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Geology topics

D. J. Hoffman

Publications and source records attributed to D. J. Hoffman.

At least 55 records · Page 3Linked to original sources
USGS2002

Sublethal effects in avocet and stilt hatchlings from selenium-contaminated sites

Excess selenium (Se) in the aquatic food chain is embryotoxic and teratogenic to avocets, stilts, and other waterbirds. American avocet ( Recurvirostra americana ) and black-necked stilt ( Himantopus mexicanus ) eggs were collected from three sites in the Tulare Lake Basin of California, USA, and hatched in the laboratory. These sites included the Tulare Lake Drainage District-north (TLDD-N, water 2.5 ppb Se), TLDD-south (TLDD-S, water 8.6 ppb Se), and Westfarmers (WF, water 190 ppb Se). Highest egg Se concentrations occurred at WF (geometric mean 31.4 ppm dry wt for avocets and 20.5 ppm dry wt for stilts). Mean egg Se concentrations were 6.7 ppm for avocets and 8.4 ppm for stilts at TLDD-S, and 3.3 ppm for avocets and 2.3 ppm for stilts at TLDD-N. Hatching success and incidence of malformations did not differ among sites, but yolk sac-free hatching weights and bone lengths were less for avocets at the WF site, whereas liver weights and liver to body weight ratios were greater at that site. With increasing Se concentration, oxidative stress was most apparent in avocet hatchlings from WF: hepatic glutathione (GSH) peroxidase activity increased, glucose-6-phosphate dehydrogenase activity decreased, and oxidized glutathione (GSSG) concentration as well as the ratio of GSSG to reduced GSH concentration increased. In stilts, hepatic GSH concentration was lower in WF hatchlings. In conclusion, our findings of Se-impaired embryo growth and hepatotoxicity in avocet hatchlings suggest that oxidative stress observed in hatchlings may be related to these biological effects and may serve as a potential bioindicator of subsequent impaired functions.

California↗
USGS2002

Effects of Phos-Chek G75-F and Silv-Ex on developing Northern Bobwhite Quail (Colinus virginianus)

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.

Archives of Environmental Contamination and Toxico↗
USGS2002

Selenium biotransformations into proteinaceous forms by foodweb organisms of selenium-laden drainage waters in California

Selenium contamination represents one of the few clear cases where environmental pollution has led to devastation of wildlife populations, most notably in agricultural drainage evaporation and power plant coal-fly ash receiving ponds. Complex biogeochemistry, in particular extensive biotransformations and foodchain transfer, governs Se ecotoxicology and toxicology, for which the mechanism(s) are still elusive. However, total waterborne Se concentration has been widely used as a criterion for regulating and mitigating Se risk in aquatic ecosystems, which does not account for Se biogeochemistry and its site-dependence. There is a need for more reliable indicator(s) that encompass Se ecotoxicity and/or toxicity. Selenomethionine warrants special attention since it simulates Se toxicosis of wildlife in laboratory feeding studies. While low in free selenomethionine, microphytes isolated from Se-laden agricultural evaporation ponds were abundant in proteinaceous selenomethionine. This prompted a more extensive survey of Se speciation in foodchain organisms including microphytes, macroinvertebrates, fish, and bird embryos residing mainly in the agricultural drainage systems of the San Joaquin Valley, California. Total Se in biomass, water-soluble fractions, and protein-rich fractions were measured along with GC-MS analysis of proteinaceous selenomethionine. In all foodchain organisms, water-soluble Se constituted the major fraction of total biomass Se, while proteinaceous Se was a substantial, if not dominant, fraction of the water-soluble Se. In turn, proteinaceous selenomethionine comprised an important fraction of proteinaceous Se. In terms of total biomass Se, an average 1400-fold of Se biomagnification from water to microphytes was observed while subsequent transfer from microphytes to macroinvertebrates exhibited an average of only 1.9-fold. The latter transfer was more consistent and greater in extent for proteinaceous Se and proteinaceous selenomethionine, which is consistent with their importance in foodchain transfer. Proteinaceous Se in the omnivorous carp (Cyprinus carpio) liver also demonstrated a relation to ovarian lesions, while deformed stilt (Himantopus mexicanus) embryo was more abundant in proteinaceous selenomethionine than were normal embryos. Although limited in the number of organisms surveyed, these findings provide an impetus for further field and laboratory feeding studies to substantiate the hypothesis that proteinaceous selenomethionine underlies Se ecotoxicity, which may in turn prove to be a reliable indicator of Se risk in aquatic ecosystems. Copyright ?? 2002 Elsevier Science B.V.

Aquatic Toxicology↗
USGS2002

Role of selenium toxicity and oxidative stress in aquatic birds

Adverse effects of selenium (Se) in wild aquatic birds have been documented as a consequence of pollution of the aquatic environment by subsurface agricultural drainwater and other sources. These effects include mortality, impaired reproduction with teratogenesis, reduced growth, histopathological lesions and alterations in hepatic glutathione metabolism. A review is provided, relating adverse biological effects of Se in aquatic birds to altered glutathione metabolism and oxidative stress. Laboratory studies, mainly with an organic form of Se, selenomethionine, have revealed oxidative stress in different stages of the mallard (Anas platyrhynchos) life cycle. As dietary and tissue concentrations of Se increase, increases in plasma and hepatic GSH peroxidase activities occur, followed by dose-dependent increases in the ratio of hepatic oxidized to reduced glutathione (GSSG:GSH) and ultimately hepatic lipid peroxidation measured as an increase in thiobarbituric acid reactive substances (TBARS). One or more of these oxidative effects were associated with teratogenesis (4.6 ppm wet weight Se in eggs), reduced growth in ducklings (15 ppm Se in liver), diminished immune function (5 ppm Se in liver) and histopathological lesions (29 ppm Se in liver) in adults. Manifestations of Serelated effects on glutathione metabolism were also apparent in field studies in seven species of aquatic birds. Reduced growth and possibly immune function but increased liver:body weight and hepatic GSSG:GSH ratios were apparent in American avocet (Recurvirostra americana) hatchlings from eggs containing 9 ppm Se. In blacknecked stilts (Himantopus mexicanus), which contained somewhat lower Se concentrations, a decrease in hepatic GSH was apparent with few other effects. In adult American coots (Fulica americana), signs of Se toxicosis included emaciation, abnormal feather loss and histopathological lesions. Mean liver concentrations of 28 ppm Se (ww) in the coots were associated with elevated hepatic GSH peroxidase, depletion of hepatic protein bound thiols and total thiols, but a small increase in GSH. Diving ducks in the San Francisco Bay area exhibited a positive correlation between hepatic Se concentration and GSH peroxidase activity (r=0.63, P<0.05), but a negative correlation between hepatic Se and GSH concentration (r=0.740, P<0.05). In willets (Catoptrophorus semipalmatus) from the San Diego area, positive correlations occurred between hepatic Se concentration and GSSG (r=0.70, P<0.001), GSSG:GSH ratio, and TBARS. In emperor geese (Chen canagica) from western Alaska, blood levels of up to 9.4 ppm occurred and were associated with increased plasma GSH peroxidase activity (r=0.62, P<0.001), but with decreased plasma GSSG reductase activity. When evaluating Se toxicity, interactive nutritional factors, including other elements and dietary protein, should also be taken into consideration. Further studies are needed to examine the relationship between different forms of environmentally occurring selenium, arsenic and mercury on reproduction, hepatotoxicity and immune function of aquatic birds. Further selenium nutritional interaction studies may also help to illucidate the mechanism of selenium induced teratogenesis, by optimizing GSH and other antioxidant defense mechanisms in a manner that would stabilize or raise the cell's threshold for susceptibility to toxic attack from excess selenium. It is concluded that Se-related manifestations of oxidative stress may serve as useful bioindicators of Se exposure and toxicity in wild aquatic birds.

Aquatic Toxicology↗
USGS2002

Selenium toxicity: cause and effects in aquatic birds

There are several manners in which selenium may express its toxicity: (1) an important mechanism appears to involve the formation of CH3Se- which either enters a redox cycle and generates superoxide and oxidative stress, or forms free radicals that bind to and inhibit important enzymes and proteins. (2) Excess selenium as selenocysteine results in inhibition of selenium methylation metabolism. As a consequence, concentrations of hydrogen selenide, an intermediate metabolite, accumulate in animals and are hepatotoxic, possibly causing other selenium-related adverse effects. (3) It is also possible that the presence of excess selenium analogs of sulfur-containing enzymes and structural proteins play a role in avian teratogenesis. l-selenomethionine is the most likely major dietary form of selenium encountered by aquatic birds, with lesser amounts of l-selenocysteine ingested from aquatic animal foods. The literature is suggestive that l-selenomethionine is not any more toxic to adult birds than other animals. l-Selenomethionine accumulates in tissue protein of adult birds and in the protein of egg white as would be expected to occur in animals. There is no suggestion from the literature that the levels of l-selenomethionine that would be expected to accumulate in eggs in the absence of environmental concentration of selenium pose harm to the developing embryo. For several species of aquatic birds, levels of Se as selenomethionine in the egg above 3 ppm on a wet weight basis result in reduced hatchability and deformed embryos. The toxicity of l-selenomethionine injected directly into eggs is greater than that found from the entry of l-selenomethionine into the egg from the normal adult diet. This suggests that there is unusual if not abnormal metabolism of l-selenomethionine in the embryo not seen when l-selenomethionine is present in egg white protein where it likely serves as a source of selenium for glutathione peroxidase synthesis in the developing aquatic chick.

Aquatic Toxicology↗
USGS2002

Nineteenth century mercury hazard to wading birds and cormorants of the Carson River, Nevada

Contemporary mercury interest relates to atmospheric deposition, contaminated fish stocks and exposed fish-eating wildlife. The focus is on methylmercury (MeHg) even though most contamination is of inorganic (IoHg) origin. However, IoHg is readily methylated in aquatic systems to become more hazardous to vertebrates. In response to a classic episode of historical (1859–1890) IoHg contamination, we studied fish-eating birds nesting along the lower Carson River, Nevada. Adult double-crested cormorants ( Phalacrocorax auritus ), snowy egrets ( Egretta thula ) and black-crowned night-herons ( Nycticorax nycticorax ) contained very high concentrations of total mercury (THg) in their livers (geo. means 134.8μg/g wet weight (ww), 43.7 and 13.5, respectively) and kidneys (69.4, 11.1 and 6.1, respectively). Apparently tolerance of these concentrations was possible due to a threshold-dependent demethylation coupled with sequestration of resultant IoHg. Demethylation and sequestration processes also appeared to have reduced the amount of MeHg redistributed to eggs. However, the relatively short time spent by adults in the contaminated area before egg laying was also a factor in lower than expected concentrations of mercury in eggs. Most eggs (100% MeHg) had concentrations below 0.80μg/g ww, the putative threshold concentration where reproductive problems may be expected; there was no conclusive evidence of mercury-related depressed hatchability. After hatching, the young birds were fed diets by their parents averaging 0.36–1.18μgMeHg/g ww through fledging. During this four to six week period, accumulated mercury concentrations in the organs of the fledglings were much lower than found in adults, but evidence was detected of toxicity to their immune (spleen, thymus, bursa), detoxicating (liver, kidneys) and nervous systems. Several indications of oxidative stress were also noted in the fledglings and were most apparent in young cormorants containing highest concentrations of mercury. This stress was evidenced by increased thiobarbituric acid-reactive substances, low activities of enzymes related to glutathione metabolism and low levels of reduced thiols, plus an increase in the ratio of oxidized to reduced glutathione. At lower concentrations of mercury, as was found in young egrets, we observed elevated activities of protective hepatic enzymes, which could help reduce oxidative stress. Immune deficiencies and neurological impairment of fledglings may affect survivability when confronted with the stresses of learning to forage and the ability to complete their first migration.

Nevada↗
USGS2001

Effects of diquat, an aquatic herbicide, on the development of mallard embryos

Bipyridylium herbicides produce embryotoxic and teratogenic effects in dipteran, amphibian, avian, and mammalian organisms. Diquat dibromide, a bipyridylium compound, is commonly used as an aquatic herbicide. Mallard (Anas platyrhynchos) eggs were exposed to diquat by immersing the eggs for 10s in solutions of 0.88, 3.5, 7, 14, or 56 g/L on either the fourth or twenty-first day of incubation. Application of diquat on day 4 yielded an estimated LC50 of 19.5 g/L through 18 days of incubation, and 9.6 g/L through hatching. Body and organ weights, and bone lengths of hatchlings did not differ between control and treatment groups with the exception of a slight increase in brain weight in the 14 g/L group. Malformations in diquat-treated embryos included defects of the brain, eye, bill, limb, and pelvis; skeletal scoliosis; and incomplete ossification. Subcutaneous edema was also present. Significant manifestations of oxidative stress were apparent in hatchlings and included increased hepatic thiobarbituric acid reactive substances (TBARS) (lipid peroxidation) and decreased brain reduced glutathione (GSH). Brain protein-bound sulfhydryls (PBSH) increased. Diquat applied on day 21 of incubation yielded an estimated LC50 of 12.6 g/L through hatching. Exposure at this late stage of development did not produce deformities. Body and organ weights, and, bone lengths of hatchlings did not differ between control and treatment groups. Significant manifestations of oxidative stress in hatchlings included decreased brain GSH, increased oxidized glutathione (GSSG) and ratio of GSSG:GSH. This study suggests that concentrations of diquat commonly used for aquatic weed control, when based upon the expected dilution effect of average water depth of the application area, would probably have little impact on mallard embryos. However, concentrations applied above ground to weeds and cattails along the edge of waters and ditches could adversely affect the survival and development of mallard embryos, and presumably other avian species nesting in such habitats.

Journal of Toxicology and Environmental Health, Pa↗
USGS2001

Differences in oxidative stress between young Canada geese and mallards exposed to lead-contaminated sediment

Lead (Pb) exposure results in an increase in tissue lipid peroxides and variation in glutathione (GSH) concentrations, which can be related to peroxidative damage of cell membranes in Pb-poisoned animals. Species and individual variation in sensitivity to Pb poisoning among animals may be due to differential resistance to oxidative stress. The effects of oxidative stress caused by Pb exposure (1.7, 414, and 828 µg/g of diet) were compared for the first 6 wk in growing young of two species of waterfowl, Canada geese ( Branta canadensis ) and mallards ( Anas platyrhynchos ), with the first species being possibly more sensitive to Pb poisoning based on previous field and laboratory observations. Blood and liver Pb concentrations increased more in mallards than in geese. This may be explained on the basis of body weight, being 3.2 times higher in geese, and by hepatic metabolism, where GSH S -transferase (GST) activity is 2.9-fold higher in geese and presumably has a role in the binding of Pb to GSH and subsequent biliary excretion. In contrast, mallards showed higher hepatic levels of GSH and activities of GSH peroxidase (GPX) and GSH reductase (GR). Although both species showed a rise in hepatic GSH concentration with Pb exposure, the relationship between increased lipid peroxidation and Pb exposure was only significant in geese. Within treatment groups, hepatic GSH concentrations were inversely related to liver Pb concentrations in both species, which may correspond to the role of GSH in Pb excretion. Hepatic GSH was also inversely related to hepatic lipid peroxidation, but only in mallards and in agreement with the species differences observed in GPX and GR activities. The lower resistance to lipid peroxidation of Canada geese may explain why geese can die in the field from Pb poisoning after ingesting fewer shot than found in the gizzards of mallards and with lower liver Pb concentrations than in mallards.

Journal of Toxicology and Environmental Health, Pa↗
USGS2001

Investigation of eggshell thickness and biochemical indicators of contaminant exposure in Great Blue Herons(Ardea herodias) from Mason Neck National Wildlife Refuge

Mason Neck National Wildlife Refuge supports the largest great blue heron (Ardea herodias) rookery in the State of Virginia. The presence of bioaccumulative compounds such as polychlorinated biphenyls and DDT in fish collected from the Potomac River and tidal tributaries along the Refuge led to this study. The objective was to determine if there were any indications of pollutant-induced eggshell thinning or evidence of biochemical exposure to contaminants. We examined eggshell thickness and biomarkers of contaminant exposure in livers of embryos collected from the refuge and Coaches Island, a reference location in Chesapeake Bay. There was no evidence of eggshell thinning. Cytochrome P450 activity, measured as ethoxyresomfin-O-dealkylase (EROD) and benzyloxy-resorufin-O-dealkylase (BROD), was not significantly different in embryos from the two colonies. Biochemical indicators of oxidative stress can be reflected as changes in levels of reduced thiols, oxidized glutathione, and thiobarbituric reactive substances (TBARS). Although there were significant differences in the levels of reduced glutathione (GSH) and total thiol (TSH) activities in the embryo livers, there were no statistically significant differences in TBARS, protein-bound sulfhydryls (PBSH), oxidized glutathione (GSSG) and the ratio of GSSG to GSH. In fact, the concentrations of GSH and TSH were higher in the Mason Neck birds relative to Coaches Island. Under conditions of increased oxidative stress at least one or more of the following would be expected: decreased concentrations of reduced thiols (GSH and TSH), increased GSSG, and increased TBARS. In conclusion, we did not detect eggshell thinning or find evidence of a biochemical response to contaminant exposure in the Mason Neck great blue herons.

Report↗
USGS2001

Environmental contaminants

The purpose of this chapter is to provide an overview of the ecotoxicology of major classes of environmental contaminants, with respect to sources, environmental chemistry, most likely routes of exposure, potential bioaccumulation and biomagification, mechanisms of toxicity, and effects on potentially vulnerable species of mammalian wildlife. Major contaminants reviewed were selected on the basis of their use patterns, availability and potential toxicity to wild mammals. These included pesticides used in agroecosystems (organochlorines, organophosphorus and carbamate compounds, anticoagulants, herbicides and fungicides), various organic pollutants (chlorobenzenes, chlorophenols, polychlorinated biphenyls, dibenzodioxins and dibenzofurans, and polycyclic aromatic hydrocarbons), heavy metals (lead, mercury, and cadmium), agricultural drainwater mixtures, leachates and radionuclides. Many of the above aspects of ecotoxicology and contaminants will be expanded upon in subsequent chapters of this book as they relate to distinct mammalian species and potential risk.

Book chapter↗
USGS2001

Ecotoxicology

Explore the source record for details and available documents.

Book chapter↗
USGS2000

Organochlorine and metal contaminant exposure and effects in hatching Black-Crowned Night Herons (Nycticorax nycticorax) in Delaware Bay

Pea Patch Island in Delaware Bay is the site of the largest heronry north of Florida. From 1989–93, the population of nine species of wading birds numbered approximately 12,000 pairs, but has recently declined to about 7,000 pairs. Because Delaware Bay is a major shipping channel and receives anthropogenic releases of toxic substances from agricultural, industrial, and municipal point and nonpoint sources, contaminant exposure and effects to the heronry have been an ongoing concern. In 1997, pipping (early hatching stage) black-crowned night herons ( Nycticorax nycticorax ) were collected from separate nests at Pea Patch Island and from a coastal reference site, Middle Island in Rehoboth Bay, Delaware. There was no evidence of malformations or hepatic histopathological lesions in embryos, and their body and liver weights did not differ between sites. Biomarkers of petroleum hydrocarbons, polyhalogenated contaminant, and metal exposure (cytochrome P450 induction and oxidative stress responses) did not differ (p > 0.05) between sites, although activities of benzyloxy- O -dealkylase and ethoxyresorufin- O -dealkylase were somewhat elevated in 3 of the 15 embryos collected from Pea Patch Island. Concentrations of 21 organochlorine pesticides and metabolites were relatively low at both sites, with p,p′ -DDE values well below the threshold associated with eggshell thinning. Although total PCB concentration was modestly elevated (p < 0.05) in Pea Patch Island heron embryos, levels of arylhydrocarbon receptor-active PCB congeners, polychlorinated dibenzodioxins and dibenzofurans, and toxic equivalents were low and did not differ between sites. Concentrations of Cd and Mn in pipping embryos from Pea Patch Island were slightly greater (p < 0.05) than values observed in Middle Island embryos, but levels of these and the other metals and metalloids ( e.g. , Hg and Se) were below values associated with toxicity. In conclusion, it seems unlikely that chlorinated hydrocarbon and metal contaminant exposure constitutes a direct threat to the reproductive success of black-crowned night herons at Pea Patch Island. However, low-level exposure to these contaminants may constitute one of many stressors that in combination could adversely affect the stability of the wading bird population at this large heronry.

Delaware↗
USGS2000

Field evaluation of lead effects on Canada geese and mallards in the Coeur d'Alene River Basin, Idaho

Hatch year (HY) mallards ( Anas platyrhynchos ) in the Coeur d'Alene (CDA) River Basin had higher concentrations of lead in their blood than HY Western Canada geese ( Branta canadensis moffitti ) (geometric means 0.98 versus 0.28 μg/g, wet weight). The pattern for adults of both species was similar, although geometric means (1.77 versus 0.41 μg/g) were higher than in HY birds. HY mallards captured in the CDA River Basin in 1987 contained significantly lower lead concentrations in their blood than in 1994–95 (0.36 versus 0.98 μg/g); however, some very young mallards were sampled in 1987, and concentrations in adults were not significantly different in 1987, 1994, or 1995 (1.52, 2.07, 1.55 μg/g, respectively). Both species in the CDA River Basin in 1994–95 showed significantly reduced red blood cell delta-aminolevulinic acid dehydratase (ALAD) activity compared to the reference areas: Canada geese (HY −65.4 to −86.0%, adults −82.3%), and mallards (HY −90.7 to −95.5%, adults −94.1%). Canada goose goslings were divided into size classes, and the two smaller classes from the CDA River Basin had significantly elevated free erythrocyte protoporphyrin (protoporphyrin) levels compared to the reference area (15.2× and 6.9×). HY and adult mallards both had significantly elevated protoporphyrin (5.9× and 7.5×). Recognizing that interspecific differences exist in response and sensitivity to lead, it appears (at least for hemoglobin and hematocrit) that Canada geese were more sensitive to lead than mallards, i.e ., adverse hematologic effects occur at lower blood lead concentrations. Only Canada geese from the CDA River Basin, in spite of lower blood lead concentrations, had significantly reduced mean hemoglobin and hematocrit values. No euthanized Canada geese (all HYs) from CDA River Basin were classified as clinically lead poisoned, but 38 Canada geese found dead in the CDA River Basin during a concurrent study succumbed to lead poisoning between 1992 and 1997. Only 6 (15.8%) of these 38 contained ingested lead shot, which contrasts greatly with the 75–94% incidence of ingested lead shot when mortality was due to lead shot ingestion. Lead from other contaminated sources ( i.e ., sediments and vegetation) in the CDA River Basin was strongly implicated in most Canada goose deaths. Based on the 31 live mallards and Canada geese collected in the CDA River Basin, which were representative of the live populations blood sampled only, the prevalence of subclinical and clinical lead poisoning (as determined by liver lead concentrations, excluding birds with ingested lead shot) was higher in mallards: subclinical (4 of 8, 50% HYs and 6 of 11, 55% adults); clinical (0% HYs and 4 of 11, 36% adults), with less data available for Canada geese (only 1 of 9, 11% HYs marginally subclinical). The clinically lead-poisoned mallards had extremely high concentrations of lead in blood (2.69–8.82 μg/g) and liver (6.39–17.89 μg/g). Eight mallards found dead in the CDA River Basin during a concurrent study were diagnosed as lead poisoned, and only one (12.5%) contained ingested lead shot, which again strongly implicates other lead sources. The finding of dead lead poisoned Canada geese together with the high percentage of live mallards classified as subclinically or clinically lead poisoned, in combination with the low incidence of ingested lead shot causes us concern for both of these species, which live in association with lead-contaminated sediment in the CDA River Basin.

Idaho↗
USGS2000

Developmental toxicity of lead-contaminated sediment to mallard ducklings

Sediment ingestion has been identified as an important exposure route for toxicants in waterfowl. The toxicity of lead-contaminated sediment from the Coeur d'Alene River Basin (CDARB) in Idaho was examined on posthatching development of mallard ( Anas platyrhynchos ) ducklings for 6 weeks. Day-old ducklings received either untreated control diet, clean sediment (24%) supplemented control diet, CDARB sediment (3,449 μg/g lead) supplemented diets at 12% or 24%, or a positive control diet containing lead acetate equivalent to that found in 24% CDARB. The 12% CDARB diet resulted in a geometric mean blood lead concentration of 1.41 ppm (WW) with over 90% depression of red blood cell ALAD activity and over threefold elevation of free erythrocyte protoporphyrin concentration. The 24% CDARB diet resulted in blood lead of 2.56 ppm with over sixfold elevation of protoporphyrin and lower brain weight. In this group the liver lead concentration was 7.92 ppm (WW), and there was a 40% increase in hepatic reduced glutathione concentration. The kidney lead concentration in this group was 7.97 ppm, and acid-fast inclusion bodies were present in the kidneys of four of nine ducklings. The lead acetate positive control group was more adversely affected in most respects than the 24% CDARB group. With a less optimal diet (mixture of two thirds corn and one third standard diet), CDARB sediment was more toxic; blood lead levels were higher, body growth and liver biochemistry (TBARS) were more affected, and prevalence of acid-fast inclusion bodies increased. Lead from CDARB sediment accumulated more readily in duckling blood and liver than reported in goslings, but at given concentrations was generally less toxic to ducklings. Many of these effects are similar to ones reported in wild mallards and geese within the CDARB.

Idaho↗
USGS2000

Mixed-function oxygenases, oxidative stress, and chromosomal damage measured in lesser scaup wintering on the Indiana Harbor Canal

During the winter of 1993-1994, male lesser scaup ( Aythya alfinis ) were collected on the heavily polluted Indiana Harbor Canal, East Chicago, Indiana, and examined for several bioindicators of chemical exposure. Livers were analyzed for activities of three cytochrome P450-associated monooxygenases and four measures of oxidative stress. Blood and spleen were analyzed by flow cytometry for chromosomal damage. In a concurrent study, scaup tissues were analyzed for organic and inorganic contaminants. Ethoxyresomfm-O-dealkylase (EROD) activity in livers of scaup collected in January 1994 was significantly higher than in livers of scaup collected in March 1994 or in livers of reference birds. Three hepatic monooxygenase activities were each significantly correlated with polycyclic aromatic hydrocarbon (PAH) concentrations in scaup carcasses. Thiobarbituric acid (TBA) activity in scaup livers was positively correlated with iron, boron, and lead concentrations in livers and polychlorinated biphenyl concentrations in carcasses. TBA activity was negatively correlated with protein-bound thiol activity and mercury concentrations in livers. The coefficient of variation of DNA content in scaup blood cells was correlated with PAH concentrations in scaup carcasses. This is the first field study with birds to demonstrate a correlation between liver monooxygenase activity and carcass PAH concentrations and to show a direct correlation between PAH concentrations in tissues and somatic chromosomal damage in blood.

Indiana↗
USGS2000

Relation of waterfowl poisoning to sediment lead concentrations in the Coeur d'Alene River Basin

For many years, waterfowl have been poisoned by lead after ingesting contaminated sediment in the Coeur d'Alene River Basin, in Idaho. Results of studies on waterfowl experimentally fed this sediment were combined with results from field studies conducted in the Basin to relate sediment lead concentration to injury to waterfowl. The first step in the model estimated exposure as the relation of sediment lead concentration to blood lead concentration in mute swans ( Cygnus olor ), ingesting 22% sediment in a rice diet. That rate corresponded to the 90th percentile of sediment ingestion estimated from analyses of feces of tundra swans ( Olor columbianus ) in the Basin. Then, with additional laboratory studies on Canada geese ( Branta canadensis ) and mallards ( Anas platyrhynchos ) fed the sediment, we developed the general relation of blood lead to injury in waterfowl. Injury was quantified by blood lead concentrations, ALAD (δ-aminolevulinic acid dehydratase) activity, protoporphyrin concentrations, hemoglobin concentrations, hepatic lead concentrations, and the prevalence of renal nuclear inclusion bodies. Putting the exposure and injury relations together provided a powerful tool for assessing hazards to wildlife in the Basin. The no effect concentration of sediment lead was estimated as 24 mg/kg and the lowest effect level as 530 mg/kg. By combining our exposure equation with data on blood lead concentrations measured in moribund tundra swans in the Basin, we estimated that some mortality would occur at a sediment lead concentration as low as 1800 mg/kg.

Idaho↗
USGS2000

Effects of lead in nestling black-crowned night-herons (Nycticorax nycticorax) experimentally dosed in the field

Lead is a known environmental toxicant, and poisoning resulting from the ingestion of lead shot has been well-documented in many species of waterfowl. However, much less is known regarding exposure and effects of free environmental lead in species of birds other than waterfowl. In an attempt to evaluate toxicity of lead to herons and to determine the usefulness of feathers as a non-invasive exposure-monitoring tool, black-crowned night-heron nestlings were dosed with lead to determine its distribution among tissues, and its effects on biochemical biomarkers, growth, and survival. Five-day-old heron nestlings (one per nest) at Chincoteague Bay, Virginia were given a single intra-peritoneal injection of dosing vehicle (control; N=7) or one of three lead solutions (as lead nitrate) (10, 50, or 250 mg/kg body weight of nestling; N=7 per dose) chosen to represent levels below, at, and above those found in moderately-polluted environments. All nestlings treated with lead exhibited dose-dependent inhibition of delta-aminolevulinic acid dehydratase (ALAD) activity compared to controls, and nestlings treated with the highest concentration showed a reduced carcass weight compared to controls. Of several measures of oxidative stress that were analyzed, significant differences were found between low- and high-dosed nestlings in hepatic total thiol and protein-bound sulfhydryl concentrations. No differences in survival were detected between dosed nestlings, controls, or uninjected siblings. Lead concentrations in several matrices, including feathers, are being determined to assess distribution among tissues and will also be examined for relationships with measures of effect.

Society of Environmental Toxicology and Chemistry,↗