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Behavioral, Clinical, and Pathological Characterization of Acid Metalliferous Water Toxicity in Mallards

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Abstract

From September to November 2000, United States Fish and Wildlife Service biologists investigated incidents involving 221 bird deaths at 3 mine sites located in New Mexico and Arizona. These bird deaths primarily involved passerine and waterfowl species and were assumed to be linked to consumption of acid metalliferous water (AMW). Because all of the carcasses were found in or near pregnant leach solution ponds, tailings ponds, and associated lakes or storm water retention basins, an acute-toxicity study was undertaken using a synthetic AMW (SAMW) formulation based on the contaminant profile of a representative pond believed to be responsible for avian mortalities. An acute oral-toxicity trial was performed with a mixed-sex group of mallards (Anas platyrhynchos). After a 24-h pretreatment food and water fast, gorge drinking was evident in both SAMW treatment and control groups, with water consumption rates greatest during the initial drinking periods. Seven of nine treated mallards were killed in extremis within 12 h after the initiation of dose. Total lethal doses of SAMW ranged from 69.8 to 270.1 mL/kg (mean ± SE 127.9 ± 27.1). Lethal doses of SAMW were consumed in as few as 20 to 40 min after first exposure. Clinical signs of SAMW toxicity included increased serum uric acid, aspartate aminotransferase, creatine kinase, potassium, and P levels. PCV values of SAMW-treated birds were also increased compared with control mallards. Histopathological lesions were observed in the esophagus, proventriculus, ventriculus, and duodenum of SAMW-treated mallards, with the most distinctive being erosion and ulceration of the kaolin of the ventriculus, ventricular hemorrhage and/or congestion, and duodenal hemorrhage. Clinical, pathological, and tissue-residue results from this study are consistent with literature documenting acute metal toxicosis, especially copper (Cu), in avian species and provide useful diagnostic profiles for AMW toxicity or mortality events. Blood and kidney Cu concentrations were 23- and 6-fold greater, respectively, in SAMW mortalities compared with controls, whereas Cu concentrations in liver were not nearly as increased, suggesting that blood and kidney concentrations may be more useful than liver concentrations for diagnosing Cu toxicosis in wild birds. Based on these findings and other reports of AMW toxicity events in wild birds, we conclude that AMW bodies pose a significant hazard to wildlife that come in contact with them.

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Acknowledgments

We thank Melanie Barnes, Gopal Coimbatore, the Colorado State University Veterinary Pathology Laboratory, and the Texas Veterinary Medical Diagnostic Laboratory for performing analytical and diagnostic procedures. George Cobb, Ann Maest, Michael Fry, Mike Hart, Amber Matthews, Toby McBride, and animal care assistants also contributed substantially to this research. We thank Kevin Reynolds, Karen Cathey, Susan Finger, Barnett Rattner, and Nelson Beyer whose reviews improved earlier versions of this manuscript. This work was funded by the Department of Interior Natural Resource Damage Assessment and Restoration Program with additional support from the U.S. Geological Survey Columbia Environmental Research Center and The Institute of Environmental and Human Health at Texas Tech University. Any use of trade, product, or firm names is for descriptive purposes only and does not imply endorsement by the U.S. Government.

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Authors and Affiliations

  1. U.S. Fish and Wildlife Service, Salt Lake City, UT, 84119, USA

    John P. Isanhart

  2. School of Public Health, Wenzhou Medical College, Wenzhou, 325035, People’s Republic of China

    Hongmei Wu

  3. Pfizer, Inc, Groton, CT, 06340, USA

    Karamjeet Pandher

  4. U.S. Fish and Wildlife Service, Spokane Valley, WA, 99206, USA

    Russell K. MacRae

  5. The Institute of Environmental and Human Health, Texas Tech University, Lubbock, TX, 79409, USA

    Stephen B. Cox

  6. U.S. Geological Survey, Columbia, MO, 65201, USA

    Michael J. Hooper

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  1. John P. Isanhart
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Correspondence to John P. Isanhart.

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Isanhart, J.P., Wu, H., Pandher, K. et al. Behavioral, Clinical, and Pathological Characterization of Acid Metalliferous Water Toxicity in Mallards. Arch Environ Contam Toxicol 61, 653–667 (2011). https://doi.org/10.1007/s00244-011-9657-z

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