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LOWER CHLORINATED PHENOLS

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Chlorinated phenols in this management will consist of the mono-, di-, tri- and tetrachlorophenols.
    B) Toxicity of the chlorinated phenols will be discussed as a whole, with individual differences being emphasized. The general effect of increasing the chlorination of phenol is a reduction of the convulsant action, but an increase in the inhibition of oxidative phosphorylation. Pentachlorophenol does not cause seizures. In general, the toxicity of chlorophenols decreases with decreasing chlorination.
    C) As a group, the chlorophenols are characterized by an odor described as unpleasant, medicinal, pungent, phenolic, strong, or persistent.

Specific Substances

    A) CHLOROPHENOL
    1) 2-Chloro-1-hydroxybenzene 2-chlorophenol (o-chlorophenol)
    2) 3-Chloro-1-hydroxybenzene 3-chlorophenol (m-chlorophenol)
    3) 4-Chloro-1-hydroxybenzene 4-chlorophenol (p-chlorophenol)
    4) m-Chlorophenol
    5) o-Chlorophenol
    6) p-Chlorophenol
    7) CHLORINATED PHENOLS
    8) CHLOROPHENOLS
    9) Molecular Formula: C6-H5-Cl-O
    10) CAS 25167-80-0 (chlorophenol)
    11) CAS 95-57-8 (o-chlorophenol)
    12) CAS 108-43-0 (m-chlorophenol)
    13) CAS 106-48-9 (p-chlorophenol)
    DICHLOROPHENOL
    1) DCP
    2) 2,4- Dichlorophenol
    3) 2,4-DCP
    4) Dichlorophenol, 2,4-
    5) Phenol, 2,4-dichloro-
    6) Molecular Formula: C6-H4-Cl2-O
    7) CAS 25167-80-0 (dichlorophenol)
    8) CAS 120-83-2 (2,4-dichlorophenol)
    TRICHLOROPHENOL
    1) 2,3,5-Trichlorophenol
    2) 2,4,5-Trichlorophenol
    3) 2,4,6-Trichlorophenol
    4) Phenol, trichloro-
    5) Molecular Formula: C6-H3-Cl3-O
    6) CAS 25167-82-2
    TETRACHLOROPHENOL
    1) 2,3,4,6-Tetrachlorophenol
    2) Phenol, tetrachloro-
    3) TCP
    4) Molecular Formula: C6-H2-Cl4-O
    5) CAS 25167-83-3 (tetrachlorophenol)
    6) CAS 58-90-2 (2,3,4,6-tetrachlorophenol)

Available Forms Sources

    A) FORMS
    1) o-Chlorophenol is a colorless liquid in its pure state, with impurities causing a light tan or slightly pink coloring (OHM/TADS , 2000; Clayton & Clayton, 1994; Exon, 1984).
    2) m-Chlorophenol is a colorless crystalline solid (needles) in its pure form, with technical grades being light tan or slightly pink due to impurities (OHM/TADS , 2000; Clayton & Clayton, 1994).
    3) p-Chlorophenol is a colorless crystalline solid (needles) in its pure form, with impurities causing a light tan to slightly pink coloring due to impurities. When placed in water, it sinks slowly and slowly dissolves (OHM/TADS , 2000; Clayton & Clayton, 1994).
    4) 2,4-Dichlorophenol is a white solid (needles) at room temperature, which liquefies at 111 to 116 degrees F (43C - 45C) (MMWR , 2000; Clayton & Clayton, 1994). It has a strong medicinal odor (Kintz et al, 1992).
    5) Trichlorophenol is a solid crystal or flake with a strong disinfectant or phenolic odor (HSDB , 2000).
    6) 2,3,4,6-Tetrachlorophenol is a colorless crystalline solid (needles) in its pure form (Clayton & Clayton, 1994).
    B) SOURCES
    1) The lower chlorinated phenols are produced by two major methods: (1) direct chlorination of phenol either in the presence of a catalyst or at elevated temperatures or (2) by alkaline hydrolysis of hexachlorobenzene or other chlorinated phenolics in methanol or another solvent (Exon, 1984).
    C) USES
    1) Chlorophenols with less than 3 chlorines are not used extensively. They may be used in the production of higher chlorinated phenols and chlorophenyloxyacetic acid herbicides.
    2) Tetrachlorophenols are used worldwide as wood preservatives or fungicides (Exon, 1984).
    3) Trichlorophenols are used as fungicides and bactericides (Clayton & Clayton, 1994).
    4) Dichlorophenol is a feedstock chemical primarily used for the production of the herbicide 2,4-dichlorophenoxyacetic acid, and is also a starting chemical to produce microbicides and insecticides as a stabilizer for pharmaceuticals (MMWR , 2000; Kintz et al, 1992).
    5) The mono-chlorophenols are used as intermediates in organic synthesis of dyes and drugs (OHM/TADS , 2000).
    6) 2,4-Dichlorophenol, which is formed by the spontaneous reaction of chlorine with phenols following chlorination of water for disinfection and deodorization, is a drinking and waste-water contaminant (Exon, 1984).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Chlorinated phenols in this management will consist of the mono-, di-, tri-, and tetrachlorophenols. They are used as biocides, antifungals, wood preservatives, disinfectants, in mothproofing and as insecticides. A separate management is available for pentachlorophenol.
    B) TOXICOLOGY: The general effect of increasing the chlorination of phenol is a reduction of the convulsant action, but an increase in the inhibition of oxidative phosphorylation. Pentachlorophenol does not cause seizures. In general, the toxicity of chlorophenols decreases with decreasing chlorination. Dermal and mucous membrane irritation may occur.
    C) EPIDEMIOLOGY: Poisoning is uncommon but can be severe. Death has occurred following accidental 10% BSA dermal exposures.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Headache, dizziness, and irritations of the eyes, skin or respiratory tract, anorexia, nausea, vomiting and chest pain may develop.
    2) SEVERE ACUTE TOXICITY: Lethargy is the first sign followed by muscular weakness, muscular fasciculation, hyperthermia, and irritability. Tremors, loss of coordination, seizures, and respiratory distress or acute lung injury can develop. This evolves to cerebral edema, paralysis, coma and death. DICHLOROPHENE: Dichlorophene ingestion resulted in multiorgan toxicity, including caustic esophageal and gastric mucosal injuries, confusion, profuse diarrhea, hypotension, electrolyte disturbances, elevated liver enzymes, rhabdomyolysis, and acute renal failure.
    3) SEVERE CHRONIC TOXICITY: Chronic toxicity of the chlorophenols in humans is not well-defined. After prolonged, higher exposures, severe dermatitis (chloracne) may be experienced. Commonly reported symptoms include night sweats, neurological disturbances, bronchitis, weight loss, headache, and fatigue. Liver and kidney damage and a depressed immune response may be associated with high levels of chronic exposure.
    0.2.20) REPRODUCTIVE
    A) Limited information on reproductive or teratologic effects indicates no significant clinical effects.
    0.2.21) CARCINOGENICITY
    A) An association between the risks of each of 3 cancers (non-Hodgkin lymphoma, multiple myeloma, and kidney cancer) with dermal exposure to chlorophenol fungicides was observed in a cohort study. In another study, there was little evidence presented for an association between hematopoietic cancers and exposure to chlorophenols containing fewer than 4 chlorines.

Laboratory Monitoring

    A) Monitor vital signs and mental status.
    B) Lower chlorinated phenol plasma concentrations are not clinically useful or readily available.
    C) Obtain an ECG and institute continuous cardiac monitoring in patients with moderate to severe toxicity.
    D) Monitor serum electrolytes, renal function, and liver enzymes in patients with significant exposures.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) The vast majority of lower chlorophenol overdoses require only supportive care; activated charcoal is indicated if patients present shortly after ingestion. For dermal exposure, remove contaminated clothing and wash skin with soap and water. Irrigate exposed eyes. Inhalation exposures should be removed from the source as quickly as possible.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Patients who experience respiratory compromise or significant CNS depression require early endotracheal intubation for airway protection. While activated charcoal is indicated in these cases, it should be performed only in patients who can protect their airway or who are intubated due to the predictable CNS depression and risk of aspiration. Those experiencing severe hyperthermia should be cooled with cooling blankets and may require sedation or paralysis.
    C) DECONTAMINATION
    1) PREHOSPITAL: Prehospital gastrointestinal decontamination is generally not recommended because of the potential for CNS depression or persistent seizures and subsequent aspiration. For dermal exposure, remove contaminated clothing and wash skin with soap and water. Irrigate exposed eyes. Inhalation exposures should be removed from the source as quickly as possible. Administer IV fluids for hypotension or tachycardia. Keep skin moist to enhance evaporative cooling if patient is hyperthermic. Use impermeable gloves and gowns to prevent exposure of healthcare workers.
    2) HOSPITAL: Activated charcoal should be given to those who are able to reliably protect their airway. gastric lavage is generally not indicated. For dermal exposure, remove contaminated clothing and wash skin with soap and water. Irrigate exposed eyes. Inhalation exposures should be removed from the source as quickly as possible. Use impermeable gloves and gowns to prevent exposure of healthcare workers.
    D) AIRWAY MANAGEMENT
    1) Perform early in patients with severe intoxication (seizures, dysrhythmias, severe delirium, CNS or respiratory depression).
    E) ANTIDOTE
    1) None
    F) SEIZURES
    1) All symptomatic patients should be placed on seizure precautions and seizures should be treated with benzodiazepines, barbiturates, or propofol.
    G) HYPERTHERMIA
    1) Remove patients clothing, keep skin moist and direct fans at the patient to enhance evaporative cooling. Ice packs may be placed in the groin and axilla, and a cooling blanket may be used. Ice water immersion can be used for extreme hyperthermia.
    H) ENHANCED ELIMINATION PROCEDURE
    1) Hemodialysis, hemoperfusion, or exchange transfusion has no benefit.
    I) PATIENT DISPOSITION
    1) HOME CRITERIA: Patients who are asymptomatic after dermal exposures to low concentration products involving small body surface areas can be observed at home. Any signs of lethargy should be referred to a healthcare facility.
    2) OBSERVATION CRITERIA: The following patients should be referred to a healthcare facility for evaluation and observation for 6 to 8 hours: Adults with large or deliberate ingestions, children with any ingestion, dermal exposures to high concentration products or those involving significant surface areas, eye or inhalation exposures with more than mild irritation, or any symptomatic patient.
    3) ADMISSION CRITERIA: Patients with significant central nervous system depression (weakness, ataxia, vertigo, coma), or those with persistent abnormal vital signs such as bradycardia, and hypotension should be admitted. Patients with coma, seizure, dysrhythmias, or end organ damage should be admitted to an intensive care setting.
    4) CONSULT CRITERIA: Consult a poison center or medical toxicologist for assistance in managing patients with severe toxicity (dysrhythmias, severe hypotension, coma), or in whom the diagnosis is not clear.
    J) PITFALLS
    1) Not identifying a possible septic patient or other agents. Giving activated charcoal to a patient whose ability to protect their airway might diminish. Underestimating the potential severity of dermal exposure (dermal exposure to high concentration products can be rapidly fatal). Healthcare providers failing to utilize personal protective equipment.
    K) TOXICOKINETICS
    1) Lower chlorinated phenols are well absorbed orally and dermally, and distributed rapidly. Onset of symptoms generally occurs within 30 minutes to 1 hour; toxicity may persist for greater than 6 hours, and may last longer in the elderly and patients with liver disease.
    L) DIFFERENTIAL DIAGNOSIS
    1) Phenol toxicity, dioxin toxicity, caustics.
    0.4.3) INHALATION EXPOSURE
    A) SUMMARY: Inhalation exposures should be removed from the source as quickly as possible. Use impermeable gloves and gowns to prevent exposure of healthcare workers.
    B) 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.
    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.
    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 must occur immediately, since these chemicals are rapidly absorbed through the skin. Exposed skin should be flushed for at least 30 minutes with water. It is important to remove all clothing from the affected area.
    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).

Range Of Toxicity

    A) TOXICITY: Toxic dose is not well quantified, that toxicity appears to be increased with increasing number of chlorines. Deaths within 20 to 30 minutes from dermal exposures, steam exposures, and oral exposures have been reported. A woman developed caustic esophageal and gastric mucosal injuries, confusion, profuse diarrhea, hypotension, electrolyte disturbances, elevated liver enzymes, rhabdomyolysis, and acute renal failure after ingesting about 200 mL of an anti-moss solution containing monosodium salt of dichlorophen (360 g/L). She recovered following supportive care.
    B) The rank order of chlorinated phenol toxicity was C5P > C4P > C3P > C2P > CP > phenol. Toxicity after oral exposure is unlikely to occur at low doses. Skin exposure to an amount of molten 2,4-DCP small enough to cover just 1% of body surface area (BSA) is potentially toxic. Adults have died rapidly after the following exposures; splash exposures of pure 2,4-DCP to 10% body surface area BSA; steam exposure of 2,4 DCP to the face and neck; splash exposure of 51% 2,4-DCP to 60% to 65% BSA; splash exposure to 2,4-DCP to the face, both forearms, right knee and thigh.

Clinical Effects

Summary Of Exposure

    A) USES: Chlorinated phenols in this management will consist of the mono-, di-, tri-, and tetrachlorophenols. They are used as biocides, antifungals, wood preservatives, disinfectants, in mothproofing and as insecticides. A separate management is available for pentachlorophenol.
    B) TOXICOLOGY: The general effect of increasing the chlorination of phenol is a reduction of the convulsant action, but an increase in the inhibition of oxidative phosphorylation. Pentachlorophenol does not cause seizures. In general, the toxicity of chlorophenols decreases with decreasing chlorination. Dermal and mucous membrane irritation may occur.
    C) EPIDEMIOLOGY: Poisoning is uncommon but can be severe. Death has occurred following accidental 10% BSA dermal exposures.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Headache, dizziness, and irritations of the eyes, skin or respiratory tract, anorexia, nausea, vomiting and chest pain may develop.
    2) SEVERE ACUTE TOXICITY: Lethargy is the first sign followed by muscular weakness, muscular fasciculation, hyperthermia, and irritability. Tremors, loss of coordination, seizures, and respiratory distress or acute lung injury can develop. This evolves to cerebral edema, paralysis, coma and death. DICHLOROPHENE: Dichlorophene ingestion resulted in multiorgan toxicity, including caustic esophageal and gastric mucosal injuries, confusion, profuse diarrhea, hypotension, electrolyte disturbances, elevated liver enzymes, rhabdomyolysis, and acute renal failure.
    3) SEVERE CHRONIC TOXICITY: Chronic toxicity of the chlorophenols in humans is not well-defined. After prolonged, higher exposures, severe dermatitis (chloracne) may be experienced. Commonly reported symptoms include night sweats, neurological disturbances, bronchitis, weight loss, headache, and fatigue. Liver and kidney damage and a depressed immune response may be associated with high levels of chronic exposure.

Vital Signs

    3.3.3) TEMPERATURE
    A) Hyperpyrexia may be expected in toxic exposures due to the uncoupling of oxidative phosphorylation, particularly with tri- and tetra-chlorophenols, as demonstrated in rats and rabbits (HSDB , 2000; Clayton & Clayton, 1994).

Heent

    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) Eye exposures may result in severe conjunctival irritation, corneal injury and iritis (HSDB , 2000). Irritation and corneal damage may result in permanent impairment of vision or blindness (EPA , 2000). Chlorinated phenol vapors may cause eye irritation.
    3.4.5) NOSE
    A) WITH POISONING/EXPOSURE
    1) Dusts and vapors from these chemicals are irritating to the nose and pharynx (HSDB , 2000; OHM/TADS , 2000).
    3.4.6) THROAT
    A) WITH POISONING/EXPOSURE
    1) Dusts and vapors from the lower chlorinated phenols are irritating to the pharynx (HSDB , 2000; OHM/TADS , 2000). Ingestion of larger amounts may cause burns of the mouth and throat (MSDS, 2000).
    2) CASE REPORT: A splash contact to over 60% of a male worker's body with a solution containing 51% 2,4-dichlorophenol (2,4-DCP) resulted in swollen, red, sloughed mucosa of the larynx, trachea, and bronchi. Blue/tan swollen esophageal mucosa was also evident (MMWR , 2000).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) TACHYCARDIA
    1) Theoretically, tri- and tetra-chlorophenols may cause tachycardia following toxic exposures due to uncoupling of mitochondrial oxidative phosphorylation cycles in tissues resulting in an increased basal metabolic rate.
    B) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Following large ingestions or dermal exposures in humans, an initial increase in respirations occurs, followed by decreased respirations and hypotension in severe poisonings (Exon, 1984; HSDB , 2000).
    b) CASE REPORT: A 74-year-old woman with a history of depression, chronic alcoholism, cardiac insufficiency, and breast cancer developed caustic esophageal and gastric mucosal injuries, confusion, profuse diarrhea, hypotension, electrolyte disturbances, and elevated liver enzymes after ingesting about 200 mL of an anti-moss solution containing monosodium salt of dichlorophen (360 g/L) in a suicide attempt. An ECG revealed first-degree atrioventricular block with a normal QRS width and a 550-ms corrected QT. Despite supportive therapy, her condition deteriorated on day 3 and she developed aspiration pneumonia and respiratory acidosis, requiring mechanical ventilation. At this time, laboratory results revealed rhabdomyolysis and acute renal failure, requiring hemodialysis on day 8. Following further supportive care, her condition gradually improved. On day 30, she was discharged to the psychiatric ward (Langrand et al, 2013).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) IRRITATION SYMPTOM
    1) These chemicals are respiratory irritants. Although not reported, it is possible that chronic exposure may result in pulmonary fibrosis (HSDB , 2000). Vapor release, causing respiratory irritation, can occur when the environmental temperature is elevated (EPA , 2000).
    B) HYPERVENTILATION
    1) Increased rate of respiration, a result of increased metabolic rate is produced in animal studies and is expected in toxic human exposures, particularly with the higher chlorinated phenols (e.g., tetrachlorophenol) (HSDB , 2000; Clayton & Clayton, 1994).
    C) ACUTE RESPIRATORY INSUFFICIENCY
    1) Severe toxic exposures may result in dyspnea, motor weakness, followed by respiratory depression and arrest (MMWR , 2000; HSDB , 2000; Clayton & Clayton, 1994).
    D) ACUTE LUNG INJURY
    1) Inhalation exposures have resulted in non-cardiogenic pulmonary edema and death (EPA , 2000; MMWR , 2000).
    2) CASE REPORT: While using steam to clear a blocked pump, a 29-year-old worker was exposed to steam containing 2,4-DCP. The patient died within an hour of the accident. Pulmonary edema was the only significant finding upon autopsy (EPA , 2000; MMWR , 2000).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) SEIZURE
    1) Toxic exposure can result in restlessness, which rapidly progresses to motor weakness, loss of coordination, tremors, tonic-clonic seizures (induced by noise or touch), dyspnea, coma, respiratory depression, and death. Seizures are more prevalent and severe with mono-chlorophenols (MMWR , 2000; HSDB , 2000; Clayton & Clayton, 1994).
    a) Di- and tri-chlorophenols produce the same toxic effects as above, but the decreased activity and motor weakness do not appear as promptly as with the mono-chlorophenols. Tetra-chlorophenols also produce tremors and seizures, although the etiology is likely due to asphyxia or hypoglycemia, a different mechanism than that noted with mono-, di-, and tri-chlorophenols.
    b) The general effect of increasing the chlorination of phenol is a reduction of the convulsant action, but an increase in the inhibition of oxidative phosphorylation.
    2) CASE REPORT: Following a dermal splash accident over portions of his right thigh and arm with pure liquid 2,4-DCP, a 33-year-old male experienced a seizure and collapsed within 20 minutes of the exposure. Resuscitation efforts were unsuccessful and death occurred within minutes (MMWR , 2000; Kintz et al, 1992).
    3) CASE REPORT: Following an upper airway exposure to steam containing 2,4-DCP, a 45-year-old male worker sustained burns to upper airway, lost consciousness and died shortly. Autopsy findings reported pulmonary congestion along with alveolar hemorrhage (MMWR , 2000; EPA , 2000).
    4) CASE REPORT: A 33-year-old male worker was splashed over 60% of his body with a solution containing 51% 2,4-DCP. He became unconscious and had seizures. He died approximately 90 minutes after the exposure (MMWR , 2000; EPA , 2000).
    B) COMA
    1) In severe intoxications, a rapidly progressing and profound coma may occur (MMWR , 2000; Clayton & Clayton, 1994).
    C) DIZZINESS
    1) Dizziness and headache are common effects following subchronic exposures or small acute exposures (Clayton & Clayton, 1994). Functional disorders of the central and peripheral nervous system have been noted in workers exposed to 4-chlorophenol (21).
    D) CLOUDED CONSCIOUSNESS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 74-year-old woman developed caustic esophageal and gastric mucosal injuries, confusion, profuse diarrhea, hypotension, electrolyte disturbances, and elevated liver enzymes after ingesting about 200 mL of an anti-moss solution containing monosodium salt of dichlorophen (360 g/L) in a suicide attempt. Despite supportive care, her condition deteriorated and she developed rhabdomyolysis and acute renal failure, requiring hemodialysis on day 8. Her condition gradually improved after further supportive care. On day 30, she was discharged to the psychiatric ward (Langrand et al, 2013).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) BURN
    1) WITH POISONING/EXPOSURE
    a) Ingestion of small amounts are not expected to cause injury. Swallowing of large amounts may cause injury, such as burns of the mouth, throat and gastrointestinal tract (MSDS, 2000). Exposure to steam containing 2,4-DCP has resulted in burns to the skin, mouth, and upper airway (MMWR , 2000; EPA , 2000).
    b) CASE REPORT: A 74-year-old woman developed caustic esophageal and gastric mucosal injuries, confusion, profuse diarrhea, hypotension, electrolyte disturbances, and elevated liver enzymes after ingesting about 200 mL of an anti-moss solution containing monosodium salt of dichlorophen (360 g/L) in a suicide attempt. On day 4, upper gastrointestinal endoscopy revealed caustic lesions with a large esophageal ulcer and 3 necrotic gastric lesions. Despite supportive care, her condition deteriorated and she developed rhabdomyolysis and acute renal failure, requiring hemodialysis. Her condition gradually improved after further supportive care. On day 30, she was discharged to the psychiatric ward (Langrand et al, 2013).
    B) DIARRHEA
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 74-year-old woman developed caustic esophageal and gastric mucosal injuries, confusion, profuse diarrhea, hypotension, electrolyte disturbances, and elevated liver enzymes after ingesting about 200 mL of an anti-moss solution containing monosodium salt of dichlorophen (360 g/L) in a suicide attempt. Despite supportive care, her condition deteriorated and she developed rhabdomyolysis and acute renal failure, requiring hemodialysis. Her condition gradually improved after further supportive care. On day 30, she was discharged to the psychiatric ward (Langrand et al, 2013).
    3.8.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) GI HEMORRHAGE
    a) RATS: Toxicity studies of mono-chlorophenols have shown hemorrhages in rat intestines (Clayton & Clayton, 1994).

Hepatic

    3.9.2) CLINICAL EFFECTS
    A) STEATOSIS OF LIVER
    1) Acute and chronic exposure may result in hepatocellular damage, including fatty changes (MSDS, 2000; Clayton & Clayton, 1994).
    2) CASE REPORT: A 45-year-old male died shortly after exposure to steam containing 2,4-DCP. Autopsy results were significant for moderately severe hepatocellular fatty change (MMWR , 2000; EPA , 2000).
    B) INCREASED LIVER ENZYMES
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 74-year-old woman developed caustic esophageal and gastric mucosal injuries, confusion, profuse diarrhea, hypotension, electrolyte disturbances, and elevated liver enzymes (peak AST on admission; peak ALT delayed on day 2, 87 IU/L) after ingesting about 200 mL of an anti-moss solution containing monosodium salt of dichlorophen (360 g/L) in a suicide attempt. Despite supportive care, her condition deteriorated and she developed rhabdomyolysis and acute renal failure, requiring hemodialysis on day 8. Her condition gradually improved after further supportive care. Her liver enzymes normalized on day 6. On day 30, she was discharged to the psychiatric ward (Langrand et al, 2013).
    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) FATTY LIVER
    a) RATS: Toxicity studies of mono-chlorophenols have shown fatty infiltration of the liver in rats (Clayton & Clayton, 1994). 2,4-Dichlorophenol has a predilection for hepatic tissues in animal toxicity studies (Exon, 1984).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) ABNORMAL RENAL FUNCTION
    1) WITH POISONING/EXPOSURE
    a) Exposure to mono- and di-chlorophenols may cause hypokalemia and may compromise renal function (EPA , 2000).
    b) CASE REPORT: A 74-year-old woman developed caustic esophageal and gastric mucosal injuries, confusion, profuse diarrhea, hypotension, electrolyte disturbances, and elevated liver enzymes after ingesting about 200 mL of an anti-moss solution containing monosodium salt of dichlorophen (360 g/L) in a suicide attempt. Despite supportive care, her condition deteriorated and she developed rhabdomyolysis and acute renal failure (peak creatinine concentration, 482 mcmol/L), requiring hemodialysis on day 8. Following further supportive care, her condition gradually improved, including renal function recovering on day 20. On day 30, she was discharged to the psychiatric ward (Langrand et al, 2013).
    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) RENAL TUBULAR DISORDER
    a) RATS: Toxicity studies of mono-chlorophenols have shown marked injury to rat kidneys, with red blood cells casts in the tubules (Clayton & Clayton, 1994). 2,4-Dichlorophenol has a predilection for renal tissues in animal toxicity studies (Exon, 1984).

Acid-Base

    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) WITH POISONING/EXPOSURE
    a) Tri- and tetra-chlorophenols cause interference with oxidative phosphorylation which theoretically, in severe poisonings, might result in increased basal metabolic rate with consequential metabolic acidosis.

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) CHEMICAL BURN
    1) On skin contact, these chemicals are corrosive and produce redness and edema; short single exposures or prolonged exposures may cause mild to moderate chemical burns (EPA , 2000; HSDB , 2000; OHM/TADS , 2000). 2,4-Dichlorophenol is classified as corrosive to the skin by DOT guidelines (EPA , 2000).
    2) CASE REPORT: An unintentional dermal splash exposure to steam containing 2,4-DCP resulted in chemical burns on the face and extremities. The patient died within one hour of the exposure (MMWR , 2000; EPA , 2000).
    3) CASE REPORT: A splash contact over 60% of a 33-year-old male workers body with a solution containing 51% 2,4-DCP resulted in first-degree chemical burns on exposed skin surfaces. The man died within about 90 minutes of the exposure (MMWR , 2000).
    B) ERUPTION
    1) Following exposures to the lower chlorinated phenols, dermatoses, including photoallergic contact dermatitis has been reported. Dermal lesions included papulofollicular lesions, comedones, sebaceous cysts, and marked hyperkeratosis (Clayton & Clayton, 1994). Contaminants (polyhalogenated dioxins and furans) in the chlorinated phenols may be responsible for some of the dermatologic effects.

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) RHABDOMYOLYSIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 74-year-old woman developed caustic esophageal and gastric mucosal injuries, confusion, profuse diarrhea, hypotension, electrolyte disturbances, and elevated liver enzymes after ingesting about 200 mL of an anti-moss solution containing monosodium salt of dichlorophen (360 g/L) in a suicide attempt. Despite supportive care, her condition deteriorated and she developed rhabdomyolysis (peak serum CPK: 1421 International Units/L 2 days postingestion) and acute renal failure (peak creatinine concentration, 482 mcmol/L), requiring hemodialysis on day 8. Her condition gradually improved after further supportive care. On day 30, she was discharged to the psychiatric ward (Langrand et al, 2013).

Endocrine

    3.16.2) CLINICAL EFFECTS
    A) HYPOGLYCEMIA
    1) Hypoglycemia may predominately be seen following toxic exposures to tetra-chlorophenols as a result of interference with oxidative phosphorylation at a mitochondrial cellular level (Clayton & Clayton, 1994).

Reproductive

    3.20.1) SUMMARY
    A) Limited information on reproductive or teratologic effects indicates no significant clinical effects.
    3.20.2) TERATOGENICITY
    A) LACK OF EFFECT
    1) Rat toxicity studies have shown no evidence of soft tissue or skeletal malformation when 3,5-dichlorophenol was administered during the period of organogenesis (Spainhour et al, 1995).
    2) Rat toxicity studies of 2,4-dichlorophenol demonstrated a slight degree of embryotoxicity or fetotoxicity, but no teratogenicity at any dose level (Rodwell et al, 1989).
    3) Six week old progeny of 2,4-DCP treated rats exhibited no signs of 2,4-DCP toxicity other than increased spleen weights in the higher dose range (Exon, 1984).
    3.20.5) FERTILITY
    A) ANIMAL STUDIES
    1) 2,4-DCP did not appear to alter reproductive performance in rat studies (Exon et al, 1984).

Carcinogenicity

    3.21.2) SUMMARY/HUMAN
    A) An association between the risks of each of 3 cancers (non-Hodgkin lymphoma, multiple myeloma, and kidney cancer) with dermal exposure to chlorophenol fungicides was observed in a cohort study. In another study, there was little evidence presented for an association between hematopoietic cancers and exposure to chlorophenols containing fewer than 4 chlorines.
    3.21.3) HUMAN STUDIES
    A) CARCINOMA
    1) 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).
    2) 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).
    3.21.4) ANIMAL STUDIES
    A) TUMOR
    1) 2,4-Dichlorophenol has produced tumors of the skin and appendages in mice and is considered carcinogenic by RTECS criteria. 2-Chlorophenol and 3-chlorophenol have produced tumors of the skin and appendages in mice and are considered equivocal tumorigenic agents by RTECS criteria (RTECS , 2001).

Genotoxicity

    A) 2,4-Dichlorophenol has been found to be mutagenic in some in-vitro studies (MSDS, 2000).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor vital signs and mental status.
    B) Lower chlorinated phenol plasma concentrations are not clinically useful or readily available.
    C) Obtain an ECG and institute continuous cardiac monitoring in patients with moderate to severe toxicity.
    D) Monitor serum electrolytes, renal function, and liver enzymes in patients with significant exposures.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Lower chlorinated phenol plasma concentrations are not clinically useful or readily available.
    2) Monitor serum electrolytes, renal function, and liver enzymes in patients with significant exposures.
    B) ACID/BASE
    1) Monitor acid-base balance and fluid status closely.
    4.1.3) URINE
    A) URINARY LEVELS
    1) Determination of urinary phenol levels (normal range, 0.5 to 81.5 mg/L) may assist in determining extent of absorption following toxic exposures (MSDS, 2000).
    4.1.4) OTHER
    A) OTHER
    1) PULMONARY FUNCTION TESTS
    a) Monitor arterial blood gases and/or pulse oximetry, respiratory function, and chest x-ray in patients with respiratory effects or following a significant exposure. Acute lung injury is a toxic effect of the lower chlorinated phenols.
    2) MONITORING
    a) CNS depression leading to coma and motor weakness can develop rapidly. Monitor closely and provide mechanical ventilation if respiratory depression develops.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) Monitor the chest x-ray in patients with significant exposure.

Methods

    A) CHROMATOGRAPHY
    1) One study described a modified gas chromatographic procedure for the analysis of 2,4-dichlorophenol in postmortem specimens, including blood, urine, bile and stomach contents. Confirmation of these results were obtained with mass spectrometry (Kintz et al, 1992).
    2) In one case report, gas chromatography/mass spectrometry was used to determine postmortem dichlorophen concentrations in blood, urine, and vitreous humor (Kintz et al, 1997).
    3) Liquid chromatography-heated electrospray ionization-tandem mass spectrometry (LC-HESI-MS/MS) was used to determine dichlorophen concentrations in serum and urine of a 74-year-old woman who ingested about 200 mL of an anti-moss solution containing monosodium salt of dichlorophen (360 g/L) in a suicide attempt (Langrand et al, 2013).
    4) Gas chromatography and liquid chromatography with electrochemical detection have been used to confirm and quantitate chlorophenols in human urine (HSDB , 2000; Kumagai & Matsunaga, 1997).
    5) Veningerova et al (1994) described the use of solid-phase extraction and gas chromatography for detection and quantification of chlorinated phenols in human urine (Veningerova et al, 1994).
    6) Hill et al (1989) described a gas chromatography with tandem mass spectrometry method for the detection of chlorinated phenols in human urine. Detection limit was 1 part per billion (Hill et al, 1989).
    B) SPECTROMETRY
    1) Detection and confirmation of trace amounts of chlorophenol residues in biological samples have been accomplished with quadruple mass spectrometry with selected-ion monitoring (SIM) (HSDB , 2000).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patients with significant central nervous system depression (weakness, ataxia, vertigo, coma), or those with persistent abnormal vital signs such as bradycardia, and hypotension should be admitted. Patients with coma, seizure, dysrhythmias, or end organ damage should be admitted to an intensive care setting.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Patients who are asymptomatic after dermal exposures to low concentration products involving small body surface areas can be observed at home. Any signs of lethargy should be referred to a healthcare facility.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a poison center or medical toxicologist for assistance in managing patients with severe toxicity (dysrhythmias, severe hypotension, coma), or in whom the diagnosis is not clear.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) The following patients should be referred to a healthcare facility for evaluation and observation for 6 to 8 hours: Adults with large or deliberate ingestions, children with any ingestion, dermal exposures to high concentration products or those involving significant surface areas, eye or inhalation exposures with more than mild irritation, or any symptomatic patient.

Monitoring

    A) Monitor vital signs and mental status.
    B) Lower chlorinated phenol plasma concentrations are not clinically useful or readily available.
    C) Obtain an ECG and institute continuous cardiac monitoring in patients with moderate to severe toxicity.
    D) Monitor serum electrolytes, renal function, and liver enzymes in patients with significant exposures.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) DERMAL EXPOSURE
    1) For dermal exposure, remove contaminated clothing and wash skin with soap and water. Keep skin moist to enhance evaporative cooling if patient is hyperthermic. Use impermeable gloves and gowns to prevent exposure of healthcare workers.
    B) EYE EXPOSURE
    1) Irrigate exposed eyes.
    C) INHALATION EXPOSURE
    1) Inhalation exposures should be removed from the source as quickly as possible.
    D) ORAL EXPOSURE
    1) Prehospital gastrointestinal decontamination is generally not recommended because of the potential for CNS depression or persistent seizures and subsequent aspiration.
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY: Activated charcoal should be given to those who are able to reliably protect their airway. Gastric lavage is generally not indicated.
    B) ACTIVATED CHARCOAL
    1) If endoscopy is to be performed, activated charcoal may interfere with visualization of involved areas.
    2) 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.
    3) 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).
    6.5.3) TREATMENT
    A) MONITORING OF PATIENT
    1) Monitor vital signs and mental status.
    2) Lower chlorinated phenol plasma concentrations are not clinically useful or readily available.
    3) Obtain an ECG and institute continuous cardiac monitoring in patients with moderate to severe toxicity.
    4) Monitor serum electrolytes, renal function, and liver enzymes in patients with significant exposures.
    B) BODY TEMPERATURE ABOVE REFERENCE RANGE
    1) Remove patients clothing, keep skin moist and direct fans at the patient to enhance evaporative cooling. Ice packs may be placed in the groin and axilla, and a cooling blanket may be used. Ice water immersion can be used for extreme hyperthermia.
    2) Administration of salicylates to reduce hyperpyrexia is absolutely CONTRAINDICATED. Salicylates can also uncouple oxidative phosphorylation and may aggravate hyperpyrexia.
    C) AIRWAY MANAGEMENT
    1) Perform early in patients with severe intoxication (seizures, dysrhythmias, severe delirium, CNS or respiratory depression).
    D) FLUID/ELECTROLYTE BALANCE REGULATION
    1) Fluids, electrolytes, and acid-base data should be monitored and intravenous replacement of losses provided. Intravenous solution should contain adequate amounts of glucose to supply the requirements of increased metabolism, particularly when toxicity is due to the higher of the chlorinated phenols.
    E) SEIZURE
    1) Seizures are most typically seen following toxic exposures to mono- and di-chlorophenols.
    2) 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).
    3) 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 .
    4) 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).
    5) 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).
    6) 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).
    7) 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).
    F) BURN
    1) There is little information regarding the use of endoscopy in the setting of concentrated lower chlorinated phenol ingestion. The following information is derived from experience with other corrosives.
    G) ENDOSCOPIC PROCEDURE
    1) SUMMARY: Obtain consultation concerning endoscopy as soon as possible, and perform endoscopy within the first 24 hours when indicated.
    2) INDICATIONS: Endoscopy should be performed in adults with a history of deliberate ingestion, adults with any signs or symptoms attributable to inadvertent ingestion, and in children with stridor, vomiting, or drooling after unintentional ingestion (Crain et al, 1984). Endoscopy should also be performed in children with dysphagia or refusal to swallow, significant oral burns, or abdominal pain after unintentional ingestion (Gaudreault et al, 1983; Nuutinen et al, 1994). Children and adults who are asymptomatic after accidental ingestion do not require endoscopy (Gupta et al, 2001; Lamireau et al, 2001; Gorman et al, 1992).
    3) RISKS: Numerous large case series attest to the relative safety and utility of early endoscopy in the management of caustic ingestion.
    a) REFERENCES: (Dogan et al, 2006; Symbas et al, 1983; Crain et al, 1984a; Gaudreault et al, 1983a; Schild, 1985; Moazam et al, 1987; Sugawa & Lucas, 1989; Previtera et al, 1990; Zargar et al, 1991; Vergauwen et al, 1991; Gorman et al, 1992)
    4) The risk of perforation during endoscopy is minimized by (Zargar et al, 1991):
    a) Advancing across the cricopharynx under direct vision
    b) Gently advancing with minimal air insufflation
    c) Never retroverting or retroflexing the endoscope
    d) Using a pediatric flexible endoscope
    e) Using extreme caution in advancing beyond burn lesion areas
    f) Most authors recommend endoscopy within the first 24 hours of injury, not advancing the endoscope beyond areas of severe esophageal burns, and avoiding endoscopy during the subacute phase of healing when tissue slough increases the risk of perforation (5 to 15 days after ingestion) (Zargar et al, 1991).
    5) GRADING
    a) Several scales for grading caustic injury exist. The likelihood of complications such as strictures, obstruction, bleeding, and perforation is related to the severity of the initial burn (Zargar et al, 1991):
    b) Grade 0 - Normal examination
    c) Grade 1 - Edema and hyperemia of the mucosa; strictures unlikely.
    d) Grade 2A - Friability, hemorrhages, erosions, blisters, whitish membranes, exudates and superficial ulcerations; strictures unlikely.
    e) Grade 2B - Grade 2A plus deep discreet or circumferential ulceration; strictures may develop.
    f) Grade 3A - Multiple ulcerations and small scattered areas of necrosis; strictures are common, complications such as perforation, fistula formation or gastrointestinal bleeding may occur.
    g) Grade 3B - Extensive necrosis through visceral wall; strictures are common, complications such as perforation, fistula formation, or gastrointestinal bleeding are more likely than with 3A.
    6) FOLLOW UP - If burns are found, follow 10 to 20 days later with barium swallow or esophagram.
    7) SCINTIGRAPHY - Scans utilizing radioisotope labelled sucralfate (technetium 99m) were performed in 22 patients with caustic ingestion and compared with endoscopy for the detection of esophageal burns. Two patients had minimal residual isotope activity on scanning but normal endoscopy and two patients had normal activity on scan but very mild erythema on endoscopy. Overall the radiolabeled sucralfate scan had a sensitivity of 100%, specificity of 81%, positive predictive value of 84% and negative predictive value of 100% for detecting clinically significant burns in this population (Millar et al, 2001). This may represent an alternative to endoscopy, particularly in young children, as no sedation is required for this procedure. Further study is required.
    8) MINIPROBE ULTRASONOGRAPHY - was performed in 11 patients with corrosive ingestion . Findings were categorized as grade 0 (distinct muscular layers without thickening, grade I (distinct muscular layers with thickening), grade II (obscured muscular layers with indistinct margins) and grade III (muscular layers that could not be differentiated). Findings were further categorized as to whether the worst appearing image involved part of the circumference (type a) or the whole circumference (type b). Strictures did not develop in patients with grade 0 (5 patients) or grade I (4 patients) lesions. Transient stricture formation developed in the only patient with grade IIa lesions, and stricture requiring repeated dilatation developed in the only patient with grade IIIb lesions (Kamijo et al, 2004).
    H) 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.
    I) 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).

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) OXYGEN
    1) If symptoms are not relieved by exposure to fresh air, oxygen should be administered until blood gases can be measured. Assisted ventilation may be required if symptoms are severe or prolonged.
    B) 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).
    8) A chest x-ray may be needed. Some irritants may cause delayed pulmonary edema.
    C) 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) IRRIGATION
    1) If in a medical facility, sterile saline should be used to irrigate the eyes until the cul de sac is returned to neutrality. A slit lamp examination should be considered following thorough irrigation. Application of an ophthalmic local anesthetic will increase patient comfort and facilitate irrigation of the eye.
    B) GENERAL TREATMENT
    1) Administration of topical antibiotics, cycloplegics, mydriatics, and patching may be necessary in rare instances of abrasion.
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DECONTAMINATION
    1) Rapid effective decontamination is critical to surviving a skin exposure episode, since chlorinated phenols are quickly absorbed through the skin. Exposed skin should be thoroughly washed with soap and water. It is important to remove all clothing from the affected area (MSDS, 2000).
    2) The lower chlorinated phenols are lipophilic, with relatively low water solubility. The use of water for skin flushing may lead to a protracted decontamination process (MMWR , 2000; EPA , 2000). Additional research is needed to identify more effective agents for skin decontamination.
    3) Because these chemicals are weak acids, it has been suggested that the dissolution rate can be influenced by adjusting the pH of the wash solution. Soap solutions, (e.g., sodium stearate) are alkaline and may be expected to promote more rapid decontamination. Alternatively, solutions of sodium bicarbonate, sodium carbonate, or phosphate buffers might be considered. It may be beneficial to use an alkaline solution since the ionized form of these compounds will be much less lipophilic, thus less readily absorbed into the skin (EPA , 2000).
    4) Undiluted polypropylene glycol or polyethylene glycol 300 or 400 may be useful solvents. Lower chlorinated phenols may be removed from the skin by repeatedly spraying/swabbing the skin with PEG, alternating with rinsing with large quantities of water for 30 minutes. It has been suggested to use PEG300/ethanol 2:1 for removal of these chemicals from the skin (MSDS, 2000).
    5) Phenol destroys nerve endings in skin; absence of pain does not mean the skin has been properly decontaminated (MSDS, 2000).
    6.9.2) TREATMENT
    A) BURN
    1) Chlorinated phenols are corrosive and irritating to the skin. Splash contact and protracted exposure have resulted in mild to moderate chemical burns.
    2) APPLICATION
    a) These recommendations apply to patients with MINOR chemical burns (FIRST DEGREE; SECOND DEGREE: less than 15% body surface area in adults; less than 10% body surface area in children; THIRD DEGREE: less than 2% body surface area). Consultation with a clinician experienced in burn therapy or a burn unit should be obtained if larger area or more severe burns are present. Neutralizing agents should NOT be used.
    3) DEBRIDEMENT
    a) After initial flushing with large volumes of water to remove any residual chemical material, clean wounds with a mild disinfectant soap and water.
    b) DEVITALIZED SKIN: Loose, nonviable tissue should be removed by gentle cleansing with surgical soap or formal skin debridement (Moylan, 1980; Haynes, 1981). Intravenous analgesia may be required (Roberts, 1988).
    c) BLISTERS: Removal and debridement of closed blisters is controversial. Current consensus is that intact blisters prevent pain and dehydration, promote healing, and allow motion; therefore, blisters should be left intact until they rupture spontaneously or healing is well underway, unless they are extremely large or inhibit motion (Roberts, 1988; Carvajal & Stewart, 1987).
    4) TREATMENT
    a) TOPICAL ANTIBIOTICS: Prophylactic topical antibiotic therapy with silver sulfadiazine is recommended for all burns except superficial partial thickness (first-degree) burns (Roberts, 1988). For first-degree burns bacitracin may be used, but effectiveness is not documented (Roberts, 1988).
    b) SYSTEMIC ANTIBIOTICS: Systemic antibiotics are generally not indicated unless infection is present or the burn involves the hands, feet, or perineum.
    c) WOUND DRESSING:
    1) Depending on the site and area, the burn may be treated open (face, ears, or perineum) or covered with sterile nonstick porous gauze. The gauze dressing should be fluffy and thick enough to absorb all drainage.
    2) Alternatively, a petrolatum fine-mesh gauze dressing may be used alone on partial-thickness burns.
    d) DRESSING CHANGES:
    1) Daily dressing changes are indicated if a burn cream is used; changes every 3 to 4 days are adequate with a dry dressing.
    2) If dressing changes are to be done at home, the patient or caregiver should be instructed in proper techniques and given sufficient dressings and other necessary supplies.
    e) Analgesics such as acetaminophen with codeine may be used for pain relief if needed.
    5) TETANUS PROPHYLAXIS
    a) The patient's tetanus immunization status should be determined. Tetanus toxoid 0.5 milliliter intramuscularly or other indicated tetanus prophylaxis should be administered if required.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) HEMODIALYSIS
    1) Hemodialysis, hemoperfusion, or exchange transfusion has no benefit.
    2) Due to the high protein binding and lipophilicity of the lower chlorinated phenols, it is anticipated that hemodialysis or hemoperfusion will not be clinically effective in the removal of these chemicals.

Abstracts

Case Reports

    A) ROUTE OF EXPOSURE
    1) DERMAL: A pure solution of 2,4-dichlorophenol was accidentally splashed over portions of the right thigh and right arm on a 33-year-old male disposing of industrial waste. The victim rinsed his skin with water, without removing any clothing, and within 20 minutes experienced a seizure and collapsed. CPR was attempted without success. Less than 10% of the victim's skin was contaminated. Post-mortem biological samples were shown to have the highest concentration of 2,4-dichlorophenol in the blood and then the bile. Because only low levels were detected in the urine, it was very suggestive that death occurred soon after splash contact (Kintz et al, 1992).

Range Of Toxicity

Summary

    A) TOXICITY: Toxic dose is not well quantified, that toxicity appears to be increased with increasing number of chlorines. Deaths within 20 to 30 minutes from dermal exposures, steam exposures, and oral exposures have been reported. A woman developed caustic esophageal and gastric mucosal injuries, confusion, profuse diarrhea, hypotension, electrolyte disturbances, elevated liver enzymes, rhabdomyolysis, and acute renal failure after ingesting about 200 mL of an anti-moss solution containing monosodium salt of dichlorophen (360 g/L). She recovered following supportive care.
    B) The rank order of chlorinated phenol toxicity was C5P > C4P > C3P > C2P > CP > phenol. Toxicity after oral exposure is unlikely to occur at low doses. Skin exposure to an amount of molten 2,4-DCP small enough to cover just 1% of body surface area (BSA) is potentially toxic. Adults have died rapidly after the following exposures; splash exposures of pure 2,4-DCP to 10% body surface area BSA; steam exposure of 2,4 DCP to the face and neck; splash exposure of 51% 2,4-DCP to 60% to 65% BSA; splash exposure to 2,4-DCP to the face, both forearms, right knee and thigh.

Minimum Lethal Exposure

    A) ADULT
    1) Following a splash accident with a pure solution of 2,4-DCP to 10% of his body area, a 33-year-old male died within 30 minutes (Kintz et al, 1992).
    2) A dermal splash exposure of 2,4-DCP to the forearms, right knee, right thigh, and face resulted in death within one hour to a 29-year-old male chemical company employee (MMWR , 2000; EPA , 2000).
    3) A 64-year-old chemical company worker died within 20 minutes of an exposure to steam containing 2,4-DCP to his face and neck (MMWR , 2000; EPA , 2000).
    4) A 33-year-old male died within 90 minutes of a dermal splash exposure to 60% to 65% of his body from a solution containing 51% 2,4-DCP (MMWR , 2000; EPA , 2000).
    5) A 59-year-old woman died after ingesting about 1 L of "Stop Mousse (dichlorophen, 360 g/L)". Postmortem dichlorophen concentrations were 9.77 mg/L in blood, 0.10 mg/L in urine, and 1.12 mg/L in vitreous humor (Kintz et al, 1997).
    B) ANIMAL DATA
    1) Acute oral LD50 studies of mono- and di-chlorophenols and pentachlorophenol in the mouse demonstrated primary signs of toxicity of increased respiration, tremors, and seizures followed by CNS depression for all compounds except pentachlorophenol, which elicited signs of CNS depression only. Death occurred in less than 24 hours for most groups (Borzelleca et al, 1985).
    C) GENERAL/SUMMARY
    1) Zhao et al (1995) reported on the structure-activity relationships of chlorophenols using human embryonic palatal mesenchymal cells (HEPM). They found a clear structure-activity relationship between toxicity of chlorinated phenols and degree of chlorine substitution. The rank order of chlorinated phenol toxicity was C5P > C4P > C3P > C2P > CP > phenol from the HEPM assay.

Maximum Tolerated Exposure

    A) ADULT
    1) Toxicity after oral exposure is unlikely to occur at low doses. Oral LD50 for rats is 2000 to 5000 milligrams/kilogram following 2,4-dichlorophenol ingestion (MSDS, 2000).
    2) Skin exposure to an amount of molten 2,4-DCP small enough to cover just 1% of body surface area is potentially toxic (EPA , 2000).
    3) CASE REPORT: A 74-year-old woman developed caustic esophageal and gastric mucosal injuries, confusion, profuse diarrhea, hypotension, electrolyte disturbances, and elevated liver enzymes after ingesting about 200 mL of an anti-moss solution containing monosodium salt of dichlorophen (360 g/L) in a suicide attempt. Despite supportive care, her condition deteriorated and she developed rhabdomyolysis and acute renal failure, requiring hemodialysis on day 8. Following further supportive care, her condition gradually improved, including renal function recovering on day 20. On day 30, she was discharged to the psychiatric ward (Langrand et al, 2013).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) ADULT
    a) Following a splash accident with a pure solution of 2,4-dichlorophenol to 10% of his body area, a 33-year-old male died. Blood concentration of 2,4-dichlorophenol was reported to be 24.3 milligrams/liter (MMWR , 2000; Kintz et al, 1992).
    b) Blood concentrations of 7.2 milligrams/liter free 2,4-DCP and 13.1 milligrams/liter total 2,4-DCP were reported in a 29-year-old male following a fatal splash exposure to 2,4-DCP. The victim died within one hour of exposure (MMWR , 2000; EPA , 2000).
    c) A 59-year-old woman died after ingesting about 1 L of "Stop Mousse (dichlorophen, 360 g/L)". Postmortem dichlorophen concentrations were 9.77 mg/L in blood, 0.10 mg/L in urine, and 1.12 mg/L in vitreous humor (Kintz et al, 1997).
    d) A 74-year-old woman developed caustic esophageal and gastric mucosal injuries, confusion, profuse diarrhea, hypotension, electrolyte disturbances, elevated liver enzymes, rhabdomyolysis, and acute renal failure after ingesting about 200 mL of an anti-moss solution containing monosodium salt of dichlorophen (360 g/L) in a suicide attempt. Following supportive care, her condition gradually resolved and she was discharged to the psychiatric ward on day 30. On admission (8 hours postingestion), serum dichlorophen concentration was 708 mcg/L. Prolonged dichlorophen elimination (serum apparent elimination half-life of 35.5 hours) with a delayed peak concentration in urine on day 2 were observed (Langrand et al, 2013).

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) 2,4,5-Trichlorophenol
    1) LD50- (ORAL)RAT:
    a) 820 mg/kg (Clayton & Clayton, 1994)
    2) LD50- (SUBCUTANEOUS)RAT:
    a) 2260 mg/kg (Clayton & Clayton, 1994)
    B) 2,4-Dichlorophenol
    1) LD50- (ORAL)MOUSE:
    a) 1276 mg/kg (NIOSH, 2000)
    2) LD50- (ORAL)RAT:
    a) 580 mg/kg (NIOSH, 2000)
    C) m-Chlorophenol
    1) LD50- (ORAL)RAT:
    a) 570 mg/kg (OHM/TADS, 2000)
    2) LD50- (SUBCUTANEOUS)RAT:
    a) 1390 mg/kg (OHM/TADS, 2000)
    D) o-Chlorophenol
    1) LD50- (ORAL)RAT:
    a) 670 mg/kg (OHM/TADS, 2000)
    2) LD50- (SKIN)RAT:
    a) 38000 mg/kg (OHM/TADS, 2000)
    3) LD50- (SUBCUTANEOUS)RAT:
    a) 950 mg/kg (OHM/TADS, 2000)
    E) p-Chlorophenol
    1) LD50- (ORAL)RAT:
    a) 500 mg/kg (OHM/TADS, 2000)
    2) LD50- (SUBCUTANEOUS)RAT:
    a) 1030 mg/kg (OHM/TADS, 2000)
    F) Tetrachlorophenol
    1) LD50- (ORAL)RAT:
    a) 140 mg/kg (RTECS, 2000)
    2) LD50- (SUBCUTANEOUS)RAT:
    a) 210 mg/kg (RTECS, 2000)

Pharmacology Toxicology

Toxicologic Mechanism

    A) SEIZURES, which are more common following exposures to mono-, di- and tri-chlorophenols, are thought to be caused by the undissociated molecule. Seizures due to tetrachlorophenol are clinically similar to seizures caused by mono-, di and tri-chlorophenols, but probably result from a different mechanism (asphyxia and/or hypoglycemia) (Clayton & Clayton, 1994).
    B) OXIDATIVE PHOSPHORYLATION - Tri- and tetra-chlorophenols cause interference with oxidative phosphorylation, possibly due to the dissociated chlorophenate ion (Clayton & Clayton, 1994). A linear relationship exists between the uncoupling of mitochondrial oxidative phosphorylation and the degree of chlorine substitution (C5P greater than C4P greater than C3P) (Phillips et al, 1991). Incorporation of phosphate into ATP (without effecting electron transport) is prevented. This occurs at mitochondrial membrane cells, which continue to metabolize, but soon are depleted of ATP necessary for energy (HSDB , 2000).
    1) Basal metabolic rate is increased and body temperature increases. This hypermetabolic state, resulting from a derangement of aerobic metabolism and characterized by hyperthermia, in severe poisonings, can lead to tachycardia, tachypnea, hyperemia, diaphoresis and metabolic acidosis.

Physicochemical

Physical Characteristics

    A) CHLOROPHENOL - The ortho, meta, and para compounds exist as a colorless liquid, as a solid with needle-like crystals, and as a solid with needle-like crystals, respectively. All three forms are soluble in alcohol and ether (Clayton & Clayton, 1994; Lewis, 2000).
    B) DICHLOROPHENOL - At room temperature, 2,4-dichlorophenol is a white solid; it liquefies at 111 degrees F - 116 degrees F (43C-45C) (MMWR , 2000). Boiling point is 209 degrees F- 210 degrees F. It is very soluble in alcohol and ether (Clayton & Clayton, 1994).
    C) TRICHLOROPHENOL - The physical state of 2,3,5- and 2,4,5- trichlorophenol is as needles/aqueous alcohol and colorless/petroleum ether, respectively. Both forms are soluble in alcohol and ether (Clayton & Clayton, 1994). Odor described as unpleasant, medicinal, pungent, phenolic, strong, or persistent (HSDB , 2000).
    D) TETRACHLOROPHENOL - The physical state of 2,3,4,6-tetrachlorophenol is a solid with needle-like crystals, which are very soluble in alcohol and ether and only very slightly soluble in water (Clayton & Clayton, 1994).

Ph

    A) The lower chlorinated phenols are weak acids (EPA , 2000).

Molecular Weight

    A) 128.56 (Chlorophenol)
    B) 163.1 (Dichlorophenol)
    C) 197.46 (Trichlorophenol)
    D) 231.90 (Tetrachlorophenol)

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