Hydrogen cyanide

CAS RN: 74-90-8

Toxicity Summary

IDENTIFICATION AND USE: Hydrogen cyanide is a colorless or pale blue liquid or gas with a faint bitter almond like odor. Hydrogen cyanide is used primarily in the production of substances such as adiponitrile, methyl methacrylate, chelating agents, cyanuric chloride, methionine and its hydroxylated analogues, and sodium and potassium cyanide. Hydrogen cyanide is also used as a fumigant in ships, railroad cars, large buildings, grain silos, and flour mills, as well as in the fumigation of peas and seeds in vacuum chambers. Hydrogen cyanide is formed during the incomplete combustion of nitrogen-containing polymers, such as certain plastics, polyurethanes, and wool. Hydrogen cyanide is also present in cigarette smoke. HUMAN STUDIES: The primary targets of cyanide toxicity in humans are the cardiovascular, respiratory, and central nervous systems. The endocrine system is also a potential target for long term toxicity, as a function of continued exposure to thiocyanate, which prevents the uptake of iodine in the thyroid and acts as a goitrogenic agent. Sequelae after severe acute intoxications may include neuropsychiatric manifestations and Parkinson type disease. Cyanide from tobacco smoke has been implicated as a contributing factor in tobacco alcohol amblyopia. Long term exposure to lower concentrations of cyanide in occupational settings can result in a variety of symptoms related to central nervous system effects. Cyanides are weakly irritating to the skin and eye. ANIMAL STUDIES: The principal features of the toxicity profile for cyanide are its high acute toxicity by all routes of administration, with a very steep and rate-dependent dose effect curve, and chronic toxicity, probably mediated through the main metabolite and detoxification product, thiocyanate. The toxic effects of cyanide ion in humans and animals are generally similar and are believed to result from inactivation of cytochrome oxidase and inhibition of cellular respiration and consequent histotoxic anoxia. The primary targets of cyanide toxicity in animals are the cardiovascular, respiratory, and central nervous systems. The endocrine system is also a potential target for long-term toxicity, as a function of continued exposure to thiocyanate, which prevents the uptake of iodine in the thyroid and acts as a goitrogenic agent. In a 13 week repeated-dose toxicity study in which cyanide was administered in drinking-water, there were no clinical signs associated with central nervous system effects or histopathological effects in the brain or thyroid of rats or mice. There were slight changes in the reproductive tract in male rats. The examination of neurotoxicity in this study was limited to clinical observation and optical microscopy in autopsy. The few available studies specifically intended to investigate neurotoxicity, while reporting adverse effects at exposure levels of 1.2 mg cyanide/kg body weight per day in rats and 0.48 mg cyanide/kg body weight per day in goats, suffer from weaknesses that preclude their quantitative assessment. In relation to characterization of concentration-response for repeated-dose toxicity for inhalation (relevant principally to the occupational environment), in three separate studies in rats, there were no adverse systemic effects in rats exposed to acetone cyanohydrin, which is rapidly hydrolyzed to hydrogen cyanide at physiological pH, at concentrations up to 211 mg/cu m (corresponding to a concentration of 67 mg hydrogen cyanide/cu m). The steepness of the dose effect curve is illustrated by the observation of 30% mortality among rats exposed part of the day to 225 mg acetone cyanohydrin/cu m (71 mg hydrogen cyanide/cu m). ECOTOXICITY STUDIES: Adverse effects of exposure to the low concentrations of cyanide that are generally present in the general environment (<1 ug/cu m in ambient air; <10 ug/L in water) are unlikely.
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