Geology topics

John D. Eisemann

Publications and source records attributed to John D. Eisemann.

5 recordsLinked to original sources

USGS2012

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

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 shorteared 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.

Ecotoxicology↗

USGS2012

Comparative risk assessment of the first-generation anticoagulant rodenticide diphacinone to raptors

New regulatory restrictions have been placed on the use of some second-generation anticoagulant rodenticides in the United States, and in some situations this action may be offset by expanded use of first-generation compounds. We have recently conducted several studies with captive adult American kestrels and eastern screech-owls examining the toxicity of diphacinone (DPN) using both acute oral and short-term dietary exposure regimens. Diphacinone evoked overt signs of intoxication and lethality in these raptors at exposure doses that were 20 to 30 times lower than reported for traditionally used wildlife test species (mallard and northern bobwhite). Sublethal exposure of kestrels and owls resulted in prolonged clotting time, reduced hematocrit, and/or gross and histological evidence of hemorrhage at daily doses as low as 0.16 mg DPN/kg body weight. Findings also demonstrated that DPN was far more potent in short-term 7-day dietary studies than in single-day acute oral exposure studies. Incorporating these kestrel and owl data into deterministic and probabilistic risk assessments indicated that the risks associated with DPN exposure for raptors are far greater than predicted in analyses using data from mallards and bobwhite. These findings can assist natural resource managers in weighing the costs and benefits of anticoagulant rodenticide use in pest control and eradication programs.

Conference Paper↗

USGS2011

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

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.

Environmental Toxicology and Chemistry↗

USGS1997

Cytochrome P450 and organochlorine contaminants in black-crowned night-herons from the Chesapeake Bay region, USA

Black-crowned night-heron ( Nycticorax nycticorax ) offspring were collected from a relatively uncontaminated coastal reference site (next to Chincoteague National Wildlife Refuge, VA, USA) and two sites in the Chesapeake Bay watershed (Baltimore Harbor, MD and Rock Creek Park, Washington, DC, USA). Hepatic microsomal activities of benzyloxyresorufin- O -dealkylase and ethoxyresorufin- O -dealkylase were significantly elevated (up to sixfold and ninefold induction, respectively) in pipping embryos from the Baltimore Harbor colony compared to the reference site, whereas values in embryos from the Rock Creek Park colony were intermediate. Concentrations of organochlorine pesticides and metabolites in pipping embryos from both sites in the Chesapeake watershed were greater than at the reference site but below the known threshold for reproductive impairment. However, concentrations of 10 arylhydrocarbon receptor-active polychlorinated biphenyl (PCB) congeners and estimated toxic equivalents were up to 37-fold greater in embryos collected from these two sites in the Chesapeake Bay region, with values for toxic congeners 77 and 126 exceeding those observed in pipping heron embryos from the Great Lakes. Monooxygenase activity of pipping embryos was associated with concentrations of several organochlorine pesticides, total PCBs, arylhydrocarbon receptor-active PCB congeners, and toxic equivalents ( r = 0.30–0.59), providing further evidence of the value of cytochrome P450 as a biomarker of organic contaminant exposure. Organochlorine contaminant levels were greater in 10-d-old nestlings from Baltimore Harbor than the reference site but had no apparent effect on monooxygenase activity or growth. These findings demonstrate induction of cytochrome P450 in pipping black-crowned night-heron embryos in the Chesapeake Bay region, probably by exposure to PCB congeners of local origin, and the accumulation of organochlorine pesticides and metabolites in nestling herons from Baltimore Harbor. Bio-monitoring with additional waterbird species (e.g., bald eagle, common tern, great blue heron) that appear to be more sensitive to PCBs than black-crowned night-herons is recommended to document health of waterbirds and remediation of the Chesapeake Bay.

Chesapeake Bay region↗

USGS1996

Developmental toxicity of PCB 126 (3,3',4,4',5-pentachlorobiphenyl) in nestling American kestrels (Falco sparverius)

Planar PCB congeners are embryotoxic and teratogenic to birds including American kestrels. The developmental toxicity of 3,3′,4,4′,5-pentachlorobiphenyl (PCB 126) was studied in the posthatching kestrel as a model for the eagle. Nestlings were dosed orally for 10 days with 5 μl/g body weight of corn oil (controls) or the planar PCB 126 at concentrations of 50, 250, or 1000 ng/g body weight. Dosing with 50 ng/g of PCB 126 resulted in a hepatic concentration of 156 ng/g wet weight, liver enlargement and mild coagulative necrosis, over 10-fold increases in hepatic microsomal ethoxyresorufin- O -dealkylase and benzyloxyresorufin- O -dealkylase, and approximately a 5-fold increase in methoxyresorufin- O -dealkylase. At this dose, mild to moderate lymphoid depletion of the spleen was apparent, as were decreased follicle size and content of the thyroid. At 250 ng/g, concentration of PCB 126 in the liver was 380 ng/g with increasing multifocal coagulative necrosis, decreased bone growth, decreased spleen weight with lymphocyte depletion of the spleen and bursa, and degenerative lesions of the thyroid. At 1000 ng/g, the liver concentration was 1098 ng/g, accompanied by decreased bursa weight, decreased hepatic thiol concentration, and increased plasma enzyme activities (ALT, AST, and LDH-L) in addition to the previous effects. Highly significant positive correlations were noted between liver concentrations of PCB 126 and the ratio of oxidized to reduced glutathone. These findings indicate that nestling kestrels are more susceptible to PCB 126 toxicity than adults, but less sensitive than embryos, and that planar PCBs are of potential hazard to nestling birds..

Fundamental and Applied Toxicology↗