Felis ISSN 2398-2950

Zinc toxicity

Synonym(s): Zn toxicosis

Contributor(s): Alexander Campbell, Rosalind Dalefield

Introduction

  • Acute zinc poisoning is less common in cats than in dogs, because they are more discriminating about what they ingest.
  • Potential sources include zinc-containing metal items such as galvanized nuts, nails, or staples, also jewelry and zippers. Zinc is present in many alloys (eg brass, bronze) and also in electrical fuses, storage batteries, and automotive parts.
  • Cats may be poisoned if they are restrained in containers or cages made of zinc-containing metals, or painted with zinc-rich paints.
  • Zinc oxide ointment may be toxic if regularly applied to and licked off the skin or paws. Severe toxicity is unlikely from single acute exposures to such ointments.
  • USA pennies minted after 1982 are 97.5% zinc.
  • Canadian pennies minted between 1997 and 2001 are 96% zinc.
  • UK £2 coins contain 20% zinc in the outer metallic ring; UK £1 coins contain 24.5% xinc & pre-1992 2p and 1p coints contained 2.5% zinc.
  • Euro coins currently contain no zinc.
  • Products containing zinc acetate, zinc sulphate Zinc or zinc undecylenate may cause zinc toxicosis.
  • Zinc is also found in calamine lotion, and in a variety of paints, suppositories, fertilizers, fungicides, antiseptics and shampoos.
  • Cats may be poisoned by licking zinc-containing substances off their coats in their efforts to clean themselves.

Pathogenesis

Pathophysiology

  • Almost all cases of zinc toxicosis in small animals are due to ingestion.
  • The toxic dose of zinc toxicosis is variable, influenced by the solubility of the zinc salt, pH of the stomach, and presence of food in the stomach. 
  • Zinc-containing pennies are retained in the stomach and dissolve slowly, releasing zinc over time.
  • Approximately 25% of ingested zinc is absorbed, primarily in the duodenum, by a carrier-mediated mechanism. Less than 50% of dietary zinc is absorbed in the small intestine.
  • Absorbed zinc is initially bound to plasma albumin and ²2-macroglobulin.
  • Zinc is deposited in the liver, kidney, prostate, muscle and pancreas, where it induces metallothionein synthesis in cells.
  • Excretion of zinc is limited, and takes place via pancreatic secretions, bile, and mucosal cells into the feces. Less than 10% is excreted in the urine.
  • The mechanism by which zinc causes toxicosis is not well characterized.
  • Initial signs are typically those of gastrointestinal distress and include vomiting, anorexia, depression and diarrhea.
  • The animal develops hemolytic anemia, which may begin within hours or may be delayed for a few days after ingestion. There is typically a regenerative response.
  • Hemoglobinuria, proteinuria Proteinuria, urinary casts and uremia Uremia indicate renal damage.
  • Late-stage signs of zinc toxicosis include oliguria/anuria, recumbency, and seizures.

Timecourse

  • Signs of zinc toxicosis may occur within 2 hours if ingestion, but latency is variable, influenced by the dose of zinc ingested and the solubility of the zinc salt or source.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

Other sources of information

  • Talcott P A (2006) Zinc. In:Small Animal Toxicology, Second Edition. Eds: M E Peterson and P A Talcott. Elsevier Inc, St Louis, MO. ISBN: 0-7216-0639-3.
  • Osweiler G D (1995) Toxicology. Philadelphia: Williams and Wilkins. ISBN: 0 6830 6664 1.

Organisation(s)


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