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At least 253 records · Page 14Linked to original sources
USGS2009

Effects of chronic ingestion of No. 2 fuel oil on mallard ducklings

No. 2 fuel oil was fed to mallard (Anas platyrhynchos) ducklings in concentrations of 0.5 and 5.0% of the diet from hatching to 18 wk of age to assess the effects of chronic oil ingestion during early development. Five growth parameters (body weight, wing length, ninth primary length, tarsal length, and bill length) were depressed in birds receiving a diet containing 5% fuel oil. There was no oil-related mortality. The 5% fuel oil diet impaired avoidance behavior of 9-d-old mallard ducklings compared with controls or ducklings fed 0.5% oil. Open-field activity was greatly increased in 16-wk-old ducklings fed 5.0% oil. Liver hypertrophy and splenic atrophy were gross evidences of pathological effects in birds on the 5.0% oil diet. More subtle effects included biochemical lesions that resulted in the elevation of plasma alanine aminotransferase and ornithine carbamoyltransferase activity.

Journal of Toxicology and Environmental Health↗
USGS2009

Effects of dietary nickel on mallards

Thirty breeding pairs of mallards (Anas platyrhynchos) were randomly assigned to one of five treatment groups and were fed breeder mash containing 0, 12.5, 50.0, 200.0, or 800.0 ppm Ni (as the sulfate) for 90 d. Ni ingestion had no effect on egg production, hatchability, or survival of ducklings. After 90 d birds were bled, sacrificed, and necropsied. There were no significant differences in hematocrit; concentrations of hemoglobin, plasma triglyceride, and cholesterol; of plasma activities of ornithine carbamoyltransferase and alanine aminotransferase. A black tarry feces was noted in the high Ni dose group at necropsy, but no gross or histopathologic lesions were observed. Although absolute concentrations of Ni in tissues were low, there were significant accumulations in kidneys of birds fed Ni at all dietary levels and in feathers, blood, and livers of birds fed high doses of Ni compared with controls.

Journal of Toxicology and Environmental Health↗
USGS2009

Effects of DDE and PCB (Aroclor 1260) on experimentally poisoned little brown bats (Myotis lucifugus): Lethal brain concentrations

Adult female little brown bats (Myotis lucifugus) were collected in a church attic in North East, Cecil County, Md. Mealworms (Tenebrio molitor) containing organochlorine pollutants were fed to the bats as follows: 5 bats were dosed at 480 ppm DDE, 12 at 150 ppm DDE, 5 at 1000 ppm polychlorinated biphenyl (PCB; Aroclor 1260), and 12 at 15 ppm PCB. Seven other bats were fed untreated mealworms. The objective was to elevate brain levels of DDE and PCB to lethality and measure these concentrations. During 40 d of dosage, one DDE-dosed bat and two PCB-dosed bats died after exhibiting the prolonged tremor that characterizes organochlorine poisoning. After dosage, surviving bats were starved to elevate brain levels of toxicants, and three additional DDE-dosed bats had tremors before dying. The mean brain concentration of DDE diagnostic of death was estimated as 603 ppm, range 540-670 ppm. This mean is 16-18% higher than means for Mexican free-tailed bats (Tadarida brasiliensis) and common grackles (Quiscalus quiscula), and may indicate less sensitivity. Lethal brain concentrations of Aroclor 1260 were 1300 and 1500 ppm. Such values appear to be higher than values (Aroclor 1254) for brown-headed cowbirds (Molothrus ater). During starvation, DDE-dosed bats lost weight about 24% faster than controls. If smaller amounts of stored DDE cause increases in metabolic rates of nonfeeding bats, as during hibernation or migration, the result could be premature energy depletion and increased mortality.

Journal of Toxicology and Environmental Health↗
USGS2009

Organochlorine concentrations in bald eagles: Brain/body lipid relations and hazard evaluation

Residue levels of 12 organochlorine compounds found In the brains of bald eagles can be predicted from the corresponding concentrations in the carcass when expressed on a hexane‐extractable lipid basis. The compounds varied by a factor of about 3 in the degree to which they accumulated In the brain. An understanding of these relations enhances our ability to assess the toxic hazards of environmental contamination.

Journal of Toxicology and Environmental Health↗
USGS2009

Recovery of cholinesterase activity in mallard ducklings administered organophosphorus pesticides

Oral doses of the organophosphorus pesticides acephate, dicrotophos, fensulfothion, fonofos, malathion, and parathion were administered to mallard ducklings ( Anas platyrhynchos ), and brain and plasma cholinesterase (ChE) activities were determined for up to 77 d after dosing. In vivo recovery of brain ChE activity to within 2 standard deviations of the mean activity of undosed birds occurred within 8 d, after being depressed an average of 25-58% at 24 h after dosing. In vivo recovery of plasma ChE appeared as fast as or faster than that of brain, but the pattern of recovery was more erratic and therefore statistical comparison with brain ChE recovery was not attempted. In vitro tests indicated that the potential for dephosphorylation to contribute to in vivo recovery of inhibited brain ChE differed among chemical treatments. Some ducklings died as a result of organophosphate dosing. In an experiment in which ducklings within each treatment group received the same dose (mg/kg), the brain ChE activity in birds that died was less than that in birds that survived. Brain ChE activities in ducklings that died were significantly different among pesticide treatments: fensulfothion > parathion> acephate > malathion (p < 0.05).

Journal of Toxicology and Environmental Health↗
USGS2009

Parathion accumulation in cricket frogs and its effect on American kestrels

Adult cricket frogs (Acris crepitans) were held individually for 96 h in static systems containing initial concentrations of either 0, 0.1, 1.0, or 10 ppm parathion in 10 ml water. Mortality of cricket frogs was directly related to the parathion concentration in the water. Frogs from the 1.0- and 10-ppm groups accumulated 0.08 and 4.6 ppm parathion, respectively. One of four American kestrels (Falco sparverius) fed frogs from the 10-ppm group died from organophosphate poisoning less than 3 h after consuming five frogs. Mortality did not occur in kestrels fed frogs from the other treatment groups, which represented more environmentally realistic levels of exposure.

Journal of Toxicology and Environmental Health↗
USGS2009

Oxychlordane, HCS-3260, and nonachlor in birds: Lethal residues and loss rates

Oxychlordane reached lethal levels in birds given dietary dosages of HCS-3260 (70.75% cis-chlordane and 23.51% trans-chlordane) at 6 levels from 50 to 500 ppm. Oxychlordane ranged from 9.4 to 22.1 ppm in brains of cowbirds (Molothrus ater ) grackles (Quiscalus quiscula , and red-winged blackbirds (Agelaius phoeniceus ) that died on dosage and from 1.3 to 4.8 ppm in sacrificed birds, providing a clear diagnostic separation. Among starlings (Sturnus vulgaris ) however, oxychlordane ranged from 5.0 to 19.1 ppm in brains of birds that died, significantly lower than in the other species, and from 1.4 to 10.5 ppm in sacrificed birds, overlapping the levels in those that died. Lethal levels, therefore, begin near 5.0 ppm, as in a previous study in which oxychlordane itself was fed, but the data from starlings emphasizes the need for confirmatory necropsy findings in diagnosis of poisoning.

Journal of Toxicology and Environmental Health↗
USGS1986

Association between PCBs and lower embryonic weight in black-crowned night herons in San Francisco Bay

Reproductive problems, including congenital malformations, reduced hatching success, and decreased survival of hatchlings, have been observed in colonial-nesting water birds at the San Francisco Bay National Wildlife Refuge (SFBNWR). Twenty-four black-crowned night heron (Nycticorax nycticorax) eggs were collected from SFBNWR in 1983. Twelve of these were collected from separate nests when late-stage embryos were pipping, and an additional egg was randomly collected from each nest for organochlorine analysis. Overt anomalies and skeletal defects were not apparent. Embryonic weights (with partially absorbed yolk sacs removed) were 15% lower (p lt 0.05) in SFBNWR embryos compared to control embryos from the Patuxent Wildlife Research Center (PWRC). Crown-rump length and femur length were shorter for SFBNWR embryos. The geometric mean polychlorinated biphenyl (PCB) concentration in SFBNWR eggs was 4.1 ppm wet weight, with a range of 0.8-52.0 ppm. A negative correlation (r = - 0.61; p lt 0.05) existed between embryonic weight and log-transformed PCB residues in whole eggs collected from the same nest at SFBNWR, suggesting a possible impact of PCBs on embryonic growth. A correlation with embryonic weight did not occur for DDE (1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene) residues. Liver microsomal aryl hydrocarbon hydroxylase activity was neither significantly elevated nor correlated with PCB, DDE, or PCB plus DDE log-transformed residues. It is unknown whether the apparent association between PCBs and lower weight is persistent through hatching.

Journal of Toxicology and Environmental Health↗
USGS1987

Oral and intramuscular toxicity of inorganic and organic mercury chloride to growing quail

The lethal toxicity of inorganic (HgCl 2 ) and organic (CH 3 HgCl) mercury chloride was compared for Coturnix (Japanese quail, Coturnix japonica) of different ages from hatch through adulthood by single‐dose acute oral and intramuscular injections and by a 5‐d dietary trial. Sublethal mercury toxicity was studied by evaluation of plasma and brain cholinesterase activity. CH 3 HgCl was more toxic than HgCl 2 in all tests at each age tested. LD50s consistently increased over the first 4 wk for both acute methods and both mercurials and then stabilized. The striking difference between single‐dose acute and 5‐d dietary tests was that CH 3 HgCl averaged about twice as toxic as HgCl 2 by both acute methods, compared to 100 times as toxic by the dietary method. For example, at 2 wk of age, the oral LD50s for CH 3 HgCl and HgCl 2 were 18 and 42 mg/kg and the dietary LC50s were 47 and 5086 ppm. When birds were fed HgCl 2 and developed clinical signs of intoxication, they could recover once treatment was withdrawn; however, on CH 3 HgCl, clinical signs often commenced after treatment was withdrawn, and then actually intensified for several days and culminated in death.

Journal of Toxicology and Environmental Health↗
USGS1988

Selenium toxicosis in wild aquatic birds

Severe gross and microscopic lesions and other changes were found in adult aquatic birds and in embryos from Kesterson Reservoir (a portion of Kesterson National Wildlife Refuge), Merced County, Calif., during 1984. Adult birds from that area were emaciated, had subacute to extensive chronic hepatic lesions, and had excess fluid and fibrin in the peritoneal cavity. Biochemical changes in their livers included elevated glycogen and non-protein-bound sulfhydryl concentrations and glutathione peroxidase activity but lowered protein, total sulfhydryl, and protein-bound sulfhydryl concentrations. Congenital malformations observed grossly in embryos were often multiple and included anophthalmia, microphthalmia, abnormal beaks, amelia, micromelia, ectrodactyly, and hydrocephaly. Mean concentrations of selenium in livers (94.4 ppm, dry weight) and kidneys (96.6 ppm) of birds collected at the Kesterson ponds were about 10 times those found at a nearby control area (8.3 and 12.2 ppm). We conclude that selenium present in the agricultural drainage water supplied to the Kesterson ponds accumulated in the food chain of aquatic birds to toxic concentrations and caused the lesion and other changes observed.

California↗
USGS1988

Embryotoxic and teratogenic effects of selenium in the diet of mallards

Mallards (Anas platyrhynchos) were fed a control diet, diets containing 1, 5, 10, or 25 ppm Se as sodium selenite, or a diet containing 10 ppm Se as seleno-DL-methionine in the first of two experiments. Selenium at 10 ppm as selenomethionine or 25 ppm as sodium selenite caused a 40-44% decrease in the total number of eggs that hatched compared to controls. Selenium at 25 ppm (sodium selenite) resulted in a 19% decrease in mean embryonic weight at 18 d of incubation, accompanied by a 6% decrease in crown-rump length. Ten parts per million Se as selenomethionine was more teratogenic than sodium selenite at 25 ppm. Selenomethionine (10 ppm Se) resulted in an incidence of 13.1% malformations that were often multiple, whereas sodium selenite (10 and 25 ppm Se) resulted in 3.6 and 4.2% malformations. The teratogenicity of selenomethionine was confirmed in a second experiment in which mallards received 1, 2, 4, 8, or 16 ppm Se as selenomethionine, resulting in 0.9, 0.5, 1.4, 6.8, and 67.9% malformations, respectively. These malformations included hydrocephaly, microphthalmia, lower bill defects, and foot defects with ectrodactyly. Both forms of selenium increased the incidence of edema and stunted embryonic growth. Selenomethionine (10 ppm Se) resulted in a significant increase of approximately 40% in plasma glutathione peroxidase activity and a 70% increase in sorbitol dehydrogenase activity (indicative of hepatotoxicity) in hatchlings. Sodium selenite (25 ppm Se) resulted in fourfold elevation in plasma uric acid concentration, indicative of renal alteration. Selenomethionine accumulated much better in eggs than did sodium selenite. These findings indicate that selenomethionine is considerably more teratogenic and generally more embryotoxic than sodium selenite, probably due to higher uptake of selenomethionine.

Journal of Toxicology and Environmental Health↗
USGS1989

Hepatic glutathione metabolism and lipid peroxidation in response to excess dietary selenomethionine and selenite in mallard ducklings

Selenium from selenomethionine accumulated in a dose-dependent manner in the liver, resulting in a decrease in hepatic-reduced glutathione with a corresponding decrease in total hepatic thiols. There was a dose-dependent increase in the oxidized to reduced glutathione ratio, and an increase in lipid peroxidation. These findings indicate that Se in the diet at 10 ppm and higher causes significant sublethal alterations in mallard ducklings, and 20-40 ppm causes significant hepatotoxicity.

Journal of Toxicology and Environmental Health↗
USGS1991

Environmental contaminants and the reproductive success of lake trout in the Great Lakes: An epidemiological approach

Epidemiological criteria were used to examine the influence of environmental contamination on reproductive success of lake trout ( Salvelinus namaycush ,) in the Laurentian Great Lakes. Most of the information was obtained from lake trout eggs collected in southeastern Lake Michigan and reared in the laboratory. Two separate end points that measure reproductive success—egg hatchability and fry survival‐were used in the evaluation. Strong evidence for maternally derived polychlorinated biphenyls causing reduced egg hatchability were observed for the time order, strength of association, and coherence criteria. Equally strong evidence for organic environmental contaminants, also of maternal origin, causing a swim‐up fry mortality syndrome were presented for the strength of association, specificity, replication, and coherence criteria. The epidemiological approach for demonstrating cause‐and‐effect relations was useful because of the difficulty in demonstrating definite proof of causality between specific environmental contaminants and reproductive dysfunction in feral fish.

Journal of Toxicology and Environmental Health↗
USGS1991

Great lakes embryo mortality, edema, and deformities syndrome (glemeds) in colonial fish-eating birds: Similarity to chick-edema disease

Several species of colonial fish-eating birds nesting in the Great Lakes basin Includ-ing herring gulls, common terns and double-crested cormorants, have exhibited chronic impairment of reproduction. In addition to eggshell thinning caused by high levels of DDT and metabolites, the reproductive impairment is characterized by high embryonic and chick mortality , edema, growth retardation, and deformities, hence the name Great Lakes embryo mortality , edema, and deformities syndrome (GLEMEDS). The hypothesis has been advanced that GLEMEDS in colonial fish-eating birds resembles chick-edema disease of poultry and has been caused by exposure to chick- edema active compounds that have a common mode of action through the cytochrome P-448 system. Detailed evidence has been collected from the following three groups of studies on herring gulls in the lower Great Lakes during the early 1970s; Forster’s terns in Green Bay, Wisconsin in 1983; and double-crested cormorants and Caspian terns in various locations in the upper Great Lakes from 1986 onwards. It has proved difficult to establish not only the onset of the disease in the various species at various locations but also the period in which chick-edema active compounds were released. Anecdotal evidence suggested that serious egg mortality . © 1988 by Hemisphere Publishing Corporation.

Illinois, Indiana, Michigan, Wisconsin, Minnesota,↗
USGS2009

Developmental toxicity of diphenyl ether herbicides in nestling American kestrels

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.

Journal of Toxicology and Environmental Health↗
USGS1993

Down-regulation of muscarinic receptors and the m3 subtype in white-footed mice by dietary exposure to parathion

The effect of ad libitum dietary exposure (as occurs in the field) to parathion for 14 d was investigated on the muscarinic acetylcholine receptor (mAChR) in brains and submaxillary glands of adults of a field species, the white-footed mouse Peromyscus leucopus. Immunoprecipitation using subtype selective antibodies revealed that the relative ratios of the m1-m5 mAChR subtypes in Peromyscus brain were similar to those in rat brain. There was little variability in acetylcholinesterase (AChE) activity in control mice brains but large variability in 39 exposed mice, resulting from differences in food ingestion and parathion metabolism. Accordingly, data on radioligand binding to mAChRs in each mouse brain were correlated with brain AChE activity in the same mouse, and AChE inhibition served as a biomarker of exposure reflecting in situ paraoxon concentrations. Exposure to parathion for 14 d reduced maximal binding (Bmax) of [3H]quinuclidinyl benzilate ([3H]QNB), [3H]-N-methylscopolamine ([3H]NMS), and [3H]-4-diphenylacetoxy-N-methylpiperidine methiodide ([3H]-4-DAMP) by up to approximately 58% without affecting receptor affinities for these ligands. Maximal reduction in Bmax of [3H]QNB and [3H]-4-DAMP binding occurred in mice with highest AChE inhibition, while equivalent maximal reduction in Bmax of [3H]NMS occurred in mice with only approximately 10% AChE inhibition, without further change at higher parathion doses. This is believed to be due to the hydrophilicity of [3H]NMS, which limits its accessibility to internalized desensitized receptors. In submaxillary glands (mAChRs are predominantly m3 subtype), there were significant dose-dependent reductions in [3H]QNB binding and m3 mRNA levels in exposed mice, revealed by Northern blot analyses. The reduction in m3 receptors is suggested to result mostly from reduced synthesis at the transcription level, rather than from translational or posttranslational events. The data suggest that down-regulation of mAChRs occurs after dietary exposure for 14 d to sublethal concentrations of parathion in a field rodent species, and that significant though incomplete recovery in AChE and mAChRs occurs in 7 d following termination of exposure.

Journal of Toxicology and Environmental Health↗
USGS2002

U.S. drinking water challenges in the twenty-first century

The access of almost all 270 million U.S. residents to reliable, safe drinking water distinguishes the United States in the twentieth century from that of the nineteenth century. The United States is a relatively water-abundant country with moderate population growth; nonetheless, current trends are sufficient to strain water resources over time, especially on a regional basis. We have examined the areas of public water infrastructure, global climate effects, waterborne disease (including emerging and resurging pathogens), land use, groundwater, surface water, and the U.S. regulatory history and its horizon. These issues are integrally interrelated and cross all levels of public and private jurisdictions. We conclude that U.S. public drinking water supplies will face challenges in these areas in the next century and that solutions to at least some of them will require institutional changes.

Environmental Health Perspectives↗
USGS1995

Contaminants and sea ducks in Alaska and the circumpolar region

We review nesting sea duck population declines in Alaska during recent decades and explore the possibility that contaminants may be implicated. Aerial surveys of the surf scoter (Melanitta perspicillata), white-winged scoter (M. fusca), black scoter (M. nigra), oldsqaw (Clangula hyemalis), spectacled eider (Somateria fischeri), and Steller's eider (Polysticta stellei) show long-term breeding population declines, especially the latter three species. The spectacled eider was recently classified threatened under the Endangered Species Act. In addition, three other diving ducks, which commonly winter in coastal areas, have declined from unknown causes. Large die-offs of all three species of scoters during molt, a period of high energy demand, were documented in August 1990, 1991, and 1992 at coastal reefs in southeastern Alaska. There was no evidence of infectious diseases in those scoters. The die-offs may or may not be associated with the long-term declines. Many scoters had elevated renal concentrations of cadmium (high of 375 micrograms/g dry weight [dw]). Effects of cadmium in sea ducks are not well understood. Selenium concentrations in livers of nesting white-winged scoters were high; however, the eggs they laid contained less selenium than expected based on relationships for freshwater bird species. Histological evaluation found a high prevalence of hepatocellular vacuolation (49%), a degenerative change frequently associated with sublethal toxic insult. Cadmium and selenium mean liver concentrations were generally higher in those birds with more severe vacuolation; however, relationships were not statistically significant. We do not know if sea duck population declines are related to metals or other contaminants.

Alaska↗