Toxicity of cyanide

Environmental. The toxicity of cyanide in the aquatic environment or natural waters is a result of free cyanide, ie, as HCN and CN . These forms, rather than complexed forms such as iron cyanides, determine the lethal toxicity to fish. Complexed cyanides may revert to free cyanide under uv radiation, but the rate is too slow to be a significant toxicity factor. Much work has been done to estabhsh stream and effluent limits for cyanide to avoid harmful effects on aquatic life. Fish are extremely sensitive to cyanide, and the many tests indicate that a free cyanide stream concentration of 0.05 mg/L is acceptable (46), but some species are sensitive to even lower concentrations. 

Some disadvantages stem from the same phenomena impeded diffusion reduces the maximum practical rate of plating to well below that possible with aquocation baths. The cyanide ion is not entirely stable both oxidation and reduction products accumulate, including carbonate. Carbonate is also formed in the alkaline cyanide baths (all cyanide baths are alkaline except some based on aurocyanides) by absorption of COj from the air, and it is necessary either to replace or purify baths periodically. Much has been made of the toxicity of cyanides, but the other process solutions used in plating are generally extremely toxic and corrosive or caustic, and it is necessary to treat them all with respect. 

The high toxicity of cyanide-containing substances requires the immediate application of a medical antidote. What simple chemical principles dictate both the toxicity of this species and the efficacy of suitable antidotes ... 

It has been more than a hundred years since MacArthur and Forrest developed a process for the leaching of gold based upon the use of an alkaline cyanide solution.29 Despite the toxicity of cyanide solutions this is still the most widely used process for both Ag and Au, and has been extensively reviewed.30-32... 

The toxicity of cyanide has led to the development of alternative lixiviants for gold and silver see also Sections 9.17.3.2 and 9.17.3.3. Thiosulfate is potentially a cheaper reagent for use in alkaline or near-neutral solutions in the presence of a mild oxidant such as dioxygen,41-48... 

Harnett (eds.). Cyanide Compounds in Biology. Ciba Found. Sympos. 140. John Wiley, Chichester. Knudson, T. 1990. Gold mining s deadly life blood. Sacramento (California) Bee (newspaper), March 21, 1990. Kovacs, T.G. and G. Leduc. 1982a. Sublethal toxicity of cyanide to rainbow trout (Salmo gairdneri) at different temperatures. Canad. Jour Fish. Aquat. Sci. 39 1389-1395. 

Kovacs, T.G. and G. Leduc. 1982b. Acute toxicity of cyanide to rainbow trout acclimated at different temperatures. Canad. Jour Fish. Aquat. Sci. 39 1426-1429. 

McGeachy, S.M. and G. Leduc. 1988. The influence of season and exercise on the lethal toxicity of cyanide of rainbow trout (Salmo gairdneri). Arch. Environ. Contam. Toxicol. 17 313-318. 

Respiratory Effects. Breathing irregularities including Cheyne-Stokes respiration developed in two persons who fell into cisterns containing copper cyanide or potassium cyanide (Dodds and McKnight 1985 Trapp 1970) or whose hands were exposed to hydrogen cyanide (Potter 1950). The effects reflect the central nervous system toxicity of cyanide. 

Food Chain Bioaccumulation. Simple cyanide compounds do not bioconcentrate in fish (ASTER 1994 Callahan et al. 1979 EPA 1985a). It would be useful to determine the bioconcentration potential for cyanide in fish from water dosed with less toxic and water-soluble cyanide complexes. There is no indication of biomagnification of cyanides in aquatic and terrestrial food chains. Because of the high toxicity of cyanides at high doses and rapid metabolism at low doses, biomagnification of cyanide in animals seems unlikely. 

Ballantyne B. 1983b. Acute systemic toxicity of cyanides by topical application to the eye. J Toxicol, Cutan, Ocular Toxicol 2 119-129. 

Blakley RL, Coop IE. 1949. The metabolism and toxicity of cyanides and cyanogenic blycosides in sheep. II. Detoxication of hydorcyanic acid. N.Z.J. Sci. Technol. 31A(3) 1-16. 

Snyder JW, Pastorino JG, Thomas AP, et al. 1993. ATP synthase activity is required for fructose to protect cultured hepatocytes from the toxicity of cyanide. Am J Physiol Cell Physiol 264(3) C709-C714. 

Bellamy, D., and J.A. Petersen (1968). Anaerobiosis and the toxicity of cyanide in turtles. Comp. Biochem. Physiol. 24 543-548. 

Ballantyne, B. 1994. Acute percutaneous systemic toxicity of cyanides. Cutaneous Ocul. Toxicol. 13 (3) 249-262. 

The majority of cyanide-bridged dinuclear complexes described for the combination of metal ions belong to the biologically relevant class of Cu —Fe dimers. These compounds serve as models for the binuclear cyanide-inhibited site of cytochrome c oxidase, an enzyme that contains the heme-copper active site responsible for the O2 reduction chemistry (59). The lethal toxicity of cyanide was traced to its irreversible binding and inhibition of this active site in the enzyme (60). The biologically relevant aspects of these complexes were the subject of many reports (61,62). Our interest is in describing their crystal structure, which will be correlated to the magnetic properties in a later section. 

CONSENSUS REPORTS Reported in EPA TSCA Inventory. EPA Genedc Toxicology Program. Cyanide and its compounds are on the Community Right-To-Know List. SAFETY PROFILE Poison by intraperitoneal route. Moderately toxic by ingesdon. Causes irritadon of the gastrointestinal tract. An herbicide. It is said to be slowly metaboUzed in the body to cyanide but does not have high toxicity of cyanides. When heated to decomposidon it emits very toxic fumes of CN and K2O. 

A similar reaction occurs between aldehydes and ketones and hydrogen cyanide, which, like bisulfite, is a weak acid but a strong nucleophile. The reaction is hazardous to carry out because of the toxicity of cyanide, but the cyanohydrins are useful synthetic intermediates ... 

The toxicity of cyanide in the aquatic environment or natural waters is a result of free cyanide, that is, as HCN and CN. Fish are extremely sensitive to cyanide. Most fish can tolerate a free cyanide stream concentration of 0.05 mg 1 , but some species are even more sensitive. 

VII. ACUTE TOXICITY OF CYANIDES A. Toxicity to Laboratory Mamaials 1. Noninhalation Routes of Exposure... 

Estimates of the acute lethal p.o. toxicity of cyanides are not too precisely defined because of uncertainties in determining the exact amounts ingested and the absorbed dose. The estimated fatal oral dose for HCN is 50-100 mg as total (DuBois and Gelling, 1959) or 0.7-3.5 mg kg (Hallstrom and Moller, 1945) for KCN a total dose of 150-250 mg has been suggested (DuBois and Gelling, 1959). 

---