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PENTACHLOROPHENOL

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Pentachlorophenol is a synthetic chemical which does not occur naturally in the environment. It is a nonpolar, lipophilic substance. Prior to 1984 it was one of the most widely used biocides in the United States. Purchase and use of this chemical is now restricted to certified applicators.
    B) Toxicity may occur as a result of dermal, inhalation or oral routes due to its lipophilicity and ease of crossing cell membranes. Absorption from these routes is rapid. Dermal and inhalation exposures may be chronic or acute.
    C) At lower concentrations, it uncouples oxidative phosphorylation in mitochondria. At higher concentrations, it inhibits mitochondrial and myosin adenosine triphosphatase (ATPase).

Specific Substances

    1) Penchlorol
    2) Chlorophen
    3) Pentachlorofenol
    4) Pentachlorofenate
    5) PCP
    6) Molecular Formula: C6-Cl5-O-H
    7) CAS 87-86-5
    8) AI3-00134
    9) CASWELL NUMBER 641
    10) CHLON
    11) CHLOROPHEN (CAS 87-86-5)
    12) DURA TREET II
    13) EPA PESTICIDE CHEMICAL CODE: 063001
    14) PCP (ABREVIATION FOR PENTACHLOROPHENOL)
    15) PENTA (COMMON NAME FOR PENTACHLOROPHENOL)
    16) PENTA CONCENTRATE
    17) PENTACHLOROL
    18) SANTOPHEN
    19) SODIUM PENTACHLORPHENATE
    20) WOODTREAT
    1.2.1) MOLECULAR FORMULA
    1) C6-H-Cl5-O

Available Forms Sources

    A) FORMS
    1) In its pure chemical form, pentachlorophenol exists as colorless crystals with a very sharp characteristic phenolic odor when heated, but very little odor at room temperature (ATSDR, 1994).
    2) BRAND NAMES: A few of the brand names used in the past for pentachlorophenol have included Santophen(R), Penta(R), Dowicide 7(R), Penchloral(R), P.C.P.(R), Cuprinol(R), Evisan(R), and Santobrite(R). Currently, the only domestic manufacturer of pentachlorophenol is Vulcan Chemicals, a division of Vulcan Materials Company in Wichita, Kansas (ATSDR, 1994).
    B) SOURCES
    1) Pentachlorophenol is prepared by a stepwise chlorination of phenols in the presence of catalysts (anhydrous aluminum chloride or ferric chloride) (Budavari, 1996; ATSDR, 1994). Outside of the United States it is also produced by the alkaline hydrolysis of hexachlorobenzene (ATSDR, 1994).
    2) Commercial preparations (not purified) of pentachlorophenol may contain trace impurities of chlorodibenzodioxins and chlorodibenzofurans (Clayton & Clayton, 1994), although content of contaminants is strictly limited by the US EPA.
    C) USES
    1) Prior to 1984 pentachlorophenol was one of the most widely used biocides in the United States. Currently, the purchase and use of this chemical is restricted to certified applicators and is no longer available to the general public. Prior to its restricted use, pentachlorophenol was widely used as a wood preservative, but is now used industrially as a wood preservative for power line poles, cross arms, fence posts, and similar objects (ATSDR, 1994). Its current principal use is as a wood preservative.
    a) Pentachlorophenol is no longer contained in wood preserving solution or insecticides and herbicides available for home and garden use because it is a restricted use pesticide (ATSDR, 1994). Pentachlorophenol is used for the formulation of fungicidal and insecticidal solutions and for incorporation into other manufactured pesticide products.
    2) Logs used for construction purposes may be treated with pentachlorophenol (PCP) and arsenical salts, and then coated with creosote (Bernstein, 1986). Wood treated with PCP is often referred to as "penta-treated". PCP is dissolved in oil and driven into the wood under pressure ("pressure-treated").
    a) Pentachlorophenols and arsenicals are preservatives against microorganisms and termites. Creosote prevents leaching of pentachlorophenol and arsenicals.
    3) Pentachlorophenol has been used to prevent fungal, mold, algae, lichens, moss, and microorganism growth on wood, paint, cellulose products, textiles, and industrial wastes. Technical grade pentachlorophenol may contain 4 to 12 percent tetrachlorophenol, which is also a pesticide-fungicide (Clayton & Clayton, 1994), as well as hexachlorinated and octachlorinated dibenzodioxins and dibenzofurans (Finkel, 1983).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Pentachlorophenol is toxic by ingestion, inhalation, and skin absorption; abuse may be fatal. This compound readily penetrates the skin. The pulmonary route of exposure may be most toxic to adults.
    B) Prolonged or frequent contact with either solution or dust may cause dermatitis or systemic symptoms including damage to the circulatory system and the heart. Hyperpyrexia and cardiac failure are common reactions during overdose.
    C) ACUTE poisoning is marked by dermatitis, weakness, tachypnea, polyuria followed by oliguria, seizures, and rapidly progressing coma in severe cases. Hyperthermia is the major factor leading to death following a fatal exposure in humans. Death may occur within a few hours following absorption.
    D) CHRONIC poisoning may produce anorexia, weight loss, weakness, dizziness, headache and anxiety.
    E) Serious exposures may leave sequelae including impaired autonomic nervous function, circulation, visual change, and an acute type of scotoma.
    0.2.4) HEENT
    A) Slight mydriasis, corneal opacity, and corneal numbness may occur after exposures to concentrations of a dust or spray.
    0.2.5) CARDIOVASCULAR
    A) Cardiac dilatation, tachycardia, and heart failure have been reported. Severe intoxications may result in initial tachycardia and tachypnea, followed by hypotension.
    B) Pentachlorophenol is a halogenated solvent and theoretically may sensitize the heart to catecholamines, increasing the risk for dysrhythmias.
    0.2.6) RESPIRATORY
    A) Bronchitis and tachypnea are common symptoms of intoxication of both animals and humans.
    0.2.7) NEUROLOGIC
    A) In severe intoxications, a rapidly progressing and profound coma may occur.
    B) Seizures may occur following significant exposures.
    C) Dizziness and headache are common effects following subchronic exposures or small acute exposures.
    0.2.8) GASTROINTESTINAL
    A) Anorexia, inflamed gastric mucosa, and GI upset may occur.
    0.2.9) HEPATIC
    A) Centrilobular necrosis has occurred in fatalities.
    0.2.10) GENITOURINARY
    A) Renal tubular degeneration has occurred in fatalities.
    0.2.11) ACID-BASE
    A) Metabolic acidosis may occur in severe cases.
    0.2.13) HEMATOLOGIC
    A) Anemia and hemolysis may occur in intoxication.
    0.2.14) DERMATOLOGIC
    A) Irritation and dermatitis generally occurs with concentrations greater than 10%.
    0.2.15) MUSCULOSKELETAL
    A) Severe poisoning may result in muscular collapse followed by death and rapid rigor mortis. Rhabdomyolysis may result when ATP stores are depleted.
    0.2.16) ENDOCRINE
    A) Hyperglycemia and glucosuria occurred in animals.
    0.2.21) CARCINOGENICITY
    A) A trend of increasing risk of cancer mortality from non-Hodgkin lymphoma, multiple myeloma, and kidney cancer with increasing dermal exposure to pentachlorophenol and tetrachlorophenol was observed in a large cohort study. Excess deaths from trachea, bronchus, and lung cancers (lung cancers); non-Hodgkin lymphoma; COPD; and medical complications were observed in another large cohort study of workers who were involved in the production of pentachlorophenol and thereby exposed to pentachlorophenol and contaminants of pentachlorophenol production. In another study, considerable evidence of an association between hematopoietic cancers and pentachlorophenol exposure was observed.
    0.2.22) OTHER
    A) Profound rigor mortis is common immediately after death.

Laboratory Monitoring

    A) Urinary levels of less than 36 ppm are usually not associated with significant symptoms.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) There is no specific antidote for these agents. The treatment is supportive and symptomatic. Monitor ABG regularly in symptomatic patients.
    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) HYPERTHERMIA - Minimize physical activity, sponge patient with tepid to cool water, and use fans to maximize evaporative heat loss; salicylates CONTRAINDICATED.
    E) Administer oxygen to patients with respiratory compromise.
    F) Replace fluid and electrolytes.
    G) 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.
    H) HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid. If hypotension persists, administer dopamine (5 to 20 mcg/kg/min) or norepinephrine (ADULT: begin infusion at 0.5 to 1 mcg/min; CHILD: begin infusion at 0.1 mcg/kg/min); titrate to desired response.
    I) RHABDOMYOLYSIS: Administer sufficient 0.9% saline (10 to 15 mL/kg/hour) to maintain urine output of at least 1 to 2 mL/kg/hour (or greater than 150 to 300 mL/hr). Monitor input and output, serum electrolytes, CK, and renal function. Diuretics may be necessary to maintain urine output, but should only be considered if urine output is inadequate after volume status is restored. Urinary alkalinization is NOT routinely recommended.
    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.
    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.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    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. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Range Of Toxicity

    A) Concentrations greater than 0.3 mg/m(3) irritate mucous membranes. Concentrations of 1 mg/m(3) cause pain in the nose and throat.
    B) Serum levels of 26 ppm were seen in asymptomatic infants, while a fatal case had a blood concentration of 162 ppm.

Clinical Effects

Summary Of Exposure

    A) Pentachlorophenol is toxic by ingestion, inhalation, and skin absorption; abuse may be fatal. This compound readily penetrates the skin. The pulmonary route of exposure may be most toxic to adults.
    B) Prolonged or frequent contact with either solution or dust may cause dermatitis or systemic symptoms including damage to the circulatory system and the heart. Hyperpyrexia and cardiac failure are common reactions during overdose.
    C) ACUTE poisoning is marked by dermatitis, weakness, tachypnea, polyuria followed by oliguria, seizures, and rapidly progressing coma in severe cases. Hyperthermia is the major factor leading to death following a fatal exposure in humans. Death may occur within a few hours following absorption.
    D) CHRONIC poisoning may produce anorexia, weight loss, weakness, dizziness, headache and anxiety.
    E) Serious exposures may leave sequelae including impaired autonomic nervous function, circulation, visual change, and an acute type of scotoma.

Vital Signs

    3.3.3) TEMPERATURE
    A) FEVER and profuse sweating may occur in both acute and chronic intoxications (Clayton & Clayton, 1994; Robson et al, 1969; ATSDR, 1994).
    B) FEVER, with temperatures as high as 42 degrees C, appears to be a common effect, and may be accompanied by extreme thirst, profuse sweating, and increased basal metabolic rate (Jorens & Schepens, 1993; ATSDR, 1994; Clayton & Clayton, 1994).

Heent

    3.4.1) SUMMARY
    A) Slight mydriasis, corneal opacity, and corneal numbness may occur after exposures to concentrations of a dust or spray.
    3.4.3) EYES
    A) 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) Corneal opacity and corneal numbness have been reported (ACGIH, 1986). Eye irritation and lacrimation have been reported following exposure to dust and vapor of pentachlorophenol (Grant & Schuman, 1993).
    C) Slight mydriasis may occur (ACGIH, 1986).
    D) CASE SERIES - 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.
    E) Serious exposures may leave sequelae including visual change, and an acute type of scotoma (ACGIH, 1986).

Cardiovascular

    3.5.1) SUMMARY
    A) Cardiac dilatation, tachycardia, and heart failure have been reported. Severe intoxications may result in initial tachycardia and tachypnea, followed by hypotension.
    B) Pentachlorophenol is a halogenated solvent and theoretically may sensitize the heart to catecholamines, increasing the risk for dysrhythmias.
    3.5.2) CLINICAL EFFECTS
    A) CARDIOMEGALY
    1) Cardiac dilatation was reported in human fatal cases; heart congestion and edema were reported in poisoned animals (Clayton & Clayton, 1994).
    B) TACHYARRHYTHMIA
    1) Tachycardia may occur, and was reported by Gray (1985). Toxicity results in increased metabolic rate which leads to tachypnea and tachycardia (JEF Reynolds , 2000).
    C) HEART FAILURE
    1) Heart failure is often the cause of death, with vascular damage reported (ACGIH, 1986; (ATSDR, 1994; Clayton & Clayton, 1994).
    D) HYPOTENSIVE EPISODE
    1) Following pentachlorophenol ingestions in humans, an initial increase in respirations occurs, followed by decreased respirations and hypotension in severe poisonings (HSDB , 2000).

Respiratory

    3.6.1) SUMMARY
    A) Bronchitis and tachypnea are common symptoms of intoxication of both animals and humans.
    3.6.2) CLINICAL EFFECTS
    A) BRONCHITIS
    1) Bronchitis and irritation may occur 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, 1981; Proctor et al, 1988; Proudfoot, 2003).
    B) HYPERVENTILATION
    1) Tachypnea is a symptom of intoxication in both animals and man (Clayton & Clayton, 1994; Gray, 1985; JEF Reynolds , 2000) and is a result of increased metabolic rate. In severe intoxications, tachypnea may be followed by decreased respirations and hypotension (HSDB , 2000).
    C) DYSPNEA
    1) CASE REPORT - Dyspnea has been reported in a 28-year-old male who applied pentachlorophenol solution to timber work for several months (Rugman & Cosstick, 1990).
    D) CHEYNE-STOKES RESPIRATION
    1) Cheyne-Stokes and Kussmaul respirations are important findings in acute pentachlorophenol poisonings (Jorens & Schepens, 1993). Respiratory failure may be one cause of death in severe poisonings; cardiac failure and hyperthermia are causes of death (Smith & Oehme, 1991; ATSDR, 1994).
    E) ACUTE LUNG INJURY
    1) CASE REPORT - In a human fatality following exposure over a 3 week period, autopsy results revealed congested and edematous lungs and widespread intraalveolar hemorrhage of the lungs. It was speculated that these effects were secondary to pentachlorophenol-induced mitochondrial derangement leading to hyperthermia (ATSDR, 1994).
    F) EMPHYSEMA
    1) WITH POISONING/EXPOSURE
    a) CHRONIC EXPOSURE - Chronic bronchitis and emphysema have been associated with pentachlorophenol exposure (Proudfoot, 2003).

Neurologic

    3.7.1) SUMMARY
    A) In severe intoxications, a rapidly progressing and profound coma may occur.
    B) Seizures may occur following significant exposures.
    C) Dizziness and headache are common effects following subchronic exposures or small acute exposures.
    3.7.2) CLINICAL EFFECTS
    A) COMA
    1) A rapidly progressing, profound coma may occur in severe cases. Cerebral edema has been reported in fatal cases (Clayton & Clayton, 1994; Gray, 1985).
    B) DIZZINESS
    1) Dizziness, headache and delirium may occur in acute intoxications (Proctor et al, 1988; Baselt, 2000).
    C) SEIZURE
    1) Asphyxial seizures have been seen in fatally poisoned animals and in humans (Clayton & Clayton, 1994; ATSDR, 1994; Gray, 1985). Ingestions have resulted in seizures (HSDB , 2000).
    D) DYSKINESIA
    1) Hyperkinetic movements, tremor, twitching, and jerking of extremities has been reported following acute ingestions (Jorens & Schepens, 1993).
    E) NEUROPATHY
    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).
    2) Workers in a pentachlorophenol chemical manufacturing plant demonstrated much slower conduction velocities of the median motor nerves in the trichlorobenzene tank area which had the highest polychlorinated dioxin contamination (Cheng et al, 1993).
    F) HEADACHE
    1) Headache has been reported following pentachlorophenol exposure while applying a solution to timber work (Rugman & Cosstick, 1990; Clayton & Clayton, 1994).
    G) DISORDER OF AUTONOMIC NERVOUS SYSTEM
    1) Serious exposures may leave sequelae including impaired autonomic nervous function (ACGIH, 1986; (ATSDR, 1994).
    H) CEREBRAL EDEMA
    1) Autopsy reports in fatal intoxications have shown cerebral edema with focal swelling of the myelin sheath (Clayton & Clayton, 1994; ATSDR, 1994). This may be a result of pentachlorophenol-induced hyperthermia.

Gastrointestinal

    3.8.1) SUMMARY
    A) Anorexia, inflamed gastric mucosa, and GI upset may occur.
    3.8.2) CLINICAL EFFECTS
    A) LOSS OF APPETITE
    1) Anorexia may occur with intoxication (Clayton & Clayton, 1994).
    B) INDIGESTION
    1) Gastrointestinal upset and nausea may occur in some cases of intoxication (Clayton & Clayton, 1994) Bergner et al; 1965; (JEF Reynolds , 2000). Inflamed mucosa has been seen on autopsy in severe cases.
    C) PANCREATITIS
    1) Suspected pentachlorophenol-induced pancreatitis was reported by Cooper & Macauley (1982). Excessive use or exposure may result in pancreatitis (Clayton & Clayton, 1994).
    3.8.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) ANOREXIA
    a) HORSES - Severe appetite suppression with significant weight loss and alopecia was reported in horses following chronic exposure to pentachlorophenol-contaminated wood shavings (Kerkvliet et al, 1992).

Hepatic

    3.9.1) SUMMARY
    A) Centrilobular necrosis has occurred in fatalities.
    3.9.2) CLINICAL EFFECTS
    A) HEPATIC NECROSIS
    1) Centrilobular necrosis has been reported in fatal human cases (Clayton & Clayton, 1994; Gray, 1985). Hepatomegaly was reported in poisoned infants (Robson et al, 1969; ATSDR, 1994).
    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HEPATIC NECROSIS
    a) HORSES - Liver biopsies of horses chronically exposed to pentachlorophenol- treated wood shavings revealed foci of individual hepatocyte necrosis with associated neutrophils and diffuse, severe vacuolar changes in hepatocytes (Kerkvliet et al, 1992).

Genitourinary

    3.10.1) SUMMARY
    A) Renal tubular degeneration has occurred in fatalities.
    3.10.2) CLINICAL EFFECTS
    A) RENAL TUBULAR DISORDER
    1) Renal tubular degeneration has been reported in fatal cases. Renal output is first increased then decreased in poisoned animals and humans (Clayton & Clayton, 1994; Gray, 1985).
    B) PORPHYRIA DUE TO TOXIC EFFECT OF SUBSTANCE
    1) Urinary porphyrins were elevated in workers at a pentachlorophenol manufacturing plant, possibly due to polychlorinated dioxin and dibenzofuran contaminants that are formed during production (Cheng et al, 1993).
    C) ABNORMAL URINE ODOR
    1) A typical odor of pentachlorophenol may be detected in the urine following massive acute intoxications (Jorens & Schepens, 1993).

Acid-Base

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

Hematologic

    3.13.1) SUMMARY
    A) Anemia and hemolysis may occur 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; ATSDR, 1994), particularly with excessive use of pentachlorophenol (Clayton & Clayton, 1994).
    B) HEMOLYSIS
    1) CASE REPORT - Intravascular hemolysis was reported in one woman who had dermal and inhalation exposure (Hassan et al, 1985).
    2) Igisu (1993) demonstrated, in vitro, the hemolysis of human erythrocytes and the decreased fluidity of purified plasma membrane by pentachlorophenol (PCP). Albumin completely abolished the hemolysis. The author concluded that hemolytic anemia would be a rare effect of PCP poisoning due to the fact that human serum contains over 3% albumin.
    C) PURPURIC DISORDER
    1) CASE REPORT - A 28-year-old male presented to a health care facility complaining of headaches, exertional dyspnea, and easy bruising associated with a chronic exposure to pentachlorophenol solution he was applying to timber work for the past several months (Rugman & Cosstick, 1990).
    D) THROMBOCYTOPENIC PURPURA
    1) CASE REPORT - A 17-year-old female presented to her physician with bruising, purpuric rash, and epistaxis. A diagnosis of idiopathic thrombocytopenic purpura was made, and all causes, other than her occupational exposure to pentachlorophenol (PCP), were ruled out. Dermal and inhalation exposure to PCP occurred during her work, which included filling and packing tins containing liquid wood preservative (Hay & Singer, 1991).
    3.13.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) THROMBOCYTOPENIA
    a) HORSE - Severe anemia, with a strong positive Coombs' reaction, and thrombocytopenia developed in a horse chronically exposed to pentachlorophenol- contaminated wood shavings (Kerkvliet et al, 1992).

Dermatologic

    3.14.1) SUMMARY
    A) Irritation and dermatitis generally occurs with concentrations greater than 10%.
    3.14.2) CLINICAL EFFECTS
    A) DERMATITIS
    1) WITH POISONING/EXPOSURE
    a) Dermatitis may be seen with as little as a 1 percent solution if contact is frequent or prolonged. Irritation generally occurs with concentrations greater than 10 percent.
    b) Concentrations of less than 0.1% are unlikely to cause symptoms (Clayton & Clayton, 1994). Prolonged skin contact may produce acneiform dermatitis (Proctor et al, 1988).
    c) Fatal poisonings have been reported after dermal exposure to concentrated PCP (Jones et al, 1986; ATSDR, 1994).
    B) BULLOUS ERUPTION
    1) WITH POISONING/EXPOSURE
    a) Pemphigus vulgaris and chronic urticaria have been reported in patients exposed to pentachloropheno l(Proudfoot, 2003; Lambert et al, 1985).
    C) CHLORINE ACNE
    1) WITH POISONING/EXPOSURE
    a) CHRONIC EXPOSURE - Chloracne has been reported from chronic exposure to pentachlorophenol. It is believed that the contaminants (dioxins and furans) are the likely causative etiological agents (Cole et al, 1985; (O'Malley et al, 1990; Cheng et al, 1993; Leet & Collins, 1991; Carpenter et al, 1991; Proudfoot, 2003).
    b) INCIDENCE - The incidence of chloracne among 648 workers assigned to pentachlorophenol production in a single plant was 7%. Direct skin contact with pentachlorophenol was associated with a significantly greater risk for developing chloracne (O'Malley et al, 1990).
    D) URTICARIA
    1) WITH POISONING/EXPOSURE
    a) Urticaria has been reported from handling pentachlorophenate (Kentor, 1986).
    E) SKIN ABSORPTION
    1) This compound readily penetrates the skin. Dermal penetration is the most dangerous pathway of exposure (ACGIH, 1986).

Musculoskeletal

    3.15.1) SUMMARY
    A) Severe poisoning may result in muscular collapse followed by death and rapid rigor mortis. Rhabdomyolysis may result when ATP stores are depleted.
    3.15.2) CLINICAL EFFECTS
    A) INCREASED MUSCLE TONE
    1) Profound and immediate onset of extreme rigor mortis is an important hallmark of fatal poisonings (Clayton & Clayton, 1994; Gray, 1985; Baselt, 2000).
    B) MUSCLE PAIN
    1) Myalgias are a relatively common complaint (Ellenhorn & Barceloux, 1988).
    C) MUSCLE WEAKNESS
    1) Mild intoxications may produce muscle weakness, while very severe poisoning may result in muscular collapse followed by death and rapid rigor mortis (Smith & Oehme, 1991; Baselt, 2000).
    D) RHABDOMYOLYSIS
    1) When ATP stores are depleted, as occurs from uncoupling of oxidative phosphorylation, rhabdomyolysis may result (ATSDR, 1994; Bouges et al, 1988).
    3.15.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) MUSCLE WEAKNESS
    a) Animals fatally poisoned developed a rapidly progressing motor weakness (Clayton & Clayton, 1981).

Endocrine

    3.16.1) SUMMARY
    A) Hyperglycemia and glucosuria occurred in animals.
    3.16.2) CLINICAL EFFECTS
    A) FINDING OF THYROID FUNCTION
    1) Chronic exposures to wood preservatives may have resulted in thyroid gland dysfunction in 6 women (Gerhard et al, 1991).
    2) A history of pentachlorophenol exposure was linked to reduced serum T3 concentrations and mild ovarian and adrenal insufficiency (Proudfoot, 2003).
    3.16.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HYPERGLYCEMIA
    a) Hyperglycemia as well as glycosuria has been reported in poisoned animals (Clayton & Clayton, 1994).

Immunologic

    3.19.2) CLINICAL EFFECTS
    A) DISORDER OF IMMUNE FUNCTION
    1) CASE SERIES - Functional immunosuppression, activated T-cells, autoimmunity, and B-cell dysregulation were found in 38 subjects exposed to pentachlorophenol in manufacturer-treated log houses (McConnachie & Zahalsky, 1991). Chronic pentachlorophenol effects include reduction of humoral and cell-mediated immunity (Clayton & Clayton, 1994; ATSDR, 1994).
    2) In-vitro studies have shown pentachlorophenol to be directly immunotoxic to human immunocompetent cells and the T helper cell subset (Lang & Mueller-Ruchholtz, 1991).
    3.19.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) IMMUNE SYSTEM DISORDER
    a) HORSES - Immunotoxicosis occurred in horses which had been chronically exposed to extremely high levels of pentachlorophenol-treated wood shavings. The immunosuppression was manifested as dermatologic disease (extreme alopecia and skin lesions), bone marrow suppression, and infections by opportunistic fungus (Kerkvliet et al, 1992).

Reproductive

    3.20.2) TERATOGENICITY
    A) HUMANS
    1) Children of fathers exposed to pentachlorophenol showed increased rates of congenital anomalies of the eye, especially congenital cataracts. Increased anencephaly or spina bifida, as well as abnormalities of genitalia, were seen with specific exposure patterns (Dimichward et al, 1996).
    B) ANIMAL STUDIES
    1) Pentachlorophenol has been embryotoxic and fetotoxic in rats (Proctor et al, 1988; Schwetz et al, 1974; Schwetz, 1978; Exon & Koller, 1982; Chou & Cook, 1979) and hamsters (Hinkle, 1973). Administration of oral doses of 5 to 50 mg/kg pentachlorophenol to pregnant rats produced resorptions, subcutaneous edema, dilated ureters, and anomalies of the ribs, skull, and vertebrae (Schwetz et al, 1974). It was teratogenic in rats, but only at high doses which were clearly toxic to the mothers (Anon, 1979).
    3.20.3) EFFECTS IN PREGNANCY
    A) MISCARRIAGES
    1) Pentachlorophenol may have been present at elevated levels in the blood of women who have had miscarriages (Mazorchuk, 1973; Gerhard et al, 1991).
    2) CASE REPORT - De Maeyer et al (1995) reported a case of a woman who had 3 successive miscarriages after successfully having 3 uneventful pregnancies. Her serum pentachlorophenol (PCP) level was elevated at 62 mcg/mL at the time of the last miscarriage, probably due to exposure to an old piece of furniture treated with timber preservative containing PCP. Following removal of the furniture, her serum PCP level dropped, and she again became pregnant and delivered a healthy baby.
    B) PARENTAL EXPOSURE AND CANCER
    1) A review of the literature found 4 studies, which showed a link between parental occupational exposure to pentachlorophenol and cancers, such as lymphoma or leukemia, in their children. However, 3 studies showed no association between parental exposure to pentachlorophenol before conception and cancers, including lymphoma, non-Hodgkin lymphoma, acute lymphoblastic leukemia, or other acute leukemia, in their children (Zheng et al, 2013).
    C) ANIMAL STUDIES
    1) In quantitative studies in rats, very little of the material crossed the placenta (Larsen, 1976; Larsen, 1975).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS87-86-5 (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) A trend of increasing risk of cancer mortality from non-Hodgkin lymphoma, multiple myeloma, and kidney cancer with increasing dermal exposure to pentachlorophenol and tetrachlorophenol was observed in a large cohort study. Excess deaths from trachea, bronchus, and lung cancers (lung cancers); non-Hodgkin lymphoma; COPD; and medical complications were observed in another large cohort study of workers who were involved in the production of pentachlorophenol and thereby exposed to pentachlorophenol and contaminants of pentachlorophenol production. In another study, considerable evidence of an association between hematopoietic cancers and pentachlorophenol exposure was observed.
    3.21.3) HUMAN STUDIES
    A) CARCINOMA
    1) Pentachlorophenol is considered a potential carcinogen because of its structural similarity to other carcinogens (Ellenhorn & Barceloux, 1988). It is in the US EPA Group B2 (probable human carcinogen). The ACGIH has not classified it as a carcinogenic hazard (ACGIH, 1992).
    2) A meta-analysis of 6 case-control studies found an increased association with pentachlorophenol exposure and non-Hodgkin lymphoma (odds ratio [OR], 2.65; 95% CI, 1.33 to 5.27), as well as all lymphomas (OR, 2.57; 95% CI, 1.52 to 4.35). However, 2 case-control studies found no significant association between pentachlorophenol exposure and Hodgkin disease (odds ratio [OR], 1.59; 95% CI, 0.51 to 4.95). A review of the literature found 4 studies, which showed a link between parental occupational exposure to pentachlorophenol before conception and cancers, such as lymphoma or leukemia, in their children. However, 3 studies showed no association between parental exposure to pentachlorophenol and cancers, including lymphoma, non-Hodgkin lymphoma, acute lymphoblastic leukemia, or other acute leukemia, in their children (Zheng et al, 2013).
    3) Excess deaths from trachea, bronchus, and lung cancers (lung cancers); non-Hodgkin lymphoma; COPD; and medical complications were observed in a cohort study of 2122 workers who were involved in the production of pentachlorophenol and thereby exposed to pentachlorophenol and contaminants of pentachlorophenol production. A total of 1165 deaths occurred in these workers from 1940 to 2005, with an overall standardized mortality ratio (SMR) of 1.01 (95% CI, 0.95 to 1.07). There were a statistically significant number of cancer deaths overall (326) in the cohort with a SMR of 1.17 (95% CI, 1.05 to 1.31). Excess deaths from lung cancers (126 deaths; SMR, 1.36; 95% CI, 1.13 to 1.62), COPD (63 deaths; SMR, 1.38; 95% CI, 1.06 to 1.77), and medical complications (5 deaths; SMR, 3.52; 95% CI, 1.14 to 8.22) were observed. Among the a priori causes of death of interest, only non-Hodgkin lymphoma was in statistically significant excess (17 deaths; SMR, 1.77; 95% CI, 1.03 to 2.84). In race- and sex-specific analyses, white males had increased non-Hodgkin lymphoma mortality (17 deaths; SMR, 1.98; 95% CI, 1.15 to 3.17) and males of other races had increased leukemia mortality (4 deaths; SMR, 4.57; 95% CI, 1.25 to 11.7). While the increased numbers of deaths from non-Hodgkin lymphoma and leukemia provide some evidence of pentachlorophenol being carcinogenic, further studies with more detailed exposure data are needed (Ruder & Yiin, 2011).
    4) A systematic review of published studies pertaining to cancer risk in relation to pentachlorophenol exposure found that the studies analyzed presented considerable evidence of an association between hematopoietic cancers and pentachlorophenol exposure, as observed in multiple studies in different locations and using different designs. However, there was little evidence presented for an association between these cancers and exposure to chlorophenols containing fewer than 4 chlorines. In addition, available data show that the risks for hematopoietic cancers were unlikely due to dioxin or other chlorophenol contaminants (Cooper & Jones, 2008).
    5) A trend of increasing risk of cancer mortality from non-Hodgkin lymphoma, multiple myeloma, and kidney cancer with increasing dermal exposure to pentachlorophenol and tetrachlorophenol was observed in a cohort study of 27,464 men who worked in Canadian sawmills for at least 1 year between 1950 and 1995. A trend of increasing risk of cancer incidence with increasing exposure was also observed for non-Hodgkin lymphoma and multiple myeloma in this study. Although the relative risks were not statistically significant compared to the general population for any of the specific cancers analyzed, strong dose-response relationships were apparent in the higher exposure categories of workers compared to the least exposed workers. These trends for all 3 cancers were stronger when the analyses were restricted to just pentachlorophenol exposure and stronger still when lagging allowed for a 20-year latency period. Overall, there were 2571 cancers, excluding non-melanoma skin cancers, diagnosed and 1495 cancer deaths in the cohort of men (Demers et al, 2006).
    6) There have been individual case reports of Hodgkin disease and leukemia associated with pentachlorophenol exposure (Roberts, 1983). There have been reported familial clusters of Hodgkin disease (Greene, 1978) in persons chronically exposed to high levels of pentachlorophenol.
    7) Pentachlorophenol is an inhibitor of sulfotransferase (Moorthy & Randerath, 1996) and an inducer of cytochrome p450 (CYP3A) (Dubois et al, 1996), and may thus act as a co-carcinogen to enhance the activity of metabolically activated carcinogens.
    8) GLIOMA - 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.
    9) CASE REPORT - A soft tissue sarcoma (malignant fibrous histiocytoma) is reported in a male worker following 10 years of dermal and inhalational exposure to the pesticides, lindane and pentachlorophenol (Brahams, 1992).
    10) Extrapolation of cancer risk of pentachlorophenol from experimental animals to humans, using a method which takes into account species differences in serum protein binding and clearance, yields virtually safe doses of pentachlorophenol which are up to 4 times smaller than those obtained using a risk assessment procedure using body surface area. The virtually safe dose derived in this study (0.25 to 1.0 micrograms/day) was lower than the average daily intakes reported for nonspecifically exposed subjects (4 to 37 micrograms/day). The risk for cancer from lifetime exposure was therefore 20 to 140 times the 10(-6) level of acceptable risk (Reigner et al, 1993).
    B) LACK OF EFFECT
    1) CARCINOMA
    a) A meta-analysis of 6 case-control studies found an increased association with pentachlorophenol exposure and non-Hodgkin lymphoma (odds ratio [OR], 2.65; 95% CI, 1.33 to 5.27), as well as all lymphomas (OR, 2.57; 95% CI, 1.52 to 4.35). However, 2 case-control studies found no significant association between pentachlorophenol exposure and Hodgkin disease (odds ratio [OR], 1.59; 95% CI, 0.51 to 4.95). A review of the literature found 4 studies, which showed a link between parental occupational exposure to pentachlorophenol before conception and cancers, such as lymphoma or leukemia, in their children. However, 3 studies showed no association between parental exposure to pentachlorophenol and cancers, including lymphoma, non-Hodgkin lymphoma, acute lymphoblastic leukemia, or other acute leukemia, in their children (Zheng et al, 2013).
    3.21.4) ANIMAL STUDIES
    A) CARCINOMA
    1) Pentachlorophenol was not carcinogenic in rats or mice exposed by the oral route, but did cause liver tumors in male mice exposed by subcutaneous injection (HSDB , 2000).
    2) Technical grade pentachlorophenol was carcinogenic in mice fed levels in the diet as high as 200 ppm; main sites of tumors were the adrenal medulla and liver. It is possible that the carcinogenicity may have been due to impurities (Hathaway et al, 1991).
    a) These results in themselves are not sufficient to consider pentachlorophenol a cancer-causing agent.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Urinary levels of less than 36 ppm are usually not associated with significant symptoms.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) In significant exposures, the victim should be monitored for electrolyte imbalance, metabolic acidosis, pancreatitis, and hepatic and renal dysfunction (Ellenhorn & Barceloux, 1988).
    2) 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).
    B) HEMATOLOGIC
    1) In significant exposures, the victim should be monitored for hemolytic anemia and methemoglobinemia (Ellenhorn & Barceloux, 1988).
    C) ACID/BASE
    1) In significant exposure, the patient should be monitored for metabolic acidosis.
    4.1.3) URINE
    A) URINARY LEVELS
    1) Urinary levels less than 36 ppm are usually not associated with significant symptoms. The ratio of blood to urine levels is approximately 10 to 2.5 (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).

Methods

    A) MULTIPLE ANALYTICAL METHODS
    1) Hemoglobin and albumin adducts of tetrachlorobenzoquinone (a metabolite of pentachlorophenol) can be detected in rats after cleavage by Raney nickel. Levels of 0.09 pmol adduct/g protein/mg PCP/kg body weight were found for hemoglobin and 8.22 pmol for albumin, respectively (Waidyanatha et al, 1994).
    2) Pentachlorophenol may be analyzed by spectrophotometry (tissue and water) or by gas-liquid chromatography. In blood, urine, fat, or clothing, it can be detected in quantities as low as parts per billion (Clayton & Clayton, 1981; Rivers, 1972).
    3) PREFERRED METHOD - The preferred method of analysis is electron-capture gas chromatography of a methyl or ethyl derivative (Benvenue et al, 1968).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Urinary levels of less than 36 ppm are usually not associated with significant symptoms.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) EMESIS/NOT RECOMMENDED
    1) Do NOT induce emesis due to the risk of CNS depression and/or seizures.
    B) ACTIVATED CHARCOAL
    1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    a) Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).
    1) In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
    2) The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).
    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).
    6.5.2) PREVENTION OF ABSORPTION
    A) EMESIS/NOT RECOMMENDED
    1) Do NOT induce emesis due to the risk of CNS depression and/or seizures.
    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) SUPPORT
    1) There is no specific antidote for these agents, and treatment is symptomatic and supportive.
    B) BODY TEMPERATURE ABOVE REFERENCE RANGE
    1) Minimize physical activity, sponge patient with tepid to cool water, and use fans to maximize evaporative heat loss.
    a) Administration of salicylates to reduce hyperpyrexia is absolutely CONTRAINDICATED. Salicylate also uncouples oxidative phosphorylation and may aggravate hyperpyrexia.
    C) OXYGEN
    1) Administer 100% oxygen in severe poisonings with respiratory compromise.
    D) FLUID/ELECTROLYTE BALANCE REGULATION
    1) 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.
    E) 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).
    7) PHENYTOIN/FOSPHENYTOIN
    a) Benzodiazepines and/or barbiturates are preferred to phenytoin or fosphenytoin in the treatment of drug or withdrawal induced seizures (Wallace, 2005).
    b) PHENYTOIN
    1) PHENYTOIN INTRAVENOUS PUSH VERSUS INTRAVENOUS INFUSION
    a) Administer phenytoin undiluted, by very slow intravenous push or dilute 50 mg/mL solution in 50 to 100 mL of 0.9% saline.
    b) ADULT DOSE: A loading dose of 20 mg/kg IV; may administer an additional 5 to 10 mg/kg dose 10 minutes after loading dose. Rate of administration should not exceed 50 mg/minute (Brophy et al, 2012).
    c) PEDIATRIC DOSE: A loading dose of 20 mg/kg, at a rate not exceeding 1 to 3 mg/kg/min or 50 mg/min, whichever is slower (Loddenkemper & Goodkin, 2011; Prod Info Dilantin(R) intravenous injection, intramuscular injection, 2013).
    d) CAUTIONS: Administer phenytoin while monitoring ECG. Stop or slow infusion if dysrhythmias or hypotension occur. Be careful not to extravasate. Follow each injection with injection of sterile saline through the same needle (Prod Info Dilantin(R) intravenous injection, intramuscular injection, 2013).
    e) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over next 12 to 24 hours for maintenance of therapeutic concentrations. Therapeutic concentrations of 10 to 20 mcg/mL have been reported (Prod Info Dilantin(R) intravenous injection, intramuscular injection, 2013).
    c) FOSPHENYTOIN
    1) ADULT DOSE: A loading dose of 20 mg phenytoin equivalent/kg IV, at a rate not exceeding 150 mg phenytoin equivalent/minute; may give additional dose of 5 mg/kg 10 minutes after the loading infusion (Brophy et al, 2012).
    2) CHILD DOSE: 20 mg phenytoin equivalent/kg IV, at a rate of 3 mg phenytoin equivalent/kg/minute, up to a maximum of 150 mg phenytoin equivalent/minute (Loddenkemper & Goodkin, 2011).
    3) CAUTIONS: Perform continuous monitoring of ECG, respiratory function, and blood pressure throughout the period where maximal serum phenytoin concentrations occur (about 10 to 20 minutes after the end of fosphenytoin infusion) (Prod Info CEREBYX(R) intravenous injection, 2014).
    4) SERUM CONCENTRATION MONITORING: Monitor serum phenytoin concentrations over the next 12 to 24 hours; therapeutic levels 10 to 20 mcg/mL. Do not obtain serum phenytoin concentrations until at least 2 hours after infusion is complete to allow for conversion of fosphenytoin to phenytoin (Prod Info CEREBYX(R) intravenous injection, 2014).
    F) MONITORING OF PATIENT
    1) Monitor ABG regularly in symptomatic patients. Monitor for signs of cardiac failure.
    G) ACIDOSIS
    1) METABOLIC ACIDOSIS: Treat severe metabolic acidosis (pH less than 7.1) with sodium bicarbonate, 1 to 2 mEq/kg is a reasonable starting dose(Kraut & Madias, 2010). Monitor serum electrolytes and arterial or venous blood gases to guide further therapy.
    H) HYPOTENSIVE EPISODE
    1) SUMMARY
    a) Infuse 10 to 20 milliliters/kilogram of isotonic fluid and keep the patient supine. If hypotension persists, administer dopamine or norepinephrine. Consider central venous pressure monitoring to guide further fluid therapy.
    2) DOPAMINE
    a) DOSE: Begin at 5 micrograms per kilogram per minute progressing in 5 micrograms per kilogram per minute increments as needed (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). If hypotension persists, dopamine may need to be discontinued and a more potent vasoconstrictor (eg, norepinephrine) should be considered (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    b) CAUTION: If ventricular dysrhythmias occur, decrease rate of administration (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). Extravasation may cause local tissue necrosis, administration through a central venous catheter is preferred (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    3) NOREPINEPHRINE
    a) PREPARATION: 4 milligrams (1 amp) added to 1000 milliliters of diluent provides a concentration of 4 micrograms/milliliter of norepinephrine base. Norepinephrine bitartrate should be mixed in dextrose solutions (dextrose 5% in water, dextrose 5% in saline) since dextrose-containing solutions protect against excessive oxidation and subsequent potency loss. Administration in saline alone is not recommended (Prod Info norepinephrine bitartrate injection, 2005).
    b) DOSE
    1) ADULT: Dose range: 0.1 to 0.5 microgram/kilogram/minute (eg, 70 kg adult 7 to 35 mcg/min); titrate to maintain adequate blood pressure (Peberdy et al, 2010).
    2) CHILD: Dose range: 0.1 to 2 micrograms/kilogram/minute; titrate to maintain adequate blood pressure (Kleinman et al, 2010).
    3) CAUTION: Extravasation may cause local tissue ischemia, administration by central venous catheter is advised (Peberdy et al, 2010).
    I) RHABDOMYOLYSIS
    1) SUMMARY: Early aggressive fluid replacement is the mainstay of therapy and may help prevent renal insufficiency. Diuretics such as mannitol or furosemide may be added if necessary to maintain urine output but only after volume status has been restored as hypovolemia will increase renal tubular damage. Urinary alkalinization is NOT routinely recommended.
    2) Initial treatment should be directed towards controlling acute metabolic disturbances such as hyperkalemia, hyperthermia, and hypovolemia. Control seizures, agitation, and muscle contractions (Erdman & Dart, 2004).
    3) FLUID REPLACEMENT: Early and aggressive fluid replacement is the mainstay of therapy to prevent renal failure. Vigorous fluid replacement with 0.9% saline (10 to 15 mL/kg/hour) is necessary even if there is no evidence of dehydration. Several liters of fluid may be needed within the first 24 hours (Walter & Catenacci, 2008; Camp, 2009; Huerta-Alardin et al, 2005; Criddle, 2003; Polderman, 2004). Hypovolemia, increased insensible losses, and third spacing of fluid commonly increase fluid requirements. Strive to maintain a urine output of at least 1 to 2 mL/kg/hour (or greater than 150 to 300 mL/hour) (Walter & Catenacci, 2008; Camp, 2009; Erdman & Dart, 2004; Criddle, 2003). To maintain a urine output this high, 500 to 1000 mL of fluid per hour may be required (Criddle, 2003). Monitor fluid input and urine output, plus insensible losses. Monitor for evidence of fluid overload and compartment syndrome; monitor serum electrolytes, CK, and renal function tests.
    4) DIURETICS: Diuretics (eg, mannitol or furosemide) may be needed to ensure adequate urine output and to prevent acute renal failure when used in combination with aggressive fluid therapy. Loop diuretics increase tubular flow and decrease deposition of myoglobin. These agents should be used only after volume status has been restored, as hypovolemia will increase renal tubular damage. If the patient is maintaining adequate urine output, loop diuretics are not necessary (Vanholder et al, 2000).
    5) URINARY ALKALINIZATION: Alkalinization of the urine is not routinely recommended, as it has never been documented to reduce nephrotoxicity, and may cause complications such as hypocalcemia and hypokalemia (Walter & Catenacci, 2008; Huerta-Alardin et al, 2005; Brown et al, 2004; Polderman, 2004). Retrospective studies have failed to demonstrate any clinical benefit from the use of urinary alkalinization (Brown et al, 2004; Polderman, 2004; Homsi et al, 1997).

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.

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).

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) Rapid decontamination is important, since this material is absorbed through the skin.
    2) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    6.9.2) TREATMENT
    A) CORTICOSTEROID
    1) Cases of chronic urticaria and pemphigus vulgaris were treated with corticosteroids such as methylprednisolone 32 to 48 mg per day (Lambert et al, 1985).
    B) CHLORINE ACNE
    1) 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).
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) EXCHANGE TRANSFUSION
    1) Robson et al (1969) reported that exchange transfusion was effective in removing PCP from seriously poisoned infants.
    B) HEMODIALYSIS
    1) Due to the high protein binding and lipophilicity of pentachlorophenol, it is anticipated that hemodialysis or hemoperfusion will not be clinically effective in the removal of this chemical.
    C) DIURESIS
    1) In one case report forced diuresis was associated with a reduction in half life from 116 to 42 hours (Baselt, 2000). Safety and efficacy of this therapy is not established.

Range Of Toxicity

Summary

    A) Concentrations greater than 0.3 mg/m(3) irritate mucous membranes. Concentrations of 1 mg/m(3) cause pain in the nose and throat.
    B) Serum levels of 26 ppm were seen in asymptomatic infants, while a fatal case had a blood concentration of 162 ppm.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The minimum lethal human dose to this agent has not been delineated.

Maximum Tolerated Exposure

    A) CONCENTRATION LEVEL
    1) Concentrations of as little as 0.3 milligram/cubic meter irritated the mucous membranes of lungs, eyes, nose, and the throat (Clayton & Clayton, 1994).
    2) Concentrations of 1 milligram/cubic meter caused pain in the nose and throat as well as sneezing and coughing (Proctor et al, 1988).
    3) Individuals with occupational exposures have had estimated net daily intakes which varied from 35 micrograms up to 24,000 micrograms (Reigner et al, 1992).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) In a fatal case reported by Gray (1985) the blood concentration was 162 parts per million.
    2) Serum levels up to 26 parts per million were reported in asymptomatic infants (Clayton & Clayton, 1994).
    3) The tissue level of one infant that died was 20 to 34 parts per million and the blood levels greater than 120 parts per million (Clayton & Clayton, 1994).
    4) Pentachlorophenol concentrations in 100 serum samples obtained from a population that had no known history of exposure ranged from 2.5 to 116.5 nanograms/milliliter (Gomez-Catalan et al, 1987).
    5) URINE
    a) Pentachlorophenol concentrations in 50 urine samples obtained from a population that had no known history of exposure ranged from 4 to 136 nanograms/milliliter (mean = 25 nanograms/milliliter) (Gomez-Catalan et al, 1987).
    b) Pentachlorophenol concentrations in 3 urine samples from 3 workers occupationally exposed ranged from 165 to 961 nanograms/milliliter (Gomez-Catalan et al, 1987).

Workplace Standards

    A) ACGIH TLV Values for CAS87-86-5 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
    a) Under Study
    1) Pentachlorophenol
    a) TLV:
    1) TLV-TWA:
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: Not Listed
    3) Definitions: Not Listed
    c) TLV Basis - Critical Effect(s):
    d) Molecular Weight:
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:
    b) Adopted Value
    1) Pentachlorophenol
    a) TLV:
    1) TLV-TWA: 0.5 mg/m(3)
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A3
    2) Codes: BEI, Skin
    3) Definitions:
    a) A3: Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.
    b) BEI: The BEI notation is listed when a BEI is also recommended for the substance listed. Biological monitoring should be instituted for such substances to evaluate the total exposure from all sources, including dermal, ingestion, or non-occupational.
    c) Skin: This refers to the potential significant contribution to the overall exposure by the cutaneous route, including mucous membranes and the eyes, either by contact with vapors or, of likely greater significance, by direct skin contact with the substance. It should be noted that although some materials are capable of causing irritation, dermatitis, and sensitization in workers, these properties are not considered relevant when assigning a skin notation. Rather, data from acute dermal studies and repeated dose dermal studies in animals or humans, along with the ability of the chemical to be absorbed, are integrated in the decision-making toward assignment of the skin designation. Use of the skin designation provides an alert that air sampling would not be sufficient by itself in quantifying exposure from the substance and that measures to prevent significant cutaneous absorption may be warranted. Please see "Definitions and Notations" (in TLV booklet) for full definition.
    c) TLV Basis - Critical Effect(s): URT and eye irr; CNS impair; card impair
    d) Molecular Weight: 266.35
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    B) NIOSH REL and IDLH Values for CAS87-86-5 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Pentachlorophenol
    2) REL:
    a) TWA: 0.5 mg/m(3)
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: [skin]
    1) Indicates the potential for dermal absorption; skin exposure should be prevented as necessary through the use of good work practices and gloves, coveralls, goggles, and other appropriate equipment.
    f) Note(s):
    3) IDLH:
    a) IDLH: 2.5 mg/m3
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS87-86-5 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Pentachlorophenol
    2) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A3 ; Listed as: Pentachlorophenol
    a) A3 :Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.
    3) EPA (U.S. Environmental Protection Agency, 2011): Likely to be carcinogenic to humans ; Listed as: Pentachlorophenol
    4) 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
    5) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Pentachlorophenol
    6) MAK (DFG, 2002): Category 2 ; Listed as: Pentachlorophenol
    a) Category 2 : Substances that are considered to be carcinogenic for man because sufficient data from long-term animal studies or limited evidence from animal studies substantiated by evidence from epidemiological studies indicate that they can make a significant contribution to cancer risk. Limited data from animal studies can be supported by evidence that the substance causes cancer by a mode of action that is relevant to man and by results of in vitro tests and short-term animal studies.
    7) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS87-86-5 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Pentachlorophenol
    2) Table Z-1 for Pentachlorophenol:
    a) 8-hour TWA:
    1) ppm:
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 0.5
    a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.
    3) Ceiling Value:
    4) Skin Designation: Yes
    5) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: RTECS, 2000
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 58 mg/kg
    2) LD50- (ORAL)MOUSE:
    a) 117 mg/kg
    3) LD50- (INTRAPERITONEAL)RAT:
    a) 56 mg/kg
    4) LD50- (ORAL)RAT:
    a) 27 mg/kg
    5) LD50- (SKIN)RAT:
    a) 96 mg/kg
    6) LD50- (SUBCUTANEOUS)RAT:
    a) 58 mg/kg

Pharmacology Toxicology

Toxicologic Mechanism

    A) Pentachlorophenol causes an uncoupling of mitochondrial oxidative phosphorylation cycles in tissues, which increases basal metabolic rate and increases body temperature (Clayton & Clayton, 1994; ATSDR, 1994). The cell membrane is the apparent site of action for pentachlorophenol. This hypermetabolic state, resulting from a derangement of aerobic metabolism and characterized by hyperthermia, leads to tachycardia, tachypnea, hyperemia, diaphoresis and metabolic acidosis.
    B) As little as 10(-6)M concentration may uncouple oxidative phosphorylation, inhibit mitochondrial and myosin adenosine triphosphatase, inhibit glycolytic phosphorylation, inactivate respiratory enzymes, and produce damage to the mitochondria (Clayton & Clayton, 1994).

Physicochemical

Physical Characteristics

    A) ODOR: Pentachlorophenol has a marked, characteristic, phenol-like smell (Clayton & Clayton, 1994); very pungent odor when hot (Budavari, 1996); phenolic odor (ACGIH, 1986)
    B) TASTE: Pungent taste (ACGIH, 1986); Taste threshold of 30 mcg/L (HSDB , 2000)
    C) COLOR: Dark-colored flakes or sublimed needle crystals (Lewis, 1996); white powder or crystals (Lewis, 1996); colorless to light brown, noncombustible solid (ACGIH, 1986); colorless crystals (pure); dark grayish powder or flakes (crude product) (HSDB , 2000)

Ph

    1) No information found at the time of this review.

Molecular Weight

    A) 266.35 (Budavari, 1996)

Other

    A) ODOR THRESHOLD
    1) Currently not available (CHRIS , 2002)

References

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