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White Phosphorus Exposure

  • Author: Lisandro Irizarry, MD, MPH, FACEP; Chief Editor: Zygmunt F Dembek, PhD, MPH, MS, LHD  more...
 
Updated: Aug 11, 2015
 

Background

White (or yellow) phosphorus is the most common and most reactive of the three allotropic forms of phosphorus. Because of its reactivity, white phosphorus has been used as an incendiary agent by the military or as an igniter for munitions. An incendiary agent is one that is primarily designed to set fires. It commonly is found in hand grenades, mortar and artillery rounds, and smoke bombs.[1]

Munitions-quality white phosphorus is generally found as a waxy, yellow, transparent solid. When exposed to air, it spontaneously ignites and is oxidized rapidly to phosphorus pentoxide. Such heat is produced by this reaction that the element bursts into a yellow flame and produces a dense white smoke. Phosphorus also becomes luminous in the dark, and this property is conveyed to "tracer bullets." This chemical reaction continues until either all the material is consumed or the element is deprived of oxygen.[2]

Most injuries associated with white phosphorus are the result of accidents due to either human or mechanical error.[3, 4, 5] Care in handling and use of munitions should serve as the primary prevention of injuries and burns associated with white phosphorus.

For patient education information, see Chemical Warfare and Personal Protective Equipment.

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Pathophysiology

White phosphorus can cause significant injury and death, and its use by the military has been highly criticized. Morbidity and mortality can occur by exposure to soft tissue, through inhalation, and by ingestion.

White phosphorus skin exposure results in painful chemical burn injuries. The resultant burn typically appears as a necrotic area with a yellowish color and characteristic garliclike odor. These burns carry a high risk of morbidity and mortality. White phosphorus is highly lipid soluble and, as such, is believed to have rapid dermal penetration once particles are embedded under the skin. This deep absorption can result in heart, liver, and kidney damage. It has also been postulated that, because of its enhanced lipid solubility, these injuries result in delayed wound healing.

Few studies have investigated the degree of tissue destruction associated with white phosphorus injuries. In the experimental animal model, most tissue destruction appears to be secondary to the heat generated by oxidation.

Systemic toxicity has been described extensively in the animal model.[6] Pathologic changes have been documented in the liver and kidney.[6] These changes result in the development of progressive anuria, decreased creatinine clearance, and increased blood phosphorus levels. Depression of the serum calcium level with an elevation in the serum phosphorus level (reversed calcium-phosphorus ratio) with electrocardiographic changes including prolongation of the QT segment, ST-segment depression, T-wave changes, and bradycardia also have been observed.

Oral ingestion of white phosphorus in humans has been demonstrated to result in pathologic changes to the liver and kidneys. The ingestion of a small quantity of white phosphorus can cause gastrointestinal complaints such as nausea, abdominal cramps, and vomiting. Individuals with a history of oral ingestion have been noted to pass phosphorus-laden stool ("smoking stool syndrome"). The accepted lethal dose is 1 mg/kg, although the ingestion of as little as 15 mg has resulted in death.

Inhalation of white phosphorus smoke is presumed to be the least severe form of exposure, as it has not been shown to cause casualties. It may result in irritation to the eyes and nose and may cause a violent cough. However, prolonged exposure to the gas does have the potential to cause death.

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Epidemiology

Mortality/Morbidity

Morbidity and mortality are related directly to trauma and burns sustained from exposure or to intentional or accidental ingestion.

Burns usually are limited to areas of exposed skin (eg, upper extremities, face). Burns frequently are second and third degree because of the rapid ignition and highly lipophilic properties of white phosphorus.

Trauma usually is a combination of blunt and penetrating. Blunt trauma results from the percussion and force of the blast, and penetrating trauma results from projectiles produced from the explosion.

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Contributor Information and Disclosures
Author

Lisandro Irizarry, MD, MPH, FACEP Chair, Department of Emergency Medicine, Wyckoff Heights Medical Center

Lisandro Irizarry, MD, MPH, FACEP is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

José Eric Díaz-Alcalá, MD, FAAEM, FACMT Medical and Executive Co-Director, Medical Toxicology Consultant, Administración de Servicios Médicos de Puerto Rico, ASEM Poison Control Center; Chief, Emergency Medicine Unit, Medical Toxicology Consultant, VA Caribbean Healthcare System

José Eric Díaz-Alcalá, MD, FAAEM, FACMT is a member of the following medical societies: American Academy of Emergency Medicine, American College of Medical Toxicology

Disclosure: Nothing to disclose.

Geri M Williams, MD Staff Physician, Department of Emergency Medicine, Brooklyn Hospital Center

Geri M Williams, MD is a member of the following medical societies: American College of Physicians, American Medical Association, Medical Society of the State of New York, National Medical Association, Emergency Medicine Residents' Association

Disclosure: Nothing to disclose.

Mollie V Williams, MD Assistant Clinical Professor, Fellow in Disaster Preparedness, Department of Emergency Medicine, State University of New York Downstate Medical Center, Brooklyn

Mollie V Williams, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Zygmunt F Dembek, PhD, MPH, MS, LHD Associate Professor, Department of Military and Emergency Medicine, Adjunct Assistant Professor, Department of Preventive Medicine and Biometrics, Uniformed Services University of the Health Sciences, F Edward Hebert School of Medicine

Zygmunt F Dembek, PhD, MPH, MS, LHD is a member of the following medical societies: American Chemical Society, New York Academy of Sciences

Disclosure: Nothing to disclose.

Additional Contributors

Mark Keim, MD Founder, DisasterDoc, LLC; Adjunct Professor, Emory University Rollins School of Public Health; Adjunct Professor, Harvard Affiliated Disaster Medicine Fellowship

Mark Keim, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

References
  1. National Research Council (US) Subcommittee on Military Smokes and Obscurants. White Phosphorous Smoke. Subcommittee on Military Smokes and Obscurants, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission on Life Sciences, National Research Council. Toxicity of Military Smokes and Obscurants. 1. Washington, D.C.: National Academies Press (US); 1999. 2: 18-44. [Full Text].

  2. Voie ØA, Johnsen A, Strømseng A, Longva KS. Environmental risk assessment of white phosphorus from the use of munitions - a probabilistic approach. Sci Total Environ. 2010 Mar 15. 408(8):1833-41. [Medline].

  3. Skaik S, Abu-Shaban N, Abu-Shaban N, Barbieri M, Barbieri M, Giani U, et al. Metals detected by ICP/MS in wound tissue of war injuries without fragments in Gaza. BMC Int Health Hum Rights. 2010 Jun 25. 10:17. [Medline]. [Full Text].

  4. Berndtson AE, Fagin A, Sen S, Greenhalgh DG, Palmieri TL. White phosphorus burns and arsenic inhalation: a toxic combination. J Burn Care Res. 2014 Mar-Apr. 35(2):e128-31. [Medline].

  5. Frank M, Schmucker U, Nowotny T, Ekkernkamp A, Hinz P. Not all that glistens is gold: civilian white phosphorus burn injuries. Am J Emerg Med. 2008 Oct. 26(8):974.e3-5. [Medline].

  6. Agency for Toxic Substances and Disease Registry (ATSDR). U.S. Department of Health and Human Services, Public Health Service. Toxicological Profile for White Phosphorus. 1997. [Full Text].

  7. Geehr EC, Salluzzo RF. Dermal injuries and burns from hazardous materials. Sullivan JB Jr,Krieger GR. Hazardous Materials Toxicology, Clinical Principles of Environmental Health. Williams and Wilkins; 1992. 415-424.

  8. Harbison RD. Phosphorus. Harbison RD. Hamilton and Hardy’s Industrial Toxicology. 5th ed. Mosby Yearbook; 1998. 194-7.

  9. Konjoyan TR. White phosphorus burns: case report and literature review. Mil Med. 1983 Nov. 148(11):881-4. [Medline].

  10. Merrifield RB. The automatic synthesis of proteins. Sci Am. 1968 Mar. 218(3):56-62 passim. [Medline].

  11. Mozingo DW, Smith AA, McManus WF, Pruitt BA Jr, Mason AD Jr. Chemical burns. J Trauma. 1988 May. 28(5):642-7. [Medline].

  12. Obermer E. Phosphorus burns. Lancet. 1943. 1:202.

  13. Pande TK, Pandey S. White phosphorus poisoning--explosive encounter. J Assoc Physicians India. 2004 Mar. 52:249-50. [Medline].

  14. Rabinowitch IM. Treatment of phosphorus burns. Can Med Assoc J. 1943. 48:291-296.

  15. Summerlin WT, Walder AI, Moncrief JA. White phosphorus burns and massive hemolysis. J Trauma. 1967 May. 7(3):476-84. [Medline].

 
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