectization and deratization. Hydrocyanic acid serves as source material in the synthesis of certain high-molecular compounds.
S. A. POGODIN
Poisoning with hydrocyanic acid and its compounds can occur during the processing of ore (cyanidation) and the galvanization of metals, as well as during disinsectization and deratization. Entering the body through the respiratory passages or, more rarely, through the skin, hydrocyanic acid blocks the respiratory enzyme cytochrome oxidase and induces oxygen starvation in tissue. Symptoms of acute poisoning include irritation of the mucous membranes, asthenia, vertigo, nausea, and vomiting. These symptoms are followed by such respiratory disorders as infrequent, deep breathing, painful dyspnea, and, finally, slow breathing and respiratory arrest. Chronic poisoning is accompanied by headache, fatigue, and low arterial pressure. Changes are observed in electrocardiograms, and the blood is seen to-have a reduced sugar level and an increased content of, among other things, hemoglobin and lactic acid. The effect of potassium and sodium cyanides on the skin can be seen in cracking and eczema.
First aid treatment for acute poisoning involves, after conveying the victim into fresh air, the administration of amyl nitrite, carbogene, and oxygen vapors, the use of lobeline, cytiton, and cardiovascular agents, and the parenteral injection of solutions of sodium nitrite and sodium thiosulfate.
Preventive measures include the observation of safety rules, the use of protective garments for the skin, and periodic medical examinations.
REFERENCENavrotskii, V. K. Gigiena truda, 2nd ed. Moscow, 1974.
A. A. KASPAROV