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' 32 B101AGICAL REPDRT 85(1.23) I~ u LJ Table 4. Continued. Species, dose, and other variables Effects R.eference• European starling, Sfurnus uulgaris 9.0 mg CN/kg BW, as NaCN Andeen condor, Vulturgryl~~.us Single oral dose of 19.1 mg CN/kg BW (36 mg NaCN/kg BW) Acute oral LD50; 95 n C.I. of 4.8 and 17 mg CN/kg BW Blood sampled immediately aRer death contained 1.2 mg free CN per liter and 0.5 mg bound CN per liter ' • 1. Krynitsky et al. 1986; 2. Wiemeyer et al. 1986; 3. Oh et el. 1987; 4. Davis 1981; 5. Comez et el. 1988: 6. Elaubier and Davis 1988b; 7. Personal communication, E. F. Hill, Patuxent Wildlife Research Center. 1 1 1 Many species of migratory birds were found dead in the immediate vicinity of gold-mine heap- leach extraction facilities and tailings ponds, pre- sumably as a result of drinking the cyanide- contaminated (>200 mg iota] cyanide per liter) wa- ters (Clark and Hothem 1991). Migratory bird mortality from cyanide toxicosis may be elimi- nated at these facilities by screening birds from toxic solutions (Hallock 1990) or lowering the cya- nideconcentrations with hydrogen peroxide to <50 mg total cyanide per liter (Allen 1990), although the latter procedure requires verification (Clark and Hothem 1991). Some birds may not die immediately after drinking lethal cyanide solutions. In Arizona, a red-breasted merganser (Mergus serraior) was found dead 20 km from the nearest known source of cyanide, and its pectoral muscle tissue tested positive for cyanide (Clark and Hothem 1991). A proposed mechanism to account for this phenome- non involves weak-acid dissociable (WAD) cyanide compounds. Cyanide bound to certain metals, usu- ally copper, is dissociable in weak acids such as stomach acids. Clark and Hothem (1991) sug- gested that drinking of lethal cyanide solutions by animals may not result in immediate death if the cyanide level is sufficiently ]ow; these animals may die later when additional cyanide is liberated by stomach acid. More research is needed on WAD cyanide compounds. Elevated cyanide concentrations were found in blood of chickens thatdied ofcyanide poisoning; however, these concentrations overlapped those in survivors. Despite this variability, blood is consid- eredmore reliable than liver as an indicator of cya- nide residues in exposed birds (Wiemeyer et al. 1986). No gross pathological changes in birds re- lated to cyanide dosing were observed at necropsy (Wiemeyer et al. 1986), similar to other taxonomic groups tested. Cyanide-nutrient interactions Ure reported for alanine, which appears to exacerbate cyanide toxicity, and for cystine, which seems to alleviate toxicity (Davis et al. 1988). Dietary cyanide-at levels that do not cause growth depression-allevi- ates selenium toxicity in chickens, bUt not the re- verse (Davis et al. 1988; Elzubier and Davis 1988a). For example, dietary seleniurry, as selenite, at 10 mg/kg for 24 days, reduced growth, food in- take, and food utilization efficiency, end produced increased liver size and elevated selenium resi- dues; the addition of 45 mg CN/l:g diet (100 mg so- dium nitroprusside per kilogram) eliminated all effects except elevated selenium residues in liver. The mechanism ofalleviation is unknown and may involve a reduction of tissue selenium through selenocyanate formation, or increased elimination of excess selenium by increasing the amount of dimethvl selenide exhaled (Elzubier and Davis 1988a ). At dietary levels oC 135 mg CN/kg plus 10 mg selenium per kilogram, chick growth was sig- nificantly decreased (Elzubier and IDavis 1988a). This interaction can be lost if there is a deficiency of certain micronutrients or an excess of vitamin K (Davis et al. 1988). Mammals Much of the toxicological interest in cyanide relating to mammals has focused on its rapid le- thal action; however, its most widely distributed toxicologic problems are due to its toxicity from