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SODIUM PENTACHLOROPHENATE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Both the sodium salt and the phenol have been used in home and industry as herbicides, disinfectants, mildew retardants, and wood preservatives. It has been used in cooling towers to control the growth of algae.

Specific Substances

    A) No Synonyms were found in group or single elements
    1.2.1) MOLECULAR FORMULA
    1) C6-Cl5-O.Na

Available Forms Sources

    A) FORMS
    1) Sodium pentachlorophenate is the sodium salt of PENTACHLOROPHENOL. It is available as a white or tan powder or buff-colored flakes, pellets, or briquets (EPA, 1985; HSDB , 1997). It has a phenolic odor (EPA, 1985). Sodium pentachlorophenate is soluble in water (21 to 29 percent weight/volume) and in ethanol and acetone; it is insoluble in benzene and petroleum oils (HSDB , 1997).
    B) SOURCES
    1) It has been banned for most uses in the USA because of its carcinogenic activity (Baselt, 1988). The toxic effects of sodium pentachlorophenate are identical to those of PENTACHLOROPHENOL (Clayton & Clayton, 1981). The following review is based on the toxicologic properties of pentachlorophenol. Effects attributed specifically to sodium pentachlorophenate are indicated.
    2) Pentachlorophenol can be absorbed in toxic amounts by all routes of exposure, but skin exposure is the most dangerous (ACGIH, 1986).
    C) USES
    1) Both the sodium salt and the phenol have been used in home and industry as herbicides, disinfectants, mildew retardants, and wood preservatives (Baselt, 1988). It has been used in cooling towers to control the growth of algae (HSDB , 1997).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) The toxic effects of sodium pentachlorophenate are identical to those of pentachlorophenol. Either or both can produce severe eye, skin, and respiratory irritation or burns, anorexia, dyspnea, anesthesia, tachycardia, hyperpyrexia, sweating and flushing of the skin, rapidly progressing coma and death.
    B) Onset of rigor mortis is especially rapid. Cerebral edema, inflammation of the gastric mucosa, pulmonary congestion, cardiac dilatation, and degenerative changes in the liver and kidney have been apparent at autopsy.
    0.2.3) VITAL SIGNS
    A) Tachypnea, hyperpyrexia, tachycardia, and elevated blood pressure can occur with pentachlorophenol intoxication.
    0.2.4) HEENT
    A) Strong irritation of the eyes, nose, throat, and mucous membranes is seen. Lacrimation occurs. Burns and permanent corneal injury may occur. Slight mydriasis, corneal opacity, and corneal numbness may be seen after exposures to concentrations of a dust or spray.
    0.2.5) CARDIOVASCULAR
    A) Cardiac dilatation has been reported from exposure to sodium pentachlorophenate. Pentachlorophenol has produced tachycardia. Heart failure may occur.
    0.2.6) RESPIRATORY
    A) Irritation of the respiratory tract can occur from exposure to fine dust or spray. Bronchitis and tachypnea are common symptoms of intoxication of both animals and humans.
    0.2.7) NEUROLOGIC
    A) Headache, dizziness, seizures, anesthesia, coma, and cerebral edema have been reported.
    0.2.8) GASTROINTESTINAL
    A) Inflammation of the gastric mucosa is caused by sodium pentachlorophenate. Anorexia occurs with severe exposure. GI upset may be seen.
    0.2.9) HEPATIC
    A) Centrilobular necrosis has been seen in fatal human cases.
    0.2.10) GENITOURINARY
    A) Renal tubular degeneration has been seen in fatal cases.
    0.2.11) ACID-BASE
    A) Metabolic acidosis may be seen in severe cases.
    0.2.12) FLUID-ELECTROLYTE
    A) Fluid and electrolyte loss may occur from excessive sweating.
    0.2.13) HEMATOLOGIC
    A) Anemia and hemolysis may be seen in intoxication.
    0.2.14) DERMATOLOGIC
    A) Pentachlorophenol is a strong skin irritant. Irritation and dermatitis generally occurs with concentrations greater than 10%.
    0.2.15) MUSCULOSKELETAL
    A) Weakness occurs frequently. Muscle spasms and tremor are indicative of severe intoxication. Unusually severe rigor mortis occurs soon after death.
    0.2.16) ENDOCRINE
    A) Hyperglycemia and glucosuria have been seen in poisoned animals.
    0.2.17) METABOLISM
    A) Sodium pentachlorophenate acts by uncoupling oxidative phosphorylation, which produces increased basal metabolism.
    0.2.18) PSYCHIATRIC
    A) Delirium has occurred in severe poisoning.
    0.2.19) IMMUNOLOGIC
    A) Changes in immune cell function have been demonstrated with acute in-vitro exposure.
    0.2.20) REPRODUCTIVE
    A) No reports of reproductive effects in humans were found; however, pentachlorophenol may have been present at elevated levels in the blood of women who had miscarriages.
    B) ANIMAL STUDIES - Pentachlorophenol has been embryotoxic, fetotoxic, and teratogenic in experimental animals.
    0.2.21) CARCINOGENICITY
    A) Pentachlorophenol is considered a potential carcinogen because of its structural similarity to other carcinogens.
    0.2.22) OTHER
    A) Sodium pentachlorophenate may be hazardous by the inhalation, dermal, or oral route. Pentachlorophenol can be rapidly absorbed in fatal amounts through the skin.

Laboratory Monitoring

    A) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    B) Monitor arterial blood gases, pulmonary function, and chest x-ray when pulmonary irritation is present.
    C) Urinary levels of less than 36 ppm are usually not associated with significant symptoms.
    D) Concentrations greater than 0.3 mg/m(3) irritate mucous membranes. Concentrations of 1 mg/m(3) cause pain in the nose and throat.
    E) Serum levels of 26 ppm were seen in asymptomatic infants, while a fatal case had a blood concentration of 162 ppm.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Do NOT induce emesis.
    B) 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.
    C) 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.
    1) CONTRAINDICATIONS: Loss of airway protective reflexes or decreased level of consciousness in unintubated patients; following ingestion of corrosives; hydrocarbons (high aspiration potential); patients at risk of hemorrhage or gastrointestinal perforation; and trivial or non-toxic ingestion.
    D) 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).
    1) Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children greater than 5 years).
    2) Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.
    E) Reduction of hyperthermia with tepid water baths is superior to alcohol sponging or ice-packs which tend to cause peripheral vasoconstriction.
    F) Replace fluid and electrolytes.
    G) There is no specific antidote for sodium pentachlorophenate. The treatment is supportive and symptomatic.
    H) Administration of salicylates to reduce hyperpyrexia is contraindicated.
    I) See treatment of oral exposure in the main body of this document for complete information.
    0.4.3) INHALATION EXPOSURE
    A) 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.
    B) Primary treatment are measures which promote heat loss, reduce anxiety, and allow for replacement of fluid and electrolytes lost through sweating.
    C) 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.
    D) 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).
    1) Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children greater than 5 years).
    2) Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.
    E) Reduction of hyperthermia with tepid water baths is superior to alcohol sponging or ice-packs which tend to cause peripheral vasoconstriction.
    F) Replace fluid and electrolytes.
    G) There is no specific antidote for sodium pentachlorophenate. The treatment is supportive and symptomatic.
    H) Administration of salicylates to reduce hyperpyrexia is contraindicated.
    I) See treatment of inhalation exposure in the main body of this document for complete information.
    0.4.4) EYE EXPOSURE
    A) 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.
    B) See treatment of eye exposure in the main body of this document for complete information.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) Rapid decontamination is important, since this material is absorbed through the skin. Primary treatment are measures which promote heat loss, reduce anxiety, and allow for replacement of fluid and electrolytes lost through sweating.
    2) 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).
    3) 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).
    a) Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children greater than 5 years).
    b) Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.
    4) Reduction of hyperthermia with tepid water baths is superior to alcohol sponging or ice-packs which tend to cause peripheral vasoconstriction.
    5) Replace fluid and electrolytes.
    6) There is no specific antidote for sodium pentachlorophenate. The treatment is supportive and symptomatic.
    7) Administration of salicylates to reduce hyperpyrexia is contraindicated.
    8) See treatment of dermal exposure in the main body of this document for complete information.

Range Of Toxicity

    A) Skin irritation occurs with brief exposure to solutions greater than 10 percent. Respiratory irritation occurs at concentrations greater than 1 mg/m(3), but acclimated persons can tolerate 2.4 mg/m(3). The minimum lethal dose is not known for humans, but fatalities have occurred.

Clinical Effects

Summary Of Exposure

    A) The toxic effects of sodium pentachlorophenate are identical to those of pentachlorophenol. Either or both can produce severe eye, skin, and respiratory irritation or burns, anorexia, dyspnea, anesthesia, tachycardia, hyperpyrexia, sweating and flushing of the skin, rapidly progressing coma and death.
    B) Onset of rigor mortis is especially rapid. Cerebral edema, inflammation of the gastric mucosa, pulmonary congestion, cardiac dilatation, and degenerative changes in the liver and kidney have been apparent at autopsy.

Vital Signs

    3.3.1) SUMMARY
    A) Tachypnea, hyperpyrexia, tachycardia, and elevated blood pressure can occur with pentachlorophenol intoxication.
    3.3.2) RESPIRATIONS
    A) Tachypnea usually occurs with pentachlorophenol intoxication (Baselt & Cravey, 1989; Morgan, 1989).
    3.3.3) TEMPERATURE
    A) Sodium pentachlorophenate raises body temperature by uncoupling oxidative phosphorylation (Finkel, 1983). Profuse sweating may be seen (Clayton & Clayton, 1994; Robson et al, 1969; Hathaway et al, 1996).
    3.3.4) BLOOD PRESSURE
    A) Elevated blood pressure was seen in dogs, rats, and guinea pigs (HSDB , 1998).
    3.3.5) PULSE
    A) Pentachlorophenol poisoning has produced tachycardia (Baselt & Cravey, 1989; Gray, 1985).

Heent

    3.4.1) SUMMARY
    A) Strong irritation of the eyes, nose, throat, and mucous membranes is seen. Lacrimation occurs. Burns and permanent corneal injury may occur. Slight mydriasis, corneal opacity, and corneal numbness may be seen after exposures to concentrations of a dust or spray.
    3.4.2) HEAD
    A) Headache has been reported following pentachlorophenol exposure while applying a solution to timber work (Rugman & Cosstick, 1990).
    3.4.3) EYES
    A) IRRITATION - Pentachlorophenol is a strong eye irritant (Finkel, 1983; Sittig, 1991). Lacrimation occurs (Grant, 1993). Concentrations of dust or spray greater than 1 mg/m(3) will cause pain in previously unexposed workers, but 2.4 mg/m(3) may be tolerated by those previously exposed. Below 1 mg/m(3) there is little effect (Clayton & Clayton, 1994).
    B) BURNS and permanent corneal injury may occur from contact of the solid or concentrated liquid (HSDB , 1991).
    C) CORNEA - Corneal opacity and corneal numbness have been reported (ACGIH, 1986).
    D) MYDRIASIS - Slight mydriasis may be seen (ACGIH, 1986).
    E) RETROBULBAR NEURITIS - There are several cases of retrobulbar neuritis associated with the use of a mixture containing pentachlorophenol (Campbell, 1952; Jindal, 1968). No cause and effect relationship has been established.
    3.4.5) NOSE
    A) IRRITATION - Pentachlorophenol irritates the nose at concentrations as low as 0.3 mg/m(3) (Clayton & Clayton, 1981).
    3.4.6) THROAT
    A) IRRITATION - Pentachlorophenol vapors irritate the throat at concentrations as low as 0.3 mg/m(3) (Clayton & Clayton, 1981).
    B) THIRST - Intense thirst is characteristic of severe pentachlorophenol intoxication (Blair, 1961; Morgan, 1989).

Cardiovascular

    3.5.1) SUMMARY
    A) Cardiac dilatation has been reported from exposure to sodium pentachlorophenate. Pentachlorophenol has produced tachycardia. Heart failure may occur.
    3.5.2) CLINICAL EFFECTS
    A) CARDIOMEGALY
    1) Cardiac dilatation has been reported from exposure to sodium pentachlorophenate (EPA, 1985).
    B) TACHYARRHYTHMIA
    1) Pentachlorophenol poisoning has produced tachycardia (Baselt & Cravey, 1989; Gray, 1985; Hathaway et al, 1996).
    C) HEART FAILURE
    1) Heart failure is often the cause of death, with vascular damage seen (ACGIH, 1986).

Respiratory

    3.6.1) SUMMARY
    A) Irritation of the respiratory tract can occur from exposure to fine dust or spray. Bronchitis and tachypnea are common symptoms of intoxication of both animals and humans.
    3.6.2) CLINICAL EFFECTS
    A) IRRITATION SYMPTOM
    1) Exposure to the fine dust or spray can cause irritation of the respiratory tract. Violent coughing and sneezing occur when it is inhaled (Sittig, 1991).
    B) BRONCHITIS
    1) Bronchitis and irritation may be seen when the concentration of dust or sprays exceed 1 mg/m(3). This may cause pain in previously unexposed workers, but 2.4 mg/m(3) may be tolerated by those previously exposed. Below 1 mg/m(3) there is little effect (Clayton & Clayton, 1994; Proctor et al, 1988).
    C) HYPERVENTILATION
    1) Tachypnea is a symptom of intoxication in both animals and man (Clayton & Clayton, 1994; Gray, 1985).
    D) DYSPNEA
    1) Dyspnea, a sense of constriction in the chest, and pulmonary congestion occur with more severe intoxication (EPA, 1985; Sittig, 1991). Dyspnea has been reported in a 28-year-old male who applied pentachlorophenol solution to timber work for several months (Rugman & Cosstick, 1990).

Neurologic

    3.7.1) SUMMARY
    A) Headache, dizziness, seizures, anesthesia, coma, and cerebral edema have been reported.
    3.7.2) CLINICAL EFFECTS
    A) HEADACHE
    1) Headache has been reported following pentachlorophenol exposure while applying a solution to timber work (Rugman & Cosstick, 1990).
    B) DIZZINESS
    1) Dizziness and headache may be seen in intoxications (Proctor et al, 1988).
    C) CENTRAL NERVOUS SYSTEM DEFICIT
    1) Signs of CNS depression from acute exposure to sodium pentachlorophenate include anesthesia (EPA, 1985).
    D) SEIZURE
    1) Asphyxial convulsions have been seen in fatally poisoned animals and in humans (Clayton & Clayton, 1994; Gray, 1985).
    E) CEREBRAL EDEMA
    1) Exposure to sodium pentachlorophenate has been reported to cause edema in the brain (Gray, 1985; EPA, 1985; Sittig, 1991).
    F) COMA
    1) Rapidly progressing coma has been reported from exposure to sodium pentachlorophenate (EPA, 1985) and pentachlorophenol (Baselt & Cravey, 1989; Sittig, 1991; Hathaway et al, 1996).
    G) LACK OF EFFECT
    1) No significant change in nerve conduction velocity could be detected, when measured 4 years apart, in 10 workers exposed to pentachlorophenol 0.3 to 180 mcg/m(3) for 4 to 24 years (Triebig et al, 1987)

Gastrointestinal

    3.8.1) SUMMARY
    A) Inflammation of the gastric mucosa is caused by sodium pentachlorophenate. Anorexia occurs with severe exposure. GI upset may be seen.
    3.8.2) CLINICAL EFFECTS
    A) GASTRITIS
    1) Inflammation of the gastric mucosa has been reported from exposure to sodium pentachlorophenate (EPA, 1985; Sittig, 1991).
    B) LOSS OF APPETITE
    1) Anorexia has been reported from severe exposure (Clayton & Clayton, 1994; EPA, 1985; Hathaway et al, 1996).
    C) INDIGESTION
    1) Gastrointestinal upset may be seen in some cases of intoxication (Clayton & Clayton, 1994) Bergner et al; 1965). Inflamed mucosa has been seen on autopsy in severe cases.
    D) PANCREATITIS
    1) Suspected pentachlorophenol-induced pancreatitis has been reported (Cooper & Maccauley, 1982).

Hepatic

    3.9.1) SUMMARY
    A) Centrilobular necrosis has been seen in fatal human cases.
    3.9.2) CLINICAL EFFECTS
    A) HEPATIC NECROSIS
    1) Liver toxicity has been reported from exposure to sodium pentachlorophenate (EPA, 1985). Centrilobular necrosis has been seen in fatal human cases (Clayton & Clayton, 1994; Gray, 1985). Hepatomegaly was seen in poisoned infants (Robson et al, 1969).

Genitourinary

    3.10.1) SUMMARY
    A) Renal tubular degeneration has been seen in fatal cases.
    3.10.2) CLINICAL EFFECTS
    A) RENAL TUBULAR DISORDER
    1) Kidney toxicity has been reported from exposure to sodium pentachlorophenate (EPA, 1985). Renal tubular degeneration has been seen in fatal cases. Renal output is first increased then decreased in poisoned animals and humans (Clayton & Clayton, 1994; Gray, 1985).

Acid-Base

    3.11.1) SUMMARY
    A) Metabolic acidosis may be seen in severe cases.
    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) Metabolic acidosis may be seen in severe cases (Gray, 1985; Robson et al, 1969).

Hematologic

    3.13.1) SUMMARY
    A) Anemia and hemolysis may be seen in intoxication.
    3.13.2) CLINICAL EFFECTS
    A) APLASTIC ANEMIA
    1) Aplastic anemia and red cell aplasia have been reported (Roberts, 1983; Roberts, 1981; Rugman & Cosstick, 1990). Documented cases have been reviewed (Roberts, 1990).
    B) HEMOLYSIS
    1) Intravascular hemolysis was reported in one woman who had dermal and inhalation exposure (Hassan et al, 1985).

Dermatologic

    3.14.1) SUMMARY
    A) Pentachlorophenol is a strong skin irritant. Irritation and dermatitis generally occurs with concentrations greater than 10%.
    3.14.2) CLINICAL EFFECTS
    A) SKIN IRRITATION
    1) Pentachlorophenol is a strong skin irritant (Finkel, 1983). Irritation generally occurs with concentrations greater than 10 percent. Concentrations of less than 0.1% are unlikely to cause symptoms (Clayton & Clayton, 1994).
    B) DEAD
    1) Fatal poisonings have been seen after dermal exposure to concentrated PCP (Jones et al, 1986).

Musculoskeletal

    3.15.1) SUMMARY
    A) Weakness occurs frequently. Muscle spasms and tremor are indicative of severe intoxication. Unusually severe rigor mortis occurs soon after death.
    3.15.2) CLINICAL EFFECTS
    A) TREMOR
    1) Muscle spasms and tremor indicate severe intoxication (Morgan, 1989).
    B) MUSCLE WEAKNESS
    1) Animals fatally poisoned developed a rapidly progressing motor weakness (Clayton & Clayton, 1994).
    C) RIGOR MORTIS
    1) Profound rigor mortis usually sets in rapidly after death by pentachlorophenol (Clayton & Clayton, 1994; Gray, 1985).

Endocrine

    3.16.1) SUMMARY
    A) Hyperglycemia and glucosuria have been seen in poisoned animals.
    3.16.2) CLINICAL EFFECTS
    A) HYPERGLYCEMIA
    1) Hyperglycemia as well as glycosuria have been seen in poisoned animals (Clayton & Clayton, 1994).

Immunologic

    3.19.1) SUMMARY
    A) Changes in immune cell function have been demonstrated with acute in-vitro exposure.
    3.19.2) CLINICAL EFFECTS
    A) CELLULAR IMMUNE DEFECT
    1) Acute exposure of human lymphocytes in-vitro impaired both cell mediated and humoral immune response (Lang & Mueller-Ruchholtz, 1991).

Reproductive

    3.20.1) SUMMARY
    A) No reports of reproductive effects in humans were found; however, pentachlorophenol may have been present at elevated levels in the blood of women who had miscarriages.
    B) ANIMAL STUDIES - Pentachlorophenol has been embryotoxic, fetotoxic, and teratogenic in experimental animals.
    3.20.2) TERATOGENICITY
    A) ANIMAL STUDIES
    1) SKELETAL MALFORMATION
    a) Post-implantation mortality, fetotoxicity and developmental abnormalities in the musculoskeletal system have been observed in rat studies (RTECS, 1990).
    b) Administration of oral doses of 5 to 50 mg/kg pentachlorophenol to pregnant rats produced resorptions, subcutaneous edema, dilated ureters, as well as anomalies of the ribs, skull, and vertebrae (Schwetz et al, 1974).
    2) EMBRYOTOXICITY
    a) Pentachlorophenol was embryotoxic and fetotoxic in rats at 15 mg/kg and higher doses. Delayed ossification of the skull was observed. Fetal death and increased resorptions were seen in hamsters given 5 mg/kg/day and higher doses (HSDB , 1998).
    3.20.3) EFFECTS IN PREGNANCY
    A) ANIMAL STUDIES
    1) IMPAIRED FERTILITY
    a) MINK - Administration of pentachlorophenol, 1 mg/kg/day, reduced fertility in mink (both sexes exposed) (Beard et al, 1997).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS131-52-2 (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):
    1) Not Listed
    3.21.2) SUMMARY/HUMAN
    A) Pentachlorophenol is considered a potential carcinogen because of its structural similarity to other carcinogens.
    3.21.3) HUMAN STUDIES
    A) RELATED COMPOUNDS
    1) Pentachlorophenol is considered a potential carcinogen because of its structural similarity to other carcinogens (Ellenhorn & Barceloux, 1988).
    B) CASE STUDIES
    1) SARCOMA
    a) One study found a correlation between 125 men with gliomas and frequent exposure to organochlorine wood preservatives and to organic solvents (Cordier et al, 1988). No cause and effect relationship could be established.
    C) OCCUPATIONAL EXPOSURE
    1) MYELOMATOSIS MULTIPLE
    a) Slightly elevated odds ratio (1.6) for multiple myeloma was found for farm workers doing fencing work (Pearce et al, 1986).
    2) LYMPHOMA-LIKE DISORDER
    a) Elevated odds ratio of 2.0 was found for non-Hodgkin's lymphoma in farming workers doing fencing work, with potential exposure to sodium pentachlorophenate (Pearce et al, 1986b).
    3.21.4) ANIMAL STUDIES
    A) ANIMAL STUDIES
    1) Pentachlorophenol was not carcinogenic in rats and mice by the oral route (Santodonato et al, 1985). In a 2-year rat study, technical and commercial pentachlorophenol in the diet (100-600 ppm) produced dose related neoplasms of liver, adrenal, and vascular endothelium (McConnell et al, 1991).

Genotoxicity

    A) Sodium pentachlorophenate has induced DNA repair in bacteria. Pentachlorophenol is mutagenic and has induced sister chromatid exchanges.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    B) Monitor arterial blood gases, pulmonary function, and chest x-ray when pulmonary irritation is present.
    C) Urinary levels of less than 36 ppm are usually not associated with significant symptoms.
    D) Concentrations greater than 0.3 mg/m(3) irritate mucous membranes. Concentrations of 1 mg/m(3) cause pain in the nose and throat.
    E) Serum levels of 26 ppm were seen in asymptomatic infants, while a fatal case had a blood concentration of 162 ppm.
    4.1.2) SERUM/BLOOD
    A) TOXICITY
    1) Seven fatal cases of pentachlorophenol intoxication averaged 107 mg/L pentachlorophenol in the blood (range of 46 to 173 mg/L) (Baselt & Cravey, 1989).
    2) Plasma samples are equally acceptable as urine for biological monitoring of exposure to pentachlorophenol. Plasma levels of free pentachlorophenol exceeding 1 mg/L are indicative of excessive exposure (Baselt, 1988).
    3) Pentachlorophenol concentrations in 100 serum samples obtained from a population with no known history of exposure ranged from 2.5 to 116.5 ng/mL (Gomez-Catalan et al, 1987).
    4) In significant exposures, the victim should be monitored for electrolyte imbalance, metabolic acidosis, hemolytic anemia, methemoglobinemia, pancreatitis, and hepatic and renal dysfunction (Ellenhorn & Barceloux, 1988).
    5) In a fatal case reported by Gray (1985), the blood concentration was 162 parts per million.
    6) Serum levels of 26 parts per million were seen in asymptomatic infants (Clayton & Clayton, 1994).
    7) The tissue level of one infant who died was 20 to 34 parts per million and the blood levels greater than 120 parts per million (Clayton & Clayton, 1994).
    8) Pentachlorophenol concentrations in 100 serum samples obtained from a population with no known history of exposure ranged from 2.5 to 116.5 nanograms/milliliter (Gomez-Catalan et al, 1987).
    4.1.3) URINE
    A) URINARY LEVELS
    1) Urinary levels of less than 36 ppm are usually not associated with significant symptoms (Clayton & Clayton, 1994).
    2) Pentachlorophenol concentrations in 50 urine samples obtained from a population with no known history of exposure ranged from 4 to 136 ng/mL (mean = 25 ng/mL) (Gomez-Catalan et al, 1987).
    3) Pentachlorophenol concentrations in 3 urine samples from workers occupationally exposed ranged from 165 to 961 ng/mL (Gomez-Catalan et al, 1987).
    4) Seven fatal cases of pentachlorophenol intoxication averaged 153 mg/L pentachlorophenol in the urine (range of 28 to 520 mg/L) (Baselt & Cravey, 1989).
    5) Levels of free pentaphenol in the urine of the general population averaged 0.044 mg/L (range of 0.003 to 0.570), and occupationally exposed persons averaged 0.465 mg/L (range of 0.003 to 38.6). There is a correlation between levels of pentaphenol in the blood and urine. Urinary levels greater than 1 mg/L are considered indicative of excessive exposure (Baselt, 1988).
    6) Pentachlorophenol concentrations in 50 urine samples obtained from a population with no known history of exposure ranged from 4 to 136 nanograms/milliliter (mean = 25 nanograms/milliliter) (Gomez-Catalan et al, 1987).
    7) Pentachlorophenol concentrations in 3 urine samples from 3 workers occupationally exposed ranged from 165 to 961 nanograms/milliliter (Gomez-Catalan et al, 1987).
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) Monitor arterial blood gases, pulmonary function, and chest x-ray when pulmonary irritation is present.
    b) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    B) Monitor arterial blood gases, pulmonary function, and chest x-ray when pulmonary irritation is present.
    C) Urinary levels of less than 36 ppm are usually not associated with significant symptoms.
    D) Concentrations greater than 0.3 mg/m(3) irritate mucous membranes. Concentrations of 1 mg/m(3) cause pain in the nose and throat.
    E) Serum levels of 26 ppm were seen in asymptomatic infants, while a fatal case had a blood concentration of 162 ppm.

Oral Exposure

    6.5.2) PREVENTION OF ABSORPTION
    A) EMESIS/NOT RECOMMENDED
    1) Do NOT induce emesis.
    B) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    C) GASTRIC LAVAGE
    1) INDICATIONS: Consider gastric lavage with a large-bore orogastric tube (ADULT: 36 to 40 French or 30 English gauge tube {external diameter 12 to 13.3 mm}; CHILD: 24 to 28 French {diameter 7.8 to 9.3 mm}) after a potentially life threatening ingestion if it can be performed soon after ingestion (generally within 60 minutes).
    a) Consider lavage more than 60 minutes after ingestion of sustained-release formulations and substances known to form bezoars or concretions.
    2) PRECAUTIONS:
    a) SEIZURE CONTROL: Is mandatory prior to gastric lavage.
    b) AIRWAY PROTECTION: Place patients in the head down left lateral decubitus position, with suction available. Patients with depressed mental status should be intubated with a cuffed endotracheal tube prior to lavage.
    3) LAVAGE FLUID:
    a) Use small aliquots of liquid. Lavage with 200 to 300 milliliters warm tap water (preferably 38 degrees Celsius) or saline per wash (in older children or adults) and 10 milliliters/kilogram body weight of normal saline in young children(Vale et al, 2004) and repeat until lavage return is clear.
    b) The volume of lavage return should approximate amount of fluid given to avoid fluid-electrolyte imbalance.
    c) CAUTION: Water should be avoided in young children because of the risk of electrolyte imbalance and water intoxication. Warm fluids avoid the risk of hypothermia in very young children and the elderly.
    4) COMPLICATIONS:
    a) Complications of gastric lavage have included: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach, fluid and electrolyte imbalance (Vale, 1997). Combative patients may be at greater risk for complications (Caravati et al, 2001).
    b) Gastric lavage can cause significant morbidity; it should NOT be performed routinely in all poisoned patients (Vale, 1997).
    5) CONTRAINDICATIONS:
    a) Loss of airway protective reflexes or decreased level of consciousness if patient is not intubated, following ingestion of corrosive substances, hydrocarbons (high aspiration potential), patients at risk of hemorrhage or gastrointestinal perforation, or trivial or non-toxic ingestion.
    6.5.3) TREATMENT
    A) SEIZURE
    1) SUMMARY
    a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
    b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
    c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).
    2) DIAZEPAM
    a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
    b) PEDIATRIC DOSE: 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 (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .
    3) NO INTRAVENOUS ACCESS
    a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
    b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).
    4) LORAZEPAM
    a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
    b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
    c) PEDIATRIC DOSE: 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 (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).
    5) PHENOBARBITAL
    a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
    b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
    c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
    d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
    e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
    f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).
    6) OTHER AGENTS
    a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):
    1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
    2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
    3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
    4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).
    B) BODY TEMPERATURE ABOVE REFERENCE RANGE
    1) Reduction of hyperthermia with tepid water baths is superior to alcohol sponging or ice packs which tend to constrict peripherally.
    2) Administration of salicylates to reduce hyperpyrexia is absolutely contraindicated. This drug is also an oxidative phosphorylation uncoupler and may aggravate hyperpyrexia.
    3) Fluids, electrolytes, and acid-base data should be monitored and intravenous replacement of losses provided. All intravenous solution should contain adequate amounts of glucose to supply the requirements of the increased metabolism.
    C) SUPPORT
    1) There is no specific antidote for these agents, and treatment is symptomatic and supportive.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.
    6.7.2) TREATMENT
    A) SEIZURE
    1) SUMMARY
    a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
    b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
    c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).
    2) DIAZEPAM
    a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
    b) PEDIATRIC DOSE: 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 (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .
    3) NO INTRAVENOUS ACCESS
    a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
    b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).
    4) LORAZEPAM
    a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
    b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
    c) PEDIATRIC DOSE: 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 (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).
    5) PHENOBARBITAL
    a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
    b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
    c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
    d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
    e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
    f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).
    6) OTHER AGENTS
    a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):
    1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
    2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
    3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
    4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).
    B) IRRITATION SYMPTOM
    1) Respiratory tract irritation, if severe, can progress to noncardiogenic pulmonary edema which may be delayed in onset up to 24 to 72 hours after exposure in some cases.
    2) There are no controlled studies indicating that early administration of corticosteroids can prevent the development of noncardiogenic pulmonary edema in patients with inhalation exposure to respiratory irritant substances, and long-term use may cause adverse effects (Boysen & Modell, 1989).
    a) However, based on anecdotal experience, some clinicians do recommend early administration of corticosteroids (such as methylprednisolone 1 gram intravenously as a single dose) in an attempt to prevent the later development of pulmonary edema.
    1) Anecdotal experience with dimethyl sulfate inhalation showed possible benefit of methylprednisolone in the TREATMENT of noncardiogenic pulmonary edema (Ip et al, 1989).
    3) Anecdotal experience also indicated that systemic corticosteroids may have possible efficacy in the TREATMENT of drug-induced noncardiogenic pulmonary edema (Zitnik & Cooper, 1990; Stentoft, 1990; Chudnofsky & Otten, 1989) or noncardiogenic pulmonary edema developing after cardiopulmonary bypass (Maggart & Stewart, 1987).
    4) It is not clear from the published literature that administration of systemic corticosteroids early following inhalation exposure to respiratory irritant substances can PREVENT the development of noncardiogenic pulmonary edema. The decision to administer or withhold corticosteroids in this setting must currently be made on clinical grounds.
    C) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) 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).
    a) 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)
    3) 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).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) 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).
    7) 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).
    D) BODY TEMPERATURE ABOVE REFERENCE RANGE
    1) Reduction of hyperthermia with tepid water baths is superior to alcohol sponging or ice packs which tend to cause peripheral vasoconstriction.
    2) Administration of salicylates to reduce hyperpyrexia is absolutely contraindicated. This drug is also an oxidative phosphorylation uncoupler and may aggravate hyperpyrexia.
    3) Fluids, electrolytes, and acid-base data should be monitored and intravenous replacement of losses provided. All intravenous solution should contain adequate amounts of glucose to supply the requirements of the increased metabolism.
    4) There is no specific antidote for these agents, and treatment is symptomatic and supportive.
    E) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: 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, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).
    6.8.2) TREATMENT
    A) OBSERVATION REGIMES
    1) Carefully observe patients with eye exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL ABSORPTION
    1) Rapid decontamination is important, since this material is absorbed through the skin. Primary treatment are measures which promote heat loss, reduce anxiety, and allow for replacement of fluid and electrolytes lost through sweating.
    B) DERMAL DECONTAMINATION
    1) 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. Rescue personnel and bystanders should avoid direct contact with contaminated skin, clothing, or other objects (Burgess et al, 1999). Since contaminated leather items cannot be decontaminated, they should be discarded (Simpson & Schuman, 2002).
    6.9.2) TREATMENT
    A) BODY TEMPERATURE ABOVE REFERENCE RANGE
    1) Reduction of hyperthermia with tepid water baths is superior to alcohol sponging or ice packs which tend to cause peripheral vasoconstriction.
    2) Administration of salicylates to reduce hyperpyrexia is absolutely contraindicated. This drug is also an oxidative phosphorylation uncoupler and may aggravate hyperpyrexia.
    3) Fluids, electrolytes, and acid-base data should be monitored and intravenous replacement of losses provided. All intravenous solution should contain adequate amounts of glucose to supply the requirements of the increased metabolism.
    B) SUPPORT
    1) There is no specific antidote for these agents, and treatment is symptomatic and supportive.
    C) SKIN DISORDER MONITORING
    1) CHRONIC URTICARIA - Cases of chronic urticaria and pemphigus vulgaris were treated with corticosteroids such as methylprednisolone 32 to 48 mg per day (Lambert et al, 1985).
    2) CHLORACNE - A 32-year-old male with pentachlorophenol-induced chloracne responded to therapy with isotretinoin 1 milligram/kilogram/day orally for 6 weeks. His chloracne did not respond to 3 months of combination therapy with tetracycline 500 milligrams orally twice daily and tretinoin 0.05 percent topical cream (Cole et al, 1986).
    D) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) EXTRACORPOREAL ELIMINATION
    1) EXCHANGE TRANSFUSION - Robson et al (1969) reported that exchange transfusion was effective in removing PCP from seriously poisoned infants.

Range Of Toxicity

Summary

    A) Skin irritation occurs with brief exposure to solutions greater than 10 percent. Respiratory irritation occurs at concentrations greater than 1 mg/m(3), but acclimated persons can tolerate 2.4 mg/m(3). The minimum lethal dose is not known for humans, but fatalities have occurred.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The minimum lethal human dose to this agent has not been delineated.
    2) Fatalities have occurred from improper handling of sodium pentachlorophenate and pentachlorophenol (Gordon, 1956).

Maximum Tolerated Exposure

    A) ROUTE OF EXPOSURE
    1) SKIN IRRITATION -
    a) Concentrations of 10 percent or greater produce irritation after brief exposure; a one percent solution will cause irritation upon repeated contact; a 0.1 percent solution will irritate from prolonged contact (HSDB , 1998).
    2) RESPIRATORY IRRITATION -
    a) Painful irritation will occur in the nose of an uninitiated persons at concentrations greater than 1 mg/m(3); 2.4 mg/m(3) can be tolerated by accustomed persons (HSDB , 1998).
    b) Concentrations of as little as 0.3 milligrams/cubic meter irritated the mucous membranes of lungs, eyes, nose, and the throat (Clayton & Clayton, 1981).
    c) Concentrations of 1 milligram/cubic meter caused pain in the nose and throat as well as sneezing and coughing (Proctor et al, 1988).
    3) INGESTION -
    a) Severe toxic effects have occurred in adults after ingestion of 2 grams of pentachlorophenol (Ellenhorn & Barceloux, 1988).

Workplace Standards

    A) ACGIH TLV Values for CAS131-52-2 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS131-52-2 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS131-52-2 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    3) 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
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS131-52-2 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: RTECS, 1998
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 63,700 mcg/kg
    2) LD50- (ORAL)MOUSE:
    a) 197 mg/kg
    3) LD50- (SKIN)MOUSE:
    a) 124 mg/kg
    4) LD50- (INHALATION)RAT:
    a) 11,700 mcg/kg
    5) LD50- (ORAL)RAT:
    a) 126 mg/kg
    6) LD50- (SUBCUTANEOUS)RAT:
    a) 66 mg/kg

Physicochemical

Molecular Weight

    A) 288.32

References

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