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<br />Cyanide hazards to Fish, Wildlife, and Invertebrates:
<br />A Synoptic Review
<br />by
<br />Ronald Eisler
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<br />U.S. Fish and Wildlijc Scruice
<br />Patuxent Wiidlije Research Center
<br />Laurel, Maryland 20708
<br />Abstract. Cyanides are used widely and extensively in the manufacture ofsyntht•tic
<br />fabrics and plastics, in electroplating baths and metal mining operations, as pesticidal
<br />agents and intermediates in agricultural chemical production, and in predator con•,rol
<br />devices. Elevated cyanide levels are normally encountered in more than 1,000 spedies
<br />of food plants and forage crops, and this probably represents the greatest source of cya-
<br />nide exposure and toxicosis to man and to range animals. Anthropogenic sources of
<br />cyanide in the environment include certain industrial processes, laboratories, fumi~s-
<br />tion operations, cyanogenic drugs, fires, cigarette smoking, and chemical warfare. Al-
<br />though cyanide is ubiquitous in the environment, levels tend to be elevated in qhe
<br />vicinity of metal processing operations, electroplaters,gold-mining tacit ities, oil re11n-
<br />eries, power plants, and solid waste combustion.
<br />Many chemical forms of cyanide are present in the environment, including flee
<br />cyanide, metallocyanide complexes, and synthetic organocyanides, also known as
<br />nitrites. But only free cyanide (i.e., the sum of molecular hydrogen cyanide, HCN, ahd
<br />the cyanide anion, CN-) is the primary toxic agent, regardless of origin.
<br />Cyanides are readily absorbed through inhalation, ingestion, or skin contact and
<br />are readily distributed throughout the body via blood. Cyanide is a potent and raptld-
<br />acting asphyxiant; it induces tissue anoxia through inactivation of cytochrort~e
<br />oxidase, causing cytotoxic hypoxia in the presence of normal hemog]obi n oxygenation.
<br />Diagnosis of acute lethal cyanide poisoning is difficult because signs and symptoms ate
<br />nonspecific, and numerous factors modify its biocidal properties, such as dietary defi-
<br />ciencies in vitamin Bps, iodine, and sulfur amino acids. Among the more consistent
<br />changes measured in acute cyanide poisoning are inhibition of brain cytochronle
<br />oxidase activity, and changes in electrical activity in heart and brain. At sublethal
<br />doses, cyanide reacts with thiosulfate in the presence of rhodanese to produce the com-
<br />parative]ynontoxic thiocyanate,most ofwhich is excreted in the urine. Rapid detoxifi-
<br />cation enables animals to ingest high sublethal doses of cyanide over extended periods
<br />without harm. Antidotes in current use to counteract cyani de poisoning include a com-
<br />bination of sodium nitrite and sodium thiosulphate (United States), cobalt edetaue
<br />(United Kingdom, Scandinavia, France), or a mixture of 4-dimethylaminophenol and
<br />sodium thiosulphate (Germany).
<br />All available evidence suggests that cyanides ere neither mutagenic, teratogenia,
<br />nor carcinogenic. Moreover, there are no reports of cyanide biomagnification or cycling
<br />in living organisms, probably owing to its rapid detoxification. Cyanide seldom perv
<br />sists in surface waters and soils owing to complexation or sedimentation, microbia9
<br />metabolism, and loss from volatilization. More data are needed on cyani de distribution
<br />and transformation in the atmosphere.
<br />Analytical methods for the determination of tree and bound cyanides and
<br />cyanogenic compounds in biological materials are under constant revision. Further,
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