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Veterinary Quarterly

ISSN: 0165-2176 (Print) 1875-5941 (Online) Journal homepage: http://www.tandfonline.com/loi/tveq20

Cyanides and their toxicity: A literature review

John O. Egekeze & Frederick W. Oehme
To cite this article: John O. Egekeze & Frederick W. Oehme (1980) Cyanides and their toxicity: A
literature review, Veterinary Quarterly, 2:2, 104-114, DOI: 10.1080/01652176.1980.9693766
To link to this article: http://dx.doi.org/10.1080/01652176.1980.9693766

Published online: 01 Nov 2011.

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Cyanides and their toxicity: A literature review

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John 0. Egekeze and Frederick W. Oehme'


Cyanide is a potent and rapidly-acting asphyxiant which prevents tissue utilization

of oxygen by inhibition of the cellular respiratory enzyme, cytochrome oxidase.
Inhalation or ingestion of cyanide produces reactions within a few seconds and
death within minutes. Cyanide toxicity of dietary origin has been implicated in
acute animal deaths and as major etiologic factors in toxic ataxic neuropathy in
man and as a cause of vision failure in humans suffering from tobacco amblyopia
and leber's hereditary optic atrophy. Diagnosis of cyanide toxicity may be
confirmed by a variety of laboratory procedures, but accurate assay is essential
for proper conclusions from analysis of animal tissues several hours after death
or from human samples in instances of chronic dietary exposure. Biological
detoxification of cyanide is available through several routes, and the application
of sodium nitrite with sodium thiosulfate or administration of methylene blue
are effective treatment procedure. The environmental availability of cyanide in its
various forms necessitates an understanding of its pathophysiology and responsible management of hazardous situations.


Cyanide is present in many industrial and

municipal waste waters. The most important source of this cyanide pollution is the
effluents of electroplating processes,
metal finishing, metallurgy, steel processing, and petroleum industries. Hydrocya-

nic acid (HCN) and its alkali salts like

sodium cyanide and potassium cyanide
are found in vermicidal fumigants, insectides, rodenticides, metal polishes (espeI

cially silver polish), electroplating solutions and photographic processes.

Hydrogen cyanide is also generated by
action of mineral acids on cyanide salts
for use as a fumigant. Several reported
deaths following the use of sodium nitro-

prusside for the elective induction of

hypotension during general ansthesia
have been attributed to the accumulation
of cyanide in the blood (1, 2, 3).

Address all correspondence to: Frederick W. Oehme, Comparative Toxicology Laboratories, College of
Veterinary medicine, Kansas State University, Manhattan, Kansas 66506 (USA).



Cyanides are widely distributed among

common plants in form of cyanogenetic
glycosides. These glycosides hydrolyze to
form hydrogen cyanide (HCN). Of chief

agricultural importance among plants

which accumulate large quantities of
cyanogenetic glycosides are the sorghums, sudan grass, and corn (4). Plants
such as flax, lima beans, cherry, apple,
peach and apricot have characteristic

sorption of cyanide across the human

ing, or stunting of the plant, free HCN

epidermis was recently reported by Dugard and Mawdsley (8). The measurements were made to assess the hazard
resulting from clothing wetted by liquor
during NaCN manufacture. Absorption
rates showed a strong pH dependence
(pH 9.0-12.0), and the permeability constant for HCN (pka = 9.2) was calculated

may be released as a result of plant cellu-

to be 25 times greater than that of the

lar activity is located in leaves and/ or

cyanide ion (CN-).

high HCN potential. Upon wilting, frost-

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readily absorbed after oral or parenteral

administration (7).
Diffusion cell measurements of the ab-

seeds of plants, and the potential for high

glycoside levels is greatest in immature
and rapidly growing plants (4).

The most common forms of cyanide are

free cyanide (HCN CN -), metallocyanide complexes, and organonitriles (both
synthetic and naturally occuring). Hydrogen cyanide (HCN) is a gas with an

odor like that of bitter almonds. It is

formed when a cyanide salt is treated
with an acid.
The liquid boils at 25.7 C and freezes at

13.2 C (5). Soluble salts such as sodium cyanide and potassium cyanide
form solutions by hydrolysis which are
alkaline. When hydrogen cyanide is dissolved in water, hydrocyanic acid is formed. This acid has a pka of 9.2 and is so

weak that it will not turn blue litmus

paper red.
Cyanide ions resemble halide ions in several ways, that they are sometimes referred to as 'pseudohalide' ions. Silver cyanide, like silver halide, is almost insoluble
in water. Cyanide ions form stable com-

plexes with many metals. For example,

sodium cyanide is used extensively in the

extraction of gold and silver from their

ores; these processes involve the formation of complex cyanides.

Cyanide is one of the most rapidly acting

poisons available to mammals. Hydrogen cyanide in aqueous solution (hydrocyanic acid) is readly absorbed from

Since the initial build up of absorption

rate was shown to depend on the diffusion constant, HCN was absorbed with
very little lag whereas CN absorption
rate increased for about 90 minutes. The
results obtained by the authors permitted
estimations of the early time courses of
absorption (by combination of CN -and
HCN contributions) for different exposures, and the resulting absorption patterns were compared with the detoxification rates of cyanide and the body burden

producing toxic effects. Their calculations showed, for example, that a large
area contact with 10% NaCN at pH 11.4
leads to clinical signs of toxicity within 25

minutes and death in about 1 hour. Observations in the small number of industrial accidents available for comparison
were in agreement with the calculations.
Therefore, cyanide absorbed by the skin
from clothing wetted with NaCN solution may lead to toxic effects in certain

A greater part of the absorbed cyanide is

rapidly detoxified by conversion to thio-

cyanate which is excreted in the urine

over a period of several days (9). Owing
to this rapid detoxification, it is possible
for animals to ingest doses of cyanogenetic glycoside only slightly less than the
lethal dose over extended periods with-

out harm. Animal and dosage factors

that influence toxicity include the size
and type of animal, the speed of ingestion, the type of food ingested simultaneously with the cyanogenic glycoside,

the skin (6), via the lungs, and from all

mucous membranes. The cyanide ion is

presence of active degradative enzymes in

the animal digestive tract, and the ability
to detoxify cyanide (9).



The median lethal dose (MLD) of cyanide is approximately 2 mg/ kg or about

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150 mg in the average adult (10). The oral

LD50 for rats is 6.44 mg NaCN/ kg or 10
mg/ kg in the case of KCN (11). In practice, is is usually only those animals
which eat rapidly that die, and intake of 4
mg/ kg body weight can be regarded as

definitely lethal if it is consumed fairly

quickly (9). HCN gas in air concentrations of 50-60 ppm may be absorbed in
sufficient quantity to cause poisoning.
Levels in plant material in excess of 200
ppm are potentially dangerous to livestock (4). Ruminants are reported to be
more susceptible to poisoning by cyanogenetic plants than are horses and pigs,
since the enzymes concerned in the release of HCN are destroyed by gastric
hydrochloric acid (9). Sheep are said to
be slightly less susceptible than cattle if
actual doses are considered.
Differences in animal toxicities of organic cyanides can be explained in terms
of different metabolic characteristics.
The toxic action of nitriles is related to
the metabolic release of the cyanide ion.
Speed and relative degree of biotransformation to release cyanide determine the
degree of poisoning (12). The appearance
of toxic signs due to organonitriles is usu-

ally delayed owing to the slowness of

decomposition and cyanide liberation.
Nitriles with biologically stable cyanide
groups generally have low toxicity.

There may be lacrimation and voiding of

faeces and urine. The animal generally

goes down, gasps for breath and may
have clonic convulsions due to anoxia.
The eyes lose their coloration in cases of
acute poisoning. The pupils are dilated,
mucous membranes are bright and the
characteristic blood color is bright cherry
red (4).

The terminal signs are slow breathing

and finally respiratory arrest.
After ingestion of cyanogenetic plants,
whether signs occur immediately or are

delayed depends not only upon the

amount of glycoside ingested, but also
upon the rate of cyanide release. It is

evident that the concentration of cyanide

within the body at any time will depend
upon the net sum of the absorption rate
from the gut minus the rate of detoxifica-

tion. It is possible for any amount of

cyanide exceeding the minimum lethal

dose to give rise to delayed signs or even
to no signs whatsoever if the cyanide
absorption is sufficiently prolonged by
slow hydrolysis of the glycoside (7).
A condition known as equine sorghum
cystitis ataxia, which is observed in horses grazing Sorghum sp. or hybrid sudan
pastures, is postulated to be caused by
either a chronic low-level exposure to
cyanide with resultant degenerative central nervous system lesions or production


of a lathyrogenic principle (nitrile related

amino acids) (14). Clinically there is urinary incontinence, posterior incoordination and cystitis. In humans, research has
shown that chronic cyanide intoxication

Cyanide is one of the most rapidly acting

caused by cassava consumption is the

poisons. Animals will commonly be

found dead since clinical signs last only a
few minutes after ingestion. The signs of
cyanide poisoning appear within a few
seconds to minutes after the ingestion of
cyanide-containing compounds or the
breathing of vapors containing the gas.
The most frequently observed first sign of
poisoning is an increase in both the rate
and depth of breathing, presumably a

consequence of the inhibition of cyto-

chrome oxidase. The other signs are variable in their severity and time of appea-

rance. There is a generalized muscle

tremor, ataxia and pronounced dyspnea.


main etiological factor in tropical ataxic

neuropathy in Nigerians (13). The disease
affects males and females equally and all
age groups, but occurs only rarely in children under 10 years. The peak incidence
is in the 40-50 year-old group.

The only consistent postmortem changes

found in animals poisoned by cyanide are

those relating to oxygenation of the

blood (4). Because oxygen cannot be utilized, venous blood has a bright red color
and often clots slowly or not at all. Ani-

mals have congestion of blood vessels,


congestion and hemorrhage of the lung,

and reddening and congestion of the

mucous membranes of the stomach (9).
As with other chemical asphyxiants, the
critical organs are those which are most
sensitive to oxygen deprivation, notably

the brain and the heart (14). Numerous

experimental studies have shown that in-

toxication by cyanide compounds can

lead to damage in the brains of rats, cats,
dogs, and monkeys (15, 20). In their research on neuropathological and physiological aspects of cyanide intoxication,
Brier ly et al. (21) concluded that cyanide
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can damage neurons only through the

medium of secondary effects on circulation and respiration. Generally, cyanide
poisoning encountered in veterinary medicine is peracute to acute and neither
gross nor microscopic lesions are consistently seen.
Tropical ataxic neuropathy (TAN), a disease compatible with chronic cyanide
poisoning, has lesions of the skin, mucous

membranes, optic and auditory nerves,

spinal cord, and peripheral nerves (13).
The neuropathology of the disease was
reported to be compatible with the effects

of chronic cyanide poisoning. Thyroid

changes, such as goiter, were also found
common in 2-5% of TAN patients (22).

The mechanism of action for cyanide is

based on its high affinity for the ferric
heme form of cytochrome a3 (cytochrome oxidase) (4, 23). The reaction in the

mitochondria forms a relatively stable

cytochrome oxidase-CN complex. With
iron in the trivalent state, electron

tabolism may result in respiratory arrest

and death.
The basic processes involved in the metabolism of cyanide are presented in Figure
1 (page 108). These processes were reported by Williams (25) and Ansell (26). In the
major path (Fig. 1), cyanide is converted
to thiocyanate by thiosulphate, which oc-

curs in the body in low concentrations.

The cytochrome oxidase-CN complex re-

leases cyanide in the presence of methemoglobin; the mitochondrial enzyme

rhodanese (also called sulfurtransferase)
mediates the transfer of sulfur from thiosulfate to the cyanide ion (27, 28). Thus,
thiocyanate is formed, the respiratory enzyme is released, and cell respiration is

restored. Up to 80% of small cyanide

doses is excreted in animal urine as thiocyanate through the major path shown in
Figure 1 (29). Tissue rhodanase is adequate to handle relatively large amounts
of cyanide, but the reaction is limited by

the endogenous supply of thiosulfate.

Upon excessive cyanide intake the rhodanase mechanism, due to limited availability of thiosulfate, is incapable of handling
all cyanide released. Under these condi-

tions, cyanide may attain toxic organ

concentrations. In the presence of high
concentrations of methemoglobin, the
formation of the cytochrome oxidaseCN complex is minimal.
The enzyme thiocyanate oxidase present
in erythrocytes catalyzes the reverse
transformation of thiocyanate to cyanide
to some extent (30). Owing to this activity, the cyanide to thiocyanate reaction in
slowly reversible, and an equilibrium is

transport along the cytochrome chain

is interrupted and oxidative metabolism and phosphorylation are inhibited (24). Electron transfer from cytochrome a3 to molecular oxygen is

set between the two ions in vivo. The

established minor pathways for the detoxification of cyanide are as follows

blocked and the chain of cellular respiration is halted. Thus, cyanide cuases cytotoxic anoxia. As a result, oxyhemoglobin

(CNO-) and formation of formate; for-

cannot relaese its oxygen for electron

transport. The clinical appearance of the
blood, then, is a bright red (oxygenated)

blood, the oxygen of which cannot be

utilized in the cells. In the central nervous

system, the inhibition of oxidative meTIIE VETERINARY QUARTERLY. VOL, 2. No. 2. APRIL 1980

(29): Oxidation of CN -to CO2, proceed-

ing through the formation of cyanate

mation of cyanocobalamin (Vitamin 1312)

resulting from the reaction of CN with

endogenous cobalamins; and combination with cystine to produce 2iminothiazolidine-4-carboxylic acid (31).

The carboxylic acid formed appears in

the urine of cyanide-dosed rats in
amounts up to 15% of the dose (31).







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I 4.r)

J= z




V/ 0

0 cc











Fig. I.

The basic processes involved in the metabolism of cyanide and treatment of cyanide poisoning.


The extreme rapidity with which cyanide

acts leaves little time for laboratory diagnosis in cases of acute poisoning. Signs of

oxygen starvation and bright colored

nide poisoning. Muscle tissues will be

more preferable for analysis than liver,
since little detoxification occurs in muscle and the rate of cyanide disappearance
is much slower. This is more so if post-

blood or mucous membranes aid in early

diagnosis (4).
A qualitative analysis for cyanogenetic
material in plant samples or rumen content may be made using the picric paper
test, but the sensitivity of the method is
very poor if less than 20kg HCN is in the
sample (32). The laboratory detection or
measurement of cyanide in forage, blood,
rumen content, liver and muscles tissues
is of great importance in confirming cya-

mortem examination is delayed after



Proper preservation of samples foranalysis is imperative in order to avoid large
variation in cyanide concentration or loss
of gaseous HCN.

Blood samples and biological tissues

should be stored at refrigeration temperature (33), while rumen contents and

forages should be stored in the frozen

state until analysis (4). Immersion of

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cyanogenetic plant samples in 1-3% mercuric chloride prevents further hydrolysis

and subsequent loss of the gaseous HCN
during storage (4). In case of legal need
for chemical analysis, all samples should
be stored frozen.

tion of the isolated cyanide. One disadvantage of the Aldridge method is that
benzidine, a reagent used in the colorimetric procedure, is carcinogenic. The
pyridine-pyrazalone reagent used in the
Epstein method is unstable, and pyridine

Levels of cyanide in plant material in

is noxious and unpleasant in routine

excess of 200 yg/ g sample are potentially

dangerous to livestock (4). Even healthy
people have a small but significant quantity of cyanide in their bodies. A detailed
survey of normal plasma cyanide levels in
10 individuals showed a maximum level
of 0.11 Ag/ ml with a mean of 0.05 /4/ ml
(34), while a maximum of 0.3 mg/ ml and
a mean of 0.075 mg/ ml were reported in
blood of 29 non-smokers (35).
The minimum whole blood cyanide concentration which will cause lethal effects

work. Two fluorometric procedures, one

in an otherwise healthy man has been

reported between 2.6 and 3.12 jig/ ml (36,

37). Observation on fire fatalities (35)

have shown that the mean level of blood

cyanide recorded in fatal cases (0.66

pg/ ml) would not be sufficient alone to
cause death. It is likely that in a fire the
main role of cyanide is its additive contribution to the effects of carbon monoxide

in producing asphyxia at the cellular

level. A five year survey (1970-1975) of
active suicides by cyanide poisoning conducted in the Allegheny county of Pittsburgh, Pennsylvania (10), showed blood

cyanide levels in the range of 4.0-45

Ag/ ml. Ansell and Lewis (26) have reviewed cyanide concentrations found in

human organs.
In rats acutely poisoned with oral doses
of potassium cyanide (KCN) the minimum lethal blood cyanide concentration
was found to be in the range 2.60-2.92
pg/ ml (38). Mean blood cyanide concen-

tration in rabbits poisoned with acute

doses of KCN or HCN was in the range
4.5-7.5 Ag/ ml (39).

Methods currently available for the isolation of cyanide from biological materials
are the microdiffusion methods (34, 40)
and distillation methods (41, 43). These
methods use modification of the colorimetric procedures developed by Aldridge
(44) and Epstein (45) for the determinaTHE VETERINARY QUARTERLY, VOL. 2, No. 2, APRIL 1980

by Morgan et al (46) and the other by

Groff et al (47), have been used to mea-

sure cyanide isolated from biological

fluids. A gas chromatographic procedure
for the determination of cyanide in biological specimen based upon its conversion to cyanogen chloride has also been
reported (48).
The cyanide determination method developed in our laboratory is a modification

of the aeration procedure described by

Pranitis and Stolman (49).
The modification involved redesigning
the gas washing bottles, reduction of the
absorbing solution volume from 20 ml to
10 ml, and most importantly the elimination of sulfide interference with 30 g/ liter
lead acetate solution.
The analysis procedure is precise and accurate and provides complete isolation of

cyanide from biological material. For

very low level cyanide determination, the
ion-selective electrode indicator technique using a silver ion-selective electrode
(50) and the colorimetric-methods mentioned earlier, have been shown more sensitive than direct measurement with the
cyanide electrode. The sensitivity of the di
rect potentiometric method used for cyanide measurement (10'6 mol/ liter) is well
below the lethal blood cyanide level 1.15
x l0 mol/ liter (36). The method is therefore sufficiently sensitive for diagnostic
application in cases of possible cyanide

An indirect atomic absorption spectrometric method has sufficent sensitivity

and precision for use in determining cyanide after isolation from biological materials. The method which was reported

by Danchik and Boltz (51) for use in

dertermining cyanide in industrial effluents and other polluted waste waters
involved the formation of a stable metalcyanide complex.
The complex was extracted and the metal

content of the extract determined by

atomic absorption. However, indirect

Thiocyanate is excreted in the urine. In

the present state of the art, the accepted
therapy is to use the combination of sodium nitrite and sodium thiosulfate

atomic absorption methods are not widely used, probably because of the general
convenience and adequacy of the competing methods.

(Na2S203) in cases where the diagnosis of

overwhelming cyanide poisoning is established. A recommended therapeutic

regimen is the intravenous administra-


tion of a mixture of 1 ml of 20% NaNO2

and 3 ml of 20% Na2S203, giving 4 ml of
this mixture per 45 kilogram bodyweight

Cyanide toxicity is effectively treated by

any means that prevents access of cyanide (CN- ) to issues, allowing for rhodanase action and a means to supply sulfur

(4). Oxygen was found to enhance the

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protective effect of the nitrite-thiosulfate

for thiocyanate formation. The treat- antidotal
combination in sheep (55, 56).
ment must promote the production of
effectiveness in treating
blood methemaglobin (Hb-Fe3+ ). The

cyanide intoxication in sheep, it was recommended that large doses of sodium

thiosulfate (660 mg/ kg) be used in combination with conventional doses of sodium nitrite (6.6 mg/ kg) (56).

antidotal effect is based on the readiness

with which free CN -combines with the
H b-Fe31- to form cyanomethemoglobin

(Hb-Fe3+ -CN). In this way, CN is

prevented from complexing with cyto-

Cobalt compounds have long been

chrome oxidase (Cyt-Fe3+ ).

known to be effective antidotes for cyanide but were themselves toxic (57, 58,

Customarily a large dose of sodium ni-

trite NaNO2) (25) is injected or amyl

nitrine is inhaled (23) to produce methemoglobin that binds with CN as

59). Their basic mechanism is to bind

cyanide by chelation. Dicobalt EDTA
(Co2EDTA) appears to be the most satisfactory of these (57). Cobaltous chloride

shown in equations 1-3 below.





Hb-Fe 3+





Hb-Fe 2--+ CN

Cyt-Fe 2+CN



Hb- Fe --CN

Thus, CN binding with cytochrome oxidase is decreased and cellular respiration

is permitted to continue. Some aminophenols are known to produce methemo-

globin more rapidly than NaNO2 and

with better safety (52). Aminopropio-


( 3)

(C0C12) and Co2EDTA were found to

induce a decreased thiocyanate excretion, suggesting that a predominant fraction of the cobalt-bound cyanide was not
further transformed into thiocyanate
(60). The difference was accounted for by
the large amounts of cobalt-cyanide com-

phenone has been used successfully in the

resuscitation of poisoned dogs (53), but is
commonly known to generate methemoglobin too slowly in man to be of value.
The injection of sodium thiosulfate pro-

cially available form of Co2EDTA, is

supplied in 20 ml ampoules, each con-

vides sulfur for thetnzyme rhodanase to

mediate the biotransformation of cya-

taining 300 mg of the compound in 20%

glucose. The manufactures recommend

nide to a much less toxic thiocyanate

(54), thereby decreasing the likelihood of
cyanide toxicity.

plexes demonstrated in the urine from

these animals. Kelocyanor, the commer-

that 20 ml be injected intravenously,

and if recovery does not ensue, a further

two doses should be given (61). Transient

2, No. 2, APRIL 1980

tachycardia and a drop in blood pressure

are to be expected.

Probably the most promising antidote

for cyanide poisoning is hydroxocobalamin (Vitamin B12a), which reverses cya-

nide toxicity by combining with cyanide

to form cyanocobalamin (Vitamin B12)

(62, 63). Hydroxocobalamin has been

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used in guinea pigs and baboons to lower

blood cyanide levels (64, 65). Its use as a
specific antidote in man after the inhalation or ingestion of cyanide compounds

has been reported (66, 67). In man, hydroxocobalamin has been shown to prevent cyanide transfer from red cells and
plasma to tissue after sodium nitroprusside (Na2FE(CN)5NO 2 H20) metabolism. It thereby prevents cyanide toxicity
from large intravenous doses of the drug

Hydroxocobalamin offers the overwhelming advantage that it is essentially

nontoxic (69). Poor solubility characteristics impose practical limits on dose, so

fields where cyanogenetic plants are

known to grow.

Cyanide is present in many industrial and

municipal wastewaters. The most impor-

tant source of cyanide pollution is from

the effluents ot electroplating processes,
metallurgy, steel processing, and petroleum industries.
The estimate for the U.S. production of
hydrogen cyanide was approximately
700 million pounds in 1976, and industrial production had increased annually
in the past decade (7). Both HCN and
CN in industrial effluent, as well as nat-

ural wastes, are toxic to aquatic life.

HCN has been determined to be the most

toxic form (72). The threshold limit of

toxicity in infinite time for fish has been
reported to be 0.1 mg/1(73). The activity
of micro-organisms responsible for self

that hydroxocobalamin is not particu-

purification of water was found to be

greatly inhibited by concentrations of
cyanide of at least 0.3 mg/1 (74). The

larly suitable for inactivation of multiple

lethal doses of cyanide (70). The use of

has been primarily based in acute toxicity

oxygen together with intravenous hydroxocobalamin and/ or sodium nitrite

with sodium thiosulfate are the specific
therapies of choice.

In order to control and prevent the occurence of cyanide poisoning, responsible

management is required in both chemi-

cal manufacturing and agricultural industries. Continuous monitoring of cyanide levels in effluents from industrial
and municipal plants, and adequate record of these levels are necessary. Farmers should be aware of factors which
influence the cyanogenetic potential of
forage crops and should conduct regular
inspection of grazing fields for cyanogenetic plants. Hays and silage should be

properly cured to enable the loss of a

majority of their cyanogenetic potentials
before feeding to livestock (4). The selective breeding of plants with low cyanogenetic content will help to reduce poisoning of livestock, but the most advisable
prevention method is to avoid grazing on

present limit for cyanides in waterways

studies where lethality is the end point.
Some consideration should be directed
toward low-level long term studies on
cyanide intoxication in mammals by the
oral and inhalation routes.
Cyanide is one of the 13 priority pollutants in raw waste and secondary effluent
samples where the concentration ranges
from 0.004 mg/1 to 0.2 mg/1(75). Under

Federal Drinking Water Standards for

cyanide, the recommended maximum
concentration is 0.01 mg/ I; 0.2 mg/ I is
considered the level of rejection (76). As
part of an industry's permit, the NPDES
(National Pollutant Discharge Elimination System) and the industrial analytical
laboratories must keep records of such
concentrations of cyanide in their wastewaters. Therefore, waste solutions containing cyanides must be disposed of in
such a way as to meet desirable standards. Continuous automatic monitoring
equipment for measuring cyanide in air

and water should be encouraged, and

these devices should include automatic
alarm systems to warn when predetermined levels are exceeded.

Cyanide-producing forages are the most

common causes of animal sickness due to
plants (77). The plants which are responsible for cyanide poisoning are the sorghums (Johnson grass, Sudan grass), arrowgrass (Triglochin spp), elderbery

(Sambucus spp.), wild cherry (Prunus

spp.), and the pits of several common
fruits (apple, peach, apricot). These plants
and fruit pits contain cyanogenetic glycosides which have the potential of releasing
cyanide upon ingestion (78). The economic importance of livestock poisoning in

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the agricultural industry has lead to the

development of several variations of

sorghums, that have a reduced capability of producing cyanide poisoning.

Substantial quantities of free HCN and

other organic cyanides are released during the thermal decomposition of polyurethane foams. As such, there is an increase in fatalities caused by inhalation of
gas or smoke from fires, possibly owing
to the increased toxicity of fire atmosphe-

res caused by the use of plastics in modern construction and furnishing.

Poisoning of humans, marine life, aquatic life or livestock due to cyanide is localized and can be minimized by responsible management.

I. Davies, D. W., Kadar, D., Steward, D. J., and Munro,
I.: A sudden death associated with the use
of sodium nitroprusside for induction of hypotension during anesthesie. Ca. Anaest h. Soc. J., 22,547,
2. Merrifield, A. Y. and Blumdell, M. D.: Toxicity of sodium
nitroprusside. Br. J. Anaesth., 46, 324,



Jack, R. D.: Toxicity of sodium nitroprusside. Br. J. Anaesth., 46, 952, (1974).
4. Buck, W. B. and Osweiler, G. D.: Cyanide, Clinical and diagnostic veterinary toxicology. Ed. G. A.
VanGelder, Kendal/ Hunt, Dubuque, Iowa, pp. 105-108, 1976.
5. The Merck Index, 9th edition, Merck and Co., Inc. Ed. Martha Windholz, New Yersey, p. 632, 1976.
6. Potter, A. L.: The successful treatment of two
recent cases of cyanide poisoning. Br. J. Ind. Med.,
7, 125, (1950).

7. Goodman, L. S. and Gilman, A.: Hydrocyanic Acid, The pharmacological basis of therapeutics.
Macmillan, New York, p. 904, 1975.

8. Dugard, P. H. and Mawdsley, S. J.: Percutaneous absorption of cyanide from aqueous sodium

cyanide. Abstracts, Seventh annual meeting, Society of Toxicology, San Francisco, California, March
12-16, p. 264, 1978.
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