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. 
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. 
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.
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.  Pathologic changes have been documented in the liver and kidney.  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.
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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