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Pentachlorophenol (penchloro, penta, PCP, others) is a chlorinated aromatic hydrocarbon that has been used as a fungicide to preserve wood (eg, telephone poles). Since 1984, its use in the United States has been restricted to industrial purposes by certified applicators. It is a ubiquitous environmental contaminant detectable in the general population. It appears to be a thyroid hormone and immune disrupter. It is a probable carcinogen (EPA). It is formed as a by-product during water disinfection with chlorinated oxidants. Moreover, it was noted that children living in the areas of pentachlorobenzene and hexachlorobenzene emissions had elevated pentachlorophenol blood concentrations.

Dinitrophenols (dinosam, DNOC, DNP, and analogs) have been used as insecticides, herbicides, fungicides, and chemical intermediaries and are used in some explosives, dyes, and photographic chemicals. Dinitrophenol has also been taken orally for weight reduction. The use of dinitrophenol as a pesticide or as a weight-reducing agent is banned in the United States, although the chemical appears to be available over the Internet.

  1. Mechanism of toxicity

    1. Pentachlorophenol and dinitrophenols uncouple oxidative phosphorylation in the mitochondria. Substrates are metabolized, but the energy produced is dissipated as heat instead of producing adenosine triphosphate (ATP). The basal metabolic rate increases, placing increased demands on the cardiorespiratory system. Excess lactic acid results from anaerobic glycolysis.

    2. Dinitrophenols may oxidize hemoglobin to methemoglobin (See Methemoglobinemia).

    3. In animal studies, pentachlorophenol is mutagenic, teratogenic, and carcinogenic. DNP is teratogenic and may be weakly carcinogenic.

  2. Toxic dose. These agents are readily absorbed through the skin, lungs, and GI tract.

    1. Inhalation. The air level of pentachlorophenol considered immediately dangerous to life or health (IDLH) is 2.5 mg/m3. The ACGIH-recommended workplace air exposure limit (TLV-TWA) is 0.5 mg/m3 as an 8-hour time-weighted average.

    2. Skin. This is the main route associated with accidental poisoning. An epidemic of intoxication occurred in a neonatal nursery after diapers were inadvertently washed in 23% sodium pentachlorophenate.

    3. Ingestion. The minimum lethal oral dose of pentachlorophenol for humans is not known, but death occurred after ingestion of 2 g. Ingestion of 1–3 g of dinitrophenol is considered lethal.

  3. Clinical presentation. The toxic manifestations of pentachlorophenol and dinitrophenol are nearly identical. Profuse sweating, fever, tachypnea, and tachycardia are universally reported in serious poisonings.

    1. Acute exposure causes irritation of the skin, eyes, and upper respiratory tract. Systemic absorption may cause headache, vomiting, weakness, and lethargy. Profound sweating, hyperthermia, tachycardia, tachypnea, convulsions, and coma are associated with severe or fatal poisonings. Pulmonary edema may occur. Death usually is caused by cardiovascular collapse or hyperthermia. After death, an extremely rapid onset of rigor mortis is reported frequently. Dinitrophenol may also induce methemoglobinemia, liver and kidney failure, and yellow-stained skin.

    2. Chronic exposure may present in a similar manner and in addition may cause weight loss, GI disturbances, fevers and night sweats, weakness, flulike symptoms, contact dermatitis, and aplastic anemia (rare). Cataracts and glaucoma have been associated with dinitrophenol.

  4. Diagnosis is based on history of exposure and clinical findings and should be ...

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