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SECTION 1. CHEMICAL IDENTIFICATION

CHEMINFO Record Number: 210
CCOHS Chemical Name: Hydrocyanic acid solutions

Synonyms:
HCN (non-specific name)
Prussic acid
Aqueous hydrogen cyanide
Hydrogen cyanide, aqueous solutions
Hydrocyanic acid (non-specific name)

Chemical Name French: Solutions d'acide cyanhydrique
Chemical Name Spanish: Acido cianhídrico
CAS Registry Number: 74-90-8
UN/NA Number(s): 1613
RTECS Number(s): MW6825000
EU EINECS/ELINCS Number: 200-821-6
Chemical Family: Inorganic acid / inorganic nitrogen compound / inorganic cyanide / hydrogen compound / hydrogen cyanide
Molecular Formula: C-H-N
Structural Formula: H-C#N (# represents a triple bond)

SECTION 2. DESCRIPTION

Appearance and Odour:
Colourless to bluish-white liquid with an odour of bitter almonds.(5)

Odour Threshold:
0.58 ppm (12,18); 0.8-4.5 ppm (cited as 0.9-5 mg/m3) (19)

Warning Properties:
POOR - up to 20% of the population is unable to smell hydrogen cyanide, which is released from hydrocyanic acid solutions, and there is wide individual variation in the minimum odour threshold. In addition, the sense of smell easily fatigues.

Composition/Purity:
Hydrocyanic acid solutions are available in concentrations of 2, 5 or 10% hydrogen cyanide in water.( 5,12) Hydrocyanic acid solutions are also made on site by dissolving hydrogen cyanide in water to produce solutions of the required concentration. This review discusses the hazards and control measures for hydrocyanic acid solutions. For information on hydrogen cyanide liquid and gas refer to the CHEMINFO review of Hydrogen cyanide. In general, a combination of sulfuric acid or phosphoric acid, and sulfur dioxide are added as a stabilizer to prevent polymerization. Oxalic acid and acetic acid are also used. The type and quantity of stabilizer used (usually less than 0.5%) depends on storage capacity, temperature and anticipated storage time in the container.(48,49)

Uses and Occurrences:
Hydrocyanic acid solutions are used to manufacture other chemicals, including adiponitrile, acetone cyanohydrin, acrylonitrile, sodium cyanide, cyanuric chloride, chelating agents, such as ethylenediaminetetracetic acid (EDTA) and methionine. Minor uses include the production of ferrocyanides, acrylates, lactic acid, pharmaceuticals and specialty chemicals. Hydrocyanic acid solutions are also used in electroplating, mining, in metallurgical and photographic processes, and in preparative chemistry as a non-aqueous, ionizing solvent.(5,12,48,49)


SECTION 3. HAZARDS IDENTIFICATION

EMERGENCY OVERVIEW:
Colourless to bluish-white liquid with an odour of bitter almonds. Hydrocyanic acid solutions containing greater than 20% hydrogen cyanide are flammable. In a fire, hydrogen cyanide will be released from the solution. Hydrogen cyanide is extremely flammable and burns with a blue flame. It can form explosive mixtures with air over a wide concentration range, and will readily ignite at room temperature. It has a low ignition energy and can be ignited by a static charge. DANGEROUSLY REACTIVE. Unstabilized hydrocyanic acid solutions or hydrogen cyanide may polymerize explosively on contact with alkaline materials, if heated, if stored longer than 90 days or if impure. During a fire, irritating/toxic nitrogen oxides may be generated. Tanks and other containers may rupture and explode if heated. VERY TOXIC. May be fatal if inhaled, absorbed through the skin or swallowed. 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. EYE IRRITANT. Causes moderate to severe eye irritation.



POTENTIAL HEALTH EFFECTS

Effects of Short-Term (Acute) Exposure

Inhalation:
Hydrocyanic acid solutions rapidly release very high concentrations of hydrogen cyanide. Hydrogen cyanide is extremely toxic and causes death at very low concentrations. It is a rapidly absorbed and a fast-acting poison, which poses a very serious inhalation hazard.
The odour threshold is very low (0.8-4.5 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.(12)
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.(13,14,15,25) With massive doses, many of the signs and symptoms may not be seen, and there is rapid onset of poisoning with convulsions, collapse, and death.(25) A characteristic sign of cyanide poisoning is the bright red colour of the blood, which may result in red skin colour.(15)
There are many reports of cyanide poisoning from accidental, suicidal and homicidal exposure to hydrogen cyanide 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.(33)

Skin Contact:
Hydrocyanic acid solutions are very toxic if absorbed through the skin. Skin contact with solutions or airborne hydrogen cyanide can cause symptoms similar to those described under "Inhalation" above. (Note: Any skin contact will also involve significant inhalation exposure).
There is no information available to assess the skin irritation potential of hydrocyanic acid solutions.
A historical case report describes airborne hydrogen cyanide being absorbed through the skin of 3 men wearing respiratory protection. Cyanide toxicity was observed 8 or 10 minutes of exposure to an extremely high concentration (approximately 20000 ppm).(7)
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 with an unspecified cyanide compound.) This person had significant long-term exposure to several metals, organic solvents and electroplating chemicals.(34)

Eye Contact:
Hydrocyanic acid solutions are very toxic if absorbed through the eye. Eye contact can cause symptoms, as described under "Inhalation" above. Direct contact with hydrocyanic acid solutions is expected to cause moderate to severe eye irritation, based on animal information.
In a case report, a man exposed to 452 ppm hydrogen cyanide for 6 minutes, while cleaning a chemical tank, experienced marked eye irritation, and was noted to have a slight loss of peripheral vision after 2 weeks. However, no baseline vision testing was available for comparison.(35)

Ingestion:
Hydrocyanic acid solutions are very toxic if ingested. Cyanide is rapidly absorbed through digestive tract resulting in the symptoms, as described under "Inhalation" above. In humans, the average lethal dose of hydrogen cyanide is estimated to be 60-90 mg.(15) 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).(36,37,38,39,40) 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 on 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.(41) Only studies with occupational exposure 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 in 36-48 hours following removal from the area of exposure.(42)
Fifty-six 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.(43)
Thirty-six employees were exposed to hydrogen cyanide 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.(44)
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.(12,41) However, this diet is also high in scopoletin, a coumarin compound, which is believed to be responsible for some of the neurotoxic effects.(45)

Lungs/Respiratory System:
Two limited studies suggest that long-term cyanide exposure may be associated with laboured breathing.
An increase in 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.(44)

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.(44)

Digestive System:
An increased incidence of nausea and/or vomiting has been 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).(42,44)

Eyes/Vision:
Eye irritation has been reported in 3 limited studies involving electroplating workers. Exposures, when specified, ranged from 4.2-15 ppm cyanide.(42,43,44) 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 a variety of chemicals that are irritating to the eyes.(12)
Degeneration of the optic nerve and the macula (part of the retina) is found in people living in tropical areas with a diet high in cassava, a root rich in cyanogenic glycosides.(41) In some cases, these effects have been attributed to cyanide exposure.(12) However, this diet is also high in scopoletin, a coumarin compound, which is believed to be responsible for some of these effects.(45)

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 levels) were observed in 34 employees exposed to unspecified concentrations of hydrogen cyanide, while engaged in case hardening and electroplating for 2-20 years.(43) 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.(46)

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.(47)
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.(47)
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.(44)
Limited animal studies have also shown impaired thyroid function.

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 hydrocyanic acid is not a developmental toxin.

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

Mutagenicity:
There is no human information available. The available evidence does not indicate that hydrocyanic acid is a mutagenic. Two tests using live mice exposed to potassium cyanide were negative. Hydrogen cyanide vapour has produced positive results in a test using 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.(12) 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.

Potential for Accumulation:
Does not accumulate. The most important route for detoxification of cyanide 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.(11) 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.(15) 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.(14)

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.(11,12) Cyanides also inhibit other enzyme systems, especially those containing iron or copper, which contributes to the symptoms observed.(12,13,14)


SECTION 4. FIRST AID MEASURES

Inhalation:
This chemical is very toxic and releases extremely flammable hydrogen cyanide. Take proper precautions to ensure your own safety before attempting rescue (e.g. wear appropriate protective equipment, use the buddy system, remove any sources of ignition). 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. As quickly as possible, remove contaminated clothing, shoes and leather goods (e.g. watchbands, belts). Flush contaminated area with lukewarm, gently flowing water for at least 20 minutes or until the chemical is removed. Immediately transport victim to an emergency care facility. Discard contaminated clothing, shoes and leather goods. NOTE: Any skin contact will also involve significant inhalation exposure and this chemical is very toxic if absorbed through the skin. See "Inhalation" above for additional procedures. See First Aid Comments below for antidote information.

Eye Contact:
Avoid direct contact. Wear chemical protective gloves, if necessary. Immediately flush the contaminated eye(s) with lukewarm, gently flowing water for 20 minutes or until the chemical is removed, while holding the eyelid(s) open. Take care not to rinse contaminated water into the unaffected eye or onto the face. Quickly transport victim to an emergency care facility. NOTE: Any eye contact will also involve significant inhalation exposure and this chemical is very toxic if absorbed through the eye. See "Inhalation" above for additional 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 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: Cyanide toxicity can occur following exposure to cyanogen chloride. 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, which can occur following exposure to adiponitrile. Specific information on antidotes which can be used as first aid and therapeutically in a medical setting is available in references 13 and 62.



SECTION 5. FIRE FIGHTING MEASURES

Flash Point:
Not available for hydrocyanic acid solutions. -17.8 deg C (0 deg F) (closed cup) (48,50) (hydrogen cyanide)

Lower Flammable (Explosive) Limit (LFL/LEL):
5.6% (50); 6% (48,51) (hydrogen cyanide)

Upper Flammable (Explosive) Limit (UFL/UEL):
40.0% (50); 41% (48,51) (hydrogen cyanide)

Autoignition (Ignition) Temperature:
537.8 deg C (1000 deg F) (48,50,51) (hydrogen cyanide)

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

Sensitivity to Static Charge:
Hydrocyanic acid solutions will not accumulate static charge. Hydrogen cyanide, at concentrations in the flammable range, can be ignited by a static charge of sufficient energy.

Electrical Conductivity:
3.3 X 10(8) pS/m at 0 deg C (48,52) (hydrogen cyanide)

Minimum Ignition Energy:
Not available

Combustion and Thermal Decomposition Products:
Carbon monoxide, carbon dioxide and nitrogen oxides.

Fire Hazard Summary:
Hydrocyanic acid solutions containing greater than 20% hydrogen cyanide are flammable. In a fire, extremely toxic and flammable hydrogen cyanide will be released from solutions. Hydrogen cyanide burns with a blue flame. Hydrogen cyanide can form explosive mixtures with air over a wide concentration range, and will readily ignite at room temperature. It has a low ignition energy. Hydrogen cyanide can be ignited by a static charge. Hazardous polymerization may occur under fire conditions. Loss of stabilizer or excessive heat from a fire may cause spontaneous polymerization. Heat from fire can cause hazardous polymerization and/or a rapid build-up of pressure inside closed containers, which may cause explosive rupture and a sudden release of large amounts of flammable gas. During a fire, irritating/toxic nitrogen oxides may be generated.

Extinguishing Media:
Carbon dioxide, dry chemical powder or "alcohol resistant" foam.(50) Water will not be effective for extinguishing a fire because it cannot cool hydrogen cyanide below its flash point.(50) Foam manufacturers should be consulted for recommendations regarding types of foams and application rates.

Fire Fighting Instructions:
Use extreme caution. Evacuate all personnel from the fire area. Explosive polymerization and explosive decomposition may occur under fire conditions and may rupture container releasing very toxic, very flammable hydrogen cyanide. Fight fire from a protected, explosion-resistant location or maximum possible distance. Approach fire from upwind to avoid extremely hazardous gas and decomposition products. Wear full protective suit if exposure is possible. See advice in Protection of Firefighters.
If venting or leaking hydrogen cyanide ignites, DO NOT extinguish the flames. Immediately cool containers with water spray from a maximum distance, taking care not to extinguish the flames and allow the fire to burn out. If the flames are accidentally extinguished, keep unprotected personal out of the area as hydrogen cyanide gas is very toxic and explosive reignition may occur.
Protect exposed materials with water spray to prevent ignition of other combustible materials.
Gas clouds may be controlled by water spray or fog. The resulting water solutions of hydrogen cyanide may be flammable and very toxic. Dike fire control water for appropriate disposal.
If a fire occurs in the vicinity of hydrogen cyanide, use unmanned monitors and hoseholders to keep cooling streams of water on fire-exposed containers, cylinders, tanks or pipelines until well after the fire is out, in order to protect their contents from the danger of polymerization. This should begin as soon as possible and should concentrate on any unwetted portions of the container. Take care not to get water inside a container. Reverse flow into a cylinder may cause rupture. No part of a cylinder or other container should be subjected to a temperature higher than 50 deg C (approximately 122 deg F), since polymerization occurs above this temperature.
Stay away from ends of tanks, but be aware that flying material from ruptured cylinders or tanks may travel in any direction. Withdraw immediately in case of rising sound from venting safety device or any discolouration of tank due to fire.
In an advanced or massive fire, the area should be evacuated; use unmanned hoseholders or monitor nozzles. If this is not possible, withdraw from fire area and do not attempt to fight the fire.
Cylinders or other 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 remain. Before entering such an area, especially confined areas, check the atmosphere with an appropriate monitoring device while wearing full protective suit.

Protection of Fire Fighters:
Water solutions of hydrogen cyanide and hydrogen cyanide gas are extremely toxic and can be absorbed through the skin. 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 - Comments:
NFPA has no listing for hydrocyanic acid solutions in Codes 49 or 325. Code 49 has a listing for 96% hydrocyanic acid, which is essentially hydrogen cyanide. For hazards and control measures of hydrogen cyanide, refer to the CHEMINFO review for Hydrogen cyanide.


SECTION 9. PHYSICAL AND CHEMICAL PROPERTIES

Molecular Weight: 27.03

Conversion Factor:
1 ppm = 1.10 mg/m3; 1 mg/m3 = 0.91 ppm at 25 deg C (calculated)

Physical State: Liquid
Melting Point: Not available.
Boiling Point: Not available
Relative Density (Specific Gravity): 0.984 (10% solution); 0.958 (20.1%); 0.829 (60%) at 18 deg C (water = 1) (48)
Solubility in Water: Soluble in all proportions
Solubility in Other Liquids: Soluble in all proportions in ethanol; soluble in diethyl ether and acetone.
Coefficient of Oil/Water Distribution (Partition Coefficient): Log P(oct) = -0.25 (experimental) (53)
pH Value: 4.62 (1M solution); 4.12 (10M) (calculated)
Acidity: Very weak acid
Dissociation Constant: pKa = 9.36 at 20 deg C (49); pKa = 9.14 at 25 deg C (Ka = 7.2 X 10(-10)) (48)
Viscosity-Dynamic: Not available
Surface Tension: Not available
Vapour Density: 0.94 (air = 1) (hydrogen cyanide) (51)
Vapour Pressure: Extremely high. Vapour pressure of hydrogen cyanide: 83 kPa (622.5 mm Hg) at 20 deg C (49); 98.9 kPa (742 mm Hg) at 25 deg C (54).
Saturation Vapour Concentration: Extremely high; 819000 ppm (81.9%) at 20 deg C; 977000 ppm (97.7%) at 25 deg C (hydrogen cyanide) (calculated).
Evaporation Rate: Extremely rapid.
Henry's Law Constant: 13.5 Pa.m3/mol (cited as 1.33 X 10(-4) atm.m3/mol) at 25 deg C (experimental) (54); log H = -2.26 (dimensionless constant; calculated)

SECTION 10. STABILITY AND REACTIVITY

Stability:
Unstable. Hydrocyanic acid solutions are stable at or below room temperature in the presence of a stabilizer.(49,55) They polymerize explosively if unstabilized and under alkaline conditions, if heated above 50 deg C, or if contaminants are present.(5,48,50,55)

Hazardous Polymerization:
In the absence of a stabilizer, hydrocyanic acid solutions undergo polymerization with the generation of heat (exothermic reaction). This polymerization can become explosively violent, especially if confined. Temperatures greater than 50 deg C contribute to the onset of polymerization.(50) Polymerization is accelerated by higher temperatures, the presence of alkaline compounds, and other contaminants, and sunlight (UV light). Since heat is generated, the polymerization reaction is autocatalytic and when the temperature reaches 184 deg C rapid explosive polymerization occurs.(55-57) Hydrocyanic acid solutions are stabilized by a combination of sulfuric, phosphoric, oxalic or acetic acid, and sulfur dioxide to prevent polymerization. The acid stabilizes the solution, while sulfur dioxide stabilizes hydrogen cyanide.(48,49) Hydrocyanic acid solutions should not be stored for longer than 90 days, particularly if the acid stabilizer is not maintained at a sufficient concentration. In addition some contaminants and surfaces may deplete the acidic stabilizer and cause polymerization. In such cases, reacidification and cooling is necessary.(48)

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.


ALKALINE MATERIALS (e.g. sodium, potassium or calcium hydroxide, ammonia, sodium carbonate) or AMINES (e.g. triethylamine) - can promote polymerization and cause explosive decomposition.(5,55)
OXIDIZING AGENTS (e.g. chlorates, hypochlorites, nitrates, perchlorates, peroxides or permanganates) - can cause a severe explosion.(5)
STRONG ACIDS (e.g. sulfuric or nitric acid) - explosively violent decomposition (hydrolysis) can occur if an excess of acid is added to hydrocyanic acid.(48)
HEAVY METAL CYANIDES (e.g. mercury cyanide) - detonates explosively in the presence of heavy metal cyanides.(55,56)

Hazardous Decomposition Products:
None reported

Conditions to Avoid:
Heat, sparks, open flames, static discharge, other ignition sources, basic conditions, impurities, depletion of stabilizer and extended storage.

Corrosivity to Metals:
Hydrocyanic acid solutions are corrosive to cast iron (gray, 3% nickel and ductile) (10% solution), copper and copper alloys, such as copper-nickel, silicon and aluminum bronze, brass, and naval and admiralty brass (solutions greater than 10%) at room temperature.(58,59) One source states that hydrocyanic acid solutions are corrosive to carbon steel (types 1010, 1020, 1075 and 1095) (solutions greater than 5%); some 400 series stainless steels (10%) and type 3003 aluminum (10%).(58) In contrast, another source indicates that these solutions do not corrode the above metals.(59) It is not known whether any of the solutions tested contained corrosive sulfuric or phosphoric acids as a stabilizer, which would influence the results of the testing. Hydrocyanic acid solutions are not corrosive to the 300 series stainless steels, Carpenter 20Cb-3 stainless steel, cast and B-356 aluminum, nickel and nickel-base alloys, such as Monel, Hastelloy, Inconel and Incoloy, tantalum and titanium at room temperature.(58,59)

Corrosivity to Non-Metals:
Hydrocyanic acid solutions attack plastics, such as nylon (solutions greater than 10%); and elastomers, such as ethylene propylene terpolymer (solutions greater than 10%), polyacrylate (concentrated solutions), polyurethane (solutions greater than 50%), polysulfide, (concentrated solutions) and chlorinated polyethylene (concentrated solutions) at room temperature.(59,60) Hydrocyanic acid solutions of greater than 10% do not attack plastics, such as Teflon and other fluorocarbons, high and low density polyethylene, polypropylene, and polyvinyl chloride (PVC); and elastomers, such as ethylene propylene, Viton, other fluorocarbons, butyl rubber, isoprene, natural rubber, nitrile Buna-N (NBR) and ethylene vinyl acetate (EVA) at room temperature.(59,60)


SECTION 11. TOXICOLOGICAL INFORMATION

LC50 (male rat): 71 ppm (4-hour exposure); cited as 158 mg/m3 (1-hour exposure) (whole-body exposure) (4)
LC50 (male rat): 40 ppm (4-hour exposure); cited as 110 ppm (30-minute exposure) (1)
LC50 (male mouse): 59 ppm (4-hour exposure); cited as 166 ppm (30-minute exposure) (3)
Note: This study was done with groups of 4 mice and only includes deaths during the exposure.
LC50 (female rabbit): 71 ppm (4-hour exposure); cited as 208 mg/m3 (35-minute exposure) (nose-only exposure) (4)
Note: Many of the LC50 values cited by secondary sources are for very short exposures. Only studies where the exposures are 30 minutes or greater have been used to more reliably determine LC50s with standardized 4-hour exposures.

LD50 (oral, female rabbit): 2.48 mg/kg (cited as 0.092 mMol/kg) (8)
LD50 (oral, female rat): 4.21 mg/kg (cited as 0.156 mMol/kg) (8)

LD50 (dermal, female rabbit): 6.90 mg/kg (solution administered to intact skin) (9)
LD50 (dermal, female rabbit): 2.34 mg/kg (solution administered to damaged skin (9)

Eye Irritation:

Hydrocyanic acid solutions are moderate to severe irritants.

Application of 0.03 mL/kg of 3.13-3.97% hydrocyanic acid in water (0.94 to 1.19 mg/kg) caused moderate inflammation and mild swelling in rabbits. In survivors, there was slight inflammation of the iris and cloudiness of the cornea after 24 hours. There was still mild inflammation after 7 days. The application also caused rapid breathing, weak movements, convulsions, irregular gasping breathing, and death.(6) LD50 (ocular, female rabbit): 1.04 mg/kg (cited as 0.039 mM/kg; administered as 3.13-3.97% solution) (6)

Skin Irritation:

The skin irritation potential of hydrocyanic acid solutions has not been determined.

No conclusions can be drawn from a study that reported vascular congestion in the skin of guinea pigs after exposure to unspecified concentrations of hydrogen cyanide for 15-97 minutes. Air temperatures during the experiment varied from -2 deg C to 6 deg C.(10)

Effects of Short-Term (Acute) Exposure:

Hydrocyanic acid solutions are very toxic by all routes of exposure. Toxic effects are primarily caused by the cyanide ion binding 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.(11,12) Cyanide also inhibits other enzyme systems, especially those containing iron or copper, which contributes to the symptoms observed.(12,13,14) Brain lesions typical of those produced by low oxygen supply have commonly been observed in animals following experimental cyanide poisoning.(15,20) Most of these studies use routes of exposure that are not relevant to occupational exposures and are not reviewed here.

Inhalation:
Exposure to 63 ppm hydrogen cyanide for 30 minutes caused a 50% decrease in the respiratory rate of male mice due to a depression of the central respiratory center. At 150 ppm, 2/4 mice died within 12-13 minutes, and at 330 ppm, 4/4 mice died within 14-30 minutes.(3) Exposure of individual monkeys to 100-150 ppm for up to 30 minutes (by facemask) caused hyperventilation, reduced activity and slow, irregular heartbeat followed by slowing of breathing and semi-consciousness. At 100 ppm, the time to incapacitation (semi-consciousness) was 16-19 minutes, while at 150 ppm it was 8 minutes. Rapid recovery occurred during the first 10 minutes following exposure.(21) In a study that examined the effects of cyanide on the central nervous system (CNS), 6 dogs were exposed for 2-10 minutes to 150-635 ppm hydrogen cyanide (cited as 0.165-0.7 mg/L) resulting in unconsciousness, convulsions, muscular rigidity, coma and 3 deaths. Extensive tissue death (necrosis) was seen in the grey matter, but not the white matter, of the CNS.(22) Rats exposed to unspecified concentrations of hydrogen cyanide for 20, 30, 45 or 60 minutes had lesions in both the grey and white matter of the brain.(23) All rats (10/10) died following a whole-body exposure to 6000 ppm for 10 seconds, 2200 ppm for 1 minute, 600 ppm for 5 minutes and 185 ppm for 1 hour.(4)

Skin Contact:
Hydrocyanic acid solutions and hydrogen cyanide are readily absorbed through the skin. Application of a hydrocyanic acid solution resulted in rapid absorption through the intact skin of rabbits in amounts sufficient to cause death (see dermal LD50s).(8) Application of an unspecified amount of hydrogen cyanide to a small area of the shaved skin of guinea pigs caused death in 7 or 8 minutes.(24) In a similar study, death occurred in guinea pigs at 45-97 minutes.(10)

Ingestion:
Studies on the short-term ingestion toxicity of cyanide have primarily been done with potassium cyanide. When potassium cyanide is given orally, it reacts rapidly with gastric acids to form hydrogen cyanide, which is readily absorbed.(25) A single dose of 8 mg/kg potassium cyanide produced slight tremors, which disappeared completely after 15 minutes, in 3/8 guinea pigs. Degenerative changes and signs of impaired kidney function were noted in rats receiving 3 mg/kg/day potassium cyanide for 15 days and degenerative liver changes were observed in animals ingesting 3 or 9 mg/kg/day. In female rats, ingestion of 0, 2, 4 or 16 mg/kg potassium cyanide for 30 days caused a dose-related decrease in body weight gain, mitochondrial function and ATP (adenosine triphosphate) levels in the liver, with statistical significance at 4 mg/kg/day. Male rats ingesting 300 mg/kg/day potassium cyanide for 14 days showed significant signs of impaired thyroid function (enlarged thyroid, increased thyroid stimulating hormone). For more details on these studies, refer to the CHEMINFO review of potassium cyanide.

Effects of Long-Term (Chronic) Exposure:

Studies on the long-term ingestion toxicity of cyanide have primarily been done with sodium or potassium cyanide. When sodium or potassium cyanide are given orally, they react rapidly with gastric acids to form hydrogen cyanide, which is readily absorbed.(25) 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.

Inhalation:
In a study, which is not available in English, laboured breathing and vomiting was observed in dogs exposed to 45 ppm hydrogen cyanide for 30 minutes/day at 2-8 day intervals for 28-96 days.(12, unconfirmed)

Ingestion:
For 2 years, rats were given a diet of dog meal fumigated with hydrogen cyanide, which produced hydrogen cyanide concentrations of 100 and 300 ppm (estimated doses averaging 5 and 15 mg/kg/day, accounting for loss from evaporation). No obvious signs of toxicity were seen. Detailed examination of the tissues showed no evidence of cyanide poisoning.(29) This study is limited by the small number of animals studied (10/sex/group). In an unconventional and limited study, 6 mongrel male dogs were fed a diet containing enough sodium cyanide to release 10.8 mg hydrogen cyanide/kg of cooked food for 14 weeks (reported dose 1.08 mg/kg). There were several biochemical changes (e.g. protein in the urine) noted. No changes were observed in the hearts or livers, but there was slight kidney injury and enlargement of the adrenal glands.(26) In earlier studies by the same author, which were conducted in a similar manner, dogs fed on this diet for 14 weeks developed decreased thyroid activity and an enlarged thyroid. Damage to the pancreas (atrophy and necrosis) with changes in glucose metabolism (indicating lowered insulin), was also observed, but the results were not statistically evaluated.(27,28)

Teratogenicity, Embryotoxicity and/or Fetotoxicity:
The available information suggests that hydrocyanic acid solutions do not cause developmental toxicity.
A study with rats ingesting 70 mg/kg/day potassium cyanide found no developmental effects. For more details on this study, refer to the CHEMINFO review of potassium cyanide. 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.(30, unconfirmed) There are insufficient details available to evaluate and interpret this study.

Reproductive Toxicity:
Some reproductive effects have been noted in studies with rats and mice exposed to sodium cyanide. However, fertility was not assessed in any confirmed study
Reproductive effects have been 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 with similar exposures, there was a significant decrease in epididymis weight at 50 mg/kg/day. For more details on this study, refer to the CHEMINFO review of sodium cyanide. In a limited, unconventional study, 6 mongrel male dogs were fed a diet containing enough sodium cyanide to release 10.8 mg hydrogen cyanide/kg of cooked food, for 14 weeks (reported dose 1.08 mg/kg/day). Significant changes were noted in the spermatogenic cycle (a decrease in relative frequency of stage 8 tubules).(26) 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.(30, unconfirmed) There are insufficient details available to evaluate and interpret this study.

Mutagenicity:
The available evidence does not indicate that hydrocyanic acid solutions are mutagenic. The available in vivo tests were done with potassium cyanide and the results are negative. In other tests done with potassium and sodium cyanide, there are both positive and negative results from in vitro tests, and a positive test in Drosophila (fruit flies). For more details on these studies, refer to the CHEMINFO reviews of potassium and sodium cyanide.
There is no specific information available for hydrocyanic acid solutions.
A positive result (point mutation) was obtained for hydrogen cyanide in bacteria, with the response weakened by the presence of metabolic activation.(31)

Toxicological Synergisms:
A study with potassium cyanide indicated that ascorbate interferes with the detoxification of cyanide in guinea pigs. When rats were co-exposed to hydrogen cyanide and carbon monoxide for 30 minutes, the effects were additive. Co-exposure of rats to 5% carbon dioxide and hydrogen cyanide caused an increase in the lethality of the hydrogen cyanide.(1) Exposure of male rats to 0, 10, 30 and 50 ppm hydrogen cyanide for 3.5 hours increased permanent noise-induced hearing loss in a dose-dependent manner. A significant enhancement of the hearing loss was noted at 30 ppm.(32)


SECTION 16. OTHER INFORMATION

Selected Bibliography:
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(2) Hydrogen cyanide. In: NIOSH pocket guide to chemical hazards. National Institute for Occupational Safety and Health, June 1997
(3) Matijak-Schaper, M., et al. Toxicity of carbon monoxide, hydrogen cyanide and low oxygen. Journal of Combustion Toxicology. Vol. 9 (Feb. 1982). p. 21-61
(4) Ballantyne, B. Acute inhalation toxicity of hydrogen cyanide vapor to the rat and rabbit. Toxic Substances Journal. Vol. 13, no. 4 (1994). p. 263-282
(5) US National Library of Medicine. Hydrogen cyanide. Last revision date: 2003-02-14. In: Hazardous Substances Data Bank (HSDB). CHEMpendium. [CD-ROM]. Canadian Centre for Occupational Health and Safety (CCOHS). Issue: 2003-2. Also available from World Wide Web: <http://ccinfoweb.ccohs.ca/chempendium/search.html>
(6) Ballantyne, B. Acute systemic toxicity of cyanides by topical application to the eye. Journal of Toxicology - Cutaneous and Ocular Toxicology. Vol. 2, nos. 2 & 3 (1983). p. 119-129
(7) Drinker, P. Hydrocyanic acid gas poisoning by absorption through the skin. The Journal of Industrial Hygiene. Vol. 14, no. 1 (Jan. 1932). p. 1-2
(8) 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
(9) Ballantyne, B. Acute percutaneous systemic toxicity of cyanides. Journal of Toxicology. Vol. 13, no. 3 (1994). p. 249-262
(10) Fairley, A., et al. The absorption of hydrocyanic acid vapour through the skin with notes on other matters relating to acute cyanide poisoning. Journal of Hygiene. Vol. 34, no. 3 (Oct. 1934). p. 283-294
(11) Basu, D.K., et al. Drinking water criteria document for cyanides (final draft). US Environmental Protection Agency, 1985
(12) Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological profile for cyanide (update). US Department of Health and Human Services, 1997
(13) Beasley, D.M.G., et al. Cyanide poisoning: pathophysiology and treatment recommendations. Occupational Medicine. Vol. 48, no. 7 (1998). p. 427-431
(14) 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
(15) Gosselin, R.E., et al. Clinical toxicology of commercial products. 5th ed. Williams and Wilkins, 1984. p. III-123-III-130
(16) Forsberg, K., et al. Quick selection guide to chemical protective clothing. 4th ed. Van Nostrand Reinhold, 2002
(17) Blank
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(19) Ruth J.H. Odor thresholds and irritation levels of several chemical substances: a review. American Industrial Hygiene Association Journal. Vol. 47 (Mar. 1986). p A-147
(20) Salkowski, A.A., et al. Cyanide poisoning in animals and humans: a review. Veterinary and Human Toxicology. Vol. 36, no. 5 (Oct. 1994). p. 455-466
(21) Purser, D.A., et al. Intoxication by cyanide in fires: a study in monkeys using polyacrylonitrile. Archives of Environmental Health. Vol. 39 (1984). p. 394-400
(22) Haymaker, W., et al. Residual neuropathological effects of cyanide poisoning: a study of the central nervous system of 23 dogs exposed to cyanide compounds. The Military Surgeon. Vol. 3, no. 4 (Oct. 1952). p. 231-246
(23) Levine, S., et al. Experimental cyanide encephalopathy. Archives of Pathology. Vol. 67 (1959). p. 80-97/306-323
(24) Walton, D.C., et al. Skin absorption of certain gases. Journal of Pharmacology and Experimental Therapeutics. Vol. 26 (1926). p. 315-324
(25) Ballantyne, B. Toxicology of cyanides. In: Clinical and experimental toxicology of cyanides. Edited by B. Ballantyne, et al. Wright, 1987. p. 41-126
(26) Kamalu, B.P. Pathological changes in growing dogs fed on a balanced cassava (Manihot esculenta Crantz) diet. British Journal of Nutrition. Vol. 69, no. 3 (May 1993). p. 921-934
(27) Kamalu, B.P. The effect of a nutritionally-balanced cassava (Manihot esculenta Crantz) diet on endocrine function using the dog as a model. 1. Pancreas. British Journal of Nutrition. Vol. 65, no. 3 (May 1991). p. 365-372
(28) Kamalu, B.P. The effect of a nutritionally-balanced cassava (Manihot esculenta Crantz) diet on endocrine function using the dog as a model. 2. Thyroid. British Journal of Nutrition. Vol. 65, no. 3 (May 1991). p. 373-379
(29) Howard, J.W., et al. Chronic toxicity for rats of food treated with hydrogen cyanide. Journal of Agriculture and Food Chemistry. Vol. 3, no. 4 (Apr. 1955). p. 325-329
(30) US Environmental Protection Agency (EPA). Hydrogen cyanide (CASRN 74-90-8). Last significant revision: 1994-09-01. [cited 2002-12]. In: Integrated Risk Information System (IRIS). Available from World Wide Web: <http://www.epa.gov/iris/subst/index.ht
(31) Kushi A., et al. Mutagen from the gaseous phase of protein pyrolyzate. Agricultural and Biological Chemistry. Vol. 47, no. 9 (1983). p.1979-1982
(32) Fechter, L.D., et al. Potentiation of noise-induced hearing loss by low concentrations of hydrogen cyanide in rats. Toxicological Sciences. Vol. 66 (2002). p. 131-138
(33) Hall, A.H., et al. Clinical toxicology of cyanide. Annals of Emergency Medicine. Vol. 15, no. 9 (Sept. 1986). p. 1067-1074
(34) Kales, S.N., et al. Paranoid psychosis after exposure to cyanide. Archives of Environmental Health. Vol. 52, no. 3 (1997). p. 245-246
(35) Bonsall, J.L. Survival without sequelae following exposure to 500 mg/m3 of hydrogen cyanide. Human Toxicology. Vol. 3 (1984). p. 57-60
(36) Rosenberg, N.L., et al. Cyanide-induced parkinsonism: clinical, MRI, and 6-fluorodopa PET studies. Neurology. Vol. 39, no. 1 (1989). p. 142-144
(37) 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
(38) 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
(39) 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
(40) Uitti, R.J., et al. Cyanide-induced parkinsonism: a clinicopathologic report. Neurology. Vol. 35, no. 6 (June 1985). p. 921-925
(41) Wilson, J. Cyanide in human disease. In: Clinical and experimental toxicology of cyanides. Edited by B. Ballantyne et al. Wright, 1987. p. 293-311.
(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) 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
(44) Blanc, P., et al. Cyanide intoxication among silver-reclaiming workers. Journal of the American Medical Association. Vol. 253, no. 3 (Jan. 1985). p. 367-371
(45) 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
(46) Dinca, C., et al. Observations on the changes in the activity of leukocytic oxidative enzymes in subjects with long term industrial exposure to hydrocyanic acid. Medicina Interna. Vol. 24, no. 11 (1972). p. 1385-1392
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(48) Pesce, L.D. Cyanides: hydrogen cyanide. In: Kirk-Othmer encyclopedia of chemical technology. 4th ed. Vol. 7. John Wiley and Sons, 1993. p. 753-765
(49) Klenk, H, et al. Cyano compounds, inorganic: hydrogen cyanide. In: Ullmann's encyclopedia of industrial chemistry. 5th completely revised ed. Vol. A 8. VCH Publishers, 1987. p. 159-165
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(51) Yaws, C.L.. Hydrogen cyanide. In: Matheson gas data book. 7th ed. McGraw-Hill, 2001. p. 453-45
(52) Britton, LG. Using material data in static hazard assessment. Plant/Operations Progress. Vol. 11, no. 2 (Apr. 1992). p. 56-70
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(54) Syracuse Research Corporation. The Physical Properties Database (PHYSPROP). Interactive PhysProp Database Demo. Date unknown. [cited 2003-07-09]. Available from World Wide Web: <http://esc-plaza.syrres.com/interkow/physdemo.htm>
(55) Urben, P.G., ed. Bretherick's reactive chemical hazards database. (CD-ROM). 6th ed. Version 3.0. Butterworth-Heinemann Ltd., 1999
(56) Armour, M-A. Hazardous laboratory chemicals disposal guide. 2nd ed. Lewis Publishers, 1996. p. 243-244
(57) Bond, J. Hydrogen cyanide tank explosion. Loss Prevention Bulletin. Vol. 101 (1991). p. 3 -7
(58) Pruett, K.M. Chemical resistance guide to metals and alloys: a guide to chemical resistance of metals and alloys. Compass Publications, 1995. p. 158-169
(59) Schweitzer, P.A. Corrosion resistance tables: metals, nonmetals, coatings, mortars, plastics, elastomers and linings, and fabrics. 4th ed. Part B, E-O. Marcel Dekker, Inc., 1995. p. 1489-1496
(60) Pruett, K.M. Chemical resistance guide for elastomers II: a guide to chemical resistance of rubber and elastomeric compounds. Compass Publications, 1994. p. C-188 to C-193
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(62) 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 from World Wide Web: <http://www.inchem.org/pages/antidote.html>
(63) Occupational Safety and Health Administration (OSHA). Airborne cyanide and hydrogen cyanide gas. In: OSHA Analytical Methods Manual. Revision Date: Oct., 31, 2001. [cited 2003-09-19]. Available from World Wide Web: http://www.osha-slc.gov/dts/sltc/methods/toc
(64) National Institute for Occupational Safety and Health (NIOSH). Hydrogen Cyanide. In: NIOSH Manual of Analytical Methods (NMAM(R)). 4th ed. Edited by M.E. Cassinelli, et al. DHHS (NIOSH) Publication 94-113 (Aug. 1994). [cited 2003-09-19]. Available from World Wide Web: http://www.cdc.gov/niosh/nmam/nmammenu.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: 2004-01-10

Revision Indicators:
EU classification 2004-11-02
Bibliography 2004-11-02
EU comments 2004-11-02



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