Acute oral toxicities of wildland fire control chemicals to birds.

Wildland fire control chemicals are released into the environment by aerial and ground applications to manage rangeland, grassland, and forest fires. Acute oral 24h median lethal dosages (LD50) for three fire retardants (Fire-Trol GTS-R, Phos-Chek D-75F, and Fire-Trol LCG-R) and two Class A fire suppressant foams (Silv-Ex and Phos-Chek WD881) were estimated for northern bobwhites, Colinus virginianus, American kestrels, Falco sparverius, and red-winged blackbirds, Agelaius phoeniceus. The LD50s of all chemicals for the bobwhites and red-winged blackbirds and for kestrels dosed with Phos-Chek WD881 and Silv-Ex were above the predetermined 2000mg chemical/kg body mass regulatory limit criteria for acute oral toxicity. The LD50s were not quantifiable for kestrels dosed with Fire-Trol GTS-R, Phos-Chek D-75F, and Fire-Trol LCG-R because of the number of birds which regurgitated the dosage. These chemicals appear to be of comparatively low order of acute oral toxicity to the avian species tested.

Dermal insecticide residues from birds inhabiting an orchard.

The US Environmental Protection Agency conducts risk assessments of insecticide applications to wild birds using a model that is limited to the dietary route of exposure. However, free-flying birds are also exposed to insecticides via the inhalation and dermal routes. We measured azinphos-methyl residues on the skin plus feathers and the feet of brown-headed cowbirds (Molothrus ater) in order to quantify dermal exposure to songbirds that entered and inhabited an apple (Malus x domestica) orchard following an insecticide application. Exposure to azinphos-methyl was measured by sampling birds from an aviary that was built around an apple tree. Birds sampled at 36 h and 7-day post-application were placed in the aviary within 1 h after the application whereas birds exposed for 3 days were released into the aviary 4-day post-application. Residues on vegetation and soil were also measured. Azinphos-methyl residues were detected from the skin plus feathers and the feet from all exposure periods. Our results underscore the importance of incorporating dermal exposure into avian pesticide risk assessments.

Field evaluation of an avian risk assessment model.

We conducted two laboratory subacute dietary toxicity tests and one outdoor subacute dietary toxicity test to determine the effectiveness of the U.S. Environmental Protection Agency's deterministic risk assessment model for evaluating the potential of adverse effects to birds in the field. We tested technical-grade diazinon and its D.Z.N 50W (50% diazinon active ingredient wettable powder) formulation on Canada goose (Branta canadensis) goslings. Brain acetylcholinesterase activity was measured, and the feathers and skin, feet, and gastrointestinal contents were analyzed for diazinon residues. The dose-response curves showed that diazinon was significantly more toxic to goslings in the outdoor test than in the laboratory tests. The deterministic risk assessment method identified the potential for risk to birds in general, but the factors associated with extrapolating from the laboratory to the field, and from the laboratory test species to other species, resulted in the underestimation of risk to the goslings. The present study indicates that laboratory-based risk quotients should be interpreted with caution.

Decomposed gosling feet provide evidence of insecticide exposure.

Canada goose goslings were exposed to turf sprayed with DZN diazinon 50W application (2.24 kg a.i./ha). The control plot was subjected to a water application. One foot from each bird was placed outdoors for 7 d to decompose and the other foot was kept frozen. Diazinon residues were analyzed on both feet. Results showed that diazinon was detected from undecomposed and decomposed feet of the birds. Diazinon residues were below the level of detection (<0.01 ppm, a.i.) on the feet from the control goslings. Decomposed feet may be used for determining insecticide exposure when the traditional matrices are not available.

Relation of fatty acid composition in lead-exposed mallards to fat mobilization, lipid peroxidation and alkaline phosphatase activity.

The increase of n-6 polyunsaturated fatty acids (PUFA) in animal tissues has been proposed as a mechanism of lead (Pb) poisoning through lipid peroxidation or altered eicosanoids metabolism. We have studied fatty acid (FA) composition in liver and brain of mallards (Anas platyrhynchos) feeding for 3 weeks on diets containing combinations of low or high levels of vitamin E (20 or 200 UI/kg) and Pb (0 or 2 g/kg). Saturated FA, n-6 PUFA and total concentrations of FA were higher in livers of Pb-exposed mallards, but not in their brains. The percentage of n-6 PUFA in liver and brain was slightly higher in Pb-exposed mallards. The increase of n-6 PUFA in liver was associated with decreased triglycerides and increased cholesterol in plasma, thus could be in part attributed to feed refusal and fat mobilization. The hepatic ratios between adrenic acid (22:4 n-6) and arachidonic acid (20:4 n-6) or between adrenic acid and linoleic acid (18:2 n-6) were higher in Pb exposed birds, supporting the existing hypothesis of increased fatty acid elongation by Pb. Among the possible consequences of increased n-6 PUFA concentration in tissues, we found increased lipid peroxidation in liver without important histopathological changes, and decreased plasma alkaline phosphatase activity that may reflect altered bone metabolism in birds.

Relationship between oxidative stress, pathology, and behavioral signs of lead poisoning in mallards.

Some of the adverse effects of lead (Pb) may be associated with oxidative damage of lipids, proteins, or DNA. In a previous study a linkage was observed between the susceptibilities of waterfowl species to Pb poisoning with oxidative stress. To investigate this relationship among the individuals of a single species, for 3 wk 4 groups of 12 mallards were fed diets containing high or low levels of vitamin E (20 or 220 UI/kg) and high or low levels of Pb (0 or 2 g/kg). During the first week of Pb exposure, mallards developed hemolytic anemia, and during the second week, signs of neurological impairment. Histological findings in the Pb-exposed mallards were hemosiderosis, demyelinization of sciatic and brachial nerves, and tumefaction of renal tubular epithelium with the presence of intranuclear inclusion bodies. Lipid peroxidation increased with Pb exposure in blood, liver, bile, and brain, but decreased in nerves. Glutathione (GSH) increased with Pb exposure in liver and bile, and its oxidized/reduced ratio only increased in bile. Pb exposure inhibited GSH peroxidase activity (GPX) in plasma, liver, and brain, and decreased protein thiols (PSH) in blood and liver. Vitamin E resulted in significantly lower lipid peroxidation in nerves of control birds relative to unsupplemented controls, but did not alleviate any sign of lead posioning. Pb-induced pathological changes associated with hepatic and nervous functions were significantly correlated with lower GPX activity and PSH concentrations in these tissues rather than lipid peroxidation. Data suggest that inhibition of antioxidant enzymes and interaction with sulfhydryl groups of proteins may play a more important role in Pb poisoning of waterfowl than lipid peroxidation.