Whole blood arsenic concentrations in cats: A diagnostic interpretation challenge

Felipe Reggeti, Jenny Tye

Animal Health Laboratory, University of Guelph, Guelph, ON (Reggeti); Derrydale Animal Hospital, Brampton, ON (Tye).

AHL Newsletter 2026;30(2):26.

A 6-year-old spayed female domestic short-haired (DSH) cat presented with a 3-week history of intermittent vomiting. The patient had been fed exclusively a commercial fish-only canned diet and was undergoing treatment for environmental allergies. Laboratory findings included increased SDMA, urea, and creatinine, and a urine specific gravity (USG) of 1.014, supporting renal disease; however, there was no evidence of proteinuria, and ultrasonographic examination of the kidneys and urinary tract was unremarkable.

Because of the fish-based diet, the owner expressed concern regarding heavy metal exposure, particularly mercury. EDTA blood samples were submitted to the toxicology section of the Animal Health Laboratory (AHL) for heavy metal analysis by ICP-MS. Blood mercury concentrations were 0.13 ppm and within the reference interval (RI: 0.10–0.30 ppm). However, the blood arsenic concentration was 0.72 ppm (720 ppb), exceeding proposed reference intervals of <0.05 ppm (50 ppb). This finding raised concerns regarding excessive arsenic exposure.

Arsenic occurs naturally in soil, and additional sources include coal, mining waste, seafood, well water, and some older pesticides and wood preservatives. Considering the clinical history, the fish-only diet was suspected as a possible source of arsenic exposure in this patient. To further assess exposure risk, feed samples were analyzed and compared with recommended maximum residue limits (MRLs) for arsenic in pet foods:

  • U.S. Food and Drug Administration (US-FDA): 12.5 ppm (12,500 ppb)
  • National Research Council (NRC): 30 ppm (30,000 ppb)

The arsenic concentration in the food was 0.92 ppm (920 ppb), which was within official recommendations. Since the cat had been fed this diet exclusively, the clinical significance of the presumably elevated blood arsenic concentration remained uncertain. To further evaluate arsenic concentrations in feline and canine blood, historical data from the AHL between 2016 and 2025 were reviewed (Table 1).

Table 1. Historical arsenic concentrations in whole blood of dogs and cats measured by ICP-MS at the AHL between 2016 and 2025.

Table 1. Historical arsenic concentrations in whole blood of dogs and cats measured by ICP-MS at the AHL between 2016 and 2025.

These data show that circulating arsenic concentrations in feline whole blood are significantly higher than those observed in dogs. A previous study evaluating blood arsenic concentrations in domestic cats and other species reported similar findings. Based on this retrospective analysis, the authors suggested considering excessive arsenic exposure in cats when blood concentrations exceed 0.17 ppm (170 ppb). Similarly, most dogs in our retrospective dataset had very low or undetectable blood arsenic concentrations.

In the present case, the blood arsenic concentration of 0.72 ppm (720 ppb) fell within the historical range observed at the AHL (16–1000 ppb), although it exceeded previously proposed thresholds for excessive exposure in cats. Acute arsenic toxicosis typically produces gastrointestinal signs including vomiting, melena, diarrhea, and hypovolemia, whereas subacute cases may show tubular damage, azotemia, and potential renal failure. These findings appear consistent with the clinical presentation in this case. Furthermore, following a change to a different batch of the same food, the clinical signs and renal parameters progressively improved. However, a causal association with the suspect food could not be established because the arsenic concentration in the diet was low relative to established MRLs for arsenic in pet foods.

Research has shown that arsenic accumulates within rat erythrocytes to a greater extent than in other species. Rats rapidly methylate inorganic arsenic into a reactive dimethylated metabolite with a high affinity for hemoglobin, specifically the cysteine residue Cys13 on the α-chain. Binding at this site stabilizes the metabolite and promotes retention of arsenic within erythrocytes. Cats appear to exhibit a similar tendency for arsenic accumulation because feline hemoglobin also contains the cysteine α-13 residue, providing a comparable binding site for dimethylated arsenic metabolites. Therefore, the relatively high arsenic concentrations observed in feline blood may reflect species-specific physiological characteristics of hemoglobin and may not necessarily indicate excessive arsenic exposure. This phenomenon should be considered when interpreting laboratory results to avoid potential misinterpretation.

Blood arsenic concentrations in cats should therefore be interpreted in conjunction with clinical signs, other laboratory findings, and assessment of dietary intake.

References

1. Puls, R. Mineral Levels in Animal Health: Diagnostic Data (2nd ed.). Sherpa International, Clearbrook, B.C. ISBN 0969342926, 1994.

2. U.S. Food and Drug Administration, Center for Veterinary Medicine. Target animal safety review memorandum, 2011. https://www.fda.gov/media/81895/download

3. National Research Council (US) Committee on Animal Nutrition. Mineral Tolerance of Animals. Washington (DC): National Academies Press; 2005.

4. Buchweitz JP, Drankhan HR, Lehner AF. Blood arsenic concentrations in felids. Vet Rec 2019;185(7):207.

5. Lu M, Wang H, Li XF, Arnold LL, Cohen SM, Le XC. Binding of dimethylarsinous acid to cys-13alpha of rat hemoglobin is responsible for the retention of arsenic in rat blood. Chem Res Toxicol 2007;20(1):27-37.