Acute toxicity of cyanide

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. 

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

As regards determination of cyanides, environmental studies are almost entirely concerned with the acute toxicity of cyanide. Although cyanide can exist in many chemical forms, hydrogen cyanide is the most toxic. The reaction ... 

Table 3. Example of the Influence of Route on the Acute Toxicity of Potassium Cyanide to the Rabbit (Female)...

Organic cyanide compounds, or nitriles, have been implicated in numerous human fatalities and signs of poisoning — especially acetonitrile, acrylonitrile, acetone cyanohydrin, malonitrile, and succinonitrile. Nitriles hydrolyze to carboxylic acid and ammonia in either basic or acidic solutions. Mice (Mus sp.) given lethal doses of various nitriles had elevated cyanide concentrations in liver and brain the major acute toxicity of nitriles is CN release by liver processes (Willhite and Smith 1981). In general, alkylnitriles release CN much less readily than aryl alkylnitriles, and this may account for their comparatively low toxicity (Davis 1981). 

Smith, L.L., S.J. Broderius, D.M. Oseid, G.L. Kimball, and W.M. Koenst. 1978. Acute toxicity of hydrogen cyanide to freshwater fishes. Arch. Environ. Contam. Toxicol. 7 325-337. 

Willhite, C.C. and R.P. Smith. 1981. The role of cyanide liberation in the acute toxicity of aliphatic nitriles. Toxicol. Appl. Pharmacol. 59 589-602. 

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

The acute toxicity of aliphatic nitriles, which are important industrial compounds, is ascribed mainly to the liberation of cyanide after oxidative de-nitrilation [118 - 120], The reaction involves cytochrome P450 mediated hy-droxylation of C(a) to form an intermediate cyanohydrin, which then breaks down to inorganic cyanide and an aldehyde ... 

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

Ballantyne, B. (1984). Comparative acute toxicity of hydrogen cyanide and its salts. In Proceedings of the Fourth Annual Chemical Defense Bioscience Review (R.E. Lindstrom, ed.), US Army Medical Research Institute of Chemical Defense, Maryland. 

The acute toxicity of HCN and cyanide is a consequence of the affinity of these substances for various heavy metals, such as iron or copper, by forming cyano complexes. The effect on cytochromes, which results in an efficient inhibition of respiration, is most important. In addition, numerous other metabolic processes are affected (for a review, see Solomonson, 1981). The lefhal dose of cyanide for humans is considered to be about 1 mg per kg... 

The influence of structure on the acute toxicity of nitriles can be used in a lecture to illustrate the fundamental structure-hazard link. Many chemists who have participated in an organic chemistry laboratory section will remember the warning that the aroma of burnt almonds may indicate that cyanide has been released. An opportunity exists for the laboratory instructor to explain where and how cyanide evolved and that it is an acutely dangerous chemical.. This example that can be incorporated into the first-day lab overview is to include a discussion of the source and toxicity of nitriles to humans. Nitriles are ubiquitous in a synthetic laboratory and can liberate cyanide under certain circumstance. The structural features that are associated with a greater chance of cyanide being liberated from a nitrile have been studied and reported (14). 

The acute toxicity of butyronitriles is thought to be due to release of cyanide through metabolism of the parent compound. Signs of acute butyronitrile intoxication including dyspnea, ataxia, and convulsions are similar to those noted with acute cyanide intoxication. The onset and duration suggests that these nitriles require metabolism to elicit toxicity. Cyanide and thiocyanate have both been found in urine and... 

The acute toxicity of metallic silver and water-soluble compounds is moderate. The oral LD50 in mice for colloidal silver was 100 mg kg and relatively similar for the water-soluble compounds silver nitrate (50-129 mg kg ) and silver cyanide (LD50 in rats, 125 mg kg ). Silver nitrate appears much less toxic in rabbits by the oral route (800 mg kg ). The insoluble silver oxide was reported to exhibit an LDlo of >2gkg Mn rats. 

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). 

Smith, M. J., and A. G. Heath. 1979. Acute toxicity of copper, zinc and cyanide to freshwater fish effect of different temperatures. Bull. Environ. Contam. Toxicol. 22(1-2) 113-19. 

Yamamoto, K. 1979. On the acute toxicities of the combustion products of various fibers, with special reference to blood cyanide values. NBS Spec. Publ. (U.S.) 540 520-21. 

The acute toxicity of hydrazoic acid through inhalation and other routes of exposure has been found to be high to very high. The symptoms and the intensity of poisoning are similar to sodium azide. It is, however, less toxic than hydrogen cyanide. In humans, inhalation of its vapors can produce irritation of eyes and respiratory tract, bronchitis, headache, dizziness, weakness, and decreased blood pressure (Matheson 1983). Prolonged exposure to high concentrations can result in collapse, convulsion, and death. An exposure to 1100 ppm for 1 hour was lethal to rats. Chronic exposure to a low level of this compound in air may produce hypotension. 

The LD50 value in mice from intravenous administration of tabun has been reported as 0.287 mg/kg (Tripathi and Dewey 1989). Gupta and coworkers (1987) investigated acute toxicity of tabun and its biochemical consequences in the brain of rats. An acute nonlethal dose of 200 pg/kg was injected subcutaneously. Within 0.5-1 hour, the toxicity was maximal it persisted for 6 hours, accompanied by a sharp decline in acetylcholinesterase activity. The prolonged inhibition of this enzyme in muscle and brain may be due to storage aud delayed release of tabun from nonenzymic sites. In addition, cyanide released from a tabun molecule could cause further delay in recovery from its toxic effects. Atropine and its combination with various compounds may offer protection against tabun (see Sections 39.2 and 39.3). 

Cyenogenic Mechanism. The acute toxicity of a third class of simple nonelectrolytes can be readily rationalized in terms of a cyanogenic mechanism, involving metabolic release of cyanide. Free cyanide is highly toxic to fish with a TLm of 0.69 mg/L (93). Some examples of cyanogenic toxicants are shown in Table IV. Lactonitrile is... 

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