Phosphorus poisoning (PP) occurs after accidental exposure to white (also synonymously termed yellow) phosphorus. This compound can have mild effects like affecting the skin upon direct contact or the eyes in case of white phosphorus gas. Further possibilities include inhalation of white phosphorus and its accidental ingestion. In this condition, the chemcial can accumulate in liver and kidney leading to liver failure and to a fatal prognosis, if more than 1 mg/kg have been absorbed.
Phosphorus poisoning (PP) presents with different symptoms depending on the kind of exposure. Direct skin contact with white phosphorus, i.e. by manipulating ammunition or firecrackers, results in painful chemical burns, quick development of necrotic skin areas, which are typically yellow and feature a garlic-like scent. Phosphorus is highly mobile in biological tissues and will be readily absorbed. Its accumulation and toxicity mainly show in liver and kidney, sometimes in the heart. PP has been speculated to be conducive to delayed wound healing. Dry skin conditions can lead to spontaneous phosphorus reignition. Localization is possible with an ultraviolet light source   .
Patients, who have been exposed to white phosphorus fumes, can show a distinct set of symptoms associated to PP, which are a burning sensation, coughs, shortness of breath, a sore throat and unconsciousness. Pulmonary edema may be observed a few hours after exposure .
Oral ingestion of white phosphorus is conducive to the fatal form of PP. Frequent symptoms after ingestion are nausea, vomiting, abdominal cramps, diarrhea, and hypotension. Patients typically deteriorate rapidly and enter a coma. The accepted lethal dose of white phosphorus is 1 mg/kg. Low-level intake can lead to accumulation in the feces ("smoking stool syndrome")  .
Accumulation of phosphorus after any kind of the above-mentioned ways of exposure mainly concerns the liver, the heart, and the kidneys. After oral ingestion, 70% of absorbed mineral will show in the liver shortly after intake, 12% will affect the heart, 4% will be recovered in the kidneys. Only traces can be found in the pancreas and brain .
PP diagnosis relies on a clinical examination and the determination of serum calcium, magnesium, phosphorus as well as urine phosphate concentrations. There is no specific method to determine PP, so diagnosis is mainly built based on observed symptoms and direct observation of phosphorus using UV light in the case of skin contact .
A major task in PP occurring by contact is skin decontamination by placing water-soaked pads or a moist gauze on the area of exposure . It is imperative to keep the skin moist to avoid spontaneous phosphorus reignition. Ingestion-caused PP may be countered with a swift gastric lavage procedure to avoid the accumulation of this chemical in the liver. Phosphorus will cause macrovesicular and microvesicular vacuolization in hepatocytes. The contaminated liver tissue is not necrotic but hepatic functions will diminish .
Experimental treatment with copper sulfate and silver nitrate is speculated to provide limited recovery perspectives after a PP diagnosis . PP fatality is highly likely for patients who present with hepatorenal failure and a cardiovascular collapse. PP has a mortality rate of 20-50%  .