CYANOGEN IODIDE
HAZARDTEXT ®
Information to help in the initial response for evaluating chemical incidents
-IDENTIFICATION
SYNONYMS
CYANOGEN IODIDE CYANOGEN MONOIODIDE IODINE CYANIDE IODINE MONOCYANIDE IODOCYANIDE JODCYAN
IDENTIFIERS
Editor's Note: This material is not listed in the Emergency Response Guidebook. Based on the material's physical and chemical properties, toxicity, or chemical group, a guide has been assigned. For additional technical information, contact one of the emergency response telephone numbers listed under Public Safety Measures.
SYNONYM REFERENCE
USES/FORMS/SOURCES
Cyanogen iodide's primary use is that of a preservative for insects and in taxidermy and systematics (Lewis, 1998). It is used "generally for destroying all lower forms of life" (HSDB , 2001).
Heating iodine and metal cyanide will produce cyanogen iodide (Lewis, 1997). It also can be "prepared by the action of iodine on sodium cyanide" (HSDB , 2001).
-CLINICAL EFFECTS
GENERAL CLINICAL EFFECTS
- Cyanogen iodide is an extremely toxic halogenated cyanide compound that releases highly toxic and irritating fumes of cyanide, iodide and oxides of nitrogen when heated to decomposition. The adverse systemic health effects of cyanogen halides are due to cyanide poisoning; however, at lower concentrations, these agents have more irritant than systemic toxic properties.
- Cyanogen iodide is a strong irritant of the skin, eyes and mucous membranes. Inhalation of fumes or vapors can produce respiratory tract irritation with possible chemical pneumonitis or noncardiogenic pulmonary edema. Dermal contact results in erythema and possible absorption, which may prove fatal. Eye contact produces redness, blepharospasm and lacrimation. Ingestion, which can be fatal, results in a bitter, acrid, burning taste.
- Exposure to low levels of cyanide systemically may produce nausea, vomiting, palpitations, confusion, hyperventilation, anxiety and vertigo. Severe hypoxic signs in the absence of cyanosis suggest this diagnosis.
- In more severe systemic exposures, initially the patient may experience flushing, tachycardia, palpitations, tightness in the chest, tachypnea, dyspnea, coughing, headache, nausea, vomiting, weakness, confusion, giddiness and dizziness.
This may progress to agitation, stupor, loss of consciousness, coma, apnea, generalized convulsions (possibly violent), paralysis, pulmonary edema, bradycardia, hypotension and death from respiratory failure. Cyanosis is generally a late finding and does not occur until the stage of circulatory collapse and apnea. Patients have survived potentially lethal cyanide exposures with supportive care only, and the absence of a rapidly deteriorating course does not exclude the diagnosis of cyanide poisoning.
- POTENTIAL HEALTH HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 157 (ERG, 2004)
TOXIC; inhalation, ingestion or contact (skin, eyes) with vapors, dusts or substance may cause severe injury, burns, or death. Reaction with water or moist air will release toxic, corrosive or flammable gases. Reaction with water may generate much heat which will increase the concentration of fumes in the air. Fire will produce irritating, corrosive and/or toxic gases. Runoff from fire control or dilution water may be corrosive and/or toxic and cause pollution.
ACUTE CLINICAL EFFECTS
- Cyanogen iodide releases highly toxic and irritating fumes of cyanide, iodide, and oxides of nitrogen when heated to decomposition (Sax & Lewis, 1989).
- Cyanogen iodide is a strong eye and skin irritant (Sax & Lewis, 1987; EPA, 1985). The adverse systemic health effects of cyanogen halides are due to cyanide poisoning; however, at lower concentrations, these agents have more irritant than systemic toxic properties (Hartung, 1982).
- Initial effects reported from acute CYANIDE poisoning include hyperpnea (increased rate and depth of breathing), tachypnea (quick, shallow breathing), tachycardia (increased heart rate), hypertension (high blood pressure), eye, skin, and respiratory tract irritation, headache, anxiety, and agitation (Vogel et al, 1981; Hall & Rumack, 1986).
- Symptoms of severe or late stages of CYANIDE poisoning include agitation, stupor, coma, apnea, generalized convulsions, metabolic acidosis, pulmonary edema, bradycardia (slow heart rate), hypotension (low blood pressure), dilated pupils, and death (Stewart, 1974; Vogel et al, 1981; Graham et al, 1977).
- Lesser CYANIDE exposures may produce nausea, vomiting, palpitations, confusion, hyperventilation, anxiety, and vertigo (Hall & Rumack, 1986). Many of these same symptoms can be caused by exposure to SIMPLE ASPHYXIANTS , central nervous system depressants, or other substances which can cause hypoxia.
CHRONIC CLINICAL EFFECTS
- At the time of this review, no data were available to assess potential effects of chronic exposure to cyanogen iodide in humans or experimental animals.
- Chronic exposure to CYANIDES has been reported to cause CNS effects, such as insomnia, loss of memory, and tremors (Chaumont, 1960). Experimental animal studies have confirmed the central nervous system as a target for the chronic toxicity of CYANIDE.
- Rats fed CYANIDE for 11 months suffered damage to the spinal cord (Philbrick, 1979). Other neurological effects include degeneration of the optic nerve, resulting in blindness.
- The neurological effects of chronic exposure to CYANIDE may be due to its metabolites THIOCYANATE and CYANATE. The exact mechanism(s) of the neurotoxicity caused by chronic CYANIDE exposure is not known. Dermatitis has also been reported (Saia, 1970).
- Another important aspect of the chronic toxicity of CYANIDE is its goiterogenic effect. A goiter-like enlargement of the thyroid gland called ENDEMIC CRETINISM occurs in regions of the world where cassava root is a major portion of the diet (Ermans et al, 1972). Cassava liberates thiocyanate in the body, which competes with iodine for uptake by the thyroid (Ermans et al, 1972).
- Enlargement of the thyroid gland has been reported with chronic occupational CYANIDE exposure, and is thought to be due to accumulation of its less toxic metabolite, thiocyanate (El Ghawabi et al, 1975). Both neurotoxic and goiterogenic effects have been produced in rats from chronic feeding of POTASSIUM CYANIDE (Philbrick, 1979), whose major metabolite is thiocyanate (Okoh, 1983; Howard & Hanzal, 1955).
- In rats the metabolites of CYANIDE may accumulate over long periods of chronic exposure (Tewe & Maner, 1981).
-MEDICAL TREATMENT
LIFE SUPPORT
- Support respiratory and cardiovascular function.
SUMMARY
- FIRST AID - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 157 (ERG, 2004)
Move victim to fresh air. Call 911 or emergency medical service. Give artificial respiration if victim is not breathing. Do not use mouth-to-mouth method if victim ingested or inhaled the substance; give artificial respiration with the aid of a pocket mask equipped with a one-way valve or other proper respiratory medical device. Administer oxygen if breathing is difficult. Remove and isolate contaminated clothing and shoes. In case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes. For minor skin contact, avoid spreading material on unaffected skin. Keep victim warm and quiet. Effects of exposure (inhalation, ingestion or skin contact) to substance may be delayed. Ensure that medical personnel are aware of the material(s) involved and take precautions to protect themselves.
CYANIDE POISONING The treatment of acetone cyanohydrin poisoning is essentially that for cyanide intoxication. Establish respiration; avoid mouth-to-mouth resuscitation if possible during CPR to prevent self-poisoning. Immediately begin therapy with 100% oxygen. Be prepared for endotracheal intubation if necessary. Rescuers must not enter areas with potential high airborne concentrations of this agent without self-contained breathing apparatus (SCBA) to avoid becoming secondary victims. Avoid direct dermal contact with cyanide contaminated patient or gastric contents. Administer 100% oxygen: Establish secure large bore IV access. A cyanide antidote, either hydroxocobalamin or the sodium nitrite/sodium thiosulfate kit, should be administered to patients with symptomatic poisoning. HYDROXOCOBALAMIN: ADULT DOSE: 5 g (two 2.5 g vials each reconstituted with 100 mL sterile 0.9% saline) administered as an intravenous infusion over 15 minutes. For severe poisoning, a second dose of 5 g may be infused intravenously over 15 minutes to 2 hours, depending on the patient's condition. CHILDREN: Limited experience; a dose of 70 mg/kg has been used in pediatric patients. The Cyanide Antidote Kit is administered as follows: SODIUM NITRITE: Adult: 10 mL (300 mg) of a 3% solution IV at a rate of 2.5 to 5 mL/minute; Child (with normal hemoglobin concentration): 0.2 mL/kg (6 mg/kg) of a 3% solution IV at a rate of 2.5 to 5 mL/minute, not to exceed 10 mL (300 mg). Repeat one-half of initial sodium nitrite dose one-half hour later if there is inadequate clinical response. Calculate pediatric doses precisely to avoid potentially life-threatening methemoglobinemia. Use with caution if carbon monoxide poisoning is also suspected. Monitor blood pressure carefully. Reduce nitrite administration rate if hypotension occurs. SODIUM THIOSULFATE: Administer sodium thiosulfate IV immediately following sodium nitrite. DOSE: ADULT: 50 mL (12.5 g) of a 25% solution; CHILD: 1 mL/kg (250 mg/kg) of a 25% solution, not to exceed 50 mL (12.5 g) total dose. A second dose, one-half of the first dose, may be administered if signs of cyanide toxicity reappear.
SODIUM BICARBONATE: Administer 1 mEq/kg IV to acidotic patients. SEIZURES: Administer a benzodiazepine; DIAZEPAM (ADULT: 5 to 10 mg IV initially; repeat every 5 to 20 minutes as needed. CHILD: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed) or LORAZEPAM (ADULT: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist. CHILD: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue). Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children greater than 5 years). Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.
METHEMOGLOBINEMIA If excessive methemoglobinemia occurs, some authors have suggested that methylene blue should not be used because it could cause release of cyanide from the cyanmethemoglobin complex. Such authors have suggested that emergency exchange transfusion is the treatment of choice. Hyperbaric oxygen therapy could be used to support the patient while preparations for exchange transfusion are being made. However, methylene or toluidine blue have been used successfully in this setting without worsening the course of the cyanide poisoning. There is some controversy over whether or not the induction of methemoglobinemia is the sodium nitrite mechanism of action in cyanide poisoning. As long as intensive care monitoring and further antidote doses (if required) are available, methylene blue can most likely be safely administered in this setting. METHEMOGLOBINEMIA: Determine the methemoglobin concentration and evaluate the patient for clinical effects of methemoglobinemia (ie, dyspnea, headache, fatigue, CNS depression, tachycardia, metabolic acidosis). Treat patients with symptomatic methemoglobinemia with methylene blue (this usually occurs at methemoglobin concentrations above 20% to 30%, but may occur at lower methemoglobin concentrations in patients with anemia, or underlying pulmonary or cardiovascular disorders). Administer oxygen while preparing for methylene blue therapy. METHYLENE BLUE: INITIAL DOSE/ADULT OR CHILD: 1 mg/kg IV over 5 to 30 minutes; a repeat dose of up to 1 mg/kg may be given 1 hour after the first dose if methemoglobin levels remain greater than 30% or if signs and symptoms persist. NOTE: Methylene blue is available as follows: 50 mg/10 mL (5 mg/mL or 0.5% solution) single-dose ampules and 10 mg/1 mL (1% solution) vials. Additional doses may sometimes be required. Improvement is usually noted shortly after administration if diagnosis is correct. Consider other diagnoses or treatment options if no improvement has been observed after several doses. If intravenous access cannot be established, methylene blue may also be given by intraosseous infusion. Methylene blue should not be given by subcutaneous or intrathecal injection. NEONATES: DOSE: 0.3 to 1 mg/kg. Concomitant use of methylene blue with serotonergic drugs, including serotonin reuptake inhibitors (SRIs), selective serotonin reuptake inhibitors (SSRIs), serotonin and norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), norepinephrine-dopamine reuptake inhibitors (NDRIs), triptans, and ergot alkaloids may increase the risk of potentially fatal serotonin syndrome.
HYPERBARIC OXYGEN AND HEMODIALYSIS: May be useful in severe cases not responsive to supportive and antidotal therapy. ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed. HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid. If hypotension persists, administer dopamine (5 to 20 mcg/kg/min) or norepinephrine (ADULT: begin infusion at 0.5 to 1 mcg/min; CHILD: begin infusion at 0.1 mcg/kg/min); titrate to desired response. ALTERNATE ANTIDOTES
INHALATION EXPOSURE INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm. ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
DERMAL EXPOSURE DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999). Some chemicals can produce systemic poisoning by absorption through intact skin. Carefully observe patients with dermal exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
EYE EXPOSURE DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
ORAL/PARENTERAL EXPOSURE In symptomatic patients, skip these steps until other major emergency measures including use of Cyanide Antidote Kit and other life support measures have been instituted. Perform gastric lavage with a large bore tube after endotracheal intubation. GASTRIC LAVAGE: Consider after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion (generally within 1 hour). Protect airway by placement in the head down left lateral decubitus position or by endotracheal intubation. Control any seizures first. ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
Administer 100% oxygen. Establish secure large bore IV. A cyanide antidote, either hydroxocobalamin OR the sodium nitrite/sodium thiosulfate kit, should be administered to patients with symptomatic poisoning. HYDROXOCOBALAMIN: ADULT DOSE: 5 g (two 2.5 g vials each reconstituted with 100 mL sterile 0.9% saline) administered as an intravenous infusion over 15 minutes. For severe poisoning, a second dose of 5 g may be infused intravenously over 15 minutes to 2 hours, depending on the patient's condition. CHILDREN: Limited experience; a dose of 70 mg/kg has been used in pediatric patients. The Cyanide Antidote Kit is administered as follows: SODIUM NITRITE: Adult: 10 mL (300 mg) of a 3% solution IV at a rate of 2.5 to 5 mL/minute; Child (with normal hemoglobin concentration): 0.2 mL/kg (6 mg/kg) of a 3% solution IV at a rate of 2.5 to 5 mL/minute, not to exceed 10 mL (300 mg). Repeat one-half of initial sodium nitrite dose one-half hour later if there is inadequate clinical response. Calculate pediatric doses precisely to avoid potentially life-threatening methemoglobinemia. Use with caution if carbon monoxide poisoning is also suspected. Monitor blood pressure carefully. Reduce nitrite administration rate if hypotension occurs. SODIUM THIOSULFATE: Administer sodium thiosulfate IV immediately following sodium nitrite. DOSE: ADULT: 50 mL (12.5 g) of a 25% solution; CHILD: 1 mL/kg (250 mg/kg) of a 25% solution, not to exceed 50 mL (12.5 g) total dose. A second dose, one-half of the first dose, may be administered if signs of cyanide toxicity reappear.
SODIUM BICARBONATE: Administer 1 mEq/kg IV to acidotic patients. SEIZURES: Administer a benzodiazepine; DIAZEPAM (ADULT: 5 to 10 mg IV initially; repeat every 5 to 20 minutes as needed. CHILD: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed) or LORAZEPAM (ADULT: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist. CHILD: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue). Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children greater than 5 years). Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.
ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed. HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid. If hypotension persists, administer dopamine (5 to 20 mcg/kg/min) or norepinephrine (ADULT: begin infusion at 0.5 to 1 mcg/min; CHILD: begin infusion at 0.1 mcg/kg/min); titrate to desired response. HYPERBARIC OXYGEN AND HEMODIALYSIS: May be useful in severe cases not responsive to supportive and antidotal therapy. If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests. Whole blood cyanide levels may be obtained to document the poisoning and response to treatment. METHEMOGLOBINEMIA If excessive methemoglobinemia occurs, some authors have suggested that methylene blue should not be used because it could cause release of cyanide from the cyanmethemoglobin complex. Such authors have suggested that emergency exchange transfusion is the treatment of choice. Hyperbaric oxygen therapy could be used to support the patient while preparations for exchange transfusion are being made. However, methylene or toluidine blue have been used successfully in this setting without worsening the course of the cyanide poisoning. There is some controversy over whether or not the induction of methemoglobinemia is the sodium nitrite mechanism of action in cyanide poisoning. As long as intensive care monitoring and further antidote doses (if required) are available, methylene blue can most likely be safely administered in this setting. METHEMOGLOBINEMIA: Determine the methemoglobin concentration and evaluate the patient for clinical effects of methemoglobinemia (ie, dyspnea, headache, fatigue, CNS depression, tachycardia, metabolic acidosis). Treat patients with symptomatic methemoglobinemia with methylene blue (this usually occurs at methemoglobin concentrations above 20% to 30%, but may occur at lower methemoglobin concentrations in patients with anemia, or underlying pulmonary or cardiovascular disorders). Administer oxygen while preparing for methylene blue therapy. METHYLENE BLUE: INITIAL DOSE/ADULT OR CHILD: 1 mg/kg IV over 5 to 30 minutes; a repeat dose of up to 1 mg/kg may be given 1 hour after the first dose if methemoglobin levels remain greater than 30% or if signs and symptoms persist. NOTE: Methylene blue is available as follows: 50 mg/10 mL (5 mg/mL or 0.5% solution) single-dose ampules and 10 mg/1 mL (1% solution) vials. Additional doses may sometimes be required. Improvement is usually noted shortly after administration if diagnosis is correct. Consider other diagnoses or treatment options if no improvement has been observed after several doses. If intravenous access cannot be established, methylene blue may also be given by intraosseous infusion. Methylene blue should not be given by subcutaneous or intrathecal injection. NEONATES: DOSE: 0.3 to 1 mg/kg. Concomitant use of methylene blue with serotonergic drugs, including serotonin reuptake inhibitors (SRIs), selective serotonin reuptake inhibitors (SSRIs), serotonin and norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), norepinephrine-dopamine reuptake inhibitors (NDRIs), triptans, and ergot alkaloids may increase the risk of potentially fatal serotonin syndrome.
ALTERNATE ANTIDOTES: Kelocyanor(R) (dicobalt-EDTA) and 4-DMAP (4-dimethylaminophenol) are alternate cyanide antidotes in clinical use in various countries outside the USA. See Treatment Sections in the Cyanide Meditext(R) Medical Management for more information.
-RANGE OF TOXICITY
MINIMUM LETHAL EXPOSURE
- The minimum lethal human dose to this agent has not been delineated.
- Ingestion of the substance can cause death, which may be preceded by paralysis and respiratory failure (Sittig, 1991).
MAXIMUM TOLERATED EXPOSURE
- At low concentrations, cyanogen iodide may behave as an irritant gas, causing lacrimation, respiratory tract irritation and possibly delayed pulmonary edema (Hartung, 1982).
- Symptoms after ingestion include the following: "anxiety, confusion, dizziness, giddiness, rapid and difficult breathing, palpitations, tightness in chest, unconsciousness, violent convulsions and death" (Sittig, 1991).
- Respiratory passage and eye irritation along with severe lacrimation and blepharospasm result from exposure to 100 mg/m(3) of cyanogen iodide (HSDB , 2001).
- Carcinogenicity Ratings for CAS506-78-5 :
ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed EPA (U.S. Environmental Protection Agency, 2011): Not Listed IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed MAK (DFG, 2002): Not Listed NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed
TOXICITY AND RISK ASSESSMENT VALUES
- EPA Risk Assessment Values for CAS506-78-5 (U.S. Environmental Protection Agency, 2011):
-STANDARDS AND LABELS
WORKPLACE STANDARDS
- ACGIH TLV Values for CAS506-78-5 (American Conference of Governmental Industrial Hygienists, 2010):
- AIHA WEEL Values for CAS506-78-5 (AIHA, 2006):
- NIOSH REL and IDLH Values for CAS506-78-5 (National Institute for Occupational Safety and Health, 2007):
- OSHA PEL Values for CAS506-78-5 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
- OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS506-78-5 (U.S. Occupational Safety and Health Administration, 2010):
ENVIRONMENTAL STANDARDS
- EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS506-78-5 (U.S. Environmental Protection Agency, 2010):
- EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS506-78-5 (U.S. Environmental Protection Agency, 2010):
- EPA RCRA Hazardous Waste Number for CAS506-78-5 (U.S. Environmental Protection Agency, 2010b):
- EPA SARA Title III, Extremely Hazardous Substance List for CAS506-78-5 (U.S. Environmental Protection Agency, 2010):
Listed as: Cyanogen Iodide Reportable Quantity, in pounds: 1000 Threshold Planning Quantity, in pounds: Note(s): Not Listed
- EPA SARA Title III, Community Right-to-Know for CAS506-78-5 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):
- DOT List of Marine Pollutants for CAS506-78-5 (49 CFR 172.101 - App. B, 2005):
- EPA TSCA Inventory for CAS506-78-5 (EPA, 2005):
SHIPPING REGULATIONS
- DOT -- Table of Hazardous Materials and Special Provisions (49 CFR 172.101, 2005):
- ICAO International Shipping Name (ICAO, 2002):
LABELS
- NFPA Hazard Ratings for CAS506-78-5 (NFPA, 2002):
-PERSONAL PROTECTION
SUMMARY
- RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 157 (ERG, 2004)
Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection. Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.
- Personnel should wear appropriate protective clothing and breathing apparatus (Sittig, 1991).
RESPIRATORY PROTECTION
- Refer to "Recommendations for respirator selection" in the NIOSH Pocket Guide to Chemical Hazards on TOMES Plus(R) for respirator information.
PROTECTIVE CLOTHING
- CHEMICAL PROTECTIVE CLOTHING. Search results for CAS 506-78-5.
-PHYSICAL HAZARDS
FIRE HAZARD
Editor's Note: This material is not listed in the Emergency Response Guidebook. Based on the material's physical and chemical properties, toxicity, or chemical group, a guide has been assigned. For additional technical information, contact one of the emergency response telephone numbers listed under Public Safety Measures. POTENTIAL FIRE OR EXPLOSION HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 157 (ERG, 2004) Non-combustible, substance itself does not burn but may decompose upon heating to produce corrosive and/or toxic fumes. Vapors may accumulate in confined areas (basement, tanks, hopper/tank cars etc.). Substance will react with water (some violently), releasing corrosive and/or toxic gases. Contact with metals may evolve flammable hydrogen gas. Containers may explode when heated or if contaminated with water.
- FLAMMABILITY CLASSIFICATION
- NFPA Flammability Rating for CAS506-78-5 (NFPA, 2002):
- FIRE CONTROL/EXTINGUISHING AGENTS
- FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 157 (ERG, 2004)
- SMALL FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 157 (ERG, 2004)
- LARGE FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 157 (ERG, 2004)
Water spray, fog or alcohol-resistant foam. Move containers from fire area if you can do it without risk. Use water spray or fog; do not use straight streams. Dike fire control water for later disposal; do not scatter the material.
- TANK OR CAR/TRAILER LOAD FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 157 (ERG, 2004)
Fight fire from maximum distance or use unmanned hose holders or monitor nozzles. Do not get water inside containers. Cool containers with flooding quantities of water until well after fire is out. Withdraw immediately in case of rising sound from venting safety devices or discoloration of tank. ALWAYS stay away from tanks engulfed in fire.
- NFPA Extinguishing Methods for CAS506-78-5 (NFPA, 2002):
- Use water spray, foam, carbon dioxide, or dry chemical to combat small cyanogen iodide fires. Use water spray, foam, or fog for large fires (Sittig, 1991).
Highly toxic vapors of nitrogen oxides, cyanide, and iodide are produced when cyanogen iodide is heated to decomposition (Lewis, 2000). Heating of cyanogen iodide may cause polymerization, thus producing highly toxic hydrogen cyanide (ILO , 1998).
DUST/VAPOR HAZARD
- Highly toxic vapors of nitrogen oxides, cyanide, and iodide are produced when cyanogen iodide is heated to decomposition (Lewis, 2000).
- Heating of cyanogen iodide may cause polymerization, thus producing highly toxic hydrogen cyanide gas (ILO , 1998).
- Contact with acids, water, or humidity also produces hydrogen cyanide gas (ILO , 1998).
REACTIVITY HAZARD
- Highly toxic vapors of nitrogen oxides, cyanide, and iodide are produced when cyanogen iodide is heated to decomposition (Lewis, 2000).
- Heating of cyanogen iodide may cause polymerization, thus producing highly toxic hydrogen cyanide (ILO , 1998).
- Contact with acids, carbon dioxide, water, or humidity also produces hydrogen cyanide gas (HSDB , 2001; ILO , 1998).
- Cyanogen iodide in contact with phosphorus or strong oxidizers results in a violent reaction (ILO , 1998; Lewis, 2000).
- The substance is incompatible with alkalis, ammonia and alcohols (HSDB , 2001).
- Cyanogen iodide plus molten phosphorus will react with incandescence, producing phosphorus iodide (NFPA, 1997).
EVACUATION PROCEDURES
- Editor's Note: This material is not listed in the Table of Initial Isolation and Protective Action Distances.
- SPILL - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 157 (ERG, 2004)
Increase, in the downwind direction, as necessary, the isolation distance of at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids in all directions.
- FIRE - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 157 (ERG, 2004)
If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions.
- PUBLIC SAFETY MEASURES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 157 (ERG, 2004)
CALL Emergency Response Telephone Number on Shipping Paper first. If Shipping Paper not available or no answer, refer to appropriate telephone number: MEXICO: SETIQ: 01-800-00-214-00 in the Mexican Republic; For calls originating in Mexico City and the Metropolitan Area: 5559-1588; For calls originating elsewhere, call: 011-52-555-559-1588.
CENACOM: 01-800-00-413-00 in the Mexican Republic; For calls originating in Mexico City and the Metropolitan Area: 5550-1496, 5550-1552, 5550-1485, or 5550-4885; For calls originating elsewhere, call: 011-52-555-550-1496, or 011-52-555-550-1552; 011-52-555-550-1485, or 011-52-555-550-4885.
ARGENTINA: CIQUIME: 0-800-222-2933 in the Republic of Argentina; For calls originating elsewhere, call: +54-11-4613-1100.
BRAZIL: PRÓ-QUÍMICA: 0-800-118270 (Toll-free in Brazil); For calls originating elsewhere, call: +55-11-232-1144 (Collect calls are accepted).
COLUMBIA: CISPROQUIM: 01-800-091-6012 in Colombia; For calls originating in Bogotá, Colombia, call: 288-6012; For calls originating elsewhere, call: 011-57-1-288-6012.
CANADA: UNITED STATES:
For additional details see the section entitled "WHO TO CALL FOR ASSISTANCE" under the ERG Instructions. As an immediate precautionary measure, isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids. Keep unauthorized personnel away. Stay upwind. Keep out of low areas. Ventilate enclosed areas.
- AIHA ERPG Values for CAS506-78-5 (AIHA, 2006):
- DOE TEEL Values for CAS506-78-5 (U.S. Department of Energy, Office of Emergency Management, 2010):
Listed as Cyanogen iodide TEEL-0 (units = mg/m3): 29.4 TEEL-1 (units = mg/m3): 29.4 TEEL-2 (units = mg/m3): 147 TEEL-3 (units = mg/m3): 147 Definitions: TEEL-0: The threshold concentration below which most people will experience no adverse health effects. TEEL-1: The airborne concentration (expressed as ppm [parts per million] or mg/m(3) [milligrams per cubic meter]) of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic, nonsensory effects. However, these effects are not disabling and are transient and reversible upon cessation of exposure. TEEL-2: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long-lasting, adverse health effects or an impaired ability to escape. TEEL-3: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience life-threatening adverse health effects or death.
- AEGL Values for CAS506-78-5 (National Research Council, 2010; National Research Council, 2009; National Research Council, 2008; National Research Council, 2007; NRC, 2001; NRC, 2002; NRC, 2003; NRC, 2004; NRC, 2004; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; United States Environmental Protection Agency Office of Pollution Prevention and Toxics, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; 62 FR 58840, 1997; 65 FR 14186, 2000; 65 FR 39264, 2000; 65 FR 77866, 2000; 66 FR 21940, 2001; 67 FR 7164, 2002; 68 FR 42710, 2003; 69 FR 54144, 2004):
- NIOSH IDLH Values for CAS506-78-5 (National Institute for Occupational Safety and Health, 2007):
CONTAINMENT/WASTE TREATMENT OPTIONS
SPILL OR LEAK PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 157 (ERG, 2004) ELIMINATE all ignition sources (no smoking, flares, sparks or flames in immediate area). All equipment used when handling the product must be grounded. Do not touch damaged containers or spilled material unless wearing appropriate protective clothing. Stop leak if you can do it without risk. A vapor suppressing foam may be used to reduce vapors. DO NOT GET WATER INSIDE CONTAINERS. Use water spray to reduce vapors or divert vapor cloud drift. Avoid allowing water runoff to contact spilled material. Prevent entry into waterways, sewers, basements or confined areas.
RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 157 (ERG, 2004) Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection. Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.
If personnel will not be put at risk, they should move containers of cyanogen iodide from the area of the fire (Sittig, 1991). Water used for fire control should be diked and fire material should not be scattered (Sittig, 1991). The spill/fire area should be isolated. Only essential containment/fire personnel should be in area. Ventilate before entering closed areas; remain upwind of spill/fire and stay away from low areas (Sittig, 1991). "Remove and isolate contaminated clothing at the site" (Sittig, 1991). If they are not put at undue risk, personnel should stop a cyanogen iodide leak (Sittig, 1991). Reduce fumes with water spray and do not touch cyanogen iodide spills (Sittig, 1991).
"At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices" (HSDB , 2001). Waste management activities associated with material disposition are unique to individual situations. Proper waste characterization and decisions regarding waste management should be coordinated with the appropriate local, state, or federal authorities to ensure compliance with all applicable rules and regulations.
-ENVIRONMENTAL HAZARD MANAGEMENT
POLLUTION HAZARD
- There was no information on pollution hazards for cyanogen iodide in available references at the time of this review.
ENVIRONMENTAL FATE AND KINETICS
ENVIRONMENTAL TOXICITY
- There was no information on environmental toxicity for cyanogen iodide in available references at the time of this review.
-PHYSICAL/CHEMICAL PROPERTIES
MOLECULAR WEIGHT
DESCRIPTION/PHYSICAL STATE
- Cyanogen iodide is a colorless to whitish needle-like solid with an acrid flavor and a very strong odor (HSDB, 2005; Budavari, 2000; Lewis, 2000; Lewis, 1998).
VAPOR PRESSURE
- 1 mmHg (at 25.2 degrees C) (Lewis, 2000)
- 0.13 kPa (at 25.2 degrees C) (ILO , 1998)
SPECIFIC GRAVITY
- TEMPERATURE AND/OR PRESSURE NOT LISTED
DENSITY
- TEMPERATURE AND/OR PRESSURE NOT LISTED
FREEZING/MELTING POINT
146.5 degrees C (ILO , 1998; Lewis, 2000) 148 degrees C (HSDB, 2005) 146-147 degrees C (Budavari, 2000)
BOILING POINT
- >45 degrees C sublimation (ILO , 1998)
SOLUBILITY
Cyanogen iodide "reacts" in water (ILO , 1998) Cyanogen iodide is soluble in water (Budavari, 2000; Lewis, 1997).
Cyanogen iodide is soluble in alcohol, ether, ethanol, and volatile oils (HSDB, 2005; Budavari, 2000; Lewis, 1997).
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