Zinc phosphide poisoning

Zinc phosphide is an inorganic compound with a dark grey, crystalline appearance. It has a characteristic smell of garlic or rotting fish. Zinc phosphide was synthesised for the first time in 1740 and initially used as a rodenticide in Italy in 1911-1912. This compound is currently used for the control of various animals, such as mice, rats, squirrels, wild rabbits and moles. In recent years it has been the cause of accidental death of children and domestic animals (dogs, cats).

KINETICS OF TOXICITY

Zinc phosphide can be absorbed following ingestion or inhalation or through skin lesions. Once ingested it reacts with water and hydrochloric acid in the stomach, releasing phosphine (a gas with a typical acetylene odour). This reaction is favoured by the acid pH in the stomach.

Zinc phosphide can be metabolised by oxidation of the phosphorus into various phosphorus oxyacids or by reduction of the phosphorus to phosphine gas. The compound is excreted in the urine; phosphine is also eliminated through the lungs.

MECHANISM OF ACTION

The toxicity of zinc phosphide is due both to the direct action of zinc and the effect of phosphine. This latter enters the circulation, damaging the lungs, liver, kidneys, heart and central nervous system.

TOXICITY

Zinc phosphide is an extremely toxic compound.

The oral LD₅₀ in various species is:

• Rat: 41 mg/kg
• Sheep: 60-70 mg/kg
• Duck: 37.5 mg/kg
• Pheasant: 9 mg/kg

The dermal LD₅₀ (through contact) is:

• Rabbit: 2000-5000 mg/kg

Animals that ingest zinc phosphide on a full stomach are at higher risk of intoxication than those who ingest this compound on an empty stomach, because in the former case the increase in gastric secretions involved in digestion makes the local environment much more acidic, enabling the rapid formation of phosphine.

Signs appear within 20-25 minutes. Death occurs within 1 hour following the intake of high doses, and between 4 and 72 hours after the intake of lower doses.

CLINICAL SIGNS

• Loss of appetite, lethargy
• Vomiting, sometimes haematemesis; abdominal pain, colic
• Convulsions, hyperthermia (dogs)
• Laboured breathing, dyspnoea, asphyxia
• Prostration, coma
• Death within 24-48 hours

LESIONS

• Venous congestion and pulmonary oedema;
• Cardiac and renal tissue degeneration;
• Dark, garlic-smelling gastric contents and mucosa.

DIAGNOSIS

Laboratory tests

Fresh samples are essential since zinc phosphide breaks down rapidly. Vomit, gastric contents and suspected bait can be analysed.

Levels of zinc phosphide  ≥ 50 ppm in the gastric contents indicate zinc phosphide intoxication.

TREATMENT

There are no antidotes. The treatment is symptomatic; 

• Emetics to induce vomiting, within 2 hours of ingestion of the poison;
• Activated charcoal;
• Gastric H₂ receptor antagonists (cimetidine, ranitidine; i.v. or i.m.) able to inhibit the secretion of acid in the stomach and, thereby, the production of phosphine;
• Calcium gluconate and sodium lactate, i.v., to counteract the acidosis;
• Ventilatory assistance, if necessary.

Suggested readings

1. BhadkambekarCA, Swain KK, Mukheriee T, et al. Zinc as a marker in viscera of suspected metal phosphide poisoning: a study by neutron activation analysis. J Anal Toxicol 2008; 32:760-2.
2. Guale FG, Stair EL, Johnson BW, et al. Laboratory diagnosis of zinc phosphide poisoning. Vet Hum Toxicol 1994;36:517-9.

Useful links

1. National Pesticide Information Center, Oregon, ZP factsheet
2. DVM360, A case of zinc phosphide toxicosis
3. Toxicology data network