Zinc toxicosis is usually a result of ingestion of objects that contain or are coated with zinc (commonly US pennies in small animals or contaminated pastures or excess dietary supplementation in large animals). GI clinical signs are common initially, with intravascular hemolysis, organ damage, pancreatitis, and DIC occurring in a second phase; lameness can be present in foals and swine. Diagnosis is on the basis of history of exposure, abnormalities on laboratory testing, or identification of a suspicious object on abdominal radiographs in small animals. Treatment consists of removal of the source of zinc and supportive therapy; chelation therapy is controversial.
Zinc is an essential trace element used by the body in the synthesis of several hundred enzymes. It plays an important role in an effective immune system and contributes to a number of normal bodily functions, including musculoskeletal growth, vision, and normal wound healing. It is ubiquitous in nature and exists in many forms.
The ingestion of some forms of zinc causes the creation of toxic zinc salts in the acidic environment of the stomach. Zinc toxicosis has been documented in humans and in a wide range of large, small, exotic, and wild animals.
Exposure to zinc in dogs, cats, and other small animals typically stems from dietary indiscretion involving metals that either contain zinc or are coated with zinc. Galvanized metals are metals coated with zinc to prevent rusting.
US pennies, specifically pennies minted since 1982, are a key source of exposure because they contain 97.5% zinc (1). This concentration is equivalent to 2,440 mg of elemental zinc per penny. US dollar coins also contain zinc, although at a much lower concentration (6%). Other coins in circulation around the world similarly contain zinc.
Additional sources of zinc include automotive parts, galvanized nails/nuts/bolts, wire/hardware, polyhedral game dice, zippers, toys, aluminum galvanized cookware, galvanized metal cages (eg, coated birdcages), BB pellets, jewelry, and zinc-coated garland and tinsel decorations (see ).
Common household items that can contain zinc include things such as zinc or galvanized nuts and bolts, zinc wire, and US pennies.
Courtesy of Dr. Michelle Carlino.
The primary sources of zinc for large animals or production animals are contaminated pastures and excess supplementation of zinc in the diet.Fumes from galvanizing factories and foundries can contain high concentrations of zinc that can settle into the soil, leading to contamination of nearby pastures. The use of fertilizers containing zinc and some wood preservatives can also contribute to increased zinc in the environment.
Pathogenesis of Zinc Toxicosis
When items containing zinc are ingested, the low pH in the stomach causes the release of free zinc, which then forms soluble, caustic zinc salts, causing zinc toxicosis. Initially, irritation and possibly GI ulceration develop; however, the longer the object stays in the stomach, the more zinc is systemically absorbed via the small intestine.
Overall, approximately 25–50% of ingested zinc is absorbed (1, 2). Zinc then rapidly accumulates in the liver, kidneys, pancreas, and spleen. The liver extracts approximately one-third of the zinc from circulating blood, releasing the remainder into the bloodstream. Zinc is eliminated primarily through feces.
Ingestion of metal objects containing zinc or high dietary concentrations of zinc cause the hallmark clinical signs of zinc toxicosis (eg, intravascular hemolysis). The exact means by which zinc causes intravascular hemolysis has not been completely established. Acute overdoses are thought to cause direct damage to the membranes of RBCs as well as oxidative damage to the cells.
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The mechanism of action by which zinc causes liver, kidney, or pancreatic damage is likewise not known, though zinc can have direct cytotoxic effects, and hemoglobinuria can cause acute kidney injury.
The LD50 of zinc salts in cases of acute toxicosis in small animals has been reported to be approximately 100 mg/kg (1).
While zinc toxicosis in small animals is often associated with indiscriminate eating behavior, diets containing high concentrations of zinc have been reported to cause chronic zinc toxicosis in large animals and production animals. The maximum tolerable amount of zinc in the diet of large animals varies depending on species and age. For example, it is common for weaned pigs to receive zinc oxide at up to 3,000 ppm in the diet for several weeks (3).
Zinc salts interfere with the metabolism of other ions, such as copper, calcium, and iron, and this can lead to dietary deficiencies of these minerals.
Clinical Findings and Lesions of Zinc Toxicosis
The nature and severity of the clinical signs of zinc toxicosis vary, depending on both the zinc source and the species of animal involved in the exposure.
Acute ingestion of zinc oxide ointment or cream, zinc lozenges, or zinc supplements represents a low toxicity risk and rarely causes more than dose-dependent GI upset (nausea, vomiting, diarrhea).
Occasionally, zinc oxide cream or ointment can also cause an allergic reaction (facial swelling, hives, erythema, pruritus).
Clinical signs of zinc toxicosis in dogs and cats develop in two phases. The initial phase is characterized by vomiting, diarrhea, anorexia, and lethargy, which can progress to ulcers and melena. These GI clinical signs can develop within minutes to several hours or even several days, depending on the source of the zinc.
A second phase of zinc toxicosis develops several hours to several days after the GI phase, because it can take days for zinc leaching from metallic objects to cause clinical signs. This phase is characterized by intravascular hemolysis, anemia (with or without an associated heart murmur), tachycardia, icterus, hemoglobinuria, hemoglobinemia, weight loss, continued GI upset, acute kidney and/or liver failure, pancreatitis, and DIC. Death can result.
Ferrets can develop the same GI clinical signs of zinc toxicosis as dogs and cats, plus GI bleeding, kidney injury, and pancreatitis.
Clinical signs in pet birds with acute zinc toxicosis include shallow respirations, partially fluffed feathers, and closed eyes. Affected birds are reluctant to move, and they sit on the floor of the cage. Anorexia, ataxia, vomiting and regurgitation, recumbency, seizures, weight loss, and polyuria/polydipsia can occur. Liver and kidney injury, pancreatitis, and death are possible. Chronic exposure results in a different clinical manifestation, with more intermittent clinical dullness and dysphagia. Death is less common with chronic zinc toxicosis in pet birds.
Foals are extremely susceptible to zinc toxicosis from chronic exposure. Joint enlargement progressing to painful joint erosions, weakened cartilage, lameness, and limb deformities can develop over the course of several weeks.
Swine exposed to excess zinc show decreased weight gain, lameness, decreased litter size, GI irritation/inflammation, pancreatitis, and an unthrifty appearance.
Ruminants with acute zinc toxicosis can develop weight loss, diarrhea, decreased appetite, decreased milk production, polyuria with secondary dehydration, and generalized listlessness. Chronic overdosing of zinc in ruminants (via dietary zinc/zinc supplements) can lead to cellular degeneration of the liver, pancreas, and kidneys. Pregnant and young animals are at greatest risk.
In laying hens, zinc toxicosis can cause decreased egg production, decreased appetite, and weight loss.
Lesions
Gross pathological findings of zinc toxicosis in dogs and cats include nonspecific hepatomegaly, splenomegaly, pancreatic nodules, red-brown kidneys, and inflammation, edema, or ulceration of the GI mucosa.
Histopathological findings of zinc toxicosis can include hemoglobin nephropathy, pancreatic acinar cell necrosis, pancreatic interstitial fibrosis, and hepatic necrosis with pigment accumulation. Macrophages in multiple organs can contain large amounts of hemosiderin.
Gross lesions in horses manifest in all limb joints as severe generalized osteochondrosis.
Possible findings in cows include renal hemorrhages, pancreatic lesions, hepatic degeneration, and pulmonary emphysema.
Diagnosis of Zinc Toxicosis
History of exposure
Laboratory testing (eg, CBC, serum chemistries, urinalysis, clotting tests)
Abdominal radiographs
Serum zinc concentration
Postmortem sampling
Feed/forage testing
Diagnosis of zinc toxicosis is on the basis of history of exposure, laboratory abnormalities, and abdominal radiographs.
A CBC can show intravascular hemolysis with regenerative anemia, spherocytes, and Heinz bodies. Leukocytosis with neutrophilia and a left shift, monocytosis, and lymphopenia can be present. Platelets can be mildly decreased.
Serum biochemical abnormalities from zinc toxicosis include increased AST, ALT, pancreatic enzymes, and bilirubin. The BUN can be disproportionately high compared with creatinine concentration, secondary to blood loss and/or dehydration.
Results of a Coombs test can be positive in cases of zinc toxicosis, although results of a saline agglutination test are usually negative.
Urinalysis can show proteinuria, hemoglobinuria, and bilirubinuria, with tubular casts observed on examination of sediment.
Coagulation tests (prothrombin time, partial thromboplastin time) can be prolonged secondary to liver damage from zinc toxicosis.
High concentrations of zinc accumulate in the liver, kidney, and pancreas. Postmortem testing of these organs is helpful in making a diagnosis of zinc toxicosis.
Abdominal radiographs can show a radiopaque foreign body (eg, a coin); however, the lack of a visible foreign body does not exclude zinc toxicosis as the diagnosis (see ).
Right lateral and ventrodorsal radiographs of a young, small-breed dog with a US penny foreign body in the stomach.
Courtesy of Dr. Raymond Cahill-Morasco.
If no metal is visible on radiographs, or if the patient is not responding to supportive care, blood should be collected for determination of serum zinc concentration.
Unless they are certified for trace mineral testing (eg, royal blue–top tube), the rubber found in stoppers for most blood tubes, such as serum separator tubes, contains zinc and can falsely elevate zinc concentrations. To minimize contamination risk and help ensure that measured zinc concentrations accurately reflect the animal’s physiological status, blood samples for zinc analysis should be allowed to clot in plastic or glass collection tubes, ensuring no contact with rubber stoppers. After complete clot formation, samples should be centrifuged and the serum transferred into a secondary container made of plastic or a trace element–certified tube for shipment to a laboratory for testing.
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A serum zinc concentration > 5 ppm is consistent with zinc toxicosis in dogs and cats (1) (or > 6 ppm in many bird species, with some bird species such as poultry being much more sensitive to levels lower than this (4).
Zinc and lead toxicosis can have similar clinical characteristics, including anemia, GI clinical signs, and a metallic foreign body visible on radiographs. To help distinguish between the two toxicities, it is important to consider other clinical signs and blood work findings.
Lead toxicosis can cause CNS effects in most species (ataxia, tremors, seizures), while CNS effects are not common in most species affected by zinc toxicosis, except pet birds. Lead can also cause dysphagia in cattle and horses and blindness in cattle and dogs, neither of which are expected with zinc. Additionally, characterizing the type of anemia and evaluating a blood smear can help differentiate between the two toxicities, with lead poisoning typically causing non-regenerative hemolytic anemia and zinc causing regenerative hemolytic anemia.
Treatment and Prevention of Zinc Toxicosis
Elevation of gastric pH with acid-reducing agents
Removal of the zinc foreign body from the GI tract
Supportive care
For small animal patients that have ingested metallic zinc, antacids such as H2 blockers (famotidine 0.5-1 mg/kg IV, SQ, IM, PO every 12-24 hours) and/or calcium carbonate (25–50 mg/kg, PO, every 2–4 hours) (5) can be administered by animal owners or in clinic to help decrease absorption of zinc until the zinc foreign body can be surgically or endoscopically removed from the GI tract.
Activated charcoal does not bind to zinc, and administration is not indicated.
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Gastroprotectants (proton pump inhibitors, H2 blockers, sucralfate, or combination thereof) should be administered for 5–7 days in clinically normal patients or for 14–21 days in clinically affected patients
Supportive care (IV fluid therapy, antiemetics) should be administered as needed.
In patients with anemia, blood transfusion may be indicated on the basis of the severity of clinical and hematological findings.
In cases of zinc toxicosis where clinical findings are consistent with pancreatitis, appropriate medical management should be instituted.
Laboratory testing (eg, CBC, serum biochemistry to monitor liver and kidney function) should be performed every 24 hours initially and then as needed until normalized.
For horses and other large animals, copper supplementation can be considered, especially if copper deficiency has been noted.
Chelation therapy for zinc toxicosis is controversial. Although it can enhance elimination of zinc and promote faster recovery, it can also increase zinc absorption from the GI tract. This is especially true if a metallic foreign body is still present in the body.
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Chelation therapy could be considered if the patient is not recovering as expected after removal of the zinc object(s). Calcium EDTA is the recommended chelation agent. Baseline serum zinc concentrations should be measured and rechecked after chelation.
With early diagnosis and treatment, the outcome is usually favorable for animals with zinc toxicosis. Eliminating exposure to zinc, either in the environment or via excessive dietary supplementation, is essential to prevent recurrence.
Key Points
Acute ingestion of zinc oxide products, zinc lozenges, or zinc supplements has a low toxicity risk that typically results in GI upset.
Ingestion of metal objects containing zinc or high doses of zinc in an animal’s diet cause the hallmark clinical signs of zinc toxicosis (eg, intravascular hemolysis).
For More Information
Henke CS, Beal MW, Walton RAL, et al. Retrospective evaluation of the clinical course and outcome of zinc toxicosis due to metallic foreign bodies in dogs (2005-2021): 55 cases. J Vet Emerg Crit Care (San Antonio). 2023;33(6):676-684.
Peterson KL. Zinc. In: Hovda LR, Brutlag AG, Poppenga RH, Epstein SE, eds. Blackwell's Five-Minute Veterinary Consult Clinical Companion Small Animal Toxicology. 3rd ed. Wiley-Blackwell; 2024:662-666.
Also see pet owner content regarding zinc poisoning.
References
Talcott PA. Zinc. In: Peterson ME, Talcott PA, eds. Small Animal Toxicology. 3rd ed. Elsevier; 2013:847-851. doi:10.1016/b978-1-4557-0717-1.00084-3
Osweiler BD. Zinc Toxicosis. In: Osweiler BD. Toxicology. Wiley-Blackwell; 1996:204-205.
Tang X, Xiong K, Zeng Y, Fang R. The mechanism of zinc oxide in alleviating diarrhea in piglets after weaning: a review from the perspective of intestinal barrier function. Int J Mol Sci. 2024;25(18):10040. doi:10.3390/ijms25181004
Poppenga RH, Tawde S. Avian toxicology. In: Veterinary Toxicology. 2nd ed. Elsevier; 2012:874-876. doi:10.1016/b978-0-12-385926-6.00099-5
Peterson KL. Zinc. In: Hovda LR, Brutlag AG, Poppenga RH, Epstein SE, eds. Blackwell's Five-Minute Veterinary Consult Clinical Companion Small Animal Toxicology. 3rd ed. Wiley-Blackwell; 2024:662-666.
