Case Definition: Phosphine

Clinical description

Exposure to phosphine gas most commonly occurs by either: 1) inhalation of gas generated by external sources such as in the workplace or 2) when phosphide-containing pesticides are ingested and come into contact with water or moisture, thus generating phosphine gas. Severe poisoning in either scenario can result in multi-organ dysfunction (e.g., convulsions, cardiac dysrhythmias, shock, and death). If one of the following lower respiratory signs and symptoms is reported, the clinical description for phosphine poisoning by inhalation has been met (1-5): chest tightness or cough; dyspnea; or pulmonary edema, which might have a delayed onset (See Phosphide Case Classification for further information). If a phosphide-containing product was ingested the person also likely will experience gastrointestinal symptoms such as vomiting, abdominal pain, and nausea. Dermal exposure to liquid phosphine can lead to skin burns.

Laboratory criteria for diagnosis

  • Biologic: No biologic marker for phosphine gas exposure is readily available. Finding measurable amounts of urinary phosphorus and phosphorus-containing compounds is not a reliable indicator of exposure.
  • Environmental: Confirmation of phosphine in environmental air samples is performed via methods detailed by NIOSH and OSHA (6,7).

Case classification

  • Suspected: A case in which a potentially exposed person is being evaluated by health-care workers or public health officials for poisoning by a particular chemical agent, but no specific credible threat exists.
  • Probable: A clinically compatible case in which a high index of suspicion—credible threat or patient history regarding location and time—exists for phosphine exposure, or an epidemiologic link exists between this case and a laboratory-confirmed case.
  • Confirmed: A clinically compatible case in which laboratory tests (not available for phosphine) have confirmed exposure.

The case can be confirmed if laboratory testing was not performed because either a predominant amount of clinical and nonspecific laboratory evidence of a particular chemical was present or the etiology of the agent is known with 100% certainty.

Additional resources

  1. Baselt RC, Cravey RH, eds. Phosphine. In: Disposition of toxic drugs and chemicals in man. 9th ed. Foster City, CA: Chemical Toxicology Institute; 1995:628.
  2. Harbison RD. Phosphorus. In: Harbison RD, ed. Hamilton and Hardy’s industrial toxicology. 5th ed. St Louis, MO: Mosby-Year Book; 1998:194-7.
  3. Hathaway GJ, Proctor NH, Hughes JP, eds. Phosphine. In: Proctor and Hughes’ chemical hazards of the workplace. 4th ed. New York, NY: John Wiley; 1996:516-7.
  4. Carter DE, Sullivan JB Jr. Intermetallic semiconductors: arsine, phosphine, and inorganic hydrides. In: Sullivan JB Jr, Krieger GR, eds. Clinical environmental health and toxic exposures. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2001:958-63.
  5. Erdman A. Chapter 81 – Phosphorous. In: Brent J, Wallace KL, Burkhard KK. Critical Care Toxicology: Diagnosis and Management of the Critically Poisoned Patient. Elsevier-Mosby: 2005:851-61.
  6. NIOSH. NIOSH manual of analytical methods [online]. 2003. [cited 2013 Apr 5]. Available from URL:
  7. OSHA. Sampling and analytical methods [online]. 2010. [cited 2013 Apr 5]. Available from URL: icon.
  8. FDA. Food: Laboratory methods [online]. 2013. [cited 2013 Apr 5]. Available from URL: icon.
  9. EPA. Selected analytical methods: chemical methods query [online]. 2013. [cited 2013 Apr 5]. Available from URL: icon.
Page last reviewed: April 4, 2018