Patients who develop hemolytic anemia may require the administration of blood products.
Patients must be closely observed for the development of hypoxia due to pulmonary edema or methemoglobinemia. 15 Treatment for phosphine toxicity includes removing the victim from the source of exposure and supportive care. OSHA exposure limits for phosphine gas are 3 ppm for an 8-hour TWA exposure to 500 ppm for 30 minutes is expected to be fatal, whereas only “a few breaths” of phosphine at a concentration of 1000 ppm can be lethal. 14 Inhalation of low levels of phosphine gas may produce symptoms of headache, dizziness, tremors, cough, chest pain, shortness of breath, nausea, vomiting, and abdominal pain. 13Ĭlinical findings in acute phosphine poisoning may include depressed mental status, pulmonary edema, hypotension, cardiac dysrhythmias, liver and kidney failure, and severe gastritis. Postmortem toxicologic analysis of this individual showed phosphine levels in all tissue samples taken. Another report describes the discovery of a 23-year-old man who was found dead after he had broken the plastic seal in a rice-filled boxcar in order to gain entry. At time of discovery, the child was dead, and the adults were complaining of nausea, vomiting, abdominal pain, headache, and dizziness.
One report described three adults who became ill and a 12-year-old boy who died after spending 18 hours in a railroad boxcar containing lima beans that had been fumigated with aluminum phosphide. Numerous deaths have been reported when stowaways attempt to use grain cars on trains and ships as transportation, not realizing that these containers have been treated with one of the phosphide chemicals to prevent pest and fungi destruction of the grain during transport. 11 Another case report of a 25-year-old man who ingested 6 g of aluminum phosphide pellets describes the development of methemoglobinemia (32%) occurring 32 hours after ingestion. This resulted in the production of denatured hemoglobin aggregates (Heinz bodies) in the erythrocyte in the course of a hemolytic anemia. One in vitro study showed that phosphine induces the formation of excess superoxide radicals in red blood cells. 10 Numerous cases have been reported of human exposures both as accidental exposures in a commercial fumigation setting and as reports of these agents being used in suicidal gestures. Small vessels appear to be affected to a greater degree than the major vessels, which may explain the extensive third spacing and profound cardiovascular collapse that may occur with phosphine poisoning. Animal studies demonstrated inhibition of the mitochondrial cytochrome oxidase system as well as interference with amino acid incorporation into proteins. Multiple mechanisms of action have been proposed for phosphine gas. This gas is highly explosive, and additives are placed within the pellets to slow the rate of gas formation to reduce the risk for explosion. For this reason, manufacturers of aluminum phosphide include ammonia-producing agents in the pellets as the more noxious ammonia odor may allow for better detection of possible phosphine gas release. However, this odor threshold does not give adequate warnings regarding possible dangerous gas concentrations. The odor is detectable at a concentration of 2 ppm. The OSHA threshold limit value (TLV) for phosphine gas is 0.3 ppm. Phosphine gas is described as having a garlic or rotten fish odor. Its formulation as pellets lends itself for use in treating transport containers. Aluminum phosphide is used primarily to treat grain and tobacco stores. Phosphine gas is produced when pellets of aluminum, calcium, magnesium, or zinc phosphide are exposed to water vapor. GREENBERG MD, MPH, in Haddad and Winchester's Clinical Management of Poisoning and Drug Overdose (Fourth Edition), 2007 PHOSPHINE (CAS ) (PH 3)
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