• 1.

    US Environmental Protection Agency. RED facts: aluminum and magnesium phosphide. Washington, DC: US Environmental Protection Agency, 1998;116.

    • Search Google Scholar
    • Export Citation
  • 2.

    Batra K, Taneja OP, Khemani LD. Acute oral toxicity of aluminum phosphide in male albino rats (Wistar). Bull Environ Contam Toxicol 1994;52:662666.

    • Search Google Scholar
    • Export Citation
  • 3.

    US Environmental Protection Agency. Chemical emergency preparedness and prevention. Washington, DC: US Environmental Protection Agency, 2006;15.

    • Search Google Scholar
    • Export Citation
  • 4.

    Beasley V. Toxicants associated with stimulation or seizures. In: Veterinary toxicology. Ithaca, NY: International Veterinary Information Service, 1999;14.

    • Search Google Scholar
    • Export Citation
  • 5.

    Grains Research and Development Corp. Keep phosphine safe. Barton, ACT, Australia: Grains Research and Development Corp, 2000;14.

  • 6.

    Singh S, Singh D, Wig N, et al. Aluminum phosphide ingestion—a clinico-pathologic study. J Toxicol Clin Toxicol 1996;34:703706.

  • 7.

    Gupta S, Sushil K, Ahlawat M. Aluminum phosphide poisoning—a review. J Toxicol Clin Toxicol 1995;33:1924.

  • 8.

    Barton MH. Disorders of the liver. In: Reed SM, Bayly WM, Sellon DC, eds. Equine internal medicine. St Louis: Saunders, 2004;953954.

  • 9.

    Abder-Rahman H. Effect of aluminum phosphide on blood glucose level. Vet Hum Toxicol 1999;41:3132.

  • 10.

    Mehrpour O, Alfred S, Shadnia S, et al. Hyperglycemia in acute aluminum phosphide poisoning as a potential prognostic factor. Hum Exp Toxicol 2008;27:591595.

    • Search Google Scholar
    • Export Citation
  • 11.

    Tiwary AK, Puschner B, Charlton BR, et al. Diagnosis of zinc phosphide in chickens using a new analytical approach. Avian Dis 2005;49:288291.

    • Search Google Scholar
    • Export Citation
  • 12.

    Chaudhry MQ. A review of the mechanisms involved in the action of phosphine as an insecticide and phosphine resistance in stored-product insects. Pestic Sci 1997;49:213228.

    • Search Google Scholar
    • Export Citation
  • 13.

    Arora B, Punia RS, Kalra R, et al. Histopathological changes in aluminum phosphide poisoning. J Indian Med Assoc 1995;93:380381.

  • 14.

    Chugh SN, Dushyant N, Ram S, et al. Incidence & outcome of aluminum phosphide poisoning in a hospital study. Indian J Med Res 1991;94:232235.

    • Search Google Scholar
    • Export Citation
  • 15.

    Sinha US, Kapoor AK, Singh AK, et al. Histopathological changes in cases of aluminum phosphide poisoning. Indian J Pathol Microbiol 2005;48:177180.

    • Search Google Scholar
    • Export Citation
  • 16.

    Tripathi SK, Pandey SK. The effect of aluminum phosphide on the human brain: a histologic study. Med Sci Law 2007;47:141146.

  • 17.

    Drolet R, Laverty S, Braselton WE, et al. Zinc phosphide poisoning in a horse. Equine Vet J 1996;28:161162.

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Phosphine intoxication following oral exposure of horses to aluminum phosphide–treated feed

Leslie Easterwood DVM1, M. Keith Chaffin DVM, MS, DACVIM2, Peggy S. Marsh DVM, DACVIM, DACVECC3, Brian Porter DVM, DACVP4, and Catherine Barr PhD, DABT5
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  • 1 Department of Large Animal Clinical Sciences, College of Veterinary Medicine, Texas A&M University, College Station, TX 77845.
  • | 2 Department of Large Animal Clinical Sciences, College of Veterinary Medicine, Texas A&M University, College Station, TX 77845.
  • | 3 Department of Large Animal Clinical Sciences, College of Veterinary Medicine, Texas A&M University, College Station, TX 77845.
  • | 4 Department of Veterinary Pathobiology, College of Veterinary Medicine, Texas A&M University, College Station, TX 77845.
  • | 5 Texas Veterinary Medical Diagnostic Laboratory, Texas A&M University, College Station, TX 77845.

Abstract

Case Description—66 horses were potentially exposed to phosphine (a gas) 14 hours after being fed a pelleted ration treated with aluminum phosphide.

Clinical Findings—28 horses had clinical signs of profuse sweating, tachycardia, tachypnea, pyrexia, ataxia, seizures, and widespread muscle tremors. Clinically relevant laboratory findings included hypoglycemia and high plasma concentrations of lactate and ammonia and activities of γ-glutamyl transpeptidase, aspartate aminotransferase, and alkaline phosphatase. At least 4 horses had signs consistent with hepatic encephalopathy. Necropsy findings included petechial and ecchymotic hemorrhages in multiple organs, widespread vascular congestion, hepatic lipidosis, and neuronal necrosis in the brain. Phosphine was detected in the stomachs of the 3 horses tested.

Treatment and Outcome—On the farm, horses were treated with gastric lavage followed by administration of di-tri-octahedral smectite, atropine, fluids, and sedatives. Six horses were hospitalized, and lactated Ringer's solution and flunixin meglumine were administered IV. Additionally, 10% dextrose, corn syrup, and di-tri-octahedral smectite were administered PO. Twenty-seven horses died within 2 days after exposure. Two survivors (1 without clinical signs of toxicosis) made a complete recovery.

Clinical Relevance—Progression of clinical signs in affected horses in this report was rapid, with few treatment options available, leading to a high case fatality rate. Fumigation with aluminum phosphide is commonly performed to eliminate weevils and other insects from stored grains. When appropriate precautions are used during fumigation, risk to livestock is typically minimal.

Abstract

Case Description—66 horses were potentially exposed to phosphine (a gas) 14 hours after being fed a pelleted ration treated with aluminum phosphide.

Clinical Findings—28 horses had clinical signs of profuse sweating, tachycardia, tachypnea, pyrexia, ataxia, seizures, and widespread muscle tremors. Clinically relevant laboratory findings included hypoglycemia and high plasma concentrations of lactate and ammonia and activities of γ-glutamyl transpeptidase, aspartate aminotransferase, and alkaline phosphatase. At least 4 horses had signs consistent with hepatic encephalopathy. Necropsy findings included petechial and ecchymotic hemorrhages in multiple organs, widespread vascular congestion, hepatic lipidosis, and neuronal necrosis in the brain. Phosphine was detected in the stomachs of the 3 horses tested.

Treatment and Outcome—On the farm, horses were treated with gastric lavage followed by administration of di-tri-octahedral smectite, atropine, fluids, and sedatives. Six horses were hospitalized, and lactated Ringer's solution and flunixin meglumine were administered IV. Additionally, 10% dextrose, corn syrup, and di-tri-octahedral smectite were administered PO. Twenty-seven horses died within 2 days after exposure. Two survivors (1 without clinical signs of toxicosis) made a complete recovery.

Clinical Relevance—Progression of clinical signs in affected horses in this report was rapid, with few treatment options available, leading to a high case fatality rate. Fumigation with aluminum phosphide is commonly performed to eliminate weevils and other insects from stored grains. When appropriate precautions are used during fumigation, risk to livestock is typically minimal.

Contributor Notes

Dr. Marsh's present address is Hagyard Equine Medical Institute, 4250 Iron Works Pike, Lexington, KY 40511.

Address correspondence to Dr. Easterwood (leasterwood@cvm.tamu.edu).