POTASSIUM PERMANGANATE
HAZARDTEXT ®
Information to help in the initial response for evaluating chemical incidents
 -IDENTIFICATION
SYNONYMS
Potassium permanganate Algae-K Argucide Chlorisol Cairox Chameleon mineral Condy's crystals Diversey Diversol CX with Arodyne Diversey Diversol CXU Hilco #88 Icc 237 Disinfectant, Sanitizer, Destainer, and Deodorizer Kaliumpermanganaat (Dutch) Kaliumpermanganat (German) Permanganate de potassium (French) Permanganate of potash Permanganato potasico (Spanish) Permanganic acid potassium salt Permanganic acid, potassium salt Potassio (permanganato di) (Italian) Potassium (permanganate de) (French) Purple salt Solo San Soo Walko Tablets KMnO4
IDENTIFIERS
C.I. NUMBER:77755 EPA PESTICIDE CHEMICAL CODE:068501 IMO CLASSIFICATION:5.1 - Potassium permanganate STANDARD INDUSTRIAL TRADE CLASSIFICATION NUMBER:52389
SYNONYM REFERENCE
- (HSDB, 2004; Pohanish, 2002; RTECS, 2004)
USES/FORMS/SOURCES
Potassium permanganate's industrial uses include bleaching resins, waxes, fats, oils, straw, cotton, silk and other fibers and chamois skins; dyeing wood; printing fabrics; purifying air and water; decontamination of skin; treatment of eczema; etching rubber and plastic; surface treatment of steel (especially in wire manufacture); and tanning leathers. It is also used as a fungicide; insecticide; miticide; algicide; bacteriocide; germicide; antiseptic; oxidizer; disinfectant; deodorant; sanitizer; chemical in photography; and reagent in analytical and synthetic organic chemistry (Goldfrank et al, 2002; HSDB, 2004; Pohanish, 2002; Budavari, 2001; Lewis, 2001; Lewis, 1998). Therapeutically, potassium permanganate is used as a topical anti-infective. In veterinary medicine it is used as a topical antiseptic, astringent, and deodorant (Budavari, 2001). Illicit uses have included the production of drugs of abuse, and induction of abortion by topical application to the vaginal wall (21 CFR 250.108, 2003; Lewis, 2000; Lewis, 2000; Lewis, 1998). Historically, potassium permanganate has been used as a urethral irrigant, lavage fluid for alkaloid poisoning, and remedy for snakebites (Goldfrank et al, 2002).
At room temperature, potassium permanganate exists as dark purple or bronze-colored, odorless, sweetish, astringent tasting orthorhombic crystals that are almost opaque by transmitted light and have a blue, metallic sheen by reflected light. It is readily soluble in water; aqueous solutions are pink to violet in color, depending on concentration, and slowly deposit manganese dioxide (HSDB, 2004; Budavari, 2001; Lewis, 2001; Lewis, 2000; Lewis, 1998; Freeman, 1998). Available grades include technical, CP (chemically pure), reagent (99+% pure), and USP(CHRIS, 2004; Lewis, 2001a). Formulations include ready-to-use solutions, pellets, tablets, crystals, and powder (HSDB, 2004).
Potassium permanganate is produced from manganese ore by electrolytic oxidation (Budavari, 2001; Lewis, 2001a). It may be prepared by oxidizing manganese dioxide with potassium chlorate in potassium hydroxide solution, then completing the oxidation with chlorine or air and carbon dioxide (HSDB, 2004). It is manufactured by a two-step process of thermal oxidation of manganese oxide (from ore) into potassium manganate, followed by electrolytic oxidation to potassium permanganate (HSDB, 2004). The reaction between manganese ore and potassium hydroxide by thermal oxidation and electrolytic oxidation produces potassium permanganate (Ashford, 2001). Treatment of a hot solution of manganate with carbon dioxide will, on cooling, result in the precipitation of potassium permanganate crystals (Lewis, 2001a). It may be manufactured by roasting processes that use manganese(IV) oxide and potassium hydroxide in a molar ratio of 1:2 to 1:3, then heating to 300-400 degrees C, and exposure to secondary oxidation at 190-210 degrees C (HSDB, 2004). A liquid-phase process can be used to manufacture potassium permanganate where manganese(IV) oxide and potassium hydroxide are in a molar ratio greater than or equal to 1:5. The molten mixture (at 200-350 degrees C) is oxygenated, and then the product may be obtained through separation (HSDB, 2004).
-CLINICAL EFFECTS
GENERAL CLINICAL EFFECTS
- USES: Potassium permanganate is an antiseptic and astringent agent with powerful oxidizing effects. Industrial uses include bleaching resins, waxes, fats, oils, straw, cotton, silk and other fibers and chamois skins. It is also used as a disinfectant, deodorant, sanitizer, chemical in photography, and reagent in analytical and synthetic organic chemistry. Illicit uses have included the production of drugs of abuse and induction of abortion by topical application to the vaginal wall. Historically, potassium permanganate has been used as a urethral irrigant, and lavage fluid for alkaloid poisoning.
- TOXICOLOGY: Potassium permanganate reacts with water to yield manganese dioxide, potassium hydroxide, and oxygen. Potassium hydroxide is a strong alkaline corrosive. In severe cases, systemic effects including disseminated intravascular coagulation (DIC), methemoglobinemia, hepatitis, pancreatitis, and acute renal failure may occur and are possibly caused by free radical generation. Chronic ingestion may cause neurotoxicity, including paresthesias, tremor, and Parkinsonism due to manganese toxicity. Neurotoxicity from manganese results from dopamine depletion and production of the neurotoxins, dopamine quinone and hydrogen peroxide.
- EPIDEMIOLOGY: Patients may be exposed to potassium permanganate by occupational contact or illicit uses.
MILD TO MODERATE TOXICITY: Skin contact with concentrated solutions may cause severe irritation and burns. Contact with diluted solutions can cause purple brown staining of the skin and hardening of the outer layer of the skin. Potassium permanganate may be irritating to the respiratory tract, causing upper airway edema, chest tightness, and coughing. Caustic injury to the mouth and gastrointestinal tract may also occur after ingestion. Eye exposure can cause conjunctival discoloration and corneal and conjunctival burns. SEVERE TOXICITY: Severe gastrointestinal burns have been reported after ingestion. Patients may also develop adult respiratory distress syndrome (ARDS), disseminated intravascular coagulation (DIC), methemoglobinemia, tachycardia, hypotension, metabolic acidosis, coagulopathy, hepatic necrosis, pancreatitis, and acute renal failure. Strictures and gastric outlet obstruction may develop as delayed complications following gastrointestinal burns. Chronic ingestion may cause neurotoxicity, paresthesias, tremor, and Parkinsonism due to manganese toxicity. Potassium permanganate use as an abortifacient may result in vaginal or cervical burns and erosions, with extensive bleeding, shock, severe scarring and miscarriage as possible complications.
- POTENTIAL HEALTH HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 140 (ERG, 2004)
Inhalation, ingestion or contact (skin, eyes) with vapors or substance may cause severe injury, burns or death. Fire may produce irritating, corrosive and/or toxic gases. Runoff from fire control or dilution water may cause pollution.
ACUTE CLINICAL EFFECTS
TOXICOLOGY: Potassium permanganate reacts with water to yield manganese dioxide, potassium hydroxide, and oxygen. Potassium hydroxide is a strong alkaline corrosive. In severe cases, systemic effects including disseminated intravascular coagulation (DIC), methemoglobinemia, hepatitis, pancreatitis, and acute renal failure may occur and are possibly caused by free radical generation. Chronic ingestion may cause neurotoxicity, including paresthesias, tremor, and Parkinsonism due to manganese toxicity. Neurotoxicity from manganese results from dopamine depletion and production of the neurotoxins, dopamine quinone and hydrogen peroxide. EPIDEMIOLOGY: Patients may be exposed to potassium permanganate by occupational contact or illicit uses. MILD TO MODERATE TOXICITY: Skin contact with concentrated solutions may cause severe irritation and burns. Contact with diluted solutions can cause purple brown staining of the skin and hardening of the outer layer of the skin. Potassium permanganate may be irritating to the respiratory tract, causing upper airway edema, chest tightness, and coughing. Caustic injury to the mouth and gastrointestinal tract may also occur after ingestion. Eye exposure can cause conjunctival discoloration and corneal and conjunctival burns. SEVERE TOXICITY: Severe gastrointestinal burns have been reported after ingestion. Patients may also develop adult respiratory distress syndrome (ARDS), disseminated intravascular coagulation (DIC), methemoglobinemia, tachycardia, hypotension, metabolic acidosis, coagulopathy, hepatic necrosis, pancreatitis, and acute renal failure. Strictures and gastric outlet obstruction may develop as delayed complications following gastrointestinal burns. Chronic ingestion may cause neurotoxicity, paresthesias, tremor, and Parkinsonism due to manganese toxicity. Potassium permanganate use as an abortifacient may result in vaginal or cervical burns and erosions, with extensive bleeding, shock, severe scarring and miscarriage as possible complications.
HYPERTENSION: Transient hypertension has been reported after ingestion and injection (Lustig et al, 1982; Middleton et al, 1990). HYPOTENSION: Profound hypotension and circulatory collapse may develop in severe cases (Gawarammana et al, 2009; Lifshitz et al, 1999; Ong et al, 1997; Young et al, 1996; Middleton et al, 1990). TACHYCARDIA: Tachycardia may develop in patients with serious exposure (Mahomedy et al, 1975; Middleton et al, 1990; Lustig et al, 1982).
ABDOMINAL PAIN: Abdominal pain may persist for weeks after ingestion (Guichardiere, 1965). BURNS: Severe burns of the esophagus, stomach, and in severe cases small intestines may develop after ingestion (Lifshitz et al, 1999; Young et al, 1996; Holzgraefe et al, 1986; Middleton et al, 1990; Desmul et al, 1968; Mayer et al, 1972). PANCREATITIS (CASE REPORT): A 75-year-old man developed severe abdominal pain, hyperglycemia and elevated serum amylase levels (3752 U/liter) after ingesting approximately 20 grams of potassium permanganate. Severe hemorrhagic pancreatitis was confirmed on autopsy (Middleton et al, 1990). STRICTURES: Esophageal strictures and gastric outlet obstruction have been reported as delayed (by weeks) complications of potassium permanganate ingestion (Dagli et al, 1973; Kochhar et al, 1986; Wang, 1994).
Acute renal failure has been reported several days after severe poisoning (Young et al, 1996; Ong et al, 1997; Gawarammana et al, 2009).
DISCOLORATION: Purple-brown staining of the mouth and tongue is common after ingestion (Southwood et al, 1987; Middleton et al, 1990; Lifshitz et al, 1999). BURNS: Burns and edema of the oral mucosa and tongue may develop after ingestion (Southwood et al, 1987; Young et al, 1996; Ong et al, 1997; Lifshitz et al, 1999). BURNS: Ocular burns have been reported after exposure (Michaels & Zugsmith, 1973; Sigg et al, 1998).
Disseminated intravascular coagulation (DIC) has been reported after large ingestions (Young et al, 1996; Ong et al, 1997). Severe methemoglobinemia has been reported after exposure (Mahomedy et al, 1975).
HEPATOTOXICITY: Hepatic injury has been described after ingestion and injection (Lustig et al, 1982; Middleton et al, 1990; Lifshitz et al, 1999). In severe cases fulminant hepatic failure and necrosis may develop (Ong et al, 1997; Young et al, 1996).
Paresthesia, tremor, Parkinsonism, and coma have been reported (Holzgraefe et al, 1986; Mahomedy et al, 1975).
LARYNGEAL STRICTURES: Laryngeal strictures have been reported as delayed (by weeks or more) complications after ingestion of potassium permanganate (Wang, 1994). BURNS AND EDEMA: Stridor and upper airway burns and edema may develop after ingestion (Justus & Gastmeier, 1967; Young et al, 1996; Ong et al, 1997; Southwood et al, 1987). ACUTE LUNG INJURY (CASE REPORT): A 75-year-old man developed adult respiratory distress syndrome (ARDS) after ingesting approximately 20 grams of potassium permanganate (Middleton et al, 1990). ACUTE RESPIRATORY DISTRESS SYNDROME (CASE REPORT): An 8-week-old infant developed acute respiratory distress syndrome, seen on chest x-ray, following the ingestion of an unknown amount of a 0.01% solution of potassium permanganate. The infant died 28 hours after admission (Lifshitz et al, 1999).
CHRONIC CLINICAL EFFECTS
- Manganese in general is a CENTRAL NERVOUS SYSTEM POISON (ILO, 1983), and potassium permanganate has also been shown to have this property. Ingestion of an 8% potassium permanganate solution over a four week period (a total of 10 grams) was followed by psychological and CNS disturbances in one person. Elevated levels of manganese in the peripheral blood confirmed systemic distribution. After nine months, progressive PARKINSON'S DISEASE developed (Holzgraefe et al, 1986).
- At the time of this review, no other studies were found on the potential effects of chronic potassium permanganate exposure in humans or experimental animals.
-FIRST AID
FIRST AID AND PREHOSPITAL TREATMENT
If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. The exact ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004). USE OF DILUENTS IS CONTROVERSIAL: While experimental models have suggested that immediate dilution may lessen caustic injury (Homan et al, 1993; Homan et al, 1994; Homan et al, 1995), this has not been adequately studied in humans. DILUENT TYPE: Use any readily available nontoxic, cool liquid. Both milk and water have been shown to be effective in experimental studies of caustic ingestion (Maull et al, 1985; Rumack & Burrington, 1977; Homan et al, 1995; Homan et al, 1994; Homan et al, 1993). ADVERSE EFFECTS: Potential adverse effects include vomiting and airway compromise (Caravati, 2004). CONTRAINDICATIONS: Do NOT attempt dilution in patients with respiratory distress, altered mental status, severe abdominal pain, nausea or vomiting, or patients who are unable to swallow or protect their airway. Diluents should not be force fed to any patient who refuses to swallow (Rao & Hoffman, 2002).
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. ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases. NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011). To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011). ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998). EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995). CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005). However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).
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.
-MEDICAL TREATMENT
LIFE SUPPORT
- Support respiratory and cardiovascular function.
SUMMARY
- FIRST AID - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 140 (ERG, 2004)
Move victim to fresh air. Call 911 or emergency medical service. Give artificial respiration if victim is not breathing. Administer oxygen if breathing is difficult. Remove and isolate contaminated clothing and shoes. Contaminated clothing may be a fire risk when dry. In case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes. Keep victim warm and quiet. Ensure that medical personnel are aware of the material(s) involved and take precautions to protect themselves.
ORAL EXPOSURE DILUTION If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. The exact ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004). USE OF DILUENTS IS CONTROVERSIAL: While experimental models have suggested that immediate dilution may lessen caustic injury (Homan et al, 1993; Homan et al, 1994; Homan et al, 1995), this has not been adequately studied in humans. DILUENT TYPE: Use any readily available nontoxic, cool liquid. Both milk and water have been shown to be effective in experimental studies of caustic ingestion (Maull et al, 1985; Rumack & Burrington, 1977; Homan et al, 1995; Homan et al, 1994; Homan et al, 1993). ADVERSE EFFECTS: Potential adverse effects include vomiting and airway compromise (Caravati, 2004). CONTRAINDICATIONS: Do NOT attempt dilution in patients with respiratory distress, altered mental status, severe abdominal pain, nausea or vomiting, or patients who are unable to swallow or protect their airway. Diluents should not be force fed to any patient who refuses to swallow (Rao & Hoffman, 2002).
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. ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases. NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011). To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011). ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998). EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995). CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005). However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).
DERMAL EXPOSURE 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.
-RANGE OF TOXICITY
MINIMUM LETHAL EXPOSURE
The probable lethal dose for a 150 lb (70 kg) adult is 10 grams (approximately 1.5 teaspoons) (Pohanish, 2002; Ong et al, 1997; Middleton et al, 1990; Cowie & Escreet, 1981) .
ADULT A 75-year-old man died after ingesting 20 grams of potassium permanganate. Complications included ARDS, hepatocellular injury, acute tubular necrosis, gastrointestinal burns, and hemorrhagic pancreatitis (Middleton et al, 1990). A 24-year-old, Chinese woman died after intentional ingestion of an unknown amount of potassium permanganate crystals. She was admitted to the hospital with initial symptoms of brownish-black staining of the hands, lips, oropharynx, and upper esophagus, and swelling of the tongue, lips, and laryngeal structures. Between hours 36 and 72 hours after admission, she developed cardiovascular instability, disseminated intravascular coagulation, hepatic and renal failure, and adult respiratory distress syndrome. Progressive cardiovascular failure developed, and the patient died on day 6. Serum manganese levels on days 5 and 6 were 756 and 1629 mcmol/L, respectively (Ong et al, 1997; Young et al, 1996).
PEDIATRIC A 33-month-old child died after ingesting one teaspoonful of potassium permanganate crystals (Justus & Gastmeier, 1967). An 8-week-old child died following ingestion of an unknown amount of a approximately 0.01% potassium permanganate solution. Upon admission to the hospital, the infant presented with a swollen tongue, drooling, inflamed oral mucosa with brownish-black staining, and severe edema of the mouth, pharynx, and epiglottis. He died 28 hours later despite intensive support, having developed hypotension, metabolic acidosis, acute respiratory distress syndrome (ARDS), E. coli bacteremia, severe bradycardia, and cardiac arrest (Lifshitz et al, 1999).
MAXIMUM TOLERATED EXPOSURE
ADULT An 18-year-old man who ingested ten 300-mg tablets of potassium permanganate developed gastric burns complicated by gastric outlet obstruction 9 weeks after ingestion (Dagli et al, 1973). A 66-year-old man ingested approximately 10 grams of potassium permanganate (approximately 125 mL of an 8% solution) over the course of a 4 week period, due to a dispensing error. He suffered severe abdominal pain and cramping, a reduction in physical capacity and ability to concentrate, visual disturbances, paresthesias of the right hand and foot, as well as increased sweating. Manganese in the blood was measured at a maximal level of 15 g/100 mL, and in the hair, 1.6 g/g. Nine months following the poisoning, the patient exhibited parkinsonian symptoms, including a resting tremor of four beats/second, a slow grade rigor of the extremities, and a shortening of gait (Holzgraefe et al, 1986). A 14 year follow-up with the patient (then 80 years old) showed that most of the initial symptoms were improved, however, the parkinsonian syndrome was unchanged (Bleich et al, 1999).
A 42-year-old man developed caustic gastric injury about 12 hours after ingesting 20 g of a household antiseptic, containing potassium permanganate dissolved in 300 mL of water. Following supportive care, including IV fluids, a proton pump inhibitor, and antibiotics, his condition gradually improved and he was discharged 4 days later (Younan et al, 2013).
PEDIATRIC A 3-year-old boy developed upper airway edema after ingesting an estimated 5 to 10 grams of potassium permanganate crystals. The child was treated with intubation, antibiotics, and corticosteroids. Liver and renal function tests remained normal and the child recovered completely (Southwood et al, 1987).
ADULT In Sri Lanka, intentional ingestion of a laundry detergent containing a sachet each of 12.5 g oxalic acid and 1.2 g potassium permanganate resulted in 115 cases of toxicity with 18 fatalities. Gastrointestinal symptoms developed within 24 hours of ingestion. Of the individuals that ingested oxalic acid only, a case fatality ratio of 25.4% was observed, while a case fatality ratio of 9.8% occurred in patients ingesting both oxalic acid and potassium permanganate. Of the 35 patients who ingested 2 or mor sachets of both potassium permanganate and oxalic acid, 16 died (46%). Of the 58 patients who ingested one sachet or less, 2 died (3%). Most deaths occurred within one hour of ingestion. No deaths were reported in the potassium permanganate only ingestion. Individuals ingesting a sublethal dose of oxalic acid and potassium permanganate (n=51), developed acute renal failure 2 to 3 days after exposure. Median serum creatinine was 1.7 (Interquartile range: 0.91-4.4). Most recovered with supportive care (Gawarammana et al, 2009).
- Carcinogenicity Ratings for CAS7722-64-7 :
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 CAS7722-64-7 (U.S. Environmental Protection Agency, 2011):
ANIMAL DATA LD- (SUBCUTANEOUS)MOUSE: LD50- (ORAL)GUINEA_PIG: LD50- (ORAL)GUINEA_PIG: LD50- (ORAL)MOUSE: LD50- (ORAL)MOUSE: LD50- (SUBCUTANEOUS)MOUSE: LD50- (ORAL)RAT: LD50- (ORAL)RAT: LDLo- (ORAL)DOG: LDLo- (INTRAVENOUS)RABBIT: LDLo- (ORAL)RABBIT: TDLo- (INTRATESTICULAR)GERBIL: TDLo- (ORAL)MOUSE: TDLo- (INTRATESTICULAR)RAT: TDLo- (ORAL)RAT: 7851 mg/kg for 39W, intermittent -- altered classical conditioning; changed serum composition (e.g., TP, bilirubin, cholesterol); affected cholinesterases (RTECS, 2004)
HUMAN LDLo- (ORAL)HUMAN: LDLo- (ORAL)HUMAN: TDLo- (ORAL)HUMAN:
-STANDARDS AND LABELS
WORKPLACE STANDARDS
- ACGIH TLV Values for CAS7722-64-7 (American Conference of Governmental Industrial Hygienists, 2010):
- AIHA WEEL Values for CAS7722-64-7 (AIHA, 2006):
- NIOSH REL and IDLH Values for CAS7722-64-7 (National Institute for Occupational Safety and Health, 2007):
- OSHA PEL Values for CAS7722-64-7 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
- OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS7722-64-7 (U.S. Occupational Safety and Health Administration, 2010):
ENVIRONMENTAL STANDARDS
- EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS7722-64-7 (U.S. Environmental Protection Agency, 2010):
- EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS7722-64-7 (U.S. Environmental Protection Agency, 2010):
- EPA RCRA Hazardous Waste Number for CAS7722-64-7 (U.S. Environmental Protection Agency, 2010b):
- EPA SARA Title III, Extremely Hazardous Substance List for CAS7722-64-7 (U.S. Environmental Protection Agency, 2010):
- EPA SARA Title III, Community Right-to-Know for CAS7722-64-7 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):
- DOT List of Marine Pollutants for CAS7722-64-7 (49 CFR 172.101 - App. B, 2005):
- EPA TSCA Inventory for CAS7722-64-7 (EPA, 2005):
SHIPPING REGULATIONS
- DOT -- Table of Hazardous Materials and Special Provisions for UN/NA Number 1490 (49 CFR 172.101, 2005):
- ICAO International Shipping Name for UN1490 (ICAO, 2002):
LABELS
- NFPA Hazard Ratings for CAS7722-64-7 (NFPA, 2002):
-HANDLING AND STORAGE
HANDLING
- Wear proper protective clothing, including chemical protective gloves, boots, and goggles. The material will attack rubber and most fibers (CHRIS, 2004; AAR, 2002; Pohanish, 2002).
Do not handle broken containers unless wearing adequate protective clothing (AAR, 2002). Contact with skin will cause burns and stain the skin a dark brown color (CHRIS, 2004).
- Isolate potassium permanganate from all other materials (Pohanish & Greene, 1997).
- Do not allow potassium permanganate (dry or solution) to come into contact with organic or other readily oxidizable substances, as fire or explosion may result (Lewis, 2001; Lewis, 2000; Lewis, 1998).
- The material should be kept out of contact with combustibles, including wood, as fire on contact may result (CHRIS, 2004).
- Use explosion-proof electrical equipment and fittings in areas where potassium permanganate is manufactured, handled, used, or stored (Pohanish, 2002).
- Sources of ignition are prohibited where the material is used, handled, or stored (Pohanish, 2002).
- Do not eat, drink, or smoke when working with or around potassium permanganate (ILO ICSC, 2003).
- Suppress the suspension of potassium permanganate dusts (OHM/TADS, 2004).
- During chemical transfer operations, metal containers should be grounded and bonded. Use automatic transfer when possible (Pohanish, 2002).
STORAGE
Aqueous solutions of potassium permanganate should be stored in steel vessels, rather than plastic or rubber containers (Freeman, 1998). Potassium permanganate is stored in bottles and cans (OHM/TADS, 2004). Containers should be tightly closed (Pohanish, 2002). Protect containers from physical damage and moisture (OHM/TADS, 2004; Pohanish, 2002).
- ROOM/CABINET RECOMMENDATIONS
Potassium permanganate should be stored in a cool, dry, well-ventilated, and dark location (Pohanish, 2002; Freeman, 1998).
Potassium permanganate will attack rubber and most fibers, and may cause ignition of wood (CHRIS, 2004; Budavari, 2001). Fire or explosion will result on contact with reducing materials, strong acids (hydrochloric, sulfuric, nitric), combustibles, organic matter, or oxidizable solids, liquids, or gases. Potassium permanganate must be stored so as to avoid contact with these types of materials (Pohanish, 2002).
-PERSONAL PROTECTION
SUMMARY
- RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 140 (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 will only provide limited protection.
- Full PPE is recommended. Potassium permanganate is a toxic and caustic compound, causing severe irritation and burns of the skin and eyes on contact and respiratory irritation and possibly pulmonary edema. It causes poisoning if ingested. Death can result from exposure to high concentrations (Goldfrank et al, 2002; Pohanish, 2002; Budavari, 2001; Lewis, 2000).
- Personal protective clothing (e.g., gloves, protective suits, boots, goggles, respirators) should be worn to prevent skin or eye contact with and inhalation of potassium permanganate (ILO ICSC, 2003; Pohanish, 2002).
EYE/FACE PROTECTION
- Wear goggles or face shield (CHRIS, 2004; ILO ICSC, 2003; Pohanish, 2002).
When working with potassium permanganate solution, wear splash-proof chemical goggles and face shield, unless full facepiece respiratory protection is being used (Pohanish, 2002). When working with the solid material in powder or dust form, wear dust-proof goggles, unless full facepiece respiratory protection is being used (Pohanish, 2002).
- Do not wear contact lenses when working with or around potassium permanganate (Pohanish, 2002).
RESPIRATORY PROTECTION
- Wear a NIOSH-approved respirator if the possibility of exposure to potassium permanganate dust or powder exists. A supplied air full-face respirator or self contained breathing apparatus (SCBA) may be necessary when working with solutions (Pohanish, 2002).
PROTECTIVE CLOTHING
- CHEMICAL PROTECTIVE CLOTHING. Search results for CAS 7722-64-7.
ENGINEERING CONTROLS
- Local exhaust ventilation is recommended to reduce worker exposure to potassium permanganate dust (ILO ICSC, 2003)
OTHER
- INDUSTRIAL DECONTAMINATION
If potassium permanganate contacts the skin, immediately wash affected area(s) with soap and water. Remove any contaminated clothing, shoes, or equipment. Seek medical attention right away (ILO ICSC, 2003; Pohanish, 2002). If potassium permanganate contacts the eye(s), remove contact lenses if present, then immediately flush the eye(s) with water for at least 15 minutes, occasionally lifting the upper and lower eyelids. Seek medical attention right away (ILO ICSC, 2003; Pohanish, 2002). Provide emergency showers and eye wash stations in areas where potassium permanganate is used (Pohanish, 2002).
-PHYSICAL HAZARDS
FIRE HAZARD
POTENTIAL FIRE OR EXPLOSION HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 140 (ERG, 2004) These substances will accelerate burning when involved in a fire. Some may decompose explosively when heated or involved in a fire. May explode from heat or contamination. Some will react explosively with hydrocarbons (fuels). May ignite combustibles (wood, paper, oil, clothing, etc.). Containers may explode when heated. Runoff may create fire or explosion hazard.
Potassium permanganate is not combustible, but enhances combustion processes (ILO ICSC, 2003). The reaction between potassium permanganate and a great number of different materials results in extreme fire hazard. Some of these hazardous reactions are detailed below (NFPA, 2002; Urben, 1999): The addition of a 20% potassium permanganate solution to nitric acid before mixing with an alcohol (methanol, ethanol, isopropanol, pentanol, or isopentanol) results in immediate ignition. Antimony and potassium permanganate will ignite on being ground together in a mortar. Pure dichloromethylsilane will ignite in the presence of potassium permanganate. Dimethyl sulfoxide and solid potassium permanganate ignite on contact. Attempted disinfection of a building using large quantities of formaldehyde (as formalin) and potassium permanganate resulted in a large fire. Contact of glycerol with solid potassium permanganate will result in a vigorous fire. Hydrogen peroxide that came in contact with packages of potassium permanganate led to a violent reaction and fire. Liquid hydrogen trisulfide will ignite on contact with solid potassium permanganate. Hydroxylamine will ignite on contact with solid potassium permanganate. Carbon and potassium permanganate mixtures will burn vigorously when heated. Mixtures of potassium permanganate and organic nitro compounds ignite easily when heated, or on contact with sulfuric acid. They are also shock-sensitive. Oxidation of 3,4,4'-trimethyldiphenyl sulfone using potassium permanganate can result in a vigorous exothermic reaction. Contact between solid potassium permanganate and wood, in the presence of moisture or mechanical friction, may lead to fire. Potassium permanganate ignited a polypropylene tube as it passed through.
Iron and potassium permanganate form shock-sensitive mixtures and may result in combustion when exposed to loud noise (percussion) (ITI, 1995). Incandescence was reported for the following reactions (Urben, 1999): Mixtures of aluminum carbide and potassium permanganate will incandesce when warmed. Oxidation of ammonia with the potassium permanganate formed in the mixture of ammonia and sulfuric acid will result in incandescence due to the permanganic acid formed during the reaction.
- FLAMMABILITY CLASSIFICATION
- NFPA Flammability Rating for CAS7722-64-7 (NFPA, 2002):
- INITIATING OR CONTRIBUTING PROPERTIES
While potassium permanganate itself is not combustible, it releases oxygen on decomposition, which will greatly intensify a surrounding fire and accelerate the combustion of combustible materials (AAR, 2002; Pohanish, 2002).
- FIRE CONTROL/EXTINGUISHING AGENTS
- SMALL FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 140 (ERG, 2004)
- LARGE FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 140 (ERG, 2004)
Flood fire area with water from a distance. Move containers from fire area if you can do it without risk. Do not move cargo or vehicle if cargo has been exposed to heat. Fight fire from maximum distance or use unmanned hose holders or monitor nozzles. Cool containers with flooding quantities of water until well after fire is out. ALWAYS stay away from tanks engulfed in fire. For massive fire, use unmanned hose holders or monitor nozzles; if this is impossible, withdraw from area and let fire burn.
- NFPA Extinguishing Methods for CAS7722-64-7 (NFPA, 2002):
- Use dry chemical or carbon dioxide extinguishers to fight fires involving potassium permanganate (Pohanish, 2002).
- Fires involving potassium permanganate should be handled similar to sodium peroxide fires (Lewis, 2000).
Potassium permanganate decomposes on heating, releasing toxic gases and irritating fumes (ILO ICSC, 2003). When heated to decomposition, toxic fumes of potassium oxide are released (Pohanish, 2002).
EXPLOSION HAZARD
- The reaction between potassium permanganate and a great number of different materials results in extreme explosion hazard. Some of these hazardous reactions are detailed below (NFPA, 2002; Urben, 1999):
Contact of potassium permanganate with acetic acid or acetic anhydride may result in explosion. Caking of solid potassium permanganate during oxidation of tert-alkylamines to nitroalkanes using 20% aqueous acetone led to a violent reaction with eruption of the flask. A mixture of 0.5% potassium permanganate solution with ammonium nitrate exploded approximately 7 hours after the chemicals were combined. The explosion was attributed to the formation and exothermic decomposition of ammonium permanganate. Arsenic and potassium permanganate will explode when ground together in a mortar. Testing of coal samples to determine sulfur content incorporates use of an aqueous mixture of potassium permanganate and the peroxoacid. This strong oxidation process can result in violent explosion if a reflux condenser is not used. The addition of potassium permanganate to dimethylformamide to get a 20% solution led to an explosion 5 minutes after the chemicals were mixed. In the preparation of chlorine, the addition of concentrated hydrochloric acid to potassium permanganate resulted in a sharp explosion. Contact between potassium permanganate and concentrated hydrogen peroxide can result in an explosion. The addition of potassium permanganate to concentrated hydrofluoric acid in the preparation of potassium hexafluoromanganate(IV) resulted in a violent exothermic reaction. Potassium permanganate mixed with phosphorus or sulfur will explode on heating or grinding. The attempted preparation of permanganyl chloride involving the addition of concentrated sulfuric acid to a mixture of potassium chloride and potassium permanganate resulted in violent explosion. Heating potassium permanganate and "Rocksil" slag wool resulted in minor explosion. The addition of concentrated sulfuric acid to slightly damp potassium permanganate led to an explosion. Potassium permanganate solutions prepared in sulfuric acid are also explosive. Mixtures of potassium permanganate and powered titanium exploded on heating. Attempted purification of trifluoroacetic anhydride by distillation from potassium permanganate resulted in explosion. The violent reaction was attributed to the formation of dimanganese heptaoxide. Explosive reactions will occur on contact with finely divided potassium permanganate and organic materials.
- The reaction of tin and potassium permanganate when heated to 170 degrees C or higher results in explosion (ITI, 1995).
- Glycerin and potassium permanganate can explode on contact due to released hydrogen (ITI, 1995).
- There is a risk of fire and explosion on contact with combustibles and reducing agents (ILO ICSC, 2003).
DUST/VAPOR HAZARD
- Potassium permanganate is a powerful oxidizing agent; its dust or finely ground powders can initiate fire or explosions when brought into contact with reducing agents, combustibles, strong acids, organic matter, or oxidizable materials (solid, liquid, gas) (Pohanish, 2002).
- Incompatibility with nitric acid will produce toxic chlorine gas (Pohanish & Greene, 1997).
- When it decomposes and is in contact with certain substances, it will release flammable oxygen gas (Pohanish, 2002).
- Inhalation of potassium permanganate dust can cause respiratory tract irritation, and at higher concentrations, pulmonary edema (Pohanish, 2002).
- On contact with acid or acid fumes, potassium permanganate can emit toxic fumes (Lewis, 2000).
REACTIVITY HAZARD
- Potassium permanganate is a strong oxidizing agent that reacts violently with numerous compounds, resulting in explosion or fire hazard (Pohanish, 2002).
Potassium permanganate ignites on reaction with the following (NFPA, 2002; Pohanish, 2002; Urben, 1999): Acetaldehyde (contact with powder) Acetic acid (contact with powder) Acetylacetone (contact with powder) Alcohols + nitric acid Antimony (on being ground) Benzaldehyde (contact with powder) 3-Chloropropane-1,2-diol (contact with powder) Dichloromethylsilane (pure material) Dimethyl sulfoxide Erythritol (contact with powder) Esters of ethylene glycol (contact with powder) Ethylene glycol (contact with powder) Glycerol Hydrogen peroxide Hydrogen trisulfide Hydroxylamine Isobutyraldehyde (contact with powder) Lactic acid (contact with powder) Mannitol (contact with powder) Organic matter Oxalic acid (contact with powder) Oxidizable solids, liquids, and gases Propane-1,2-diol (contact with powder) Reducing materials Strong acids Triethanolamine (contact with powder) Wood (presence of moisture or friction)
Potassium permanganate explodes on reaction with the following (NFPA, 2002; Urben, 1999; Pohanish & Greene, 1997) : Acetic acid Acetic anhydride Anhydrous ammonia Ammonium nitrate Arsenic Dimethylformamide Formaldehyde Glycerol Hydrochloric acid (concentrated) Hydrogen peroxide Hydroxylamine Organic matter Phosphorus (upon grinding) Potassium chloride + sulfuric acid Powdered sulfur (when heated) Sulfuric acid + water Titanium (powdered metal; when heated)
Potassium permanganate forms sensitive explosive mixtures with the following (Lewis, 2000): Violent reactions or ignition may occur from contact between potassium permanganate and the following (Lewis, 2000): Acetone + tert-butylamine Alcohols + nitric acid Aluminum carbide Ammonia + sulfuric acid Antimony Carbon Coal + peroxomonosulfuric acid Dichloromethylsilane Dimethyl sulfoxide Ethanol + sulfuric acid Gylcerol Hydrofluoric acid (concentrated) Hydrogen peroxide Hydrogen trisulfide Hydroxylamine Organic nitro compounds Polypropylene 3,4,4'-Trimethyldiphenyl sulfone
- Mixtures of aluminum carbide and potassium permanganate will incandesce when warmed (Urben, 1999).
- Oxidation of ammonia with the potassium permanganate formed in the mixture of ammonia and sulfuric acid will result in incandescence due to the permanganic acid formed during the reaction (Urben, 1999).
- Potassium permanganate reacts with nitric acid to produce toxic chlorine fumes (Pohanish & Greene, 1997).
- Potassium permanganate reacts violently with most metal powders (HSDB, 2004).
- Potassium permanganate is incompatible with (Budavari, 2001):
Alcohol Arsenites Bromides Charcoal Ferrous salts Hydrochloric acid Hypophosphites Hyposulfites Iodides Mercurous salts Organic substances Oxalates Peroxides Sulfites
- It is also incompatible with (Pohanish, 2002):
EVACUATION PROCEDURES
- Editor's Note: This material is not listed in the Table of Initial Isolation and Protective Action Distances.
- LARGE SPILL - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 140 (ERG, 2004)
- FIRE - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 140 (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 140 (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 closed spaces before entering.
- Relocate any persons in the vicinity of the spill to areas of fresh air, and seek medical care for victims of exposure (AAR, 2002).
- AIHA ERPG Values for CAS7722-64-7 (AIHA, 2006):
- DOE TEEL Values for CAS7722-64-7 (U.S. Department of Energy, Office of Emergency Management, 2010):
Listed as Potassium permanganate TEEL-0 (units = mg/m3): 0.575 TEEL-1 (units = mg/m3): 8.63 TEEL-2 (units = mg/m3): 14.4 TEEL-3 (units = mg/m3): 500 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 CAS7722-64-7 (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 CAS7722-64-7 (National Institute for Occupational Safety and Health, 2007):
CONTAINMENT/WASTE TREATMENT OPTIONS
SPILL OR LEAK PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 140 (ERG, 2004) Keep combustibles (wood, paper, oil, etc.) away from spilled material. Do not touch damaged containers or spilled material unless wearing appropriate protective clothing. Stop leak if you can do it without risk. Do not get water inside containers.
RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 140 (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 will only provide limited protection.
Evacuate persons not wearing personal protective equipment until the spill clean up is complete (Pohanish, 2002). Remove or extinguish all sources of ignition from the area of the spill (Pohanish, 2002). For spills or leaks of potassium permanganate solution, ventilate the area of release (Pohanish, 2002). Do not absorb spills of potassium permanganate with sawdust or other combustible absorbents (ILO ICSC, 2003). Absorb potassium permanganate solution in vermiculite, dry sand, earth, peat, or other absorbant material. Collect and deposit in sealed containers for disposal (Pohanish, 2002). Solid potassium permanganate spills should be collected in the safest manner possible. Prevent dispersion of dusts. After spill is cleaned up, ventilate the area (Pohanish, 2002). Sweep the solid material into containers to be sealed and removed to a safe location (ILO ICSC, 2003). Prevent potassium permanganate from entering confined spaces, such as a sewer, due to the explosion hazard (Pohanish, 2002). Prevent this chemical from entering the environment and water. Notify downstream users if it or contaminated runoff enters the waterways (ILO ICSC, 2003; Pohanish, 2002). In situ clean-up can be accomplished through use of an anion exchanger. Use ferrous salts, alcohols, and charcoal to decompose the potassium permanganate, only if these substances themselves do not pose a threat to the environment. Seek professional environmental engineering assistance (OHM/TADS, 2004).
SMALL LIQUID SPILL PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 140 (ERG, 2004) SMALL DRY SPILL PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 140 (ERG, 2004)
LARGE SPILL PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 140 (ERG, 2004) Dike far ahead of liquid spill for later disposal. Following product recovery, flush area with water.
Only trained personnel should perform spill clean up (Pohanish, 2002): Cover the potassium permanganate with weak a reducing agent (e.g., sodium thiosulfate, bisulfates or ferrous salts). Transfer the material into a large container of water. Neutralize with soda ash.
For a spill on land, contain the spilled material in a holding area, and if necessary, cover with a plastic tarp to prevent it from dissolving in rain or firefighting water. Neutralize the potassium permanganate with sodium bisulfate (AAR, 2002). For a spill in water, add dilute caustic acid (NaOH) or sodium bisulfite (NaHSO3); use mechanical dredges or lifts to remove the material (AAR, 2002).
Add potassium permanganate to a large volume of reducing agent, then neutralize with soda ash or dilute hydrochloric acid (OHM/TADS, 2004). 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
- Release of potassium permanganate to the environment can occur through its use in aquatic systems (Cruz & Tamse, 1989).
- Occupational exposure has been reported (HSDB, 2004).
- Direct release to the environment occur through its use as an effective algaecide in reservoirs (OHM/TADS, 2004).
ENVIRONMENTAL FATE AND KINETICS
SURFACE WATER Potassium permanganate will sink and dissolve in water, and it rapidly oxidizes any organic material present. It is reduced to manganese dioxide, a brown precipitate (OHM/TADS, 2004).
ABIOTIC DEGRADATION
- In an aquatic environement, potassium permanganate will sink and dissolve in the water column (OHM/TADS, 2004).
ENVIRONMENTAL TOXICITY
LC - MINUTE CRUSTACEANS: 5 mg/L (OHM/TADS, 2004) LC5 - MILKFISH, fingerling (Chanos chanos): 1.2317 ± 0.0315 for 96H (Cruz & Tamse, 1989) LC5 - MILKFISH, fingerling (Chanos chanos): 1.5070 mg/L ± 0.0325 for 24H (Cruz & Tamse, 1989) LC50 - CHANNEL CATFISH (Ictalurus punctatus): 0.75 mg/L for 96H (HSDB, 2004) LC50 - CHANNEL CATFISH (Ictalurus punctatus): 4.5 mg/L for 96H (single dose; chemical oxygen demand of 21 mg/L) (HSDB, 2004) LC50 - CHANNEL CATFISH (Ictalurus punctatus): 9.0 mg/L for 96H (four doses, applied equally at 30 minute intervals; relatively lower chemical oxygen demand) (HSDB, 2004) LC50 - CHANNEL CATFISH (Ictalurus punctatus): 17.6 mg/L for 96H (single dose; chemical oxygen demand of 118 mg/L) (HSDB, 2004) LC50 - CHANNEL CATFISH (Ictalurus punctatus): 25.6 mg/L for 96H (four doses, applied equally at 30 minute intervals; relatively higher chemical oxygen demand) (HSDB, 2004) LC50 - GOLDFISH (Carassius auratus): 3.6 mg/L for 96H (HSDB, 2004) LC50 - MILKFISH, fingerling (Chanos chanos): 1.4757 ± 0.0227 for 96H (Cruz & Tamse, 1989) LC50 - MILKFISH, fingerling (Chanos chanos): 1.4860 ± 0.0200 for 24H (Cruz & Tamse, 1989) LC50 - STRIPED BASS, fingerling: 4 mg/L for 48-96H (OHM/TADS, 2004) LC50 - STRIPED BASS, fingerling: 5 mg/L for 24H -- static conditions (OHM/TADS, 2004) LC50 - STRIPED BASS, larvae: 1 mg/L for 48 - 96H -- static conditions (OHM/TADS, 2004) LC50 - STRIPED BASS, larvae: 1.5 mg/L for 24H -- static conditions (OHM/TADS, 2004) LC50 - FISH (Trachinotus carolinus), juvenile: 1.6 - 2.9 mg/L for 96H -- static conditions (OHM/TADS, 2004) LC95 - MILKFISH, fingerling (Chanos chanos): 1.6980 ± 0.0530 for 96H (Cruz & Tamse, 1989) LC95 - MILKFISH, fingerling (Chanos chanos): 1.7257 ± 0.0227 for 24H (Cruz & Tamse, 1989) LD50 - BLUEGILL SUNFISH (Lepomis macrochirus): 2.7 - 3.6 mg/L for 96H (HSDB, 2004) TC - BLUEGILL: 3 mg/L (OHM/TADS, 2004) TC - EEL, young: 11.8 mg/L for 8H (OHM/TADS, 2004) TC - FATHEAD MINNOW: 5 mg/L (OHM/TADS, 2004) TC - FISH (unspecified): 22 - 62 mg/L for 0.5H (OHM/TADS, 2004) TC - GOLDFISH: 10 mg/L for 12 - 18H (OHM/TADS, 2004) TC - LARGEMOUTH BASS: 4 mg/L (OHM/TADS, 2004) TC - TROUT: 6.25 mg/L for 24H (OHM/TADS, 2004) TLm - BLUEGILL: 4.2 mg/L for 24H, 48H, and 96H (OHM/TADS, 2004) TLm - BLUEGILL: 5.2 mg/L for 24H (OHM/TADS, 2004) TLm - BLUEGILL: 5.4 mg/L for 48H (CHRIS, 2004; OHM/TADS, 2004) TLm - CATFISH, fingerling: 3.2 mg/L for 24H (OHM/TADS, 2004) TLm - CREEK CHUB: 3.7 mg/L for 96H (OHM/TADS, 2004) TLm - MOSQUITOFISH: 12 mg/L for 24H and 96H (OHM/TADS, 2004)
- Milkfish fingerlings (Chanos chanos) from a commercial fish farm were exposed to potassium permanganate at concentrations ranging from 1.0 mg/L to 1.8 mg/L. An avoidance response was observed in all fish immediately following addition of the potassium permanganate to the test waters. Following the addition of sublethal concentrations (1.0 - 1.25 mg/L), the fish had increased activity levels for approximately 15 minutes, after which time they slowed; the fish were able to tolerate this concentration for the entire 96 hours of the test. At lethal concentrations (1.8 mg/L), the fish swam rapidly for 30 minutes, and evidence of oxidation, including blackening of the snouts, fin tips, and dorsal body region, was apparent; at this level, all fish died within 6 to 24 hours (Cruz & Tamse, 1989).
- Potassium permanganate is extremely toxic to fish and other aquatic organisms, even in low concentrations (CHRIS, 2004; OHM/TADS, 2004; ILO ICSC, 2003).
-PHYSICAL/CHEMICAL PROPERTIES
MOLECULAR WEIGHT
DESCRIPTION/PHYSICAL STATE
- At room temperature, potassium permanganate exists as dark purple or bronze-colored, odorless, sweetish, astringent tasting crystals, that are described as having a blue, metallic sheen. It is readily soluble in water; aqueous solutions are pink to violet in color and slowly deposit manganese dioxide (Budavari, 2001; Lewis, 2001; Lewis, 2000; Lewis, 1998; Freeman, 1998).
SPECIFIC GRAVITY
- OTHER TEMPERATURE AND/OR PRESSURE
- TEMPERATURE AND/OR PRESSURE NOT LISTED
2.7 (Budavari, 2001) 2.703 (Lewis, 2000) 2.7032 (Lewis, 2001)
DENSITY
- TEMPERATURE AND/OR PRESSURE NOT LISTED
FREEZING/MELTING POINT
SOLUBILITY
Potassium permanganate is soluble in water (Ashford, 2001; Lewis, 2001; Lewis, 2000). 63.8 g/L (at 20 degrees C) (Bingham et al, 2001) 64 g/L (at 20 degrees C) (HSDB, 2004) 65 g/L (at 20 degrees C) (Freeman, 1998) Soluble in 14.2 parts cold water or 3.5 parts boiling water (Budavari, 2001)
Potassium permanganate is soluble in acetone and methanol (Lewis, 2001). Moderately soluble in methanol, alcohol, acetone, and pyridine (Lewis, 2000) Soluble in acetic acid, trifluoroacetic acid, acetic anhydride, pyridine, benzonitrile, and sulfolane (HSDB, 2004)
OTHER/PHYSICAL
- DECOMPOSITION TEMPERATURE
<240 degrees C (Pohanish, 2002; Ashford, 2001; Bingham et al, 2001; Lewis, 2001; Lewis, 2000) ~240 degrees C (Budavari, 2001)
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