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<br />BIOLOGICAL REPORT 85(1.23)
<br />1948, cyanide, in appropriate doses, was used
<br />therapeutically in England for the treatment of
<br />pulmonary diseases and tuberculosis, and as a
<br />sedative. By 1830, cyanogenic glycosides contain-
<br />ing HCN were isolated from cassava; today, more
<br />than 800 species of cyanogenic plants have been
<br />identified. In 1876, it was first demonstrated that
<br />cyanide inhibited tissue oxidation. In 1894, cobalt
<br />compounds were suggested as antidotes due to
<br />their marked cyanide-binding capacity. Studies on
<br />cyanide detoxification conducted between 1877
<br />and 1894 showed that thiosulphate administra-
<br />tion caused the formation of thiocyanate-a rela-
<br />tively harmless metabolite. By the late 1800•x,
<br />cyanide was regarded as a common plant
<br />metabolite rather than as an unusual poison. In
<br />1929, it was conclusively demonstrated that cya-
<br />nide combines with the trivalent iron atom in
<br />cytochrome oxidase, a respiratory enzyme that
<br />]inks the tricarboxylic acid cycle and formation of
<br />metabolic water. Many reviews have been pub-
<br />lished on cyanide in the environment; particularly
<br />useful are those by Doudoroff (1976), Towill et al.
<br />(1978), Smith et al. (1979), Egekeze and Oehme
<br />(1980), EPA (1980, 1989), Vennesland et al.
<br />(1981a), Leduc et al. (1982), Leduc (1984), Way
<br />(1984), Ballantyne and Marrs (1987a), and Evered
<br />and Harnett (1988).
<br />Cyanide hazards to fish, wildlife, and live-
<br />stock are well documented. Massive kills of fresh-
<br />water fish by accidental discharges of cyanide
<br />wastes are fairly common tHolden and Marsden
<br />1964; Leduc 1978; Towill et al. 1978; EPA 1980). In
<br />one case, cyanide-containing mine effluents from a
<br />Canadian tailings pond released into a nearby
<br />creek killed more than 20,000 steelhead (Oncor-
<br />hynchus myhiss; Leduc et al. 1982). Many species
<br />of birds were found dead near burrows oftheblack-
<br />tailed prairie dog (C,}•nom}•s ludouicianusl after
<br />the burrows had been treated with calcium cya-
<br />nide to control prairie dog populations; dead birds
<br />included the burrowing owl (Athenc cunicularia),
<br />the bald eagle (Holiaeetus leucocephalus), and the
<br />golden eagle (Aquila chrysaetos; Wiemeyer et al.
<br />1986). An endangered California condor (Gym-
<br />nogyps californianus) found dead in Bern Count}•,
<br />California, in November 1983 had particles of a
<br />yellow fluorescent tracer in its mouth; these parti-
<br />cles were similar to those mixed with sodium cya-
<br />nide in M-44 spring-loaded ejector mechanism
<br />devices used in a U.S. Fish and Wildlife Service
<br />Animal Damage Control Program in that vicinity,
<br />suggesting that cyanide was a possible cause of
<br />death (lirynitsky et al. 1986). M-44 devices are
<br />known to have caused the death of magpies (Pica
<br />sp.), ravens and crows (Coruus spp.), wild turkeys
<br />(Meleagrfs gallopauo), and various unidentified
<br />species of hawks and vultures (R'iemeyer et al.
<br />19$6). Between 1980 and 1989, 519 mammals-
<br />mostly rodents (35^~) and bats (3440-were found
<br />dead atcyanide-extraction, gold-mine leach ponds
<br />in California, Nevada, and Arizpna; the list in-
<br />cluded coyote (Canis tatrans), foxes, skunks,
<br />badger(Taxidea taxus}, weasels, r$bbits, deer, and
<br />beavers (Clark and Hothem 1991). Also foun d dead
<br />at these same leach ponds were 38 reptiles, 55 am-
<br />phibians, and 6,997 birds (Clark and Hothem
<br />1991), including many species of waterfowl and
<br />songbirds (Allen 1990). The inRugnce of cyanide-
<br />extraction gold-mining operations on wildlife is
<br />currently under investigation by gcientists at the
<br />Patuxent Wildlife Research Centel.
<br />The major threat of cyanide poisoning to live-
<br />stock and terrestrial mammalian wildlife is
<br />through ingestion of plants containing high levels
<br />of cyanogenic glycosides (Towill et al. 1978; Marrs
<br />and Ballazttyne 1987). Plants implicated in cya-
<br />nide poisoning of animals include the sorghums
<br />(Johnson grass, Sorghum hatepenst; Sudan grass,
<br />Sorghum sudanensc), arrowgraSs (Triglochin
<br />spp.), elderberry (Sambucus spp.), wild cherry
<br />(Prunus spp.), and the pits of several common
<br />fruits, such as apple, peach, and apricot; these
<br />plants and fruit pits have the potentlial ofreleasing
<br />c}':•nide upon ingestion (Egekez4 and Oehme
<br />19801. Domestic goats (Capra spp.) died of cyanide
<br />poisoning after eating leaves and fruit of the crab
<br />apple (Malus syluestris•); the crab fipple contains
<br />cyanogenic glycosides in its leaves atr~d fruit (Shaw
<br />1986). Cyanide poisoning ofcattle (loos spp.) by for-
<br />age sorghums and various hybrid cultivars has
<br />been reported in India (Bapat arld Abhyankar
<br />1984 i and elsewhere (Cade and Rubira 1982; Bieh]
<br />1984 ~. Cattle appear to be more vulnerable to cya-
<br />nide poisoning than are sheep (Oafs arics), horses
<br />(Equus caballus), and pigs (Sus spp.; Cade and
<br />Rubira 1982). Equine sorghum cystdtis ataxia is a
<br />condition ubserved in horses grazing on Sorghum
<br />or hybrid Sudan grass pastures; it is characterized
<br />by urinaryincontinence, posterior incoordination,
<br />and degenerative central nervous system lesions
<br />(Egekeze and Oehme 1980). Grazigg cyanogenic
<br />plants can induce sulfur deficiency in sheep, pre-
<br />sumab]}• because sulfur detoxifies the released
<br />cyanide (Towill et al. 1978). The increasing use of
<br />cassava and other cyanogenic plants in animal
<br />feeding portends a greater exposure to dietary cya-
<br />nides (Davis 1981).
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