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<br />medication in Tylenol capsules in drugstores in
<br />various cities in the United States. In fact, cya-
<br />nidesare responsible for more human deaths than
<br />any other chemicals known, owing to their deliber-
<br />ateuse insuicide, murder, chemical warfare, geno-
<br />cide, and judicial execution (Way 1981, 1984;
<br />Ballantyne and Marrs 1987a; Gee 1987; Marrs and
<br />Ballantyne 19B7;Yamamoto 19891. High sublethal
<br />doses of cyanide are rapidly detoxified, and acci-
<br />dentalacute cyanide poisonings in humans are un-
<br />common (Towill et al. 1978).
<br />Cyanide compounds are useful to society in
<br />terms of their key role in synthetic and industrial
<br />processes, for certain fumigation and agricultural
<br />uses, and for some therapeutic applications (Bal-
<br />lan tyneand Marrs 1987a). Cyanides are present in
<br />effluents from iron and steel processing plants, pe-
<br />troleum refineries, and metal-plating plants, and
<br />constitute a hazard to aquatic ecosystems in cer-
<br />tain waste-receiving waters (Smith et al. 1979),
<br />and to livestock (EPA 1980; Towill et al. 1978).
<br />Cyanide serves no useful purpose in the human
<br />body, yet it is present in our food, air, and water
<br />(Becker 1985).
<br />Natural sources of cyanide include various
<br />species of bacteria, algae, fungi, and higher plants
<br />that form and excrete cyanide (Way 1984), The
<br />most widely distributed major food crop with a
<br />high content of cyanogenic glycosides is cassava
<br />(Manihot esculenia), also known as manioc. Cas-
<br />sava is a staple food in human diets in over 80
<br />countries, and it is sometimes added to animal
<br />feeds as a substitute for more expensive cereal
<br />grains (Gomez et al. 1988). In humans, chronic
<br />cyanide intoxication caused by consumption ofcas-
<br />sava is the main etiological Cactor in the debilitat-
<br />ing tropical ataxic neuropathy (Egekeze and
<br />Oehme 1980). Other plants having comparatively
<br />elevated cyanide content include fruit pits, sweet
<br />potatoes (lpomoea batatas), corn (Zee mays), bam-
<br />boo shoots (Bambusa spp.), linseed, iLinum sp.),
<br />lima beans (Phaseolus lunatus), and millet
<br />(Ponicum miliaceum; Way 1984). In higher plants
<br />that contain cyanogenic glycosides, at least 20 of
<br />these compounds have been identified (EPA 1980).
<br />Amygdalin--one of the more intensively studied
<br />cyanogenic glycosides-is found in seeds of the
<br />cherry fPrunus spp.), plum (Prunus spp.l, peach
<br />(Prunus persica), apricot (Prunus armenaical, ap-
<br />ple (iilalus domestical, pear (Pyrus communise,
<br />and many parts of the cherry laurel (Prunus
<br />laurocerasus; EPA 1980). Apricot seeds and peach
<br />kernels are food delicacies in Turkey, and have
<br />caused at ]east nine poisonings (two fatal) in chil-
<br />dren Crom that. country (Gee 1987). Acute cyanide
<br />poisoning has occurred in the United States from
<br />the ingestion of almond-flavored milkshakes pre-
<br />pared from apricot kernels (Way 19$4 ). Amygdalin
<br />is also the chiefingredient in laetrile, a medication
<br />prescribed by some physicians to control tumors.
<br />Both laetrile and amygdalin-cpntaining fruit pits
<br />have been implicated as the cpuses of acute cya-
<br />nide poisoning in humans (EpA 1980). Another
<br />naturally occurring group of organic cyanides
<br />(nitrites) is the highly toxic pseudocyanogenic
<br />glycosides, especially cycasin, apd these have been
<br />implicated in a variety of tropical diseases of the
<br />nervous system, and partial pr total blindness
<br />(EPA 1980). Other nitrites found in plants include
<br />the ]athyrogenic compounds, glucosinolates, and
<br />the cyanopyridine alkaloids (EPA 1980).
<br />That certain plants, such ~s bitter almonds
<br />(Prunus dulcls), cherry laurel le8ves, and cassava,
<br />are poisonous if consumed in su1<iicient quantities
<br />has been known for at least 2,000 years. But it was
<br />not until the 1700's that cyanide was recognized as
<br />the basis for their lethal toxicity. The first account
<br />otan experimental administration of extract of bit-
<br />ter almonds and other poisons to dogs (Canis
<br />jamitiarls) dates from 1679, as reviewed by Sykes
<br />(1981) and Ballantyne (1987a). In 1731, two fatal
<br />cases of human poisoning in Ireland were caused
<br />by drinking cherry laurel water, in this instance
<br />used as a flavoring agent in cooking and to dilute
<br />brand}'. In that same year it was shown that cherry
<br />laurel water administered to dpgs by various
<br />routes proved rapidly fatal. By 1781, it was well es-
<br />tablished that mammals, birds, reptiles, amphibi-
<br />ans, fish, and insects could all be killed with small
<br />doses of laurel water, and that death was more
<br />rapid than that produced by other poisons tested.
<br />It was also at this time that cyanide was first impli-
<br />cated as a homicidal agent in England. In 1782,
<br />hydrocyanic acid was isolated from Prussian blue
<br />la dye) by the Swedish chemist Scheele. In 1786,
<br />Scheele accidentally broke a via] of the material
<br />and died from vapor poisoning. In 17$7, it was de-
<br />termined that hydrocyanic acid contained hydro-
<br />gen, carbon, and nitrogen, but did not contain
<br />oxygen, formerly believed to be an essential compo-
<br />nent of all acids. Between 1802 and 1815,
<br />hydrocyanic acid was found to be lethal in small
<br />quantities to birds and dogs, and to act rapidly
<br />when given orall}~, intravenously, or $pplied to the
<br />eye surface. By 1803, it was known that cyanide oc-
<br />curred naturally and could be extracted from apri-
<br />cots or almonds. In 1815, hydrocyanic acid was
<br />prepared in a semipure form. Between 1817 and
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