Development of Dietary-Based Toxicity Reference Values to Assess the Risk of Chlorophacinone to Non-Target Raptorial Birds

Regulatory changes in the use of some second-generation anticoagulant rodenticides in parts of North America may result in expanded use of first-generation anticoagulant rodenticides (FGARs). Recent toxicological studies with captive raptors have demonstrated that these species are considerably more sensitive to the FGAR diphacinone than traditional avian wildlife test species (mallard, bobwhite). We have now examined the toxicity of the FGAR chlorophacinone (CPN) to American kestrels fed rat tissue mechanically amended with CPN, or rat tissue containing biologically-incorporated CPN, for 7 days. Nominal CPN concentrations in these diets were 0.15, 0.75, and 1.5 µg/g food wet weight, and actual CPN concentration in diets were analytically verified as being close to target values. Food intake was consistent among groups, body weight fluctuated by less than 6%, exposure and adverse effects were generally dose-dependent, and there were no dramatic differences in toxicity between mechanically-amended and biologically-incorporated CPN diets. Using benchmark dose statistical methods, toxicity reference values at which clotting times were prolonged in 50% of the kestrels was estimated to be about 80 µg CPN consumed/kg body weight-day for prothrombin time and 40 µg CPN/kg body weight-day for Russell’s viper venom time. Based upon carcass CPN residues reported in rodents from field baiting studies, empirical measures of food consumption in kestrels, and dietary-based toxicity reference values derived from the 7-day exposure scenario, some free-ranging raptors consuming CPN-exposed prey might exhibit coagulopathy and hemorrhage. These sublethal responses associated with exposure to environmentally realistic concentrations of CPN could compromise survival of exposed birds.

[1]  R. Lazarus,et al.  Toxicokinetics and coagulopathy threshold of the rodenticide diphacinone in eastern screech‐owls (Megascops asio) , 2014, Environmental toxicology and chemistry.

[2]  C. Rice,et al.  Evidence of Songbird Intoxication From Rozol® Application at a Black-Tailed Prairie Dog Colony , 2013 .

[3]  M. Taylor,et al.  Monitoring agricultural rodenticide use and secondary exposure of raptors in Scotland , 2013, Ecotoxicology.

[4]  C. Rice,et al.  Chlorophacinone residues in mammalian prey at a black‐tailed prairie dog colony , 2012, Environmental toxicology and chemistry.

[5]  N. B. Vyas,et al.  Critique on the Use of the Standardized Avian Acute Oral Toxicity Test for First Generation Anticoagulant Rodenticides , 2012 .

[6]  R. Lazarus,et al.  Assessment of toxicity and potential risk of the anticoagulant rodenticide diphacinone using Eastern screech-owls (Megascops asio) , 2012, Ecotoxicology.

[7]  R. Lazarus,et al.  Comparative risk assessment of the first-generation anticoagulant rodenticide diphacinone to raptors , 2012 .

[8]  C. Meteyer,et al.  Acute toxicity, histopathology, and coagulopathy in American kestrels (Falco sparverius) following administration of the rodenticide diphacinone , 2011, Environmental toxicology and chemistry.

[9]  P. Mineau,et al.  Anticoagulant Rodenticides in Three Owl Species from Western Canada, 1988–2003 , 2010, Archives of environmental contamination and toxicology.

[10]  D. Bird,et al.  The Use of Captive American Kestrels (Falco sparverius) as Wildlife Models: A Review , 2009 .

[11]  R. Engeman,et al.  CHLOROPHACINONE BAITING FOR BELDING’S GROUND SQUIRRELS , 2007 .

[12]  Salomon Sand,et al.  The Benchmark Dose Method—Review of Available Models, and Recommendations for Application in Health Risk Assessment , 2003, Critical reviews in toxicology.

[13]  J. Okoniewski,et al.  Anticoagulant Rodenticides and Raptors: Recent Findings from New York, 1998–2001 , 2003, Bulletin of environmental contamination and toxicology.

[14]  G. H. Matschke,et al.  Chlorophacinone Residues in Rangeland Rodents: An Assessment of the Potential Risk of Secondary Toxicity to Scavengers , 2001 .

[15]  F. Lamarque,et al.  Field evidence of secondary poisoning of foxes (Vulpes vulpes) and buzzards (Buteo buteo) by bromadiolone, a 4-year survey. , 1997, Chemosphere.

[16]  R. Poche,et al.  Biodeterioration of chlorophacinone in voles, hawks and an owl , 1992 .

[17]  C. Massari,et al.  Effects of chlorophacinone on captive kestrels , 1988, Bulletin of environmental contamination and toxicology.

[18]  L. Pank,et al.  Secondary poisoning of owls by anticoagulant rodenticides , 1980 .