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There are two naturally occurring types of elemental phosphorus: red and yellow. Red phosphorus is not absorbed and is essentially nontoxic. In contrast, yellow phosphorus (also called white phosphorus) is a highly toxic cellular poison. Yellow/white phosphorus is a colorless or yellow waxlike crystalline solid with a garlic-like odor and is almost insoluble in water.

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Phosphorus is used to make fertilizers, as an additive in food and beverages, and as a cleaning compound, and it has been used in matches, fireworks, and as a pesticide. It is also used in the manufacture of methamphetamine and as an incendiary in military ammunition.

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  1. Mechanism of toxicity

    1. Phosphorus is highly corrosive and is also a general cellular poison. Cardiovascular collapse occurring after ingestion probably results not only from fluid loss caused by vomiting and diarrhea but also from a direct toxic effect on the heart and vascular tone.

    2. Yellow/white phosphorus spontaneously combusts in air at room temperature to yield phosphorus oxide, a highly irritating fume.

  2. 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 yellow or 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.

  3. Clinical presentation

    1. Acute inhalation may cause mucous membrane irritation, cough, wheezing, chemical pneumonitis, and noncardiogenic pulmonary edema. Chronic inhalation of phosphorus (over at least 10 months) may result in mandibular necrosis (“phossy jaw”).

    2. Skin or eye contact may cause conjunctivitis or severe dermal or ocular burns.

    3. Acute ingestion may cause GI burns and hemorrhage, severe vomiting and abdominal pain, and diarrhea with “smoking” stools (due to spontaneous combustion on exposure to air). Systemic effects include headache, delirium, shock, seizures, coma, and arrhythmias (atrial fibrillation, QRS and QT prolongation, ventricular tachycardia, and fibrillation). Metabolic derangements, including hypocalcemia, hyperkalemia, and hyperphosphatemia (or hypophosphatemia), may occur. Fulminant hepatic or renal failure may occur after 2–3 days. Reversible bone marrow toxicity with neutropenia has been described.

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

    1. Specific levels. Because serum phosphorus may be elevated, depressed, or normal, it is not a useful test for diagnosis or estimation of severity.

    2. Other useful laboratory studies include BUN, creatinine, potassium, calcium, liver aminotransferases, urinalysis, arterial blood gases or oximetry, ECG, and chest radiography (after acute inhalation).

  5. 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 (See Perform endotracheal intubation). Administer supplemental oxygen. Treat bronchospasm (See Hypoxia) and pulmonary edema (See Hypoxia) if they occur.

      2. Treat fluid losses from gastroenteritis with aggressive IV crystalloid fluid ...

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