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1 <br /> <br /> <br /> <br /> <br /> <br /> <br />1 <br /> <br /> <br /> <br /> <br /> <br /> <br /> <br /> <br /> <br /> <br /> <br />BIOLOGICAL REPORT 85(1.23) <br />unless tissue samples are obtained promptly after cyanide exposure and analyzed im- <br />mediately, erroneous analytical values will result. <br />Higher plants are adversely alrected by cyanide through cytochrome oxidase inhi- <br />bition; the rate of production and release of cyanide by plants to the environment <br />through death and decomposition is unknown. Nonacclimatized soil bacteria ere ad- <br />versely affected at 0.3 mg HCN/kg; acclimatized populations, however, can degrade <br />wastes containing up to 60 mg total cyanide per kilogram. In some cases, soil bacteria <br />and fungi produce cyanides as secondary metabolites, with adverse effects on certain <br />plants. Several species of arthropods normally contain elevated whole-body cyanide <br />concentrations, and these confer protection against predators and allow conaumptibn <br />of cyanogenic plants. <br />Fish were the most sensitive aquatic organisms tested. Adverse effects on awi>h- <br />mingand reproduction were observed between 5 and 7.2 µg free cyanide per liter; Ye- <br />thal effects usually occurred between 20 and 76 µg/L. Biocide) properties of cyanide in <br />aquatic environments were significantly modified by water pH, temperature, and oz~- <br />gen content; life stage, condition, and species assayed; previous exposure to cyanides; <br />presence of other chemicals; and initial dose tested. <br />Birds that feed predominantly on flesh were more sensitive to cyanide than wets <br />herbivores. Free cyanide levels associated with high avian death rates include 0.12 <br />mg/L in air, 2.1--4.6 mg/kg body weight (BW) via acute oral exposure, end 1.3 mg/Ifg <br />BW administered intravenously. Dietary levels of 135 mg total cyanide per kilogram <br />ration resulted in growth reduction of chicks, but 103 mg total cyanide per kilogram <br />ration had no measurable eRect an domestic chickens. <br />cyanogenic plants represent a problem for various range animals and wildlife, <br />primarily among species that eat rapidly. Intakes of 4 mg HCN/kg BW are lethal W <br />these species if it is consumed quickly. Cassava (Manihol escalenla) is a cyanogenic <br />plant that accounts for up to 70'R, of human calnric intake in some areas, and this is <br />associated with serious, long-term toxic effects including ataxia, optic nerve lesion, <br />altered thyroid function, demyelination, and increases in tissue thiocyanate 3eve1$. <br />Acute oral LD50 values for representative species of mammals ranged between 2 and <br />3.6 mg HCN/kg BW. Despite the high lethality of large single exposures, repeated sub- <br />lethal doses--especially in diets-can be tolerated by many species for extended peri- <br />ods,perhaps indefinitely. Mammalian deaths were also recorded at air concentrations <br />of 140 mg HCN/m3 (exposure for 60 min) and 9,400 mg HCN/m3 (exposure for 1 mint, <br />and at dermal applications between 2.3 mg HCN/kg BW for abraded skin and 100 mg <br />HCN/kg BW for intact skin. Adverse nonlethal e(fects were noted at drinking watet <br />concentrations >150 mg HCN/L and at dietary concentrations >720 mg HCN/kg ram <br />lion. <br />Free cyanide criteria currently proposed for natural resource protection includd <br />c3 µg1L medium for aquatic life, and <100 mg/kg diet for birds and livestock. For hu. <br />man health protection, free cyanide values aze <10 µg/L drinking water, <50 mg/kg <br />diet, and <5 mg/m3 air. <br />Key words: Cyanide, toxic effects, wildlife, cyanogenic plants, aquatic organisms, <br />criteria. <br />The origin of terrestrial life probably de- <br />~ended on the presence and reactivity of hydro- <br />gen cyanide and its derivatives; paradoxically, hy- <br />drogen cyanide is toxic to the majority of living <br />matter (Marrs and Ballantyne 1987). Cyanide is a <br />general respiratory poison-although uptake can <br />also occur through ingestion or derma] absorp- <br />tion-producing reactions within seconds, and <br />death within minutes (Towil] et al. 1978; Environ- <br />mental Protection Agency [EPA] 1980). The toxic <br />mechanism of cyanide primarily involves the inhi- <br />bition of cvt.ochrome oxidase, the terminal oxida- <br />tive enzyme of the mitochondria) electron <br />transport chain, producing blockage of aerobic <br />ATP synthesis (Egekeze and Oehme 1979; Younes <br />and Strubelt 1988). Because of their highly effec- <br />tive lethal potency, cyanides were uged for geno- <br />cidal programs in Germany in Worid V~'ar I1, in <br />mass suicides by members of the People's Temple <br />religious sect in Guyana, and in the substitution of <br /> <br />