Toxicokinetics and coagulopathy threshold of the rodenticide diphacinone in eastern screech‐owls (<i>Megascops asio</i>)

Rattner, Barnett A.; Horak, Katherine E.; Lazarus, Rebecca S.; Goldade, David A.; Johnston, John J.

doi:10.1002/etc.2390

Cited by 56 publications

(43 citation statements)

References 26 publications

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“…Fibrinogen deficiency resulting from improper sample collection can prolong clotting time, and in rodenticide toxicity studies it is important to verify that its concentration is adequate to promote clot formation. The conduct, performance, and use of these assays in raptors have been previously described (Rattner et al 2011, Rattner et al 2012a, Rattner et al 2014.…”

Section: Clotting Time Assaysmentioning

confidence: 99%

“…These firstgeneration compounds are considered to be less hazardous to non-target wildlife than SGARs (Erikson andUrban 2004, US EPA 2011a), although recent diphacinone studies with captive raptors indicate that they may be more hazardous than previously recognized (Rattner et al 2011, Rattner et al 2012a, Rattner et al 2012b, Rattner et al 2014.…”

Section: Introductionmentioning

confidence: 99%

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

Rattner¹,

Lazarus²,

Schultz³

et al. 2014

vertebrate_pest_conference

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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. Proc. 26 th Vertebr. Pest Conf. (R. M. Timm and J. M. O'Brien, Eds.) Published at Univ. of Calif., Davis. 2014. Pp. 347-352.

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Section: Clotting Time Assaysmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

Rattner¹,

Lazarus²,

Schultz³

et al. 2014

vertebrate_pest_conference

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“…Several toxicokinetic of avian species have been studied. Compared to mammals, eastern screech-owls ( Megascops asio ) have a long elimination half-life of diphacinone in the liver [39]. Furthermore, owls have very low CYP-dependent warfarin metabolic activity compared to rats and other avian species [62].…”

mentioning

confidence: 99%

A review: poisoning by anticoagulant rodenticides in non-target animals globally

Nakayama

Morita

Ikenaka

et al. 2019

The Journal of Veterinary Medical Science

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Worldwide use of anticoagulant rodenticides (ARs) for rodents control has frequently led to secondary poisoning of non-target animals, especially raptors. In spite of the occurrence of many incidents of primary or secondary AR-exposure and poisoning of non-target animals, these incidents have been reported only for individual countries, and there has been no comprehensive worldwide study or review. Furthermore, the AR exposure pathway in raptors has not yet been clearly identified. The aim of this review is therefore to comprehensively analyze the global incidence of primary and secondary AR-exposure in non-target animals, and to explore the exposure pathways. We reviewed the published literature, which reported AR residues in the non-target animals between 1998 and 2015, indicated that various raptor species had over 60% AR- detection rate and have a risk of AR poisoning. According to several papers studied on diets of raptor species, although rodents are the most common diets of raptors, some raptor species prey mainly on non-rodents. Therefore, preying on targeted rodents does not necessarily explain all causes of secondary AR-exposure of raptors. Since AR residue-detection was also reported in non-target mammals, birds, reptiles and invertebrates, which are the dominant prey of some raptors, AR residues in these animals, as well as in target rodents, could be the exposure source of ARs to raptors.

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“…Symptoms documented in these studies, and in the veterinary and medical literature, include lethargy, anorexia, ataxia, anemia, lameness or immobility due to bleeding in the joints, and difficulty breathing (DuVall et al 1989, Merola 2002, Spahr et al 2007, Murray and Tseng 2008, Valchev et al 2008. Work by Rattner et al on captive kestrels (Falco sparverius) (Rattner et al 2011) and Eastern screech-owls (Megascops asio) , Rattner et al 2014a) examined the pharmacokinetics of first generation anticoagulant exposure and developed toxicity reference values for a range of sublethal effects, including coagulopathy and hemorrhaging. Their most recent research, presented at the Symposium, investigated the sublethal effects of sequential exposures to a FGAR (chlorophacinone) and a SGAR (brodifacoum).…”

Section: Effects Of Anticoagulant Rodenticide Exposurementioning

confidence: 99%

What Do We Need to Know to Assess Individual and Population-level Effects on Wildlife from Anticoagulant Rodenticides?

Quinn¹,

Swift²

2018

vertebrate_pest_conference

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Anticoagulant rodenticides have been detected in many species of wildlife worldwide; yet the origins, exposure pathways, and effects of this exposure are not well understood. Furthermore, to accurately characterize the risks from rodenticide use, information is needed on what proportion of populations are being exposed, what proportion of the exposed individuals are affected, and in what ways. The relationship between anticoagulant rodenticide concentrations found in wildlife and the rate of mortality or illness is the subject of much current research. Residue levels observed in liver and whole body analyses vary, and overlap extensively among apparently healthy asymptomatic individuals and sublethal and lethal cases. Results from laboratory studies also show there can be wide variability in lethal and sublethal effects among and within taxonomic groups. Correlating the sublethal and reproductive effects observed in laboratory studies with realistic exposure scenarios and effects in the wild is needed to improve risk assessments. For species with limited numbers/declining populations, a critical question is whether the rodenticide exposure documented in individual animals inhibit population growth or contribute to population declines by lowering survival and reproductive success. This information is essential to the regulatory agencies that must weigh the risks and benefits of rodenticide uses and identify restrictions that are effective in reducing risks to wildlife. A primary objective of this symposium was to facilitate communication between regulators and researchers. Current research on many of these topics was presented, and was followed by discussions on how to improve our understanding of what factors lead to wildlife exposure and improve our ability to assess the effects of exposure on individuals and populations. A collaborative approach will be developed to design studies that provide regulatory and wildlife management agencies with additional science on which to base their decisions.

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Toxicokinetics and coagulopathy threshold of the rodenticide diphacinone in eastern screech‐owls (Megascops asio)

Cited by 56 publications

References 26 publications

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

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

A review: poisoning by anticoagulant rodenticides in non-target animals globally

What Do We Need to Know to Assess Individual and Population-level Effects on Wildlife from Anticoagulant Rodenticides?

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