Analysis of tissues of mallard ducks fed two phthalate esters
No abstract available.
Geology topics
Publications and source records attributed to J. W. Spann.
No abstract available.
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 72 mallards were fed diets containing high or low levels of vitamin E (20 or 220 Ul/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.
Beginning the day after hatching, American kestrel (Falco sparverius) nestlings were orally dosed for 10 consecutive days with 5 microliters/g of corn oil (controls) or one of the diphenyl ether herbicides (nitrofen, bifenox, or oxyfluorfen) at concentrations of 10, 50, 250, or 500 mg/kg in corn oil. At 500 mg/kg, nitrofen resulted in complete nestling mortality, bifenox in high (66%) mortality, and oxyfluorfen in no mortality. Nitrofen at 250 mg/kg reduced nestling growth as reflected by decreased body weight, crownrump length, and bone lengths including humerus, radiusulna, femur, and tibiotarsus. Bifenox at 250 mg/kg had less effect on growth than nitrofen, but crownrump, humerus, radiusulna, and femur were significantly shorter than controls. Liver weight as a percent of body weight increased with 50 and 250 mg/kg nitrofen. Other manifestations of impending hepatotoxicity following nitrofen ingestion included increased hepatic GSH peroxidase activity in all nitrofentreated groups, and increased plasma enzyme activities for ALT, AST, and LDHL in the 250mg/kg group. Bifenox ingestion resulted in increased hepatic GSH peroxidase activity in the 50and 250mg/kg groups. Nitrofen exposure also resulted in an increase in total plasma thyroxine (T4) concentration. These findings suggest that altricial nestlings are more sensitive to diphenyl ether herbicides than young or adult birds of precocial species.
Wildland fire control chemicals are released into the environment by aerial and ground applications to manage rangeland, grassland, and forest fires. Acute oral 24 h 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 2000 mg 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.
Effects of field application levels of wildfire control chemicals, Phos-Chek ® G75-F (PC) and Silv-Ex ® (SE), were examined on red-winged blackbird ( Agelaius phoeniceus ) embryos. Embryos were more sensitive to PC and SE when eggs were immersed for 10 s at an early developmental stage (days 3–5 of incubation) than at a later stage (days 6–9 of incubation). The LC 50 (concentration causing 50% mortality) for early stage embryos exposed to PC was 213.3 g/L (slope = 1.6; 95% confidence interval [CI] = 129.1–326.1). The no observed effect concentration (NOEC) was below 135 g PC/L, which caused a significant increase in embryonic mortality and represents the lowest field coverage level of 1 gal/100 feet 2 . The LC 50 for early stage embryos exposed to SE was 19.8 g/L (slope = 1.5; 95% CI = 11.7–52.2). Significant mortality was observed at 10 g SE/L and marginal at 7.5 g SE/L with an apparent NOEC around 5 g SE/L. Neither chemical resulted in apparent developmental malformations.
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.
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.
Canada goose goslings were exposed to turf sprayed with D · Z · N® 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.
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.
Nine brown-headed cowbirds ( Molothrus ater ) were exposed to turf sprayed with either EarthCare® (25% diazinon; 4.77 L a.i./ha) or Ortho-Klor® (12.6% chlorpyrifos; 5.21 L a.i./ha). Birds were euthanized and one foot from each bird was weathered outdoors for up to 28 days and the other foot was kept frozen until residue analysis. When compared to the unweathered feet, feet weathered for 28 days retained 43% and 37% of the diazinon and chlorpyrifos, respectively. Insecticide residues were below the level of detection (1.0 ppm) on control feet. Weathered feet may be used for determining organophosphorus insecticide exposure to birds.
The illegal use of pesticide-laced baits for predator control is a wildlife crime that is underreported, inadequately documented, and insufficiently punished. The crime occurs when some ranchers, farmers, and hunting groups illegally lace baits with pesticides to control avian and mammalian predators. The activity has poisoned birds protected by the Endangered Species Act, Migratory Bird Treaty Act, and the Bald and Golden Eagle Protection Act. However, because of difficulties in discovering, reporting, and confirming the baitings and the wildlife kills, the crimes often appear inconsequential. The limited knowledge of these crimes in the public, regulatory, and judicial arenas distorts their importance .for some prosecutors and judges. The United States pesticide regulatory system has positioned federal and state prosecutors and judges in a critical role for protecting wildlife from the illegal practice of lacing baits with pesticides. In this article, the authors provide an overview of the crime and describe the ways in which the crime is investigated. They then present investigative and experimental evidence on the extent of the illegal practice and the magnitude of the kills in order to elucidate their importance with respect to prosecution and sentencing. The authors conclude by recommending that sufficient resources be made available, public awareness and education increased, and persistent prosecution occur in order to improve the effectiveness of all federal wildlife enforcement.
Eggs of nesting birds situated in peripheral areas serving as fire breaks are at risk of being sprayed with fire control chemicals. Acute toxicity tests were conducted by immersing northern bobwhite quail eggs for 10 s in different water-based concentrations of Silv-Ex® (SE), a foam-suppressant chemical, and Phos-Chek® G75-F (PC), a fire retardant chemical, on day 4 or day 11 of incubation. An attempt was made to relate the treatment concentrations to the actual field application levels. Mortality appeared higher in most groups exposed on day 11 than on day 4, suggesting that on day 11 the extensive chorioallantoic vascular network permitted greater uptake of chemical. Only 24–60% of the embryos survived to hatch at exposure concentrations of 202, 269, and 454 g/L PC when treated on incubation day 11. At higher concentrations including 681, 956, and 1,211 g/L PC, the compound did not completely dissolve in water and clumped on eggshells, resulting in greater hatching success. Exposures to SE at 100 g/L on incubation day 11 did not significantly affect hatching success of embryos but did significantly reduce the percent hematocrit in blood compared with controls. Incubation day 11 exposure to 202 and 1,211 g/L PC led to a significant increase in plasma aspartate aminotransferase, and day 4 exposure to 1,211 g/L PC resulted in a significant increase in alanine aminotransferase. In addition to elevated liver enzymes, these treatments resulted in a decrease in the number of hepatocyte profiles (1,211 g/L PC at day 4 and day 11) and an increase in hepatocyte size (202 and 1,211 g/L PC at day 11) in hatchlings. A combination of SE and PC was synergistic (202 g/L PC and 50 g/L SE) at day 11 of incubation with respect to decreased hatching success and reduced bone lengths. However, lower concentrations of SE (10 g/L or 30 g/L) combined with 202 g/L of PC appeared antagonistic. This may be due to SE, as a surfactant, altering the ability of PC to penetrate the egg. Our results show fewer adverse effects following exposure to SE than to PC; therefore application of SE may be less harmful to breeding bird populations.
American kestrels ( Falco sparverius ) were fed diets containing 0 (control), 1, 3, 10, and 30 μg/g (wet wt) of Kelthane®. Residues of dicofol and its metabolites were then analyzed in the eggs and carcasses of females. Significant differences occurred among treatments for residues of both p,p ′‐dicofol and p,p ′‐dechlorodicofol (DCD) in both eggs and carcasses and for p,p ′‐dicholorbenzophenone (DCBP) in eggs. Residue concentrations increased with increasing treatment exposure. Residues of p,p ′‐dicofol, p,p ′‐DCD, and p,p ′‐DCBP in eggs were significantly correlated with eggshell quality parameters. Significant correlations also occurred among contaminants in eggs and for individual contaminants between eggs and carcasses. The lowest‐observed‐dietary‐effect concentration for eggshell thinning was 3 μg/g, whereas 1 μg/g may be considered to be near a no‐observable‐adverse‐effect concentration. Concentrations of dicofol in potential prey items and eggs of wild birds generally have been lower than dietary‐effect concentrations or concentrations in tissues or eggs associated with eggshell thinning and reduced reproductive success.
This study evaluated the toxicity of a single size 7.5 lead shot to passerines. No mortalities or signs of plumbism were observed in dosed cowbirds (Molothrus ater) fed a commercial diet, but when given a more natural diet, three of 10 dosed birds died within 1 day. For all survivors from which shot were recovered, all but one excreted the shot within 24 h of dosing, whereas, the dead birds retained their shot. Shot erosion was significantly greater (P < 0.05) when weathered shot were ingested compared to new shot, and the greatest erosion was observed in those birds that died (2.2-9.7%). Blood lead concentrations of birds dosed with new shot were not significantly different (P=0.14) from those of birds exposed to weathered shot. Liver lead concentrations of birds that died ranged from 71 to 137 ppm, dry weight. Despite the short amount of time the shot was retained, songbirds may absorb sufficient lead to compromise their survival.
Our objective was to determine if ground foraging passerines in a woodland surrounding a trap and skeet range were subject to lead poisoning. Lead availability to birds was determined by shot counts and soil and earthworm analysis. Avian exposure to lead was identified by measuring free-erythrocyte protoporphyrin levels in blood and lead in tissues of three passerine species. Results showed that most shot were found in the top 3 cm of soil. Lead measurements ranged from 110 to 27,000 ppm (dry wt) in soil and were 660 and 840 ppm in earthworms. Sparrows held in an aviary at the range (p = 0.02) and free-flying juncos (p = 0.0005) mistnetted at the range displayed significantly higher protoporphyrin levels than those at an uncontaminated site. Sparrow and cowbird carcasses from the aviary carried 37 and 39 ppm lead (dry wt), respectively, whereas a junco liver contained 9.3 ppm lead.
The effects of polychlorinated biphenyl (PCB) congeners, PCB 126 (3,3′,4,4′,5-pentaCB) and PCB 77 (3,3′4,4′-tetraCB), were examined in chicken ( Gallus gallus ), American kestrel ( Falco sparverius ), and common tern ( Sterna hirundo ) embryos through hatching, following air cell injections on day 4. PCB 126 caused malformations and edema in chickens starting at 0.3 ppb, in kestrels at 2.3 to 23 ppb, but in terns only at levels affecting hatching success (44 ppb). Extent of edema was most severe in chickens and least in terns. Defects of the beak were common in all species but with crossed beak most prevalent in terns. Effects on embryo growth were most apparent for PCB 126 in chickens and kestrels. The approximate 50% lethal dose (LD50) for PCB 126 in chickens was 0.4 ppb, in kestrels was 65 ppb, and in terns was 104 ppb. The approximate LD50 for PCB 77 in chickens was 2.6 ppb and in kestrels was 316 ppb. Induction of cytochrome P450 associated monooxygenase activity (ethoxyresorufin- O -dealkylase activity) by PCB 126 in chick embryo liver was about 800 times more responsive than in tern and at least 1,000 times more responsive than in kestrel. High concentrations of PCB 126 found in bald eagle eggs are nearly 20-fold higher than the lowest toxic concentration tested in kestrels. Concentrations of PCB 126 causing low-level toxic effects in common tern eggs are comparable to highest levels in common terns and Forster's terns in the field, suggesting additional involvement of other compounds in the Great Lakes.
No abstract available.
Arsenic (As) and selenium (Se) occur together in high concentrations in the environment and can accumulate in aquatic plants and invertebrates consumed by waterfowl. Ninety-nine pairs of breeding mallards ( Anas platyrhynchos ) were fed diets supplemented with As (sodium arsenate) at 0, 25, 100, or 400 μg/g, in combination with Se (seleno-DL-methionine) at 0 or 10 μg/g, in a replicated factorial experiment. Ducklings produced were placed on the same treatment combination as their parents. Arsenic accumulated in adult liver and egg, reduced adult weight gain and liver weight, delayed the onset of egg laying, decreased whole egg weight, and caused eggshell thinning. Arsenic did not affect hatching success and was not teratogenic. In ducklings, As accumulated in the liver and reduced body weight, growth, and liver weight. Arsenic did not increase duckling mortality, but it did decrease overall duckling production. Selenium accumulated in adult liver and egg, was teratogenic, and decreased hatching success. Selenium did not affect adult weight, liver weight, survival, onset of egg laying, egg fertility, egg weight, or eggshell thickness. In ducklings, Se accumulated in the liver and reduced body weight and growth, and increased liver weight. Selenium increased duckling mortality and decreased overall duckling production. Antagonistic interactions between As and Se occurred whereby As reduced Se accumulation in liver and egg, and alleviated the effects of Se on hatching success and embryo deformities. It was demonstrated that As and Se, in the chemical forms and at the dietary levels administered in this study, can adversely affect mallard reproduction and duckling growth and survival, and that As can alleviate toxic effects of Se.