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At least 1,405 records · Page 78Linked to original sources
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

Subchronic hepatotoxicity of selenomethionine ingestion in mallard ducks

Twoyearold male mallards (Anas platyrhynchos) received a control diet (0.2 ppm Se) or diets containing 1, 2, 4, 8, 16, or 32 ppm Se as selenomethionine for 14 wk. Se accumulated readily in the liver in a dosedependent manner, reaching a mean concentration of 29 ppm (wet weight) in the 32 ppm group. Dietary Se of 2 ppm or greater increased plasma glutathione peroxidase activity. Mortality (10%) and histopathological effects, including bile duct hyperplasia and hemosiderin pigmentation of the liver and spleen, occurred in the 32 ppm group. These histopathological effects were accompanied by lower hemoglobin concentrations (16 and 32 ppm groups) and hematocrit (32 ppm group), and elevated plasma alkaline phosphatase activity (32 ppm group) indicative of cholestatic liver inJury. Other manifestations of hepatotoxicity included significant linear dose responses for hepatic oxidized glutathione (GSSG) concentrations and ratio of GSSG to reduced glutathione (GSH). Means for both of these responses differed from controls in groups receiving 832 ppm Se. Mean hepatic GSH and malondialdehyde (a measure of lipid peroxidation) concentrations were significantly elevated in the 16 and 32 ppm groups. Subchronic effects of selenomethionine, which occurs in vegetation, are of particular interest with respect to the health of wild aquatic birds in seleniferous locations.

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↗
USGS2018

Method to characterize inorganic particulates in lung tissue biopsies using field emission scanning electron microscopy

Humans accumulate large numbers of inorganic particles in their lungs over a lifetime. Whether this causes or contributes to debilitating disease over a normal lifespan depends on the type and concentration of the particles. We developed and tested a protocol for in situ characterization of the types and distribution of inorganic particles in biopsied lung tissue from three human groups using field emission scanning electron microscopy (FE-SEM) combined with energy dispersive spectroscopy (EDS). Many distinct particle types were recognized among the 13 000 particles analyzed. Silica, feldspars, clays, titanium dioxides, iron oxides and phosphates were the most common constituents in all samples. Particles were classified into three general groups: endogenous , which form naturally in the body; exogenic particles, natural earth materials; and anthropogenic particles, attributed to industrial sources. These in situ results were compared with those using conventional sodium hypochlorite tissue digestion and particle filtration. With the exception of clays and phosphates, the relative abundances of most common particle types were similar in both approaches. Nonetheless, the digestion/filtration method was determined to alter the texture and relative abundances of some particle types. SEM/EDS analysis of digestion filters could be automated in contrast to the more time intensive in situ analyses.

Toxicology Mechanisms and Methods↗
USGS2025

Derivation and characterization of environmental hazard concentrations for chemical prioritization: A case study in the Great Lakes tributaries

Ongoing anthropogenic activities and analytical advancements yield continuously expanding lists of environmental contaminants. This represents a challenge to environmental managers, who must prioritize chemicals for management actions (e.g., restriction, regulation, remediation) but are often hindered by resource limitations. To help facilitate prioritization efforts, this study presents several strategies for deriving environmental hazard concentrations using publicly accessible data and open-source computational tools. Using a Great Lakes tributaries aquatic monitoring dataset as a case study, environmental hazard concentrations were obtained or derived for 334 organic chemicals. These concentrations were based on (1) current water quality guidelines; (2) apical screening values; (3) apical and (4) nonapical effect concentrations from the ECOTOXicology Knowledgebase; (5) in vitro effect concentrations from the ToxCast database; (6) cytotoxic burst concentrations collated from the Comptox Dashboard; (7) “estimated screening values” derived from modeled or estimated data and available from various regulatory and nonregulatory agencies; (8) pharmaceutical potency estimates from the MaPPFAST database; and (9) quantitative structure-activity relationship (QSAR)–derived acute toxicity estimates. Environmental fate data included aquatic half-lives and bioconcentration factors collated from the Comptox Dashboard or estimated using QSARs. To identify patterns that could be used for characterization, availability of ecotoxicological concentrations and environmental fate data were evaluated. Furthermore, exceedances of hazard concentrations were evaluated and compared across diverse ecotoxicological data types. Altogether, by providing detailed methodology and practical examples generated with real monitoring data, this study demonstrated that these hazard concentration derivation strategies can be efficiently and effectively used with large, complex datasets and identified critical considerations for future prioritization efforts.

Great Lakes region↗
USGS2025

Methylmercury in subarctic amphibians: Environmental gradients, bioaccumulation, and estimated flux

Rapid warming in polar regions is causing large changes to ecosystems, including altering environmentally available mercury (Hg). Although subarctic freshwater systems have simple vertebrate communities, Hg in amphibians remains unexplored. We measured total Hg (THg) in wetland sediments and methylmercury (MeHg) in multiple life-stages (eggs to adults) of wood frogs ( Rana sylvatica ) and larval boreal chorus frogs ( Pseudacris maculata ) from up to 25 wetlands near Churchill, Manitoba (Canada), during the summers of 2018–2019. We used egg mass counts for wood frogs from 24 wetlands (2015–2019) and per-ovum MeHg concentrations to estimate site-level MeHg flux by metamorphs from wetlands to the terrestrial environment. Total Hg in wetland sediment was unrelated to MeHg concentrations of amphibian larvae, but sediment THg increased with from coastal tundra vegetation to inland boreal forests. Methylmercury concentrations of wood frog eggs (geometric mean = 35.9; range: 6.7–77.9 ng/g dry wt) exceeded previous reports for amphibians, including from sites contaminated by industrial sources of Hg. Methylmercury concentrations of adult wood frogs (298.9 ng/g dry wt) were also higher than that for frogs included in a recent assessment of MeHg in amphibians across the contiguous United States. Within wetlands, MeHg concentrations of wood frog larvae were strongly correlated with MeHg concentrations in eggs earlier in the summer, and concentrations increased with each life stage. We estimate there would have been 1,971.8–3,286.4 ng MeHg exported from wetlands by wood frog metamorphs, which is 3.4–5.6 times more MeHg than inputted by eggs. Collectively, these data provide an initial assessment of Hg concentrations, body burdens, and dynamics in subarctic food webs that are expected to experience large changes from climate warming.

Manitoba↗
USGS2025

Evaluation of the sensitivity of a federally endangered freshwater mussel (Venustaconcha trabalis) to selected chemicals

Protection of critically endangered species requires identification of factors limiting their survival and growth. Previous studies have demonstrated that unionid mussels are sensitive to some chemicals and the sensitivity was similar among different taxonomic families and tribes of mussels. However, common species of mussels were generally used in these previous studies; little is known about the sensitivity of endangered and threatened mussels relative to common species. The objective of this study was to evaluate the sensitivity of a critically endangered mussel (Tennessee bean, Venustaconcha trabalis ) to seven chemicals with different modes of toxic action (ammonia, chloride, nitrite, potassium, cobalt, manganese, nickel) in acute 96-h exposures and to three chemicals (nitrite, cobalt, iron) in chronic 28-d exposures conducted following standard methods. A commonly tested mussel (fatmucket, Lampsilis siliquoidea ) was also tested side-by-side with Tennessee bean in chronic exposures. Test chemicals were selected based on (1) chemicals of potential concern found in a review of existing data for the river where a population of Tennessee bean occurs or was historically present, (2) chemicals to which other mussels are sensitive, or (3) chemicals that had not been previously tested with mussels. Acute 50% effect concentrations (EC50s) for the seven chemicals from the Tennessee bean tests were within or close to the range of EC50s for other mussel species tested in previous studies, and chronic 20% effect concentrations for the three chemicals were similar between Tennessee bean and fatmucket, indicating the endangered species has sensitivity similar to other tested mussel species. Inclusion of the new mussel data in existing toxicity databases for freshwater organisms would rank one or more mussel species among the four most sensitive species to ammonia, chloride, potassium, and nickel in acute exposures and to nitrite, cobalt, and iron in chronic exposures.

Environmental Toxicology and Chemistry↗