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Phenol (carbolic acid) was introduced into household use as a potent germicidal agent but has limited use today because less toxic compounds have replaced it. Phenol is now most commonly found in topical skin products (eg, Campho-phenique contains 4.7% phenol) and is also used cosmetically as a skin-peeling agent. Hexachlorophene is a chlorinated biphenol that was used widely as a topical antiseptic and preoperative scrub until its adverse neurologic effects were recognized. Other phenolic compounds include creosote, creosol, cresol, cresylic acid, hydroquinone, eugenol, and phenylphenol (bisphenol, the active ingredient in Lysol). Pentachlorophenol and dinitrophenols are discussed in Pentachlorophenol and Dinitrophenol.

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  1. Mechanism of toxicity. Phenol denatures protein, disrupts the cell wall, and produces a coagulative tissue necrosis. It may cause corrosive injury to the eyes, skin, and respiratory tract. Systemic absorption may result in cardiac arrhythmias and CNS stimulation, but the mechanisms of these effects are not known. Some phenolic compounds (eg, dinitrophenol and hydroquinone) may induce hemolysis and methemoglobinemia (See Methemoglobinemia).

  2. Toxic dose. The minimum toxic and lethal doses have not been well established. Phenol is well absorbed via inhalation, skin application, and ingestion.

    1. Inhalation. The ACGIH-recommended workplace exposure limit (TLV-TWA) for pure phenol is 5 ppm (19 mg/m3) as an 8-hour time-weighted average. The level considered immediately dangerous to life or health (IDLH) is 250 ppm.

    2. Skin application. Death has occurred in infants from repeated dermal applications of small doses (one infant died after a 2% solution of phenol was applied for 11 hours on the umbilicus under a closed bandage). Cardiac arrhythmias occurred after dermal application of 3 mL of an 88% phenol solution. Solutions of more than 5% are corrosive.

    3. Ingestion. Deaths have occurred after adult ingestions of 1–32 g of phenol; however, survival after ingestion of 45–65 g has been reported. As little as 50–500 mg has been reported as fatal in infants.

    4. Pharmacokinetics. Phenol is rapidly absorbed by all routes. Its elimination half-life is 0.5–4.5 hours.

  3. Clinical presentation. Toxicity may result from inhalation, skin or eye exposure, or ingestion.

    1. Inhalation. Vapors of phenol may cause respiratory tract irritation and chemical pneumonia. Smoking of clove cigarettes (clove oil contains the phenol derivative eugenol) may cause severe tracheobronchitis.

    2. Skin and eyes. Topical exposure of the skin may produce a deep white patch that turns red, after which the skin stains brown. This lesion is often relatively painless. Irritation and severe corneal damage may occur if concentrated phenolic compounds come in contact with eyes.

    3. Ingestion usually causes vomiting and diarrhea, and diffuse corrosive GI tract injury may occur. Systemic absorption may cause agitation, confusion, seizures, coma, hypotension, arrhythmias, and respiratory arrest.

    4. Injection. Accidental injection of high concentrations of phenol has resulted in acute renal failure and acute respiratory distress syndrome.

  4. Diagnosis is based on a history of exposure, the presence of a characteristic odor, and painless skin burns with white discoloration.

    1. Specific levels. Normal urine phenol levels are less than 20 mg/L. Urine phenol levels may be elevated ...

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