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Introduction

There are two naturally occurring types of elemental phosphorus: red and white. Red phosphorus is not well absorbed and has limited toxicity. In contrast, white phosphorus (also called yellow phosphorus) is a highly toxic cellular poison. White phosphorus is a colorless or yellow wax-like crystalline solid with a garlic-like or match-like odor and is almost insoluble in water but glows with exposure to air.

White phosphorous is used in the manufacture of fertilizers, food additives, cleaning compounds, and incendiaries in military ammunition. Historically, it has been used as a rodenticide and in the manufacture of fireworks. Red phosphorous is used in the manufacture of methamphetamine.

Mechanism of Toxicity

  1. White phosphorous ignites spontaneously in air to form phosphorous pentoxide, which reacts with water to form phosphoric acid. White phosphorus is also a cellular poison.
  2. Toxicity resulting from red phosphorous is largely associated with methamphetamine production. This process may involve the inadvertent conversion of red phosphorous to white phosphorous and the generation of phosphine gas.

Toxic Dose

  1. Ingestion. The fatal oral dose of yellow/white phosphorus is approximately 1 mg/kg.
  2. Inhalation. The ACGIH-recommended workplace limit (TLV-TWA) for white phosphorus is 0.1 mg/m3 (0.02 ppm) as an 8-hour time-weighted average. The air level considered immediately dangerous to life or health (IDLH) is 5 mg/m3. Occupational exposure limits are not well established for red phosphorous.

Clinical Presentation

(white phosphorous)

  1. Acute inhalation may cause mucous membrane irritation, cough, wheezing, chemical pneumonitis, and noncardiogenic pulmonary edema.
  2. Eye contact may cause conjunctivitis and foreign body sensation. Blepharospasm, tearing, and photophobia can occur. Phosphorus particles can cause caustic corneal injury.
  3. Skin contact can cause partial or full-thickness burns that have a garlic-like odor and an emission of smoke from the burn. Absorption through skin can occur.
  4. Acute ingestion may cause GI burns, inflammation and hemorrhage, severe abdominal pain, and “smoking” vomiting and diarrhea with a garlic-odor (“smoking” due to spontaneous combustion on exposure to air). Vomitus and feces can cause dermal burns on contact with skin. Death may occur within 24-48 hours due to cardiovascular collapse.
  5. Systemic effects include headache, delirium, shock, seizures, coma, and arrhythmias (atrial fibrillation, QRS and QT prolongation, ventricular tachycardia, and fibrillation). Acute renal injury, hepatic injury, and electrolyte derangements including hypocalcemia, hyperkalemia, and hyperphosphatemia may occur. Multisystem organ failure and death may result within days of exposure.
  6. Chronic exposure to phosphorous is associated with “phossy jaw” or mandibular osteonecrosis.

Diagnosis

Is based on a history of exposure and the clinical presentation. Cutaneous burns, a garlic odor of the skin, vomitus, feces, and “smoking” or luminescent stools and vomitus caused by spontaneous combustion of elemental phosphorus suggest ingestion. Wood lamp examination of the skin or eyes will cause embedded phosphorus particles to fluoresce.

  1. Specific levels. Serum phosphorous concentrations are not useful in diagnosing phosphorous poisoning.
  2. Other useful laboratory studies include BUN, creatinine, potassium, calcium, liver aminotransferases, urinalysis, blood gases, pulse oximetry, ECG, and chest radiography (after acute inhalation).

Treatment

  1. Emergency and supportive measures
    1. Observe a victim of inhalation closely for signs of upper airway injury and perform endotracheal intubation and assist ventilation if necessary. Administer supplemental oxygen. Treat bronchospasm and non-cardiogenic pulmonary edema if they occur.
    2. Treat fluid losses from gastroenteritis with aggressive IV crystalloid fluid and electrolyte replacement.
    3. Consider endoscopy if oral, esophageal, or gastric burns are suspected.
    4. Consider consultation with a burn specialist for skin burns and an ophthalmologist for eye injuries.
  2. Specific drugs and antidotes. There is no specific antidote.
  3. Decontamination . Rescuers should wear appropriate NIOSH-recommended protective gear to prevent accidental skin, eye, or inhalation exposure. Solid phosphorus or phosphorous particles should be covered with water to prevent spontaneous ignition. Contaminated clothing should be put under water.
    1. Inhalation. Remove the victim from exposure and give supplemental oxygen.
    2. Skin and eyes
      1. Remove contaminated clothing and wash exposed areas thoroughly with soap and water.
      2. Cover exposed areas with moist dressings or submersion in water to help prevent spontaneous combustion of white phosphorus. Avoid use of oily or greasy dressings because they may facilitate absorption of lipid-soluble phosphorus into tissue.
      3. Manually debride remaining phosphorus particles from skin while affected area remains moistened or immersed in water. A Wood's lamp may help visualize embedded phosphorus, which fluoresces under ultraviolet light.
      4. Irrigate affected eyes for 15 minutes with cool water and then cover with wet compresses.
    3. Ingestion. Consider gastric lavage and whole bowel irrigation after acute white phosphorus ingestion. Activated charcoal is of unknown benefit.
  4. Enhanced elimination. There is no effective method of enhanced elimination.