Pentachlorophenol is a chlorinated aromatic hydrocarbon that was widely used as a pesticide to preserve wood products from insect and fungal damage (eg, power line poles). Since 1984, its use in the United States has been restricted to industrial purposes by certified applicators. It is synthetically manufactured and also formed as a by-product during water disinfection with chlorinated oxidants, and is a ubiquitous environmental contaminant detectable in the general population. Moreover, children living in the areas of pentachlorobenzene and hexachlorobenzene emissions had elevated pentachlorophenol serum and urine concentrations. It is an endocrine and immune disrupter. The EPA classifies pentachlorophenol as a likely human carcinogen and it has been designated as an IARC Group 1 carcinogen.

Dinitrophenols and analogs have been used as insecticides, herbicides, fungicides, and chemical intermediates and are used in some explosives, dyes, and photographic chemicals. In the 1930s, 2,4-dinitrophenol was prescribed as a weight reducing agent, but was later discontinued due to health risks. The use of dinitrophenol as a pesticide or as a weight-reducing agent is now banned in the United States, although the chemical is available from unregulated sources on the internet.

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. Anaerobic respiration results in the production of excess lactic acid.
2. Dinitrophenols may oxidize hemoglobin to methemoglobin.
3. In animal studies, pentachlorophenol and dinitrophenol are mutagenic, teratogenic, and carcinogenic.

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. There is insufficient data for minimal risk level derivation after inhalational exposure to dinitrophenol.
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 in an adult is considered lethal.

The toxic manifestations of pentachlorophenol and dinitrophenol are nearly identical. Profuse sweating, fever, tachypnea, and tachycardia are universally reported in serious poisonings and can manifest as early as 3.5 hours after intentional overdose.

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, intravascular hemolysis, pancreatitis, jaundice, and acute renal failure have been reported. Death usually is caused by cardiovascular collapse or hyperthermia. After death, an extremely rapid onset of rigor mortis is frequently reported. Dinitrophenol may also induce methemoglobinemia and yellow-stained skin.
2. Chronic exposure may present in a similar manner as acute systemic poisoning and may cause weight loss, GI disturbances, fevers and night sweats, weakness, flulike symptoms, contact dermatitis and chloracne, and aplastic anemia (rare). In addition, impaired fertility and hypothyroidism have been reported. Cataracts and glaucoma have been associated with dinitrophenol.

Is based on history of exposure and clinical findings and should be suspected in patients with fever, metabolic acidosis, diaphoresis, and tachypnea.

1. Specific levels. Blood levels are not readily available or useful for emergency management.
2. Other useful laboratory studies include CBC, electrolytes, glucose, BUN, creatinine, creatine kinase (CK), liver aminotransferases, lipase, lactate, urine dipstick for occult blood (positive with hemolysis or rhabdomyolysis), arterial blood gases, methemoglobin level, and chest radiography.

1. Emergency and supportive measures
   1. Maintain a patent airway and assist ventilation if necessary.
   2. Treat coma, seizures, hypotension, and hyperthermia if they occur. Dehydration from tachypnea, fever, and sweating is common and may require large-volume fluid replacement.
   3. Monitor asymptomatic patients for at least 6 hours after exposure.
   4. Do not use salicylates or anticholinergic agents, as they may worsen hyperthermia. Paralysis with neuromuscular blockers may not be helpful because of the intracellular mechanism for hyperthermia. Barbiturates may be of some value.
2. Specific drugs and antidotes. There is no specific antidote. Treat methemoglobinemia with methylene blue.
3. Decontamination
   1. Inhalation. Remove the victim from exposure and administer supplemental oxygen if available.
   2. Skin and eyes. Remove contaminated clothing and store in a plastic bag; wash exposed areas thoroughly with soap and copious water. Irrigate exposed eyes with copious saline or tepid water. Rescuers should wear appropriate protective clothing and respirators to avoid exposure.
   3. Ingestion. Administer activated charcoal orally if conditions are appropriate (see Table I-37,). Gastric lavage is not necessary after small-to-moderate ingestions if activated charcoal can be given promptly.
4. Enhanced elimination. There is no evidence that enhanced elimination procedures are effective.