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Find information on animal health topics, written for the veterinary professional.

Zinc Phosphide

By Safdar A. Khan, DVM, MS, PhD, DABVT, Director of Toxicology Research, ASPCA Animal Poison Control Center, Urbana, Illinois ; Mary M. Schell, DVM, DABVT, DABT, Senior Toxicologist, ASPCA Animal Poison Control Center, Urbana, Illinois

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Zinc phosphide is a component in a number of mole, gopher, ground squirrel, and vole baits intended for outdoor use only. It is a dark gray powder, not soluble in water, and is commonly sold in 2%–5% bait pellets, paste, or tracking powder. In the past several years, an oat-based bait labeled for killing prairie voles has been marketed. There is evidently no way to identify this grain mixture, and bait ingestion has resulted in lethal exposure to a number of horses. The clinical effects of aluminum phosphide, used as a grain fumigator, are similar to those of zinc phosphide.

Lethal doses of zinc phosphide vary markedly between species and are much more toxic to species unable to vomit. The phosphide salts are unstable in an acid environment. At gastric pH, they degrade rapidly to form phosphine gas. Presence of food in the stomach, which will trigger release of gastric acid, increases the rate of this transition. Phosphine gas, when inhaled, results in acute noncardiogenic pulmonary edema. Vomiting, often hemorrhagic, is a common presenting sign in animals capable of vomiting. Tachypnea, ataxia, weakness, trembling, collapse, seizures, and death may ensue.

If there is no food in the stomach, undegraded zinc phosphide can be absorbed systemically. An animal surviving for 48 hr can then have liver and/or renal failure within 5–14 days due to absorption of intact zinc phosphide. Zinc phosphide is thought to block cytochrome C oxidase, leading to formation of highly reactive oxygen compounds, which cause most of the tissue injury; the most severe damage is in tissues with the highest oxygen demand, ie, brain, lungs, liver, and kidney.

Phosphine gas is a public health hazard. Animal owners and veterinary staff members must be cautious while inducing emesis, because they can be exposed to phosphine gas from the presence of zinc phosphide bait in the stomach contents after vomiting. The gas is reported to have a garlic-like or fishy odor.

Management of zinc phosphide ingestion relies on effective decontamination. If the animal has not already vomited, emesis can be induced by use of apomorphine. Decreasing gastric acid may be beneficial, via oral magnesium hydroxide antacid or using famotidine at 1 mg/kg, SC. IV fluid support is recommended while the animal is under observation. Use of activated charcoal may be considered; although metals are poorly bound by activated charcoal, the larger zinc phosphide molecule may be. If vomiting is ongoing, administration of activated charcoal should be avoided because of the aspiration risk. Obtaining a baseline biochemical profile, with repeat evaluation of liver and renal values at 24, 48, and possibly 72 hr, is recommended. Use of N-acetylcysteine may be beneficial, with a loading dose of 140 mg/kg, followed by 70 mg/kg every 6 hr for six total doses. Administration of S-adenosyl methionine (SAM-e) may also be beneficial. Seizures should be controlled with diazepam or barbiturates, and other signs treated symptomatically.