Vertebrate Pesticide Toxicology Manual (Poisons)


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1.2 Cyanide

Chemical Name: Sodium cyanide

Synonyms: Cyanide

Cyanide paste and pellets are favoured by commercial hunters. Because it kills so quickly, animals die no more than a few feet from where the poison was laid so recovery of carcasses and skins is easy. Cyanide can only be purchased and used by licensed operators.

Pea-sized pieces of paste are placed with a little flour and icing sugar (or other lures such as cinnamon or eucalyptus oil) on a rock, leaf, or stick. However, cyanide paste rapidly loses its toxicity in wet conditions and possums that receive a sub-lethal dose become bait shy. This shyness problem may be compounded by the hydrogen cyanide gas (also hazardous for hunters) emitted by the paste. Bait and poison shyness is a problem in many areas where cyanide paste has been used intensively.

Feratox® (a pea-sized encapsulated cyanide pellet) was developed to increase the effectiveness of cyanide and reduce the risk of exposure of operators to hydrogen cyanide gas. The pellets are placed in a bait station with either similar-sized cereal feed pellets, or in a peanut-butter paste.

1.2.1 Physical and chemical properties

The empirical formula for sodium cyanide is NaCN and the molecular weight is 49. It is a white powder with a melting point of 563ºC. Potassium cyanide (KCN) is also available in New Zealand. Both compounds have similar properties. They are both highly soluble in water. KCN has a melting point of 623ºC, molecular weight.

1.2.2 Historical development, use, and occurrence in nature

Cyanide has been used in New Zealand for several decades for killing possums, but has limited use in other countries. Because of its fast action, cyanide is considered in a number of countries to be too hazardous for pest control. Cyanides are used widely and extensively in the manufacture of synthetic fabric and plastics, in electroplating baths, and metal-mining operations. Other sources of cyanide in the environment include fumigation operations, cyanogenic drugs, fires, cigarette smoke, and chemical warfare agents. Although the natural occurrence of cyanide is widespread in the environment, levels tend to be elevated in the vicinity of metal-processing operations, electroplaters, gold-mining facilities, oil refineries, power plants, and solid-waste combustion.

Cyanogenic (cyanide-containing) compounds occur in plants (see Table 4) and also in some fungi and bacteria. More than 2000 plants are known to be cyanogenic, including food plants and forage crops.

Some common sources for humans include cassava, sweet potatoes, yams, maize, millet, bamboo, sugar cane, peas, beans, almond kernels, lemons, limes, apples, pears, cherries, apricots, prunes, and plums. There are reports from overseas that yields of hydrogen cyanide (HCN) from common food and feed sources range from 0 to 912 mg/100 g. There are also numerous overseas reports of livestock that have been acutely poisoned by young sorghum and sugar gums (Towill et al. 1978; Webber et al. 1984). Young bamboo shoots and peach leaf ‘tea’ are examples of dietary sources of HCN poisoning in children (Hayes 1994). Cyanogenic lipids are another group of precursors from plants that contain, instead of sugars, long-chain fatty acids and yield carbonyl compound and hydrogen cyanide upon hydrolysis. Like fluoroacetate, cyanogenic glycosides are considered to be a chemical plant-defence to deter browsing animals.

Table 4. Examples of plants with cyanogenic potential (Osweiler et al. 1985)

Botanical name Common name

Holcus lanatus velvet grass

Hydrangea spp. hydrangea

Linum spp. flax

Lotus corniculatus birdsfoot trefoil

Phaseolus lunatus lima bean

Prunus spp. cherry, apricot, peach

Malus spp. apple

Pyrus spp. pear

Sambucus canadensis elderberry

Sorghum spp. Sudan grass, Johnson grass

Suckleya suckleyana poison suckleya

Trifolium repens white clover

Triglochin maritima arrow grass

Vicia sativa vetch seed

Zea mays maize

Under natural conditions the hydrolysis of cyanogenic glycosides in plants is inhibited, since the degradative enzymes of plants that can cause release of cyanide from the glycoside are kept spatially separated from the glycoside in intact plant cells. Upon wilting, frosting, or stunting of the plant, free HCN may be released as a result of plant cellular damage, which allows enzymatic degradation of the glycoside.

Rapid hydrolysis and release of HCN occurs only when plant cell structure is disrupted. Thus when the leaves of cyanogen-containing plants that possess glycosidase enzyme are eaten or damaged by herbivores, HCN will be released.

Cyanide has been recognised as a poison since very early times, having been used by the ancient Egyptians and early Romans. In the USA and Australia it is used in predator control devices and in New Zealand it is used in pastes or in a pellet (Feratox®) for controlling possums. The pastes contain oil, which protects the cyanide from exposure to air and hence slow down the release of hydrogen cyanide gas. Nevertheless, cyanide paste has a characteristic smell produced by the hydrogen cyanide gas liberated on hydrolysis. It is thought that ‘shy’ possums avoid cyanide paste because of this smell. The paste contains 55% NaCN and Feratox® pellets contain 80 mg. Cyanide has not been the toxicant of choice in the past, because cyanide pastes are only moderately effective and some possums have an innate aversion to the smell (Warburton & Drew 1994). Feratox® became available in 1997 and has become increasingly popular as field experience with the product has been gained. Feratox® products for other species (e.g. ferrets) are being developed, but at present these are still at the prototype phase (Spurr et al. 1999). A rodent repellent has been added to the Feratox® delivery system to increase its specificity for possum control (Morgan & Rhodes 2000).

1.2.3 Fate in the environment

There are no formally published data on the fate of cyanide from possum pastes used in New Zealand. However, cyanide paste is fairly unstable. It is thought that the cyanide dissipates into the environment by gaseous diffusion as hydrogen cyanide. The stability of the cyanide is increased by the oil present in the paste bait. The length of time that baits remain toxic depends on rainfall and on how well they are protected from the rain. The baits are not considered safe until they are broken down and unrecognisable (Rammell & Fleming 1978). Feratox® pellets that fall from bait stations will disintegrate slowly over a period of 2–4 months.

Cyanide ions are not strongly absorbed or retained in soils. Leaching into water will occur. Cyanide salts may also be degraded by some soil micro-organisms (Eisler 1991). Bacteria exposed to high concentrations of cyanide can be adversely affected, but acclimatised populations can degrade cyanide to yield a variety of products, including carbon dioxide and ammonia (Towill et al. 1978).

1.2.4 Toxicology and pathology

Onset of symptoms

Cyanide is a potent and rapid-acting asphyxiant. At lethal doses inhalation or ingestion of cyanide produces adverse reactions within seconds and death within minutes. Of all the poisons currently used for possum control, cyanide is considered the most humane (Gregory et al. 1996, 1998). However, death from lower doses can in some cases take from 1 to 4 hours, hence the importance of using high-quality baits and baiting practices to ensure maximum efficacy.

The minimal lethal dose of HCN in humans is 0.5–3.5 mg/kg. Information on the LD50 values of specific species is detailed in Tables 5 and 6. Signs of acute poisoning in humans are hyperventilation, headache, nausea and vomiting, generalised weakness and coma, followed by respiratory depression and death (Hayes 1994). In animals, clinical effects also occur in rapid succession. Initially there can be excitement and generalised muscle tremor. Animals may salivate, void faeces and urine, and gasp for breath. Convulsions will follow due to anoxia. In possums there appears to be minimal signs of distress, and convulsions occur after unconsciousness (Gregory et al. 1998).

The first signs of cyanide toxicosis in birds appear between 0.5 and 5 minutes after exposure, and include panting, eye blinking, salivation, and lethargy (Wiemeyer et al. 1986). Breathing becomes laboured and intermittent prior to death.

Mode of action

Cyanide disrupts energy metabolism by preventing the use of oxygen in the production of energy. Cyanide’s toxic effect is due to its affinity for the ferric haem form of cytochrome a3 (also known as cytochrome c oxidase), the terminal oxidase of the mitochondrial respiratory chain. Formation of a stable cytochrome c oxidase – CN complex in the mitochondria produces a blockage of electron transfer from cytochrome oxidase to molecular oxygen and cessation of cellular respiration, causing cytotoxic hypoxia in the presence of normal haemoglobin oxygenation. Tissue anoxia induced by the inactivation of cytochrome oxidase causes a shift from aerobic to anaerobic metabolism, resulting in the depletion of energy-rich compounds such as glycogen, phosphocreatine, and adenosine triphosphate, and the accumulation of lactic acid with decreased blood pH.

The combination of cytotoxic hypoxia with lactate acidosis depresses the central nervous system, the most sensitive site of anoxia, resulting in respiratory arrest and death (Eisler 1991). Cyanide is known to produce a range of biochemical changes in the brain associated with poisoning. Some of these changes will be associated with acute toxicity, anoxia, and death. Others, such as the depletion of dopamine (a central nervous system neurotransmitter), may be associated with chronic toxicity, such as the development of delayed progressive Parkinsonism and dystonia in humans following sub-lethal cyanide intoxication (Kanthasamy et al. 1994).

Pathology and regulatory toxicology

Cyanide causes subendocardial and subepicardial haemorrhage and petechial haemorrhage in the intestine. However, the only consistent post-mortem changes are those related to the oxygenation of the blood. Mucous membranes are pink and appear well oxygenated. The blood is usually a bright cherry-red colour. Chronic exposure to sub-lethal doses may lead to multiple foci of degeneration in the central nervous system (Osweiler et al. 1985), and histological examination of the brain has associated extensive destruction of dopaminergic neurones in the basal ganglia with neurotoxicity associated with acute cyanide intoxication (Kanthasamy et al. 1994).

The authors were unable to access regulatory toxicology studies on cyanide, which are conducted in in vitro test systems and laboratory animals to assess risk to humans with regard to issues such as mutagenicity, teratogenicity, and to define no-effect levels.

Fate in animals
Absorption, metabolism, and excretion

Cyanide is rapidly absorbed through the lungs by inhalation or through the gastrointestinal tract following ingestion. It is less readily absorbed through the skin. However, it should be noted that the LD50 for a solution of KCN on intact skin in rabbits is as low as 22.3 mg/kg (Eisler 1991). Free cyanide is rapidly distributed in tissue and body fluids, resulting in the prompt onset of the signs of acute cyanide poisoning.

In animals surviving a sub-lethal dose, the great majority of the absorbed cyanide reacts with sulphane sulphur in the presence of enzymes to produce thiocyanate, which is excreted in the urine for several days afterwards. Owing to this rapid detoxification, animals can ingest sub-lethal doses of cyanide over extended periods without apparent harm (Mengel et al. 1989). Species vary considerably in both the extent to which thiocyanate is formed and the rate at which it is eliminated from the body. Thiocyanate metabolites resulting from the transulphuration process are about 120 times less toxic than the parent cyanide compound. However, thiocyanate may accumulate in tissues, and has been associated with developmental abnormalities and other adverse effects. The development of delayed progressive central nervous system disorders, including Parkinsons disease in humans, following acute cyanide intoxication (Kanthasamy et al. 1994) suggests that there is a risk of permanent brain damage in animals and humans after apparent recovery from acute exposure. Although cyanide is not cumulative, as with other toxic materials, the damage caused from repeated exposure could be cumulative.

Minor detoxification pathways for cyanide include exhalation in breath as HCN and as CO2 from oxidative metabolism of formic acid; conjugation with cystine to form 2 aminothiazolidene 4 carboxylic acid or 2 aminothiazoline 4 carboxylic acid; combining with hydroxocobalamin (B12) to form cyanocobalamin, which is excreted in urine and bile; and binding by methaemoglobin in the blood.

Inhalation and skin absorption are the primary hazardous routes in cyanide toxicity in relation to occupational exposure. Skin absorption is most rapid when the skin is cut, abraded, or moist. Inhalation of cyanide salts is also particularly hazardous because the cyanide dissolves readily on contact with moist mucous membranes. Regardless of route of exposure, cyanide is readily absorbed into the bloodstream and distributed throughout the body. Cyanide concentrates in erythrocytes through binding to methaemoglobin. Because of the affinity of cyanide for the mammalian erythrocyte, the spleen may contain elevated cyanide concentrations when compared to blood. Accordingly, the spleen should always be taken for analysis in cases of suspected cyanide poisoning (Eisler 1991). The brain is the major target organ of cytotoxic hypoxia, and brain cytochrome oxidase may be the most active site of lethal cyanide action, as judged by distribution of cyanide.

Species variation in response to cyanide

Cyanide is a broad-spectrum toxin and is likely to be toxic to a range of vertebrates and invertebrates. The LD50s on a mg/kg basis are similar for a range of mammals and birds (see Table 5). The insecticidal properties are utilised when HCN is used as a fumigant (e.g. to kill weevils in grain warehouses).

Table 5. Acute oral toxicity (LD50mg/kg) of cyanide (Hone & Mulligan 1982; Marks & Gigliotti 1996)
Species LD50 (mg/kg)

Duck 1.43

American kestrel 2.12

Cattle 2.00

Sheep 2.30

Deer Approx. 3.5–4.5

Pig Approx. 3.5–4.5

Goat Approx. 3.5–4.5

Rabbit Approx. 3.5–4.5

Hare Approx. 3.5–4.5

Japanese quail 4–5

Rodents 6.40

Possum 8.70

European starling 9.00

It has been suggested that the rapid recovery of some birds exposed to sub-lethal doses of cyanide may be due to the rapid metabolism of cyanide to thiocyanate and its subsequent excretion. Species sensitivity to cyanide is not related to body size, but may be associated with diet. For example, raptors are more sensitive to cyanide than are species that feed mainly on plant material, with the exception of mallard duck (Eisler 1991).

There are limited data on the toxicity of cyanide to reptiles, though it would appear that cold-blooded animals such as frogs are less susceptible. The lethal dose in frogs is approximately 60 mg/kg (Hone & Mulligan 1982).

Aquatic toxicology

There are numerous publications on the toxicity of cyanide to aquatic invertebrates and fish, and some examples of these are given below (Table 6).

Table 6. Acute toxicity (96-hour LD50) of cyanide to daphnia and fish from aquaria (Hone & Mulligan 1982)

Species Cyanide concentration (ppb)

Rainbow trout 28 at 6ºC

Yellow perch 76–108

Fat minnow 82–113

Daphnia magna 160

However, these data are principally relevant to accidental spills of large quantities of sodium or potassium cyanide into rivers and streams (Eisler 1991) and are of very limited relevance to the use of cyanide baits for possum control in New Zealand.

1.2.5 Diagnosis and treatment of cyanide poisoning

First aid for human exposure

Lethal exposures to cyanide can cause unconsciousness in 10 seconds and death within a few minutes. Symptoms in humans include hot flushes with diaphoresis (perspiration), headache, nausea, vomiting, lethargy/weakness, anxiety, confusion, coma, convulsions, increased respiratory rate at low doses, but rapid onset of apnea (respiratory arrest) at high doses, tachycardia (increased heart rate) early, which progresses to bradycardia (decreased heart rate) with hypotension, arrhythmias, and asystole (cardiac arrest).

Fatalities usually result from intentional ingestion of bait or cyanide salts. By contrast, pest managers are most likely to be exposed to inhalation of hydrogen cyanide (HCN) fumes in an enclosed space, such as a storeroom or vehicle. Serious risks to health are rare under these circumstances, but prompt treatment is essential if any of the above symptoms are observed in the presence of cyanide baits.

First aid for persons who have inhaled HCN gas includes (Meredith et al. 1993):

  • Move the victim to a safe environment, being careful to avoid exposing the rescuers.

  • Ensure adequate ventilation.

  • Establish clear airway and provide 100% oxygen, if possible.

  • If victim is still breathing, break a capsule of amyl nitrite in a handkerchief and hold it under the nose and mouth for 30 seconds of every minute until the condition stabilises. Note that inhalation of amyl nitrite is rather ineffective at producing methaemoglobinemia, and is meant to be a temporising measure until intravenous sodium nitrite can be administered. In the field, it is far more important to adequately ventilate and oxygenate the victim than to administer amyl nitrite (Chen & Rose 1952).

  • If breathing has ceased, begin artificial respiration, preferably with an endotracheal tube and bag, or bag-mask-valve ventilation. Hold a crushed capsule of amyl nitrite in front of the intake valve of the ventilation bag for 30 seconds of every minute. Direct mouth-to-mouth resuscitation should be avoided because of risk to the rescuers.

  • Initiate cardiopulmonary resuscitation if there is no pulse.
  • Remove any contaminated clothing and wash cyanide from the skin.

  • Keep victim warm and transport to hospital immediately.

It is important to note that a person who has only inhaled HCN gas but has escaped to a safe environment without becoming seriously ill is unlikely to develop delayed adverse health effects (Peden et al. 1986).

Diagnosis of non-target poisoning in domestic animals

Cyanide poisoning is an extremely acute syndrome, and non-target animals that receive a lethal dose are usually found dead close to the source of the toxin. However, in cases where exposure is observed directly, and the dose is not immediately fatal, veterinary intervention may increase the chance of survival. Diagnosis of cyanide toxicosis is based on exposure history, clinical signs, laboratory analysis of appropriate specimens, and in lethal cases, lesions. Differential diagnoses in livestock include nitrate and urea poisoning.

Clinical signs

Clinical signs generally begin within 5B10 minutes of oral exposure to toxic levels of cyanide, and are characterised by anxiety, salivation, lacrimation (flow of tears), and tachypnoea (rapid respiratory rate), progressing rapidly to dyspnoea (difficult breathing), weakness, pink-coloured mucous membranes, muscle fasciculations and tremors, urination, defaecation, pupillary dilatation, staggering, and tachycardia (rapid heart rate). Terminal signs include lateral recumbency, cardiac arrhythmias, opisthotonus (spasm in which the head and hind legs are bowed backward), clonic/tonic convulsions, and death from respiratory paralysis. Death can occur in as little as 10B20 minutes, or more swiftly if large doses are absorbed, or up to 3B4 hours after exposure. However, most animals that survive 2 hours after exposure will recover completely without treatment (Radostits et al. 1994; Osweiler 1996a; Beasley et al. 1997b).

Laboratory diagnosis

Since cyanide exposure causes no specific, definitive pathologic changes, and many animals are found dead (rather than sub-lethally exposed), it is difficult to confirm a diagnosis of cyanide poisoning without demonstrating cyanide residues in stomach contents or blood or other tissue (Osweiler et al. 1985; Beasley et al. 1997b). Stomach or rumen contents, liver, or skeletal muscle samples should be collected and immediately frozen in airtight containers. Samples should be shipped frozen to an appropriate laboratory. Low concentrations of cyanide in tissues are indicative of intoxication. Whole, heparinised blood samples collected in airtight containers with no head space (submitted immediately or frozen) can also be analysed for cyanohaemoglobin concentration.


Blood and mucous membranes may be bright red in colour, especially in cases of rapid death, and when post-mortem examination is performed promptly. This distinct colouration is caused by high oxygen levels in the venous blood secondary to cyanide inhibition of mitochondrial cytochrome c oxidase, with resultant inability to utilise molecular oxygen at the cellular level. Peripheral tissue oxygen rises, preventing unloading of arterial oxygen, and the consequent increase in oxyhaemoglobin in the venous return (Smith 1996). However, this clinical sign is not consistently present. In the terminal stages, many poisoned animals become cyanotic (bluish or purple discolouration of skin and mucous membranes resulting from the accumulation of deoxyhaemoglobin in peripheral blood), as a result of respiratory paralysis, low cardiac output, and shock (Curry 1992).

Because death associated with cyanide exposure is so rapid, gross and microscopic lesions induced by the toxin are frequently absent (Jones et al. 1997). Many of the gross post-mortem changes that may be observed are attributable to death from anoxia, often accompanied by terminal seizures, and are not specific for cyanide. Subepicardial and subendocardial haemorrhage are often observed, as is congestion with petechial haemorrhages in the lungs, trachea, abomasum, and intestine. If death is somewhat delayed, or animals have been repeatedly exposed to cyanide, focal lesions of gray and white matter may be seen in the brain (Jones et al. 1997). A bitter-almond smell may be detectable in the rumen contents in some cases (Osweiler et al. 1985; Radostits et al. 1994).

Treatment of cyanide toxicosis in domestic animals

Cyanide poisoning is an urgent medical emergency, and veterinary treatment should be initiated rapidly in order to maximise the probability of survival. Therapeutic goals are (1) to decrease toxin absorption; (2) to split the cyanide-cytochrome oxidase bond and facilitate cyanide excretion; and (3) to support respiration and cardiac function. Recommendations for the treatment of cyanide toxicosis in animals are as follows (Osweiler 1996a; Beasley et al. 1997b):

  • Peracute onset of signs precludes the induction of emesis as a means of decontamination.

  • Administer activated charcoal (1B2 g/kg).

  • Livestock

  • Sodium nitrite at 10B20 mg/kg IV (as a 20% solution) to induce measured methaemoglobinemia. The Fe+3 in methaemoglobin binds cyanide (forming cyanomethaemoglobin) and reduces the amount of toxin available and bound to Fe+3 in cytochrome oxidase. Nitrite may also act as a vasodilator.

  • Sodium thiosulphate at 30B40 mg/kg IV (as a 20% solution), to provide a sulphur substrate to enable rhodanase-catalysed conversion of cyanomethaemoglobin to hydrogen thiocyanate, which is excreted in the urine. Repeat at half the initial dose in 30 minutes if no clinical response.

  • Recent reports indicate that high doses of sodium thiosulphate (660 mg/kg IV) may be effective without the use of nitrites (and the attendant risk of excessive methaemoglobinemia).

  • Small animals
  • Administer 1.65 mL of a 25% solution of sodium thiosulphate per kilogram, and 16 mg of sodium nitrite per kilogram body weight IV over several minutes. Repeat at half the initial dose in 30 minutes if no clinical response.

1.2.6 Non-target effects

In general it is perceived that fewer land-bird species have been reportedly killed by cyanide than by trapping or 1080. Smaller numbers of individual birds have been killed by cyanide than caught in traps. The most commonly poisoned native bird species have been weka and kiwi. For example, in 1947/48, extensive use of cyanide in Poverty Bay killed thousands of possums, but only a small number of native birds, mainly weka. However, in 1984, 66 hunters reported 37 kiwi poisoned by cyanide, about a quarter of the number caught in traps (Spurr 1991). No kiwi have been reported poisoned after 1080 operations. A short-tailed bat has been found dead, presumably poisoned on a cyanide bait laid for possums (Daniel & Williams 1984). The use of Feratox® baits and improved delivery systems should limit non-target mortality. The risks of secondary poisoning are low, but freshly killed carcasses are likely to be hazardous to non-target species.

1.2.7 Summary



Cheap (1–2 cents per bait)

Hazardous to users

Humane (very rapid action)

Toxicity of paste deteriorates rapidly in wet weather

Suitable for skin/carcass recovery

Paste can result in very poor kills if possums are cyanide-shy, hence not favoured by pest control agencies

Low secondary-poisoning risk

Can induce poison aversion

Achieves moderate to high kills (70–90%)

Antidotes are available but their use is controversial

Encapsulated cyanide does not produce HCN gas so is safer for hunters to use and is suitable for cyanide-shy possums

Encapsulated cyanide pellets can be recovered and reused

Encapsulated cyanide is not adversely affected by wet weather as cyanide paste is

Biodegradable in the environment

  • Cyanide has been used since ancient times. It is used in New Zealand in a concentrated paste bait or pellet for controlling possums.

  • Cyanide is the most humane poison available for vertebrate pest control.
  • Naturally occurring cyanogenic compounds are considered to be a plant defence mechanism to deter browsing animals. When animals eat the leaves of cyanogen-containing plants, hydrogen cyanide gas is released.

  • Cyanide in paste bait is fairly unstable and has low persistence in the environment. Cyanide dissipates by gaseous diffusion. The length of time that a bait remains toxic will depend on rainfall. Some cyanide may be washed into the ground, but it will not be strongly absorbed or retained in soil, and cyanide salts can be degraded by micro-organisms.

  • Cyanide is toxic to a wide range of aquatic organisms; however, significant contamination of waterways after ground use of cyanide paste is most unlikely.

  • Cyanide is a fast-acting broad-spectrum toxin and in both birds and mammals it causes tissue anoxia through inactivation of cytochrome oxidase and death due to respiratory failure.

  • Sub-lethal doses of cyanide will be metabolised to less toxic thiocyanides and excreted in the urine over a period of several days.

  • Cyanide biomagnification in food webs is most unlikely and has not been reported, possibly due to rapid detoxification of sub-lethal doses by most species and death at higher doses.

  • Cyanide baits have been reported to kill non-target species, including kiwi, weka, and short-tailed bats.

  • Cyanide bait is a potential hazard to users and the public if not handled, dispensed, and disposed of with diligence.

  • Cyanide in paste can change into a gaseous state (HCN). Risk of inhalation of HCN is perhaps the greatest risk associated with cyanide. One or two cyanide capsules (Feratox®) contain enough cyanide to be lethal to humans.

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