Phosphine is a colorless gas that is heavier than air. It is odorless in its pure form, but impurities give it a characteristic fishy or garlic-like odor. It has been used for fumigation, and it is a serious potential hazard in operations producing metal phosphides, in which phosphine can be released in the chemical reaction of water and metal alloys. Workers at risk include metal refiners, acetylene workers, firefighters, pest control operators, and those in the semiconductor industry. Magnesium phosphide and aluminum phosphide are available in pellets or tablets and are used as fumigants and rodenticides. Zinc phosphide is a crystalline, dark gray powder mixed into food as rodent bait. Phosphides are a leading cause of fatal suicides and accidental ingestions in India and many developing countries.

Phosphine is a highly toxic gas, especially to the lungs, brain, kidneys, heart, and liver. It is also flammable on contact with air. The pathophysiologic action of phosphine is not clearly understood but may be related to inhibition of electron transport in mitochondria. Phosphides liberate phosphine gas upon contact with moisture, and this reaction is enhanced in the acidity of the stomach. Phosphine is then absorbed through the GI and respiratory tracts.

1. Phosphine gas. The ACGIH-recommended workplace exposure limit (TLVTWA) is 0.3 ppm (0.42 mg/m³), which is much lower than the minimal detectable (fishy odor) concentration of 1-3 ppm. Hence, the odor threshold does not provide sufficient warning of dangerous concentrations. An air level of 50 ppm is considered immediately dangerous to life or health (IDLH). Chronic exposure to sublethal concentrations for extended periods may produce toxicity.
2. Phosphides. Ingestion of as little as 500 mg of aluminum phosphide has caused death in an adult. In a reported case series, survivors had ingested about 1.5 g (range, 1.5-18 g), whereas fatal cases had ingested an average of 2.3 g (range, 1.5-36 g). The 50% lethal dose (LD₅₀) for zinc phosphide in rats is 40 mg/kg; the lowest reported lethal dose in humans is 4 g. A 36-year-old man who ingested 6 mg/kg of zinc phosphide and was treated with ipecac and activated charcoal remained asymptomatic.

Inhalation of phosphine gas is associated with cough, dyspnea, headache, dizziness, and vomiting. Phosphide ingestion may cause nausea, vomiting, diarrhea, refractory hypotension, and a rotten fish or garlicky odor sensed by caregivers. Adult respiratory distress syndrome (ARDS), acute renal failure, hepatitis, seizures, and coma may occur. Myocardial injury manifested by elevated cardiac enzymes, ST-T-wave changes, global hypokinesia, and various atrial and ventricular arrhythmias have been reported, as well as pericardial and pleural effusions, adrenal necrosis, and pancreatitis. Methemoglobinemia has also been reported. The onset of symptoms is usually rapid, although delayed onset of pulmonary edema has been described. Survivors of acute poisoning have been reported to develop esophageal complications including strictures and tracheoesophageal fistulas.

Is based on a history of exposure to the agent. Caution: Pulmonary edema may have a delayed onset, and initial respiratory symptoms may be mild or absent.

1. Specific levels. Body fluid phosphine levels are not clinically useful.
2. Other useful laboratory studies include BUN, creatinine, electrolytes, liver aminotransferases, blood gases or oximetry, and chest radiography.

1. Emergency and supportive measures
   1. Maintain an open airway and assist ventilation if necessary. Administer supplemental oxygen and treat noncardiogenic pulmonary edema if it occurs.
   2. Treat seizures and hypotension if they occur.
   3. Patients with a history of significant phosphine inhalation or phosphide ingestion should be admitted and observed for 48-72 hours for delayed onset of pulmonary edema.
   4. IV magnesium has been used to treat cardiac arrhythmias otherwise unresponsive to treatment.
   5. In severe poisoning, adrenal function may be compromised, and IV hydrocortisone should be considered, especially if hypotension does not respond to fluids and vasopressors.
   6. In several small human studies, acetylcysteine demonstrated a mortality benefit.
   7. In a small prospective unblinded study, high-dose insulin demonstrated a survival benefit and improvement in cardiovascular parameters.
2. Specific drugs and antidotes. There is no specific antidote.
3. Decontamination
   1. Caregivers are at a low risk for secondary contamination, but off-gassing of phosphine may occur if the patient vomits or if gastric lavage fluid is not isolated.
   2. Administer activated charcoal orally if conditions are appropriate (see Table I-37,), although studies have not determined its binding affinity for phosphides. Consider gastric lavage for large recent ingestion. Use of 3-5% sodium bicarbonate in the lavage fluid has been proposed (to reduce stomach acid and resulting production of phosphine) but is not of proven benefit. Lavage using potassium permanganate also has no proven benefit and has the potential to produce severe complications including hemolysis, methemoglobinemia, and exothermic reactions.
4. Enhanced elimination. Dialysis and hemoperfusion have not been shown to be useful in hastening elimination of phosphine.