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Results for “Journal of Toxicology and Environmental Health”

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At least 37 records · Page 2Linked to original sources
USGS2010

Evidence of weak contaminant-related oxidative stress in glaucous gulls (Larus hyperboreus) from the Canadian arctic

Environmental contaminants are transported over great distances to Arctic ecosystems, where they can accumulate in wildlife. Whether contaminant concentrations in wildlife are sufficient to produce adverse effects remains poorly understood. Exposure to contaminants elevates oxidative stress with possible fitness consequences. The glaucous gull ( Larus hyperboreus ), an Arctic top predator, was used as a bioindicator for investigating relationships between contaminant levels (organochlorines and polychlorinated biphenyls [OC/PCB], mercury [Hg], and selenium [Se]) and measures of oxidative stress (glutathione [GSH] metabolism and lipid peroxidation) in Canadian Arctic ecosystems. Contaminant levels were low and associations between contaminant exposure and oxidative stress were weak. Nevertheless, glutathione peroxidase activity rose with increasing hepatic Se concentrations, levels of thiols declined as Hg and OC/PCB levels rose, and at one of the two study sites levels of lipid peroxidation were elevated with increasing levels of hepatic Hg. These results suggest the possibility of a deleterious effect of exposure to contaminants on gull physiology even at low contaminant exposures.

Arctic↗
USGS2011

Meat and bone meal and mineral feed additives may increase the risk of oral prion disease transmission

Ingestion of prion-contaminated materials is postulated to be a primary route of prion disease transmission. Binding of prions to soil (micro)particles dramatically enhances peroral disease transmission relative to unbound prions, and it was hypothesized that micrometer-sized particles present in other consumed materials may affect prion disease transmission via the oral route of exposure. Small, insoluble particles are present in many substances, including soil, human foods, pharmaceuticals, and animal feeds. It is known that meat and bone meal (MBM), a feed additive believed responsible for the spread of bovine spongiform encephalopathy (BSE), contains particles smaller than 20 μm and that the pathogenic prion protein binds to MBM. The potentiation of disease transmission via the oral route by exposure to MBM or three micrometer-sized mineral feed additives was determined. Data showed that when the disease agent was bound to any of the tested materials, the penetrance of disease was increased compared to unbound prions. Our data suggest that in feed or other prion-contaminated substances consumed by animals or, potentially, humans, the addition of MBM or the presence of microparticles could heighten risks of prion disease acquisition.

Journal of Toxicology and Environmental Health, Pa↗
USGS2011

Diversity and distribution of white-tailed deer mtDNA lineages in chronic wasting disease (CWD) outbreak areas in southern Wisconsin, USA

Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy affecting North American cervids. Because it is uniformly fatal, the disease is a major concern in the management of white-tailed deer populations. Management programs to control CWD require improved knowledge of deer interaction, movement, and population connectivity that could influence disease transmission and spread. Genetic methods were employed to evaluate connectivity among populations in the CWD management zone of southern Wisconsin. A 576-base-pair region of the mitochondrial DNA of 359 white-tailed deer from 12 sample populations was analyzed. Fifty-eight variable sites were detected within the sequence, defining 43 haplotypes. While most sample populations displayed similar levels of haplotype diversity, individual haplotypes were clustered on the landscape. Spatial clusters of different haplotypes were apparent in distinct ecoregions surrounding CWD outbreak areas. The spatial distribution of mtDNA haplotypes suggests that clustering of the deer matrilineal groups and population connectivity are associated with broad-scale geographic landscape features. These landscape characteristics may also influence the contact rates between groups and therefore the potential spread of CWD; this may be especially true of local disease spread between female social groups. Our results suggest that optimal CWD management needs to be tailored to fit gender-specific dispersal behaviors and regional differences in deer population connectivity. This information will help wildlife managers design surveillance and monitoring efforts based on population interactions and potential deer movement among CWD-affected and unaffected areas.

Wisconsin↗
USGS2009

Sublethal effects of chronic lead ingestion in mallard ducks

Mallard drakes (Anas platyrhynchos) fed 1, 5, or 25 ppm lead nitrate were bled and sacrificed at 3‐wk intervals. No mortality occurred, and the pathologic lesions usually associated with lead poisoning were not found. Changes in hematocrit and hemoglobin concentration did not occur. After 3 wk ducks fed 25 ppm lead exhibited a 40% inhibition of blood δ‐aminolevulinic acid dehydratase activity that persisted through 12 wk exposure. After 12 wk treatment similar enzyme inhibition was present in the ducks fed 5 ppm lead. At 3 wk there was a small accumulation of lead (less than 1 ppm) in the liver and kidneys of ducks fed 25 ppm lead; no further increases occurred throughout the exposure. No significant accumulation of lead occurred in the tibiae or wing bones. Groups of ducks fed 5 and 25 ppm diets for 12 wk were placed on clean feed and examined through a 12 wk posttreatment period. After 3 wk on clean diet δ‐aminolevulinic acid dehydratase activity and lead concentrations in the blood had returned to pretreatment levels. Even though lead concentrations in the blood, soft organs, and bone were low, a highly significant negative correlation between blood lead and blood enzyme activity was obtained. This enzyme bioassay should provide a sensitive and precise estimate for monitoring lead in the blood for waterfowl.

Journal of Toxicology and Environmental Health↗
USGS2009

Experimental feeding of DDE and PCB to female big brown bats (Eptesicus fuscus)

Twenty-two female big brown bats (Eptesicus fuscus) were collected in a house attic in Montgomery County, Maryland. Seventeen were fed mealworms (Tenebrio molitor larvae) that contained 166 ppm DDE; the other five were fed uncontaminated mealworms. After 54 days of feeding, six dosed bats were frozen and the remaining 16 were starved to death. In a second experiment, 21 female big brown bats were collected in a house attic in Prince Georges County, Maryland. Sixteen were fed mealworms that contained 9.4 ppm Aroclor 1254 (PCB). After 37 days, two bats had died, four dosed bats were frozen, and the remaining 15 were starved to death. Starvation caused mobilization of stored residues. After the feeding periods, average weights of all four groups (DDE-dosed, DDE control, PCB-dosed, PCB control) had increased. However, weights of DDE-dosed bats had increased significantly more than those of their contols, whereas weights of PCB-dosed bats had increased significantly less than those of their controls. During starvation, PCB-dosed bats lost weight significantly more slowly than controls. Because PCB levels in dosed bats resembled levels found in some free-living big brown bats, PCBs may be slowing metabolic rates of some free-living bats. It is not known how various common organochlorine residues may affect metabolism in hibernating bats. DDE and PCB increased in brains of starving bats as carcass fat was metabolized. Because the tremors and/or convulsions characteristic of neurotoxicity were not observed, we think even the maximum brain levels attained (132 ppm DDE, 20 ppm PCB) were sublethal. However, extrapolation of our DDE data predicted lethal brain levels when fat reserves declined sufficiently. PCB-dosed bats were probably in no danger of neurotoxic poisoning. However, PCB can kill by a nonneurotoxic mode, and this could explain the deaths of two bats on PCB dosage.

Journal of Toxicology and Environmental Health↗
USGS1977

Effects of DDE on experimentally poisoned free-tailed bats (Tadarida brasiliensis): Lethal brain concentrations

Adult female free-tailed bats (Tadarida brasiliensis) were collected at Bracken Cave, Texas, and shipped to the Patuxent Wildlife Research Center. Treated mealworms (Tenebrio molitor) containing 107 ppm DDE were fed to 17 bats; five other bats were fed untreated mealworms. After 40 days on dosage, during which one dosed bat was killed accidentally, four dosed bats were frozen and the remaining 17 were starved to death. The objective was to elevate brain levels of DDE to lethality and measure these concentrations. After the feeding period, dosed bats weighed less than controls. After starvation, the body condition of dosed bats was poorer than that of controls even though there was no difference in the amounts of carcass fat. During starvation, dosed bats lost weight faster than controls. Also, four dosed bats exhibited the prolonged tremoring that characterizes DDE poisoning. DDE increased in brains of starving bats as fat was metabolized. The estimated mean brain concentration of DDE diagnostic of death was 519 ppm with a range of 458-564 ppm. These values resemble diagnostic levels known for two species of passerine birds, but they exceed published levels for two free-tailed bats from Carlsbad Caverns, New Mexico.

Journal of Toxicology and Environmental Health↗
USGS1978

Effects of dietary vanadium in mallard ducks

Adult mallard ducks fed 0, 1, 10, or 100 ppm vanadyl sulfate in the diet were sacrificed after 12 wk on treatment; tissues were analyzed for vanadium. No birds died during the study and body weights did not change. Vanadium accumulated to higher concentrations in the bone and liver than in other tissues. Concentrations in bones of hens were five times those in bones of drakes, suggesting an interaction between vanadium and calcium mobilization in laying hens. Vanadium concentrations in most tissues were significantly correlated and increased with treatment level. Lipid metabolism was altered in laying hens fed 100 ppm vanadium. Very little vanadium accumulated in the eggs of laying hens.

Journal of Toxicology and Environmental Health↗
USGS1978

Influence of laying on lead accumulation in bone of mallard ducks

Paired mallard ducks (Anas platyrhynchos) were given No. 4 lead shot, and bone lead concentrations were compared in drakes and in laying and nonlaying hens. Lead accumulation was significantly greater in bones with a high medullary content (femur and sternum) compared with bones with a lower medullary content (ulna-radius or wingbones). In dosed groups, hens always contained higher bone lead residues than drakes. After dosage with one shot (approximately 200 mg lead), lead in femurs of laying hens averaged 488.4 ppm compared with 113.6 ppm in nonlaying hens. Femurs of drakes averaged 9.4 ppm lead. Dosage with the second lead shot did not result in further accumulation of bone lead in hens, but increased bone lead concentrations threefold in drakes, suggesting that saturation levels for bone lead had already been reached in the hens after ingestion of one shot. There was no demonstrable relationship between egg production and bone lead residues. The high lead residues, found in medullary bones of laying hens indicate that sex and physiological condition are major factors influencing lead absorption by bone.

Journal of Toxicology and Environmental Health↗
USGS1978

Histopathologic effects of dietary cadmium on kidneys and testes of mallard ducks

Mallard ducks fed 2, 20, or 200 ppm cadmium chloride were sacrificed at 30, 60, and 90 d. No mortality occurred during the study and body weights remained unchanged. Kidney weights of the 200-ppm group were significantly greater after 60 and 90 d than those of controls; also, testis weights were significantly lower after 90 d. Kidneys of ducks fed 2 and 20 ppm cadmium were relatively unaffected; however, slight to severe kidney lesions were found in the 200-ppm group after 60 d of treatment. No significant lesions were found in mallard testes after feeding 2 ppm cadmium in the diet, and only a few birds in the 20-ppm group showed slight to moderate gonad alterations. After 90 d of treatment, however, testes of males fed 200 ppm had atrophied and the spermatogenic process had ceased. This study should provide important information for the interpretation of cadmium levels found in kidneys and testes of wild ducks.

Journal of Toxicology and Environmental Health↗
USGS2009

Embryotoxic and teratogenic effects of petroleum hydrocarbons in mallards (Anas platyrhynchos)

Egg surface applications of microliter quantities of crude and refined oils of high aromatic content are embryotoxic to mallards (Anas platyrhynchos) and other avian species; applications of aliphatic hydrocarbons have virtually no effect. Mallard eggs at 72 h of development were exposed to a mixture of aromatic hydrocarbons or to aromatic compounds representative to those present in crude oil to assess their toxicity. The class composition of the mixture was similar to that of South Louisiana crude oil, an American Petroleum Institute reference oil. Application of 20 microliter of the mixture reduced embryonic survival by nearly 70%. The temporal pattern of embryonic death was similar to that after exposure to South Louisiana crude oil. Embryonic growth was stunted, as reflected by weight, crown-rump length, and bill length, and there was a significant increase in the incidence of abnormal survivors. When individual classes of aromatic hydrocarbons were tested, tetracyclics caused some embryonic death at the concentrations in the mixture. When classes were tested in all possible combinations of two, no combination appeared to be as toxic as the entire mixture. Addition of the tetracyclic compound chrysene to the aromatic mixture considerably enhanced embryotoxicity, but could not completely account for the toxicity of the crude oil. The presence of additional unidentified polycyclic aromatic hydrocarbons as well as methylated derivatives of polycyclic aromatic compounds such as chrysene may further account for the embryotoxicity of the crude oil.

Journal of Toxicology and Environmental Health↗
USGS2009

Embryotoxic effects of benzo[a]pyrene, chrysene and 7,12-dimethylbenz[a]-anthracene in petroleum hydrocarbon mixtures in mallard ducks

Studies with different avian species have revealed that surface applications of microliter amounts of some crude and fuel oils that coat less than 70% of the egg surface result in considerable reduction in hatching with teratogenicity and stunted growth. Other stUdies have shown that the embryo toxicity is dependent on the aromatic hydrocarbon content, further suggesting that the toxicity is due to causes other than asphyxia. In the present study the effects of three polycyclic aromatic hydrocarbons identified in petroleum were examined on mallard (Anas platyrhynchos) embryo development. Addition of benzo[a]pyrene (BaP), chrysene, or 7,7 2-dimethylbenz[ a]anthracene (DMBA) to a synthetic petroleum hydrocarbon mixture of known composition and relatively low embryotoxicity resulted in embryo toxicity that was enhanced or equal to that of crude oil when 10 :I was applied externally to eggs at 72 h of development. The order of ability to enhance embryo toxicity was DMBA > BaP > chrysene. The temporal pattern of embryonic death was similar to that reported after exposure to crude oil, with additional mortality occurring after outgrowth of the chorioallantois. Retarded growth, as reflected by embryonic body weight, crown-rump length, and bill length, was accompanied by teratogenicity. Abnormal embryos exhibited extreme stunting; eye, brain, and bill defects; and incomplete ossification. Gas chromatographic-mass spectral analysis of externally treated eggs showed the passage of aromatic hydrocarbons including chrysene through the shell and shell membranes to the developing embryos. These findings suggest that the presence of polycyclic aromatic hydrocarbons in petroleum, including BaP, chrysene, and DMBA, significantly enhances the overall embryotoxicity in avian species.

Journal of Toxicology and Environmental Health↗
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↗