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SECTION 1. CHEMICAL IDENTIFICATION

CHEMINFO Record Number: 341
CCOHS Chemical Name: Potassium cyanide

Synonyms:
Cyanide of potassium
Hydrocyanic acid, potassium salt
KCN
Potassium cyanide (K(CN))

Chemical Name French: Cyanure de potassium
Chemical Name Spanish: Cianuro potásico
CAS Registry Number: 151-50-8
UN/NA Number(s): 1680 3413
RTECS Number(s): TS8750000
Chemical Family: Potassium and compounds / inorganic potassium compound / alkali metal compound / inorganic nitrogen compound / alkali metal cyanide / cyanide salt
Molecular Formula: C-K-N
Structural Formula: K.C#N (# represents a triple bond)

SECTION 2. DESCRIPTION

Appearance and Odour:
White granular powder or crystalline solid; odourless when dry; slight odour of bitter almonds in moist air or when damp.(13,14,15) Deliquescent (absorbs moisture from the air and forms wet solid or solution).(15,16)

Odour Threshold:
Pure, dry potassium cyanide is odourless, but gives off hydrogen cyanide in the presence of moisture. The odour threshold of hydrogen cyanide is 0.6-4.5 ppm.(10,49,50)

Warning Properties:
POOR - neither potassium cyanide nor hydrogen cyanide are detectable by odour or irritation at concentrations providing a significant margin of safety.

Composition/Purity:
Commercial potassium cyanide is about 99-99.5% pure.(16) The main impurities are potassium carbonate, potassium formate and potassium hydroxide.(16) It is sold as granules, pillow-shaped briquettes, cylindrical tablets, a coarse-grained powder, and as a 40% solution in water.(14)

Uses and Occurrences:
Potassium cyanide is used mainly for fine silver plating. It is also used for electroplating, electrolytic refining, extracting gold or silver from ore, case-hardening of steel, nitriding steel, and photographic film processing; in the manufacture of dyes and specialty chemicals; for metal colouring by chemical or electrolytic processes and as an analytical chemical reagent, fumigant and insecticide. It is a component of the electrolyte for the analytical separation of gold, silver and copper from platinum.(13,16)


SECTION 3. HAZARDS IDENTIFICATION

EMERGENCY OVERVIEW:
White granular powder or crystalline solid; odourless when dry; slight odour of bitter almonds and ammonia in moist air or when when damp. Deliquescent (absorbs moisture from the air and forms wet solid or solution). Does not burn. Contact with acid quickly releases extremely toxic and very flammable hydrogen cyanide gas. Decomposes slowly to hydrogen cyanide in presence of moisture and/or carbon dioxide in moist air. VERY TOXIC. May be fatal if absorbed through the skin or swallowed. Inhalation of hydrogen cyanide, which is formed when potassium cyanide reacts with moisture or carbon dioxide, may be fatal. The early symptoms of cyanide poisoning may include headache, nausea, dizziness, drowsiness, anxiety, rapid breathing, incoordination and confusion. More severe exposures can cause red skin colour, laboured breathing, convulsions, collapse and death. Inhalation of the dust can be very irritating to the nose and throat. CORROSIVE to the skin and eyes. May cause blindness or permanent scarring.



POTENTIAL HEALTH EFFECTS

Effects of Short-Term (Acute) Exposure

Inhalation:
Potassium cyanide is a solid, which does not form a vapour at room temperature. However, inhalation to potassium cyanide can occur following exposure to the dust and to mists or vapours from heated or misted solutions. In general, dusts or mists can be very irritating to the nose and throat. More importantly, potassium cyanide releases hydrogen cyanide when combined with water or acid. Hydrogen cyanide is an extremely toxic gas, which causes death at very low concentrations. It is a rapidly absorbed and fast-acting poison, which poses a very serious inhalation hazard.
The odour threshold of hydrogen cyanide is very low (0.6-4.5 ppm), but it does not provide a reliable warning of exposure. Some people (up to 20% of the population) are unable to smell cyanide, even at highly toxic concentrations.(10)
The early symptoms of cyanide poisoning may include anxiety and excitement, weakness, headache, nausea, vomiting, metallic taste, chest tightness, facial flushing, drowsiness, dizziness, irritation of the eyes, nose and throat, rapid breathing, a rise in blood pressure and a decrease in pulse. Laboured breathing, falling blood pressure, rapid, weak irregular heartbeat, unconsciousness, and convulsions follow these symptoms. In severe cases, cardiovascular collapse, shock, and fluid accumulation in the lungs (pulmonary edema) are followed by death.(4,17,18,19) With massive doses, many of the signs and symptoms may not be seen, and there is a rapid onset of poisoning with convulsions, collapse and death.(19) A characteristic sign of cyanide poisoning is the bright red colour of blood, which may result in red skin colour.(4)
There are many reports of cyanide poisoning from accidental, suicidal and homicidal exposure to HCN or its salts (most commonly potassium or sodium cyanide). The majority of people who survive short-term cyanide poisoning do not have long-lasting effects. However, depending on the degree of exposure, there may be enduring effects from low oxygen, including impaired memory and mathematical abilities, personality changes, and altered control and coordination of movement.(36)

Skin Contact:
Potassium cyanide is very toxic if absorbed through the skin. Skin contact with potassium cyanide solutions can cause symptoms similar to those described under "Inhalation" above.
Potassium cyanide solutions are expected to be corrosive, based on pH. Corrosive materials can cause severe skin burns with blistering, permanent scarring and, in severe cases, death.
No conclusions can be drawn from a case report that describes an electroplater and metal worker who developed a unique neurobehavioural disorder, diagnosed as an acute psychosis, following a significant short-term exposure to cyanide. (He was splashed in the face by an unspecified cyanide compound.) This person also had significant long-term exposure to several metals, organic solvents and electroplating chemicals.(35)

Eye Contact:
Potassium cyanide is very toxic if absorbed through the eye. Eye contact can cause symptoms as described under "Inhalation" above.
Potassium cyanide solutions are expected to be corrosive, based on pH. Corrosive materials can cause very severe eye irritation and, in some cases, permanent damage to vision, including blindness.

Ingestion:
Potassium cyanide is very toxic if ingested. It is rapidly absorbed through the digestive tract resulting in symptoms as described under "Inhalation" above. Immediately following ingestion, a bitter, acrid, burning taste may be noted, followed by constriction or numbness in the throat. There is rapid ventilation and shortness of breath, the stomach lining is irritated and nausea and vomiting may occur. Then, unconsciousness, convulsions, muscular contraction of the jaw, rapid and irregular pulse, gasping, paralysis and death may occur.(4,9) In humans, the average lethal dose of hydrogen cyanide is estimated to be 60-90 mg.(4) A few cases of Parkinsonism (a syndrome characterized by decreased mobility, muscular rigidity, and tremor) have been reported in survivors of acute cyanide poisoning. All case reports involved non-occupational exposure to high oral doses (where specified).(37,38,39,40,41) Ingestion is not a typical route for occupational exposure.

Effects of Long-Term (Chronic) Exposure

Several human population studies have evaluated the potential health effects of long-term cyanide exposure. In general, these studies are limited by factors such as the small number of employees evaluated and the possibility of concurrent exposure to other potentially harmful chemicals (particularly in the electroplating industry). In addition, few studies report reliable measurements of cyanide exposures and even when airborne concentrations are reported, exposure may also have occurred by skin absorption. Despite these limitations, the available evidence suggests that long-term occupational cyanide exposure may be associated with harmful effects in the thyroid gland and the nervous system.
Long-term exposure to cyanide also occurs from smoking, eating foods containing cyanogenic glycosides, and infection with cyanide-producing bacteria.(43) Only studies with occupational exposures are reviewed here.

Nervous System:
Limited information suggests that long-term exposure to cyanides may be associated with harmful effects on the nervous system. Some of the symptoms observed are non-specific (e.g. headaches) and could be associated with many causes. Nevertheless, there does seem to be an association between some nervous system symptoms and cyanide exposure.
Thirty-six male, non-smoking employees were exposed for 5-15 years to 4.2-12.4 ppm cyanide from electroplating baths containing sodium and copper cyanide. Nervous system symptoms were, in order of frequency, headache, weakness, changes in taste and smell, visual difficulties, and nervous instability. Two employees experienced psychotic episodes, which they recovered from within 36-48 hours following removal from the area of exposure.(42)
Fifty-six male employees were exposed to hydrogen cyanide (concentrations not reported) while engaged in case hardening and electroplating for 2-20 years. A significant increase in impairment of memory, visual ability, visual learning and psychomotor ability was observed in exposed employees, compared to 34 matched controls. Headaches were more frequently reported in exposed workers.(44)
Thirty-six employees were exposed to hydrogen and sodium cyanide in a silver-reclaiming factory by inhalation (15 ppm, 24-hour average concentration), skin contact and possibly oral exposure. An employee died of acute cyanide poisoning and the plant was closed for 7 months before the study was carried out. An overall exposure index was calculated based on job category, frequency of handling cyanide and ingesting food or drink in the production areas. Nervous system symptoms, which had a significant positive correlation with exposure, were numbness or tingling (paresthesia) of the extremities, easy fatigue and a symptom complex including headache, dizziness, and fainting.(45)
Neuropathies in people living in tropical areas with a diet high in cassava, a root rich in cyanogenic glycosides, have previously been attributed to cyanide.(10,43) However, this diet is also high in scopoletin, a coumarin compound, which is believed to be responsible for some of the neurotoxic effects.(46)

Lungs/Respiratory System:
Two limited studies suggest that long-term cyanide exposure may be associated with laboured breathing.
An increased incidence of effort-induced, laboured breathing was observed in 36 male, non-smoking employees exposed for 5-15 years to 4.2-12.4 ppm cyanide from electroplating baths containing sodium and copper cyanide.(42)
An association between laboured breathing and cyanide exposure was also observed in 36 employees exposed to hydrogen and sodium cyanide in a silver-reclaiming factory, by inhalation (15 ppm, 24-hour average concentration), skin contact and possibly oral exposure. An employee had died of acute cyanide poisoning and the plant was closed for 7 months before the study was carried out. An overall exposure index was calculated based on job category, frequency of handling cyanide and ingesting food or drink in the production areas.(45)

Skin:
An association between development of a skin rash and cyanide exposure was also observed in 36 employees exposed to hydrogen and sodium cyanide in a silver-reclaiming factory, by inhalation (15 ppm, 24-hour average concentration), skin contact and possibly oral exposure. An employee had died of acute cyanide poisoning and the plant was closed for 7 months before the study was carried out.(45)

Digestive System:
An increased incidence of nausea and/or vomiting was reported in two studies that evaluated employees with long-term exposure to cyanide concentrations up to 15 ppm (with possible concurrent ingestion and skin contact).(42,45)

Eyes/Vision:
Eye irritation was reported in 3 limited studies involving electroplating workers. Exposures, when specified, ranged from 4.2-15 ppm cyanide.(42,44,45) However, it is not possible to draw any specific conclusions about the eye irritation potential of long-term cyanide exposure, because electroplating workers are exposed to many chemicals that are irritating to the eyes.(10)
Degeneration of the optic nerve and part of the retina (the macula) is found in people living in tropical areas with a diet high in cassava, a root rich in cyanogenic glycosides.(43) In some cases, these effects have been attributed to cyanide exposure.(10) However, this diet is also high in scopoletin, a coumarin compound, which is believed to be responsible for some of these effects.(46)

Blood/Blood Forming System:
There is very limited information that long-term exposure to cyanide is associated with harmful effects on the blood.
Blood chemistry changes (increased white blood cells and red blood cell sedimentation rate, and decreased hemoglobin level) was observed in 34 employees exposed to unspecified concentrations of hydrogen cyanide, while engaged in case hardening and electroplating for 2-20 years.(44) Statistical analysis of the results was not conducted.
Blood chemistry changes (increased hemoglobin and lymphocyte counts and red blood cell damage) were observed in 36 male, non-smoking employees exposed for 5-15 years to 4.2-12.4 ppm cyanide during electroplating operations.(42) However, exposure to copper, an agent known to have toxic effects on blood also occurred.
Changes in white blood cell enzyme activity were noted in 43 employees exposed to an average concentration of 0.23 ppm hydrogen cyanide for 0.25-16 years (average 5.4 years) during metal coating operations.(47)

Endocrine System:
Evidence from human and animal studies indicates that long-term exposure to cyanide can result in impaired thyroid function and enlargement of the thyroid (goiter). Thiocyanate, the main metabolite of cyanide, is believed to cause these effects by inhibiting the uptake of iodine by the thyroid.(48)
Findings consistent with impaired thyroid function were observed in 35 male employees, all non-smokers, who were exposed to cyanide salts for at least 5 years, while working with an electroplating process. Cyanide concentrations were not reported.(48)
Mild to moderate thyroid enlargement was observed in 20/36 male electroplating workers, who were exposed to 4.2-12.4 ppm cyanide for 5-15 years. Measurement of radioactive iodine uptake showed a significantly higher iodine uptake in the exposed workers than for the control group.(42)
The health of 36 employees exposed to hydrogen and sodium cyanide in a silver-reclaiming factory was assessed. Inhalation (15 ppm, 24-hour average concentration), skin contact and possibly oral exposure had occurred. An employee died of acute cyanide poisoning and the plant was closed for 7 months before the study was carried out. An overall exposure index was calculated based on job category, frequency of handling cyanide and ingesting food or drink in the production areas. In tests done 7-30 months after the last exposure, the thyroid-stimulating hormone was significantly higher in high exposure index employees, compared to the mean laboratory control value. However, thyroxine levels were normal and no thyroid enlargement was found.(45)
Limited animal information suggests that long-term exposure to cyanide compounds may harm the thyroid gland.

Carcinogenicity:

There is no human or animal information available.

The International Agency for Research on Cancer (IARC) has not evaluated the carcinogenicity of this chemical.

The American Conference of Governmental Industrial Hygienists (ACGIH) has not assigned a carcinogenicity designation to this chemical.

The US National Toxicology Program (NTP) has not listed this chemical in its report on carcinogens.

Teratogenicity and Embryotoxicity:
There is no human information available. The limited animal information available suggests that potassium cyanide is not a developmental toxin.

Reproductive Toxicity:
There is no human information available. In an animal study, changes suggestive of reproductive effects were observed in rats and mice. However, fertility was not evaluated.

Mutagenicity:
There is no human information available. The available evidence does not indicate that potassium cyanide is mutagenic. Two tests using live mice were negative. Both positive and negative results have been obtained in short-term tests using mammalian cells and bacteria.

Toxicologically Synergistic Materials:
Co-exposure to hydrogen cyanide and 5% carbon dioxide (not lethal by itself) resulted in an increase in the lethality of hydrogen cyanide.(10) Oral pre-treatment of guinea pigs with ascorbate enhanced the toxic effects of oral administration of potassium cyanide. It was suggested that the ascorbate interfered with the reaction to detoxify cyanide.(20)

Potential for Accumulation:
Does not accumulate. The most important route for detoxification is by a mitochondrial enzyme, rhodanese, which adds sulfur to the cyanide ion to form thiocyanate. Thiocyanate is less toxic, and is excreted in the urine.(9) This enzyme is widely distributed in the tissues, but has its greatest activity in the liver. The body has a large capacity to detoxify cyanide but the reaction is dependent on an adequate supply of sulfur.(4) The maximum detoxification rate for humans is 0.6-0.9 micrograms/kg body weight/minute, which is considerably lower than for lab rodents or dogs. Most absorbed cyanide is excreted in the urine as thiocyanate, but small amounts are eliminated in exhaled air and urine as hydrogen cyanide, carbon dioxide and other metabolic products. The average half time for excretion of thiocyanate has been reported to be 2.7 days in healthy volunteers.(18)

Health Comments:
The cyanide ion binds with iron ions in the enzyme cytochrome oxidase, which prevents body cells from using oxygen. Thus, cyanide impairs the body's ability to use oxygen and the primary target organs for acute cyanide poisoning are the central nervous system and the heart.(9,10) Cyanides also inhibit other enzyme systems, especially those containing iron or copper, which contributes to the symptoms observed.(10,17,18)


SECTION 4. FIRST AID MEASURES

Inhalation:
This chemical is very toxic. Take proper precautions to ensure your own safety before attempting rescue (e.g. wear appropriate protective equipment, use the buddy system). Remove source of contamination or move victim to fresh air. If breathing is difficult, oxygen may be beneficial if administered by trained personnel, preferably on a doctor's advice. DO NOT allow victim to move about unnecessarily. Symptoms of pulmonary edema can be delayed up to 48 hours after exposure. If breathing has stopped, trained personnel should begin artificial respiration (AR) or, if the heart has stopped, cardiopulmonary resuscitation (CPR) immediately. Avoid mouth-to-mouth contact by using mouth guards or shields. Immediately transport victim to an emergency care facility. See First Aid Comments below for antidote information.

Skin Contact:
Avoid direct contact. Wear chemical protective clothing, if necessary. Flush contaminated area with lukewarm, gently flowing water for at least 20-30 minutes, by the clock. If irritation persists, repeat flushing. DO NOT INTERRUPT FLUSHING. If necessary, keep emergency vehicle waiting. Immediately transport victim to an emergency care facility. Discard contaminated clothing, shoes and leather goods. NOTE: This chemical is very toxic by skin absorption. See "inhalation" for general procedures. See First Aid Comments below for antidote information.

Eye Contact:
Immediately flush the contaminated eye(s) with lukewarm, gently flowing water for at least 20-30 minutes, by the clock, while holding the eyelid(s) open. Neutral saline solution may be used as soon as it is available. DO NOT INTERRUPT FLUSHING. If necessary, keep emergency vehicle waiting. Take care not to rinse contaminated water into the unaffected eye or onto the face. Quickly transport victim to an emergency care facility. NOTE: This chemical is very toxic by eye absorption. See "inhalation" for general procedures. See First Aid Comments below for antidote information.

Ingestion:
NEVER give anything by mouth if victim is rapidly losing consciousness, is unconscious or convulsing. Have victim rinse mouth thoroughly with water. DO NOT INDUCE VOMITING. Have victim drink 240 to 300 mL (8 to 10 oz) of water to dilute material in stomach. If milk is available, it may be administered AFTER the water is given. If vomiting occurs naturally, rinse mouth and repeat administration of water. If breathing is difficult, oxygen may be beneficial if administered by trained personnel, preferably on a doctor's advice. If breathing has stopped, trained personnel should begin artificial respiration (AR) or, if the heart has stopped, cardiopulmonary resuscitation (CPR) immediately. Avoid mouth-to-mouth contact by using mouth guards or shields. Quickly transport victim to an emergency care facility. See First Aid Comments below for antidote information.

First Aid Comments:
Provide general supportive measures (comfort, warmth, rest).
Consult a doctor and/or the nearest Poison Control Centre for all exposures.
Some recommendations in the above sections may be considered medical acts in some jurisdictions. These recommendations should be reviewed with a doctor and appropriate delegation of authority obtained, as required.
All first aid procedures should be periodically reviewed by a doctor familiar with the material and its conditions of use in the workplace.

ANTIDOTE: Amyl nitrite, which can be used as a first aid measure, is antidotal to cyanide toxicity. Consult with a doctor familiar with cyanide toxicity to determine the appropriateness of using amyl nitrite as first aid measure in your workplace and to arrange training for first aiders who may be required to administer amyl nitrite.

Note to Physicians:
There are antidotes available for cyanide toxicity. Specific information on antidotes which can be used as first aid and therapeutically in a medical setting is available in references 17 and 61.



SECTION 5. FIRE FIGHTING MEASURES

Flash Point:
Not combustible (does not burn).

Lower Flammable (Explosive) Limit (LFL/LEL):
Not applicable

Upper Flammable (Explosive) Limit (UFL/UEL):
Not applicable

Autoignition (Ignition) Temperature:
Not applicable

Sensitivity to Mechanical Impact:
Probably not sensitive. Stable material.

Sensitivity to Static Charge:
Potassium cyanide will not accumulate static charge and is not a combustible dust. Since it does not burn, potassium cyanide will not be ignited by a static discharge.

Electrical Conductivity:
Not available

Minimum Ignition Energy:
Not applicable

Combustion and Thermal Decomposition Products:
Decomposes in a fire to produce hydrogen cyanide, nitrogen oxides, oxides of carbon, ammonia and dipotassium oxide.(13)

Fire Hazard Summary:
Potassium cyanide does not burn or support combustion. It decomposes in a fire to form very flammable and extremely toxic hydrogen cyanide and toxic and irritating nitrogen oxides. Hydrogen cyanide can accumulate in confined spaces, resulting a toxicity hazard. The heat from a fire can cause a rapid build-up of pressure inside closed containers, which may cause explosive rupture. If small amounts of water come into contact with larger amounts of solid potassium cyanide, dangerous amounts of hydrogen cyanide can form.

Extinguishing Media:
Potassium cyanide does not burn. Use extinguishing agents compatible with potassium cyanide and appropriate for surrounding fire. Use water spray to keep fire-exposed containers cool.(51)

Extinguishing Media to be Avoided:
DO NOT use carbon dioxide since extremely toxic and very flammable hydrogen cyanide will be released.(51)

Fire Fighting Instructions:
Evacuate area and fight fire from a protected location or maximum possible distance. Approach fire from upwind to avoid extremely hazardous vapours and very toxic decomposition products, such as hydrogen cyanide. Wear full protective gear if exposure is possible. See Protection of Firefighters.
If possible, isolate containers exposed to heat, but not directly involved in the fire. Move containers from the fire area if this can be done without risk. Protect personnel. Otherwise, use water in flooding quantities as a spray to keep fire-exposed containers and tanks cool and absorb heat to help prevent rupture. Cooling should begin as soon as possible (within several minutes) and should concentrate on any unwetted portions of the container. Apply water from the side and a safe distance. Cooling should continue until well after the fire is out. Water spray may also be used to knock down irritating/toxic combustion products which may be produced in a fire. Note that the resulting water solutions of hydrogen cyanide may be flammable. Dike fire control water for appropriate disposal. Stay away from ends of tanks, but be aware that flying material (shrapnel) from ruptured tanks may travel in any direction. Withdraw immediately in case of rising sound from venting safety device or any discolouration of tank. In an advanced or massive fire, the area should be evacuated.
Containers should not be approached after they have been involved in a fire until they have completely cooled down. After the fire has been extinguished, explosive and toxic atmospheres may be present. Before entering such an area, especially confined areas, check the atmosphere with an appropriate monitoring device while wearing full protective gear.

Protection of Fire Fighters:
Potassium cyanide decomposes to extremely flammable and toxic hydrogen cyanide and toxic and irritating nitrogen oxides when heated in a fire. Do not enter without wearing specialized protective equipment suitable for the situation. Firefighter's normal protective clothing (Bunker Gear) will not provide adequate protection. A full-body encapsulating chemical protective suit with positive pressure self-contained breathing apparatus (NIOSH approved or equivalent) may be necessary.



NATIONAL FIRE PROTECTION ASSOCIATION (NFPA) HAZARD IDENTIFICATION

NFPA - Health: 3 - Short exposure could cause serious temporary or residual injury.
NFPA - Flammability: 0 - Will not burn under typical fire conditions.
NFPA - Instability: 0 - Normally stable, even under fire conditions, and not reactive with water.

SECTION 9. PHYSICAL AND CHEMICAL PROPERTIES

Molecular Weight: 65.12

Conversion Factor:
Not applicable

Physical State: Solid
Melting Point: 634 deg C (1173.2 deg F) (14,52)
Boiling Point: Not available
Relative Density (Specific Gravity): 1.55 at 20 deg C; 1.56 at 25 deg C (water = 1) (14)
Solubility in Water: Very soluble (71.6 g/100 g water at 25 deg C) (16,53)
Solubility in Other Liquids: Soluble in methanol, formamide and glycerol; slightly soluble in ethanol, dimethylformamide and phosphorus oxychloride.(14,16)
Coefficient of Oil/Water Distribution (Partition Coefficient): LogP(oct) = -1.69 (estimated) (54)
pH Value: 11.7 (10% solution); 12 (72% solution) (calculated)*
Basicity: Water solutions are strongly alkaline.
Dissociation Constant: pKa = approximately 9.2 (Ka = 2.51 x 10 (-5)) (sodium cyanide) (62); pKb = approximately 4.8 (1.6 x 10(-5)) (calculated)
Viscosity-Dynamic: Not applicable
Surface Tension: Not applicable
Vapour Density: Not applicable
Vapour Pressure: Approximately zero at room temperature.(53)
Saturation Vapour Concentration: Not applicable (does not form a vapour)
Evaporation Rate: Not applicable
Henry's Law Constant: Not available

Physical Properties Comments:
*NOTE: Because potassium cyanide hydrolyzes in water to form hydrogen cyanide and potassium hydroxide, water solutions of potassium cyanide are always strongly alkaline. Commercial products always contain small amounts of potassium hydroxide to enhance stability and suppress formation of hydrogen cyanide.(12) Therefore, the actual pH values of solutions measured are usually higher than those calculated and as given above.


SECTION 10. STABILITY AND REACTIVITY

Stability:
Normally stable. Reacts slowly with water or moist carbon dioxide to form extremely toxic and flammable hydrogen cyanide.(14) In some cases, this reaction may produce enough hydrogen cyanide to pose a health hazard, but not a flammability hazard.

Hazardous Polymerization:
Does not occur.

Flammable Gases Released Upon Contact with Water:
Hydrogen cyanide is slowly released in the presence of moisture or in water solutions of potassium cyanide at room temperature.(12,16) However, this reaction does not pose a flammability hazard because the reaction is slow and not enough hydrogen cyanide is given off.

Incompatibility - Materials to Avoid:

NOTE: Chemical reactions that could result in a hazardous situation (e.g. generation of flammable or toxic chemicals, fire or detonation) are listed here. Many of these reactions can be done safely if specific control measures (e.g. cooling of the reaction) are in place. Although not intended to be complete, an overview of important reactions involving common chemicals is provided to assist in the development of safe work practices.


ACIDS (e.g. sulfuric acid, hydrochloric acid or acetic acid) - very flammable and extremely toxic hydrogen cyanide is released.(14,16,51)
STRONG OXIDIZING AGENTS (e.g. chlorates, nitrates, nitrites, perchlorates or peroxides) - violent or explosive reaction occurs.(14,15,51)
MERCURY(II) NITRATE - may explode when heated.(55)
NITROGEN TRICHLORIDE - can explode on contact.(51,55)
PERCHLORYL FLUORIDE - react explosively at 100 deg C.(55)
HALOGEN GASES - react exothermically to form toxic cyano halide compounds.
ORGANIC HALIDES (e.g. benzyl chloride, ethyl chloroacetate) - depending on the type of halide, may react rapidly under normal conditions.(43,62)
CARBON DIOXIDE - reacts slowly in the presence of moisture or moist air to produce hydrogen cyanide.(14)

Hazardous Decomposition Products:
Hydrogen cyanide, ammonia, potassium hydroxide, potassium formate.

Conditions to Avoid:
Moisture, moist air, heat, acidic conditions.

Corrosivity to Metals:
All concentrations of potassium cyanide is corrosive to aluminum (types 3003, Cast and B-356) (at any temperature), gray cast iron, copper and its alloys (e.g. silicon bronze, aluminum bronze, copper-nickel, and brass (including admiralty and naval), and lead.(56,57) Potassium cyanide is not corrosive (rate less than 0.5 mm/year) to stainless steel (most 300 series, except 321, 347 and 348, 400 series, 17-4 and Carpenter 20 Cb-3), carbon steel (types 1010, 1020 and 12L14); high nickel cast iron, nickel, nickel-base alloys, such as Monel, Hastelloy and Incolloy, tantalum and titanium.(56, 57,58) Solutions are corrosive to metals and alloys such as aluminum, zinc, steel, lead, silver and several copper base alloys.

Corrosivity to Non-Metals:
Potassium cyanide does not attack plastics, such as acrylonitrile-styrene-butadiene (ABS), chlorinated polyvinyl chloride (CPVC), Teflon and other fluorocarbons, nylon, polyesters, polyethylene, polypropylene and polyvinyl chloride (PVC); elastomers, such as butyl rubber, chloroprene, ethylene-propylene, Viton and other fluorocarbons, natural rubber, isoprene, neoprene, nitrile Buna-N (NBR), polyurethane, and styrene-butadiene (SBR); and coatings, such as coal tar epoxy, chemical resistant epoxy, polyester and vinyls.(57,59)

Stability and Reactivity Comments:
When water solutions of potassium cyanide are stored for a long time or heated, potassium cyanide is slowly converted to toxic and corrosive ammonia and potassium formate. The decomposition rate accelerates with increasing temperature. This situation can pose a hazard in closed containers because of possible pressure build-up.(14,16)


SECTION 11. TOXICOLOGICAL INFORMATION

LD50 (oral, male mouse): 8.5 mg/kg (2)
LD50 (oral, female rabbit): 5.86 mg/kg (cited as 0.09 mMol/kg) (3)
LD50 (oral, female rat): 7.49 mg/kg (cited as 0.115 mMol/kg) (3)
LD50 (oral, male rat): 10 mg/kg (5,7)

LD50 (dermal, female rabbit): 22.3 mg/kg (solution administered to intact skin) (8)
LD50 (dermal, female rabbit): 14.3 mg/kg (solution administered to damaged skin) (8)

Eye Irritation:

Based on the pH of solutions, potassium cyanide is predictably corrosive. Limited animal information has shown severe irritation.

Application of 0.03-0.04 mL/kg of 19.8-40% potassium cyanide in water (6.3-16.0 mg/kg) caused moderate inflammation and mild swelling in rabbits. In survivors, there was also slight inflammation of the iris and cloudiness of the cornea after 24 hours. After 7 days, there was still mild inflammation. The application also caused rapid breathing, weak movements, convulsions, irregular gasping breathing, and deaths.(1) LD50 (ocular, female rabbit): 7.88 mg/kg; cited as 0.121 mMol/kg (administered as a 19.8-40% solution) (1,3)

Effects of Short-Term (Acute) Exposure:

Potassium cyanide is very toxic by skin contact and by ingestion. Effects are attributed primarily to the binding of the cyanide ion with iron ions in the enzyme cytochrome oxidase, thereby preventing cells from using oxygen. The primary target organs for acute cyanide poisoning are the central nervous system (CNS) and the heart, because they are the most sensitive to oxygen deprivation.(9,10) Cyanide also inhibits other enzyme systems, especially those containing iron or copper, which contributes to the symptoms observed.(10,17,18)

Skin Contact:
Potassium cyanide solutions are readily absorbed through the skin. Application of potassium cyanide in water resulted in rapid absorption through the intact skin of rabbits in amounts sufficient to cause death.(8)

Ingestion:
When potassium cyanide is given orally, it reacts with gastric acids rapidly to form hydrogen cyanide, which is readily absorbed.(19) Slight tremors, which disappeared completely after 15 minutes, were observed in 3/8 guinea pigs given a single dose of 8 mg/kg potassium cyanide.(20) Rats ingesting 0, 0.3, 0.9, 3.0 or 9.0 mg/kg/day potassium cyanide in drinking water for 15 days were studied for harmful effects on the liver and kidneys. Animals exposed to 9.0 mg/kg/day had a significant decrease in body weight gain. A dose-dependent increase in thyroid gland changes was observed in all treated animals, which could represent the earliest step in enlargement of the thyroid. At 9.0 mg/kg/day, degenerative liver changes, and at 3.0 and 9.0 mg/kg/day, degenerative kidney changes were observed (statistical significance not reported). Functional changes consistent with liver and kidney injury were noted.(21) Female rats ingesting 0, 50, 100 or 500 ppm cyanide as potassium cyanide in their drinking water for 30 days (reported approximate doses 0, 2, 4, or 16 mg/kg/day) had no differences in food consumption. However, there were dose-related decreases in water consumption, which was significant at 16 mg/kg/day, and in body weight gain, which was significant at 4 mg/kg/day. Dose-dependent decreases in mitochondrial function were found in liver and heart tissues with significance at 4 and 16 mg/kg/day. Tissue ATP levels showed a dose-dependent decrease in the liver, and heart, reaching significance in the liver at 4 mg/kg/day, and in the heart at 16 mg/kg/day.(22) Male rats on low protein, low iodide diets, given potassium cyanide as 0.2% of their diet (approximately 300 mg/kg/day) for 14 days, experienced significant increases in thyroid weight and in plasma thyroid-stimulating hormone. The addition of iodine to the diet for a further 14 days eliminated the thyroid effects. Rats fed the same dose of potassium cyanide as part of a high protein, low iodide diet, had no thyroid effects.(23)

Effects of Long-Term (Chronic) Exposure:

When sodium or potassium cyanide are given orally, they react rapidly with gastric acids to form hydrogen cyanide, which is readily absorbed.(19) In a well-conducted study, significant signs of toxicity were not observed in rats or mice exposed to sodium cyanide in drinking water at doses up to 23.5 mg/kg/day for rats and 50 mg/kg/day for mice. For a review of this study, refer to the relevant CHEMINFO review of sodium cyanide. Limited studies suggest that long-term cyanide exposure may affect the thyroid gland.

Ingestion:
Ten male rats ingesting a diet containing 1500 ppm potassium cyanide (approximately 90 mg/kg/day) for 11 months had a significant reduction in body weight gain and modest myelin degeneration in the spinal tract (statistical significance not reported). Depressed thyroid gland function (a significant decrease in thyroxine secretion and in plasma thyroxine) was noted at 4 months. At 11 months, the thyroxine secretion was still decreased, but plasma thyroxine levels were not, and the thyroid glands were significantly larger than the controls. There were no deaths or clinical signs of toxicity.(24) This study is limited by the relatively small number of animals and the fact that only one dose was administered. In a limited study, female rats were fed diets with 5 or 10 g potassium cyanide/100 g laboratory diet for 14 weeks (approximate dose 2500 or 5000 mg/kg/day). The treated animals had loss of hair and were apathetic, with dose-related signs of anemia, significant decreases in body weight, thyroid activity, and spleen weight, and a significant enlargement of the thyroid gland.(11) The results of this study are questionable as these daily doses are much higher than the oral LD50s for rats.

Teratogenicity, Embryotoxicity and/or Fetotoxicity:
The available information suggests that potassium cyanide is not a developmental toxin.
Female rats were fed a diet with 500 ppm cyanide as potassium cyanide (approximate dose 25 mg/kg/day potassium cyanide; 10.6 mg/kg/day cyanide) throughout breeding, pregnancy and lactation. There were no significant signs of toxicity in the mothers or their offspring at birth. Two female offspring/mother were continued on the control or treatment diet for 28 days to assess their growth. The treated offspring had a significant reduction in feed consumption and growth rate.(12) In a study, which is not available in English, mice exposed to 0.05 mg/kg/day cyanide obtained from drinking water had decreased fertility and survival rate in the F1 generation and 100% mortality in the F2 generation.(25, unconfirmed) There are insufficient details available to evaluate and interpret this study.

Reproductive Toxicity:
It is not possible to conclude that potassium cyanide is a reproductive toxicity hazard based on the available information. Some reproductive effects (e.g. reduced sperm motility) were observed in a well-conducted study using rats and mice exposed to the closely related chemical sodium cyanide. However, fertility was not assessed in any confirmed study.
Reproductive effects were observed in rats exposed to sodium cyanide in their drinking water for 13 weeks (sperm motility at 0.3 mg/kg/day and higher, altered fertility cycle in females at 9 mg/kg/day and higher, and decreased testes and epididymis weights and sperm counts at 23.5 mg/kg/day). In mice, there was a significant decrease in epididymis weight at 50 mg/kg/day. For more details on this study, see the CHEMINFO review of sodium cyanide. In a limited study, female rats fed diets containing 5 or 10 g potassium cyanide/100 g laboratory diet (approximate dose 2500 or 5000 mg/kg/day) for 2 weeks premating and then through the mating period (total time not reported) did not become pregnant.(11) The results of this study are questionable as these doses are much higher than the oral LD50s for rats. In a study, which is not available in English, mice exposed to 0.05 mg/kg/day of cyanide obtained from drinking water had decreased fertility and survival rate in the F1 generation and 100% mortality in the F2 generation.(25, unconfirmed) There are insufficient details available to evaluate and interpret this study.

Mutagenicity:
The available evidence does not indicate that potassium cyanide is mutagenic. Two in vivo tests are negative. In tests done with hydrogen, potassium and sodium cyanide, there are both positive and negative results from in vitro tests, and a positive result in Drosophila (fruit flies).
Negative results (chromosome aberrations) were obtained in a limited study where male mice received 16 daily oral doses of 5 mg/kg/day potassium cyanide.(26) Negative results (inhibition of testicular DNA synthesis) were also obtained in mice treated intraperitoneally with a single dose of 2.5 mg/kg potassium cyanide.(27) This route of exposure is not considered relevant to occupational situations.
In mammalian cells, positive results (chromosome aberrations (28) and DNA fragmentation (29)) and negative results (DNA synthesis inhibition (30)) were obtained for potassium cyanide. Treatment of mammalian cells with potassium cyanide for 7 days, resulted in a dose-dependent increase in morphologically transformed cells, with a significant increase first seen at cyanide concentration of 200 micromolar. Oxidative DNA damage was seen with 500 micromolar cyanide after 1 and 2 days of exposure but not after 7 days.(31) Negative results (point mutation) were obtained for potassium cyanide in several strains of bacteria, with and without metabolic activation.(32,33,34)

Toxicological Synergisms:
Guinea pigs pretreated orally with 1300 mg/kg/day ascorbate before oral administration of 8 mg/kg potassium cyanide all developed a severe tremor, incoordination, muscle twitches, paralysis and convulsions. Only 38% of the animals developed these symptoms when treated with potassium cyanide alone. It was suggested that the ascorbate interfered with the detoxification of cyanide.(20)


SECTION 16. OTHER INFORMATION

Selected Bibliography:
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(2) Sheehy, M., et al. Effect of oxygen on cyanide intoxication. III. Mithridate. Journal of Pharmacology and Experimental Therapeutics. Vol. 161 (1968). p. 163-168
(3) Ballantyne, B. The influence of exposure route and species on the acute lethal toxicity and tissue concentrations of cyanide. In: Developments in the science and practice of toxicology. Edited by A.W. Hayes, et al. Elsevier, 1983. p. 583-586
(4) Gosselin, R.E., et al. Clinical toxicology of commercial products. 5th ed. Williams & Wilkins, 1984. p. III-123-III-130
(5) Gaines, T.B. Acute toxicity of pesticides. Toxicology and Applied Pharmacology. Vol. 14, no. 3 (1969). p. 515-534
(6) Potassium cyanide. In: NIOSH pocket guide to chemical hazards. National Institute for Occupational Safety and Health, June 1997. p. 262-263
(7) Hayes, Jr., W.J. The 90-dose LD50 and a chronicity factor as measures of toxicity. Toxicology and Applied Pharmacology. Vol. 11 (1967). p. 327-335
(8) Ballantyne, B. Acute percutaneous systemic toxicity of cyanides. Journal of Toxicology. Vol. 13, no. 3 (1994). p. 249-262
(9) Basu, D.K., et al. Drinking water criteria document for cyanides (final draft). US Environmental Protection Agency, 1985
(10) Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological profile for cyanide (update). US Department of Health and Human Services, 1997
(11) Olusi, S.O., et al. Effects of the cyanogenic agents on reproduction and neonatal development in rats. Biology of the Neonate. Vol. 36 (1979). p. 233-243
(12) Tewe, O.O., et al. Long-term and carry-over effect of dietary inorganic cyanide (KCN) in the life cycle performance and metabolism of rats. Toxicology and Applied Pharmacology. Vol. 58 (1981). p. l-7
(13) US National Library of Medicine. Potassium cyanide. Last revision date: 2002-11-08. In: Hazardous Substances Data Bank (HSDB). CHEMpendium. [CD-ROM]. Canadian Centre for Occupational Health and Safety (CCOHS). Also available at: <ccinfoweb.ccohs.ca/chempendium/search.html>
(14) Klenk, H, et al. Cyano compounds, inorganic: alkali-metal cyanides. In: Ullmann's encyclopedia of industrial chemistry. 5th completely revised ed. Vol. A 8. VCH Publishers, 1987. p. 165-170
(15) Armour. M-A. Potassium cyanide. In: Hazardous laboratory chemicals disposal guide. 2nd ed. Lewis Publishers, 1996. p. 413-414
(16) Pesce, L.D. Cyanides: potassium cyanide. In: Kirk-Othmer encyclopedia of chemical technology. 4th ed. Vol. 7. John Wiley and Sons, 1993. p. 774-776
(17) Beasley, D.M.G., et al. Cyanide poisoning: pathophysiology and treatment recommendations. Occupational Medicine. Vol. 48, no. 7 (1998). p. 427-431
(18) Consensus report for hydrogen cyanide, sodium cyanide and potassium cyanide. Scientific Basis for Swedish Occupational Standards XXII. Edited by J. Montelius. Arbete Och Halsa. No. 20 (2001). p. 43-59
(19) Ballantyne, B. Toxicology of cyanides. In: Clinical and experimental toxicology of cyanides. Edited by B. Ballantyne, et al. Wright, 1987. p. 41-126
(20) Basu, T.K. High-dose ascorbic acid decreases detoxification of cyanide derived from amygdalin (laetrile): Studies in guinea pigs. Canadian Journal of Physiology and Pharmacology. Vol. 61 (1983). p. 1426-1430
(21) Sousa, A.B., et al. Does prolonged oral exposure to cyanide promote hepatotoxicity and nephrotoxicity? Toxicology. Vol. 174 (2002). p. 87-95
(22) Pritsos, C.A., et al. Mitochondrial dysfunction and energy depletion from subchronic peroral exposure to cyanide using the Wistar rat as a mammalian model. Toxic Substance Mechanisms. Vol. 15 (1996). p. 219-229
(23) Kreutler, P.A., et al. Interactions of protein deficiency, cyanide and thiocyanate on thyroid function in neonatal and adult rats. American Journal of Clinical Nutrition. Vol. 31, no. 2 (Feb. 1978). p. 282-289
(24) Philbrick, D.J., et al. Effects of prolonged cyanide and thiocyanate feeding in rats. Journal of Toxicology and Environmental Health. Vol. 5 (1979). p. 579-592
(25) US Environmental Protection Agency (EPA). Hydrogen cyanide. Last revision: 1997-09. [cited 2002-12]. In: Integrated Risk Information System (IRIS). Available at: <www.epa.gov/iris/subst/index.ht>
(26) Rabello-Gay, M.N., et al. Acrylonitrile: In vivo cytogenetic studies in mice and rats. Mutation Research. Vol. 79, no. 3 (1980). p. 249-255
(27) Friedman, M.A., et al. Inhibition of mouse testicular DNA synthesis by mutagens and carcinogens as a potential simple mammalian assay for mutagenesis. Mutation Research. Vol. 37 (1976). p. 67-76
(28) Umeda, M., et al. Inducibility of chromosomal aberrations by metal compounds in cultured mammalian cells. Mutation Research. Vol. 67 (1979). p. 221-229
(29) Bhattacharya, R., et al. Cyanide induced DNA fragmentation in mammalian cell cultures. Toxicology. Vol. 123 (1997). p. 207-215
(30) Painter, R.B., et al. The HeLa DNA-synthesis inhibition test as a rapid screen for mutagenic carcinogens. Mutation Research. Vol. 92 (1982). p. 427-437
(31) Kamendulis, L.M., et al. Morphological transformation and oxidative stress induced by cyanide in Syrian hamster embryo (SHE) cells. Toxicological Sciences. Vol. 68, no. 2 (2002). p. 437-443
(32) De Flora, S., et al. Study of 106 organic and inorganic chemical compounds in the Salmonella/microsome test. Carcinogenesis. Vol. 2, no. 4 (1981). p. 283-291
(33) De Flora, S., et al. Genotoxic activity and potency of 135 compounds in the Ames reversion test and in a bacterial DNA-repair test. Mutation Research. Vol. 133, no. 3 (1984). p. 161-198
(34) De Flora, S., et al. Mutagenicity testing with TA97 and TA102 of 30 DNA-damaging compounds, negative with other Salmonella strains. Mutation Research. Vol. 134, no. 2-3 (1984). p. 159-165
(35) Kales, S.N., et al. Paranoid psychosis after exposure to cyanide. Archives of Environmental Health. Vol. 52, no. 3 (1997). p. 245-246
(36) Hall, A.H., et al. Clinical toxicology of cyanide. Annals of Emergency Medicine. Vol. 15, no. 9 (Sept. 1986). p. 1067-1074
(37) Rosenberg, N.L., et al. Cyanide-induced parkinsonism: clinical, MRI, and 6-fluorodopa PET studies. Neurology. Vol. 39, no. 1 (1989). p. 142-144
(38) Messing, B., et al. Computer tomography and magnetic resonance imaging in cyanide poisoning. European Archives of Psychiatry and Neurological Science. Vol. 237, no. 3 (1988). p. 139-143
(39) Grandas, F., et al. Clinical and CT scan findings in a case of cyanide intoxication. Movement Disorders. Vol. 4, no. 2 (1989). p. 188-193
(40) Carelli, F., et al. Dystonic-Parkinsonian syndrome after cyanide poisoning: Clinical and MRI findings. Journal of Neurology, Neurosurgery, and Psychiatry. Vol. 51, no. 10 (1988). p. 1345-1348
(41) Uitti, R.J., et al. Cyanide-induced parkinsonism: a clinicopathologic report. Neurology. Vol. 35, no. 6 (June 1985). p. 921-925
(42) El Ghawabi, S.H., et al. Chronic cyanide exposure: a clinical, radioisotope and laboratory study. British Journal of Industrial Medicine. Vol. 32 (1975). p. 215-219
(43) Wilson, J. Cyanide in human disease. In: Clinical and experimental toxicology of cyanides. Edited by B. Ballantyne et al. Wright, 1987. p. 293-311.
(44) Kumar, P., et al. Health status of workers engaged in heat treatment (case hardening) plant and electroplating at cyanide bath. Indian Journal of Environmental Protection. Vol. 12, no. 3 (1992). p. 179-183
(45) Blanc, P., et al. Cyanide intoxication among silver-reclaiming workers. Journal of the American Medical Association. Vol. 253, no. 3 (Jan. 18, 1985). p. 367-371
(46) Obidoa, A., et al. Coumarin compounds in cassava diets: 2 Health implications of scopoletin in gari. Plant Foods for Human Nutrition. Vol. 41 (1991). p. 283-289
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(48) Banerjee, K.K., et al. Evaluation of cyanide exposure and its effects on thyroid function of workers in a cable industry. Journal of Occupational and Environmental Medicine. Vol. 39 (1997). p. 258-260
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(54) Syracuse Research Corporation. Interactive LogKow (KowWin) Database Demo. Date unknown. Available at: <syrres.com/esc/kowdemo.htm>
(55) Urben, P.G., ed. Bretherick's reactive chemical hazards database. (CD-ROM). 6th ed. Version 3.0. Butterworth-Heinemann Ltd., 1999
(56) Pruett, K.M. Chemical resistance guide to metals and alloys: a guide to chemical resistance of metals and alloys. Compass Publications, 1995. p. 278-289
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(61) IPCS/CEC Evaluation of Antidotes Series. Vol. 2. Antidotes for poisoning by cyanide. Edited by T.J. Meredith, et al. Published by Cambridge University Press on behalf of the World Health Organization and of the Commission of European Communities. Cambridge University Press, 1993. Also available at: <www.inchem.org/pages/antidote.html>
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Information on chemicals reviewed in the CHEMINFO database is drawn from a number of publicly available sources. A list of general references used to compile CHEMINFO records is available in the database Help.


Review/Preparation Date: 2004-11-30

Revision Indicators:
pH 2006-01-06
US transport 2007-01-10
UN/NA No 2007-01-10



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