Probabilistic risk assessment for snails, slugs, and endangered honeycreepers in diphacinone rodenticide baited areas on Hawaii, USA

Johnston, John J.; Pitt, William C.; Sugihara, Robert T.; Eisemann, John D.; Primus, Thomas M.; Holmes, Melvin; Crocker, Joe; Hart, Andy

doi:10.1897/04-255r.1

Cited by 32 publications

(30 citation statements)

References 22 publications

(24 reference statements)

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“…Invertebrates have different bloodclotting mechanisms to vertebrates and so are less susceptible to anticoagulant rodenticides than birds and mammals (Shirer, 1992;Pain et al, 2000;Craddock, 2002;Johnston et al, 2005). However, ground-dwelling invertebrates can access and feed on rodenticides, including those placed in bait stations (Spurr and Drew, 1999;Dunlevy et al, 2000;Craddock, 2002), and retain ingested compound in their predation of contaminated invertebrates is likely to be a major pathway by which hedgehogs are exposed to anticoagulant rodenticides.…”

Section: Discussionmentioning

confidence: 99%

Accumulation of anticoagulant rodenticides in a non-target insectivore, the European hedgehog (Erinaceus europaeus)

Dowding

Shore

Worgan

et al. 2010

Environmental Pollution

111

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Article (refereed)Dowding (Singleton et al., 1999;Stenseth et al., 2003).72 Consequently, a range of methods is employed to reduce rodent density and 73 associated damage. This is most commonly done in developed countries using 74 anticoagulant rodenticides, vitamin K antagonists that prevent the synthesis of 75 functional prothombrin and related blood-clotting factors. Extensive use of first-76 generation anticoagulant rodenticides (FGARs) during the 1950s, however, led to the 77 evolution of genetic resistance in brown rats (Rattus norvegicus), with widespread 78 cross-resistance to other compounds (Cowan et al., 1995;Thijssen, 1995). As a 79 result, more potent second-generation anticoagulant rodenticides (SGARs) were 80 developed which have a greater affinity to binding sites, resulting in greater 81 accumulation, persistence and toxicity (Parmar et al., 1987; Huckle and Warburton, 82 1986). 83Given their mode of action, both FGARs and SGARs are potentially harmful to all 84 vertebrates, and so users are expected to adopt measures that limit direct exposure 85 to non-target species. However, the degree to which these preventive measures are 86 adhered to, particularly by non-professionals, is unknown. For example, in Britain 87 some products are readily available to householders who may be less aware of the 88 risks of non-target poisoning and/or less likely to follow manufacturer's guidelines.89 Non-target species may also be deliberately poisoned (Barnett et al., 2006). 90Most studies investigating indirect exposure of non-target species to 91 anticoagulant rodenticides have focussed on the consumption of poisoned rodents by 92 predatory birds and mammals (Newton et al

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Section: Discussionmentioning

confidence: 99%

Accumulation of anticoagulant rodenticides in a non-target insectivore, the European hedgehog (Erinaceus europaeus)

Dowding

Shore

Worgan

et al. 2010

Environmental Pollution

111

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“…In addition, a probabilistic-based exposure model was developed using Crystal Ball Software (Oracle Inc., Redwood City, CA) and used to estimate the quantity of rodent liver consumption that would be required to exceed various toxicological endpoints (Johnston et al 2005). For each iteration, a single value was Monte-Carlo sampled from each model input distribution.…”

Section: Statistical and Risk Analysesmentioning

confidence: 99%

“…Using the sublethal threshold for anemia and prolonged clotting time (0.24 mg/kg/day) and the aforementioned rodent liver residue data in the probabilistic-based exposure model of Johnston and coworkers (Johnston et al 2005), it was determined that a small fraction (1%) of the population of male Hawaiian short-eared owls would exceed the LOAEL if they consumed more than 3.72 g of liver per day, and 10% of the male population would exceed the LOAEL if 19.6 g of liver from DPN poisoned mice were consumed for 7 days (Fig. 6).…”

Section: Risk Assessment Of Dietary Exposure To Diphacinonementioning

confidence: 99%

Assessment of toxicity and potential risk of the anticoagulant rodenticide diphacinone using Eastern screech-owls (Megascops asio)

Rattner

Horak²,

Lazarus

et al. 2012

Ecotoxicology

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In the United States, new regulatory restrictions have been placed on the use of some second-generation anticoagulant rodenticides. This action may be offset by expanded use of first-generation compounds (e.g., diphacinone; DPN). Single-day acute oral exposure of adult Eastern screech-owls (Megascops asio) to DPN evoked overt signs of intoxication, coagulopathy, histopathological lesions (e.g., hemorrhage, hepatocellular vacuolation), and/or lethality at doses as low as 130 mg/kg body weight, although there was no dose-response relation. However, this single-day exposure protocol does not mimic the multiple-day field exposures required to cause mortality in rodent pest species and non-target birds and mammals. In 7-day feeding trials, similar toxic effects were observed in owls fed diets containing 2.15, 9.55 or 22.6 ppm DPN, but at a small fraction (<5%) of the acute oral dose. In the dietary trial, the average lowest-observed-adverse-effect-level for prolonged clotting time was 1.68 mg DPN/kg owl/week (0.24 mg/kg owl/day; 0.049 mg/owl/day) and the lowest lethal dose was 5.75 mg DPN/kg owl/week (0.82 mg/kg owl/day). In this feeding trial, DPN concentration in liver ranged from 0.473 to 2.21 μg/g wet weight, and was directly related to the daily and cumulative dose consumed by each owl. A probabilistic risk assessment indicated that daily exposure to as little as 3-5 g of liver from DPN-poisoned rodents for 7 days could result in prolonged clotting time in the endangered Hawaiian short-eared owl (Asio flammeus sandwichensis) and Hawaiian hawk (Buteo solitarius), and daily exposure to greater quantities (9-13 g of liver) could result in low-level mortality. These findings can assist natural resource managers in weighing the costs and benefits of anticoagulant rodenticide use in pest control and eradication programs.

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“…As part of a Special Local Needs pesticide registration (FIFRA Section 24c) for broadcast application of diphacinone (0.005% in a grain-based pellet) for the control of rodents and wild pigs in Hawaii, its hazard to various species of birds was evaluated by both deterministic [37] and probabilistic [38] risk assessments. Using the greatest quantity of diphacinone found in a pig liver (3.07 mg/kg) and the available toxicity data for game birds (LD50 > 400 mg/kg for bobwhite), Eisemann and Swift [37] estimated the quantity of pig liver that would have to be scavenged by a Hawaiian hawk (Buteo solitarius; Federally listed as endangered) or a Hawaiian short-eared owl (Asio flammeus sandwichensis; State of Hawaii listed as endangered) to receive a median lethal dose would be 58.6 kg and 45.6 kg, respectively.…”

Section: Risk Evaluationmentioning

confidence: 99%

“…These quantities of liver are far greater than the weight of both the Hawaiian hawk and short-eared owl, so the risk associated with a single-day exposure to diphacinone would be low. However, applying the kestrel dose-response curve for lethality and the rodent liver residue data in the probabilistic-based 1-d exposure model described by Johnston et al [38], 50% of male Hawaiian hawks would have a 1% probability of mortality if they consumed 0.0035 kg of liver from diphacinone-poisoned rats (Supplemental Data, Fig. S2).…”

Section: Risk Evaluationmentioning

confidence: 99%

Acute toxicity, histopathology, and coagulopathy in American kestrels (Falco sparverius) following administration of the rodenticide diphacinone

Rattner

Horak

Warner

et al. 2011

Enviro Toxic and Chemistry

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The acute oral toxicity of the anticoagulant rodenticide diphacinone was found to be over 20 times greater in American kestrels (Falco sparverius; median lethal dose 96.8 mg/kg body weight) compared with Northern bobwhite (Colinus virginianus) and mallards (Anas platyrhynchos). Modest evidence of internal bleeding was observed at necropsy, although histological examination of heart, liver, kidney, lung, intestine, and skeletal muscle revealed hemorrhage over a wide range of doses (35.1-675 mg/kg). Residue analysis suggests that the half-life of diphacinone in the liver of kestrels that survived was relatively short, with the majority of the dose cleared within 7 d of exposure. Several precise and sensitive clotting assays (prothrombin time, Russell's viper venom time, thrombin clotting time) were adapted for use in this species, and oral administration of diphacinone at 50 mg/kg increased prothrombin time and Russell's viper venom time at 48 and 96 h postdose compared with controls. Prolongation of in vitro clotting time reflects impaired coagulation complex activity, and generally corresponded with the onset of overt signs of toxicity and lethality. In view of the toxicity and risk evaluation data derived from American kestrels, the involvement of diphacinone in some raptor mortality events, and the paucity of threshold effects data following short-term dietary exposure for birds of prey, additional feeding trials with captive raptors are warranted to characterize more fully the risk of secondary poisoning.

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Probabilistic risk assessment for snails, slugs, and endangered honeycreepers in diphacinone rodenticide baited areas on Hawaii, USA

Cited by 32 publications

References 22 publications

Accumulation of anticoagulant rodenticides in a non-target insectivore, the European hedgehog (Erinaceus europaeus)

Accumulation of anticoagulant rodenticides in a non-target insectivore, the European hedgehog (Erinaceus europaeus)

Assessment of toxicity and potential risk of the anticoagulant rodenticide diphacinone using Eastern screech-owls (Megascops asio)

Acute toxicity, histopathology, and coagulopathy in American kestrels (Falco sparverius) following administration of the rodenticide diphacinone

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