CHAPTER 2-126: PHENOL AND RELATED COMPOUNDS

Phenol (carbolic acid) was introduced into household use as a potent germicidal agent but today is found in fewer products because less toxic compounds have replaced it. Phenol can be found in topical skin products (eg, Campho-phenique containing 4.7% phenol) and in surface deodorizers and disinfectants (eg, Creolin^®). Phenol is used in the production of fertilizers, wood preservatives, paint removers, and other chemicals. 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 chloroxylenol, the active ingredient in Dettol^®. Pentachlorophenol and dinitrophenols are discussed

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.

The minimum toxic and lethal doses are not well defined. Most phenolic compounds can be absorbed following inhalation, skin exposure, and ingestion.

1. Inhalation. The OSHA recommended workplace permissible exposure limit 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. A 9-year-old child developed brief runs of ventricular tachycardia, became obtunded and required intubation after application of Creolin^® to her head and upper torso. Cardiac arrhythmias occurred after dermal application of 3 mL of an 88% phenol solution. Solutions of more than 5% can be 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.

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

1. Inhalation. Vapors from 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. Dermal exposure may produce a deep white patch that turns red, after which the skin stains brown. This lesion is often initially 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 a mild transaminitis, 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.

Is based on a history of exposure, the presence of a characteristic odor, and painless skin burns with white discoloration. Dark colored urine has also been seen after skin exposure and ingestion.

1. Specific levels. Normal urine phenol levels are less than 20 mg/L. Urine phenol levels may be elevated in workers exposed to benzene and after the use of phenol-containing throat lozenges and mouthwashes. These tests are not routinely available in hospital laboratories.

2. Other useful laboratory studies include CBC, electrolytes, glucose, BUN, creatinine, chest x-ray, and ECG. Obtain a methemoglobin level after hydroquinone exposures.

1. Emergency and supportive measures

   1. Maintain an open airway and assist ventilation if necessary.

   2. Treat coma, seizures, hypotension, and arrhythmias if they occur.

   3. If corrosive injury to the GI tract is suspected, consult a gastroenterologist for possible endoscopy.

2. Specific drugs and antidotes. No specific antidote is available. If methemoglobinemia occurs, administer methylene blue.

3. Decontamination

   1. Inhalation. Remove victims from exposure and administer supplemental oxygen if available.

   2. Skin and eyes. Remove contaminated clothing and wash exposed skin with very soapy water or, if available, polyethylene glycol 300, mineral oil, or olive oil. Immediately flush exposed eyes with copious tepid water or normal saline for at least 15 minutes.

   3. Ingestion. Administer activated charcoal orally if conditions are appropriate (see Table I–38). Use caution because phenol can cause convulsions, increasing the risk for pulmonary aspiration. Charcoal may also interfere with endoscopy. Gastric lavage is not necessary after small-to-moderate ingestions if activated charcoal can be given promptly.

4. Enhanced elimination. Enhanced removal methods are generally not effective because of the large volume of distribution of these lipid-soluble compounds. Hexachlorophene is excreted in the bile, and repeat-dose activated charcoal may possibly be effective in increasing its clearance from the gut.