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1 1 1 1 46 BIOIAGICnL REPORT 85(1.23) brat oxidative responses to cyanide may be due to redistribution of intracellular oxygen supply to mi- tochondria respiring in an oxygen-dependent manner or by branching effects within brain mito- chondria (Lee et al. 1988). Hyperammonemia and the increase of neutral and arom;itic amino acids may also be important in lass of consciousness in- duced by cyanide (Yamamoto 1989). Organic cyanide compounds, or nitrites, have been implicated in numerous human fatalities and signs ofpoisoning-especially acetonitrile, acrylo- nitri]e,acetone cyanohydrin, malonitrile, and suc- cinonitrile. Nitrites hydrolyze to carboxylic acid and ammonia in either basic or acidic solutions. Mice (Mus sp.) gi yen lethal doses of various nitrites had elevated cyanide concentrations in liver and brain; the major acute toxicity of nitrites is CN re- lease byliver processes (Willhite and Smith 1981). In general, alkylnitriles release CN much less readily than aryl alkylinitriles, and this may ac- count for their comparatively low toxicity (Davis 1981). No human cases of illness or death due to cya- nide in water supplies are known (EPA 1980). Ac- cidental acute cyanide poisonings in humans are uncommon (Towill et al. 1975); however, a man ac- cidentally splashed with molten sodium cyanide died about 10 h later (Curry 1963). Human cyanide deaths usu~]ly involve suicides, where relatively large amounts ofsodium cyanide or potassium cya- nideare ingested and the victims die rapidly in ob- viouscircumstances. Recovery after oral ingestion is rare. In one case, a spouse emptied capsules con- taining medicine and repacked them with 40°rc solid NaC'A'. The victim took one capsule and in- gested about 0.05 g, but vomited and recovered completely (Curry 1963). Human deaths are in- creasing Irom gas or smoke inhalation from urban fires, possibly owingto the increased toxicity offire atmospheres caused b}• the use of organoc}•anide plastics in modern construction and furnishings (Egekeze and Oehme 1980). Hydrogen cyanide may be important in some fires in producing rapid incapacitation, causing the victims to remain in the fire and die from carbon monoxide or other fac- tors, although HCN concentrations of 60 mg/L air and lower had minima] effects (Purser 1984). Ex- posure to the mixture of HCIQ and carbon monox- ide, with accompanying changes in cerebral blood flow during attempts to escape from fires, maybe a cause of collapse and subsequent death (Purser 1984). Fur example, cynomolgus monkeys (Macaca spp.) exposed to pyrolysis products of poly- acrylonitrile (PAN) and to ]ow-]eve] HCN gas had similar physiological effects in both atmospheres, specifically: hyperventilation, followed by loss of consciousness after 1-5 min; and brachycardia, with arrhvthmias and T-wave abnotmalities. Re- covery was rapid following cessation of exposure (Purser et al. 1984). Because HCN is the major toxic product formed by the pyrolysis of ]'AN, Purser et al. (19841 suggested that IfCN may pro- ducerapid incapacitation at low blood levels ofcya- nide in fires, while death may occut later due to carbon monoxide poisoning or other factors. Finally, cyanide does not appear to be muta- genic, teratogenic, or carcinogenic in mammals (EPA 1980; Ballantyne 1987a). In f8ct, there has been along-standing hypothesis for an anticancer effect of the cyanogenic glycoside anhygdalin (also called laetrile). The hypothesis is based on amyg- dalin's selective hydrolysis by a betA glucosidase, liberating cyanide and benzaldehyde at the neo- plastic site. The cyanide then selectively attacks the cancer cell, which is presumed' to be ]ow in rhodanese, whereas normal cells at'e assumed to possess sutiicient rhodanese and sulfur to detoxify the cyanide (Way 1981). However, many tumors are neither selectively enriched in beta glucosidase nor low in rhodanese (Way 1981). Recommendations Proposed free cyanide criteria suggest that sensitive species of aquatic organisms are pro- tected at <3 µg/L, birds and livestock at <100 mg/ kg diet, and human health at conoentrations of <10 µg/L drinking water, <50 mgl'kg diet, and <5 mg/m3 air (Table 6). Analytical methodologies need to be devel- opedthat difl'erentiate between free cyanide (HCN and CN-) and other forms of cyanide, and that are simple, sensitive (i.e., in the µg2 range), and accu- rate (Smith et al. 1979; Leduc et al. 1982). Proce- dures need to be standardized that etrtsure prompt refrigeration and analysis of al] samples for cya- nide determination because some sflored samples generate cyanide while others show decreases (Gee 1987). Periodic monitoring of cyanide in waterways is unsatisfactory for assessing potential hazards because of cyanide's rapid action, high toxicity, and ]oH• environmental persistence. A similar case is made for cyanide in the atmosphere. Develop- ment of a continuous monitoring system of cya- nides in waterv.•ays and air is recommended, with 1