Cyanide compounds toxicity

Cyanide compounds are classified as either simple or complex. It is usually necessary to decompose complex cyanides by an acid reflux. The cyanide is then distilled into sodium hydroxide to remove compounds that would interfere in analysis. Extreme care should be taken during the distillation as toxic hydrogen cyanide is generated. The cyanide in the alkaline distillate can then be measured potentiometricaHy with an ion-selective electrode. Alternatively, the cyanide can be determined colorimetricaHy. It is converted to cyanogen chloride by reaction with chloramine-T at pH <8. The CNCl then reacts with a pyridine barbituric acid reagent to form a red-blue dye. 

Cyanides are dangerously toxic materials that can cause instantaneous death. They occur in a number of industrial situations but are commonly associated with plating operations, and sludges and baths from such sources. Cyanide is extremely soluble and many cyanide compounds, when mixed with acid, release deadly hydrogen cyanide gas. Cyanide is sometimes formed during the combustion of various nitrile, cyanohydrin, and methacrylate compounds. Cyanides (CN ) are commonly treated by chlorine oxidation to the less toxic cyanate (CNO ) form, then acid hydrolyzed to COj and N. Obviously, care should be taken that the cyanide oxidation is complete prior to acid hydrolysis of the cyanate. 

A mixture of 1.5 1. of water and 624 g. (6.00 moles) of sodium bisulfite in a 5-1. beaker equipped with a mechanical stirrer is stirred until solution is complete. Benzaldehyde (Note 1) (636 g., 6.00 moles) is added and the mixture is stirred for 20 minutes, during which time a slurry of the benzaldehyde-bisulfite addition product is formed. A 25% aqueous solution of dimethylamine (1100 g.) containing 275 g. (6.13 moles) of the amine is run in, and stirring is continued as most of the addition compound dissolves. The beaker is immersed in an ice bath, and 294 g. (6.00 moles) of sodium cyanide (CautionI Toxic) is added over a period of 20-25 minutes. 

Thiocyanate metabolites resulting from the transulfuration process are about 120 times less toxic than the parent cyanide compound. 

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). 

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. 

Plasma-chemical sample preparation allows breaking-up of cyanide compounds to non-toxic forms, which may be used for purification of technological solutions and galvanic production wastewaters, posing hazard to people s health in the event they are purposely used by terrorists. 

Oral exposure to cyanide usually results from accidental, homicidal, or suicidal ingestion of cyanide salts. Sodium cyanide and potassium cyanide are the most frequently studied cyanide compounds. Copper cyanide, potassium silver cyanide, silver cyanide, and calcium cyanide are other compounds that humans could encounter through oral or dermal exposure. Cassava roots and certain fruit pits contain compounds that can be broken down to form cyanide. Cassava roots form the staple diet of some populations in Africa, Central and South America, and Asia. However, it must be noted that cassava roots are notoriously deficient in protein and other nutrients and contain many other compounds, in addition to cyanide, that could be responsible for some of the observed toxic effects. Thiocyanate is a metabolite of cyanide that is formed in the body after exposure to cyanide compounds. When possible, all oral exposures are expressed as mg CN/kg/day. 

When comparing the available acute lethal toxicity information for cyanide compounds, it was concluded that, for oral exposure, the molar lethal toxicities of hydrogen cyanide, sodium cyanide, and potassium cyanide are similar. Rabbits appeared to be more susceptible to the lethal toxicity of these three compounds than rats (Ballantyne 1988). 

The Toxics Release Inventory (TRI), which contains this information for 1992, became available in May of 1994. This database will be updated yearly and should provide a list of industrial production facilities and emissions. Information in the TRI93 (1995) data base pertains only to U.S. industrial facilities that manufacture or process hydrogen cyanide. There is a need for similar information on releases and off-site transfer from facilities that manufacture or process other cyanide compounds covered in this profile. 

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. 

Westley, J. 1988. Mammalian cyanide detoxification with sulphane sulphur. Pages 201-218 in D. Evered and S. Harnett (eds.). Cyanide Compounds in Biology. Ciba Eound. Sympos. 140. John Wiley, Chichester. Wiemeyer, S.N., E.E. Hill, J.W. Carpenter, and A.J. Krynitsky. 1986. Acute oral toxicity of sodium cyanide in birds. Jour. Wildl. Dis. 22 538-546. 

Caution. Because of the toxicity of metal cyanide compounds, all reactions must be carried out in a well-ventilated fume hood, in particular avoiding exposure to acid. 

Official statements at the time, and to an extent even now, refer to only the less-toxic defoliants. However, Assistant Secretary of Defence, Cyrus Vance, when asked in 1965 whether arsenic and cyanide compounds were being sprayed over South Vietnam, replied, We are making limited use of them in the southern part of Vietnam but not yet in the north. 52 It is hard to escape the conclusion then that aerial spraying of cacodylic acid continued unabated to at least 1971 and caused unknown casualties to human and animal life below. 

U.S. Environmental Protection Agency (U.S. EPA). 2000. Technology transfer network air toxics Web site. Cyanide compounds. Hazard summary, April 1992. Revised in January 2000 (updated 2007). Washington, D.C. U.S. EPA. 

CONSENSUS REPORTS Reported in EPA TSCA Inventory. Cyanide compounds are on the Community Right-To-Know List. SAFETY PROFILE Poison by inhalation. Moderately toxic by ingestion and intraperitoneal routes. Mildly toxic by skin... 

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