Exposure pathways of anticoagulant rodenticides to nontarget wildlife.

Second-generation anticoagulant rodenticides are widely reported to contaminate and poison nontarget wildlife, primarily predatory birds and mammals. Exposure pathways, however, have not been well defined. Here, we examined potential movement of rodenticides from deployment of bait to exposure of small mammals and other biota. At two adjacent working farms, we placed baits containing either brodifacoum or bromadiolone. We monitored movement of those compounds to the surrounding environment by collecting small mammals, birds, and invertebrates. Similar collections were made at a third agricultural setting without active bait deployment, but located among intensive livestock production and regular rodenticide use by farmers. Livers and whole invertebrate samples were analyzed for rodenticides using a sensitive LC-MSMS method. Norway rats (Rattus norvegicus) from both baited and non-baited farms had residues of brodifacoum or bromadiolone, implicating rats as an important exposure pathway to wildlife. Among 35 analyzed nontarget small mammals, a single vole had high hepatic residues (18.6 µ/g), providing some indication of a small mammal pathway. One song sparrow (Melospiza melodia) sample from a baited farm contained 0.073 µg/g of brodifacoum in liver, while 0.39 µg/g of diphacinone was measured in a pool of carrion beetles (Dermestes spp.) from the non-baited farm area, implicating avian and invertebrate components in exposure pathways. Regurgitated pellets of barn owl (Tyto alba) selected randomly from baited farms contained no detectable rodenticide residues, while 90% of owl pellets collected from a variety of farms, and selected for the presence of rat fur, contained detectable anticoagulant residues. We recorded behavior of a captive sample of a representative songbird, the house sparrow (Passer domesticus); they readily entered bait stations and fed on (unloaded) bait.

Anticoagulant rodenticides in three owl species from Western Canada, 1988-2003.

Anticoagulant rodenticides are widely used to control rodent infestations. Previous studies have shown that nontarget organisms, such as birds, are at risk for both primary and secondary poisoning. This paper presents rodenticide residue information on the livers from 164 strigiformes which included barn owls (Tyto alba), barred owls (Strix varia), and great horned owls (Bubo virginianus), collected from 1988 to 2003 in the province of British Columbia and the Yukon Territory, Canada. Livers were analyzed for brodifacoum, bromadiolone, chlorophacinone, diphacinone, difethialone, and warfarin. Our results show that, of the 164 owl livers analyzed, 70% had residues of at least one rodenticide, and of these 41% had more than one rodenticide detected. Of the three species of owls examined, barred owls were most frequently exposed (92%, n = 23); brodifacoum and bromadiolone were most often detected, with liver concentrations ranging from 0.001 to 0.927 mg/kg brodifacoum, and 0.002 to 1.012 mg/kg bromadiolone. Six of the owls (three barred owls, two barn owls, and one great horned owl) were diagnosed as having died from anticoagulant poisoning; all six owls had brodifacoum residues in the liver.

Dose-dependent uptake, elimination, and toxicity of monosodium methanearsonate in adult zebra finches (Taeniopygia guttata).

Monosodium methanearsonate (MSMA), an arsenic-based pesticide, has been used for the past 10 years in attempts to suppress mountain pine beetle (Dendroctonus ponderosae) outbreaks in British Columbia, Canada. Previous studies have shown that cavity nesting forest birds such as woodpeckers forage and breed in MSMA treated pine stands. Here we examined the effects of MSMA in the laboratory using the zebra finch (Taeniopygia guttata), with the objective to examine tissue distribution and sublethal toxic effects in a model avian species. Zebra finches were exposed to this pesticide at doses similar to those found in bark beetle samples from MSMA stands of trees treated in the southern interior of British Columbia (8, 24, and 72 microg/g/d and a control group). Results showed high excretion (>90%) of arsenic in all dose groups, as well as dose-dependent trends in accumulation of arsenic in the blood (p < 0.001) and specific tissues. Monomethylarsonic acid, MMA (V), was the predominant form of arsenic in the blood plasma. Dimethylarsinic acid was the major form of arsenic found in the liver (83%) and kidney (61%) tissues. The brain tissue contained primarily the MMA (V) form (57%). Significant weight loss occurred in the two highest dose groups (p < 0.05). Birds in the highest dose group lost up to 15% of initial body mass.

Arsenic accumulation in bark beetles and forest birds occupying mountain pine beetle infested stands treated with monosodium methanearsonate.

The arsenic-based pesticide, monosodium methanearsonate (MSMA), is presently being evaluated for re-registration in Canada and the United States and has been widely used in British Columbia to help suppress Mountain Pine Beetle (MPB) outbreaks. We assessed the availability and exposure of MSMA to woodpeckers and other forest birds that may prey directly on contaminated bark beetles. Total arsenic residues in MPB from MSMA treated trees ranged from 1.3-700.2 microg g(-1) dw (geometric mean 42.0 microg g(-1)) with the metabolite monomethyl arsonic acid (MMAA) contributing 90-97% to the total arsenic extracted. Live adult and larval beetles were collected from treated trees and reached concentrations up to 327 microg g(-1) dw. MPBs from reference trees had significantly lower arsenic concentrations averaging 0.19 microg g(-1) dw. Woodpeckers foraged more heavily on MSMAtreesthat contained beetles with lower arsenic residues, suggesting those trees had reduced MSMAtranslocation and possibly greater live beetle broods. Blood samples from five species of woodpeckers and other forest passerines breeding within 1 km of MSMA stands contained elevated levels of total arsenic but with large individual variability (geometric mean = 0.18 microg g(-1) dw, range 0.02-2.20 microg g(-1). The results indicate that there is significant accumulation and transfer of organic arsenic within the food chain at levels that may present a toxicity risk to avian wildlife.