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G. H. Heinz

Publications and source records attributed to G. H. Heinz.

At least 37 records · Page 2Linked to original sources

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↗

Lead poisoning of passerines at a trap and skeet range

Our objective was to determine if ground foraging passerines in a woodland surrounding a trap and skeet range were subject to lead poisoning. Lead availability to birds was determined by shot counts and soil and earthworm analysis. Avian exposure to lead was identified by measuring free-erythrocyte protoporphyrin levels in blood and lead in tissues of three passerine species. Results showed that most shot were found in the top 3 cm of soil. Lead measurements ranged from 110 to 27,000 ppm (dry wt) in soil and were 660 and 840 ppm in earthworms. Sparrows held in an aviary at the range (p = 0.02) and free-flying juncos (p = 0.0005) mistnetted at the range displayed significantly higher protoporphyrin levels than those at an uncontaminated site. Sparrow and cowbird carcasses from the aviary carried 37 and 39 ppm lead (dry wt), respectively, whereas a junco liver contained 9.3 ppm lead.

Environmental Pollution↗

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↗

Approaches for assessment of terrestrial vertebrate responses to contaminants: moving beyond individual organisms

Conclusions: A need for a broader range ofinformation on effects of contaminants on individuals exists among the 4 classes of terrestrial vertebrates, especially mammals, reptiles, and amphibians. Separation of contaminant effects from other effects and reduction of speculative extrapolation within and among species requires information that can be produced only by combined field and laboratory investigations that incorporate seasonal or annual cycles and important spatial and interaction conditions. Assessments of contaminant effects at the population level and higher are frequently dependent on extrapolations from a lower organizational level. Actual measurements of the effects of contaminants on populations or communities, possibly in conjunction with case studies that establish relations between effects on individuals and effects on populations, are needed to reduce the uncertainty associated with these extrapolations. Associated with these assessment levels is the need for acceptable definitions of what we mean when we refer to a 'meaningful population change' or an 'effect on communities or ecosystems.' At these higher levels of organization we are also confronted with the need for procedures useful for separating contaminant effects from effects caused by other environmental conditions. Although the bulk of literature surveyed was of the focused cause-and-effect type that is necessary for proving relations between contaminants and wildlife, community or ecosystem field assessments, as sometimes performed with reptiles and amphibians, might be a useful alternative for estimating the potential of a contaminant to cause environmental harm. Assumptions about the special usefulness of reptiles and amphibians as environmental indicators ought to be tested with comparisons to mammals and birds. Information on the effects of contaminants above the individual level is needed to generate accurate estimates of the potential consequences of anthropogenic pollution (e.g., ecological risk assessments). However, realized population, or higher, levels of effects should not be part of regulatory guidelines because the threshold of harm would be too high to be used as a catalyst for action. Measures of realized population or community effects could be used to evaluate the effectiveness of regulatory actions and assess chronic or difficult environmental problems. Some of these information needs can be satisfied with modest effort and expense, but much of the suggested work that incorporates great complexity or long duration is likely to be difficult to accomplish. Cooperation among investigators with different specialties and a willingness by government, academia, and corporate organizations to support the most challenging work will be necessary. Because we are unlikely to have the financial resources to evaluate more than a small number of contaminants for effects at the levels of population, community, or ecosystem, we might need to thoroughly study a few contaminants and then extend the findings to functionally similar contaminants. If sufficient cooperation and organizational support does not materialize, the pursuit of estimation methods will overshadow the collection of actual information on relations between contaminants and wildlife.

Book chapter↗

Toxicity of lead-contaminated sediment to mallards

Because consumption of lead-contaminated sediment has been suspected as the cause of waterfowl mortality in the Coeur d?Alene River basin in Idaho, we studied the bioavailability and toxicity of this sediment to mallards (Anas platyrhynchos). In experiment 1, one of 10 adult male mallards died when fed a pelleted commercial duck diet that contained 24% lead-contaminated sediment (with 3,400 μg/g lead in the sediment). Protoporphyrin levels in the blood increased as the percentage of lead-contaminated sediment in the diet increased. Birds fed 24% lead-contaminated sediment exhibited atrophy of the breast muscles, green staining of the feathers around the vent, viscous bile, green staining of the gizzard lining, and renal tubular intranuclear inclusion bodies. Mallards fed 24% lead-contaminated sediment had means of 6.1 μg/g of lead in the blood and 28 μg/g in the liver (wet-weight basis) and 1,660 μg/g in the feces (dry-weight basis). In experiment 2, we raised the dietary concentration of the lead-contaminated sediment to 48%, but only about 20% sediment was actually ingested due to food washing by the birds. Protoporphyrin levels were elevated in the lead-exposed birds, and all of the mallards fed 48% lead-contaminated sediment had renal tubular intranuclear inclusion bodies. The concentrations of lead in the liver were 9.1 μg/g for mallards fed 24% lead-contaminated sediment and 16 μg/g for mallards fed 48% lead-contaminated sediment. In experiment 3, four of five mallards died when fed a ground corn diet containing 24% lead-contaminated sediment (with 4,000 μg/g lead in this sample of sediment), but none died when the 24% lead-contaminated sediment was mixed into a nutritionally balanced commercial duck diet; estimated actual ingestion rates for sediment were 14% and 17% for the corn and commercial diets. Lead exposure caused elevations in protoporphyrin, and four of the five mallards fed 24% lead-contaminated sediment in a commercial diet and all five fed the contaminated sediment in a corn diet had renal intranuclear inclusion bodies. Lead was higher in the livers of mallards fed 24% lead-contaminated sediment in the corn diet (38 μg/g) than in the commercial diet (13 μg/g).

Idaho↗

Methylmercury chloride and selenomethionine interactions on health and reproduction in mallards

Adult mallards ( Anas platyrhynchos ) were fed a control diet or diets containing 10 ppm mercury as methylmercury chloride, 10 ppm selenium as seleno- DL -methionine, or 10 ppm mercury plus 10 ppm selenium. One of 12 adult males fed 10 ppm mercury died, and eight others suffered paralysis of the legs by the time the study was terminated. However, when the diet contained 10 ppm selenium in addition to the 10 ppm mercury, none of 12 males became sick. In contrast to the protective effect of selenium against mercury poisoning in males, selenium plus mercury was worse than selenium or mercury alone for some measurements of reproductive success. Both selenium and mercury lowered duckling production through reductions in hatching success and survival of ducklings, but the combination of mercury plus selenium was worse than either mercury or selenium alone. Controls produced an average of 7.6 young per female, females fed 10 ppm selenium produced an average of 2.8 young, females fed 10 ppm mercury produced 1.1 young, and females fed both mercury and selenium produced 0.2 young. Teratogenic effects also were worse for the combined mercury plus selenium treatment; deformities were recorded in 6.1% of the embryos of controls, 16.4% for those fed methylmercury chloride, 36.2% for those fed selenomethionine, and 73.4% for those fed methylmercury chloride and selenomethionine. The presence of methylmercury in the diet greatly enhanced the storage of selenium in tissues. The livers of males fed 10 ppm selenium contained a mean of 9.6 ppm selenium, whereas the livers of males fed 10 ppm selenium plus 10 ppm mercury contained a mean of 114 ppm selenium. However, selenium did not enhance the storage of mercury. The results show that mercury and selenium may be antagonistic to each other for adults and synergistic to young, even within the same experiment.

Environmental Toxicology and Chemistry↗

Effects of mercury and selenium on glutathione metabolism and oxidative stress in mallard ducks

Earlier studies have reported on the toxicity and related oxidative stress of different forms of Se, including seleno- D ,L-methionine, in mallards ( Anas platyrhynchos ). This study compares the effects of Se (seleno- D ,L-methionine) and Hg (methylmercury chloride) separately and in combination. Mallard drakes received one of the following diets: untreated feed (controls), or feed containing 10 ppm Se, 10 ppm Hg, or 10 ppm Se in combination with 10 ppm Hg. After 10 weeks, blood, liver, and brain samples were collected for biochemical assays. The following clinical and biochemical alterations occurred in response to Hg exposure: hematocrit and hemoglobin concentrations decreased; activities of the enzymes glutathione (GSH) peroxidase (plasma and liver), glutathione- S -transferase (liver), and glucose-6-phosphate dehydrogenase (G-6-PDH) (liver and brain) decreased; hepatic oxidized glutathione (GSSG) concentration increased relative to reduced glutathione (GSH); and lipid peroxidation in the brain was detected by increased thiobarbituric reactive substances (TBARS). Effects of Se alone included increased hepatic GSSG reductase activity and brain TBARS concentration. Selenium in combination with Hg partially or totally alleviated effects of Hg on GSH peroxidase, G-6-PDH, and GSSG. These findings are compared in relation to field observations for diving ducks and other aquatic birds. It is concluded that since both Hg and excess Se can affect thiol status, measurement of associated enzymes in conjunction with thiol status may be a useful bioindicator to discriminate between Hg and Se effects. The ability of Se to restore the activities of G-6-PDH, GSH peroxidase, and glutathione status involved in antioxidative defense mechanisms may be crucial to biological protection from the toxic effects of methylmercury.

Environmental Toxicology and Chemistry↗

Contaminant effects on Great Lakes' fish-eating birds: a population perspective

Preventing environmental contaminants from reducing wildlife populations is the greatest concern in wildlife toxicology. In the Great Lakes, environmental contaminants have a history of reducing populations of many species of fish-eating birds. Endocrine effects may have contributed to declines in fish-eating bird populations, but the overriding harm was caused by DDE-induced eggshell thinning. Toxic effects may still be occurring today, but apparently they are not of a sufficient magnitude to depress populations of most fish-eating birds. Once DDE levels in the Great Lakes declined, eggshells of birds began to get thicker and reproductive success improved. Populations of double-crested cormorants (Phalacrocorax auritus) and ring-billed gulls (Larus delawarensis) have increased dramatically since the bans on DDT and other organochlorine pesticides. Bald eagles (Haliaeetus leucocephalus) are still not reproducing at a normal rate along the shores of the Great Lakes, but success is much improved compared to earlier records when eggshell thinning was worse. Other species, such as herring gulls (Larus argentatus) and black-crowned night-herons (Nycticorax nycticorax), seem to be having improved reproductive success, but data on Great Lakes'-wide population changes are incomplete. Reproductive success of common terns (Sterna hirundo), Caspian terns (Sterna caspia), and Forster's terns (Sterna forsteri) seems to have improved in recent years, but, again, data on population changes are not very complete, and these birds face many habitat related problems as well as contaminant problems. Although contaminants are still producing toxic effects, and these effects may include endocrine disfunction, fish-eating birds in the Great Lakes seem to be largely weathering these effects, at least as far as populations are concerned. A lack of obvious contaminant effects on populations of fish-eating birds in the Great Lakes, however, should not be equated with a lack of any harm to these birds or with a conclusion that certain contaminants do not need additional control.

Book chapter↗

Effects of boron and selenium on mallard reproduction and duckling growth and survival

Boron (B) and selenium (Se) sometimes occur together in high concentrations in the environment and can accumulate in plants and invertebrates consumed by waterfowl. One hundred twenty-six pairs of breeding mallards (Anas platyrhynchos) were fed diets supplemented with B (as boric acid) at 0, 450, or 900 ppm, in combination with Se (as seleno-DL-methionine) at 0, 3.5, or 7 ppm, in a replicated factorial experiment. Ducklings produced received the same treatment combination as their parents. Boron and Se accumulated in adult liver, egg, and duckling liver. In adults, B and Se caused weight loss, and B decreased hemoglobin concentration, egg weight, and egg fertility. Both B and Se reduced hatching success and duckling weight, and B reduced duckling growth and duckling production, and caused several alterations in duckling liver biochemistry. Duckling survival was not reduced by B or Se, and neither B nor Se had histopathologic effects on adult or duckling liver, kidney, or spleen. There was little evidence of interaction between B and Se. This study demonstrated that B and Se, in the chemical forms and at the dietary levels administered in this study, can adversely affect mallard reproduction and duckling growth.

Environmental Toxicology and Chemistry↗

Toxicity and oxidative stress of different forms of organic selenium and dietary protein in mallard ducklings

Concentrations of over 100 ppm (mg/kg) selenium (Se) have been found in aquatic plants and insects associated with irrigation drainwater and toxicity to fish and wildlife. Composition of diet for wild ducklings can vary in selenium-contaminated environments. Earlier studies have compared toxicities and oxidative stress of Se as selenite to those of seleno-DL-methionine (DL) in mallards ( Anas platyrhynchos ). This study compares DL, seleno-L-methionine (L), selenized yeast (Y) and selenized wheat (W). Day-old mallard ducklings received an untreated diet (controls) containing 75% wheat (22% protein) or the same diet containing 15 or 30 ppm Se in the above forms except for 30 ppm Se as W. After 2 weeks, blood and liver samples were collected for biochemical assays and Se analysis. All forms of selenium caused significant increases in plasma and hepatic glutathione peroxidase activities. Se as L at 30 ppm in the diet was the most toxic form, resulting in high mortality (64%) and impaired growth (>50%) in survivors and the greatest increase in ratio of oxidized to reduced hepatic glutathione (GSH). Se as both L and DL decreased the concentrations of hepatic GSH and total thiols. Se as Y accumulated the least in liver (approximately 50% of other forms) and had less effect on GSH and total thiols. In a second experiment, in which the basal diet was a commercial duck feed (22% protein), survival was not affected by 30 ppm Se as DL, L, or Y and oxidative effects on GSH metabolism were less pronounced than with the wheat diet.

Archives of Environmental Contamination and Toxico↗

Toxicity of seleno-l-methionine, seleno-dl-methionine, high selenium wheat, and selenized yeast to mallard ducklings

The toxicity of four chemical forms of selenium (seleno-L-methionine, seleno-DL-methionine, selenized yeast, and high selenium wheat) was compared in day-old mallard ducklings ( Anas platyrhynchos ). In the first experiment, in which the basal diet was 75% wheat, survival after 2 weeks was lower for ducklings fed 30 μg/g selenium as seleno-L-methionine (36%) than for ducklings fed 30 μg/g selenium as seleno-DL-methionine (100%) or 30 μg/g selenium from high selenium yeast (88%). The concentration of selenium at 2 weeks in the livers of survivors was similar for ducklings fed 15 μg/g selenium as seleno-DL-methionine (12 μg/g, wet weight), seleno-L-methionine (11 μg/g), and high selenium wheat (11 μg/g), but was lower when the selenium came from selenized yeast (6.2 μg/g). When fed 30 μg/g selenium from the various sources, the selenium concentrations in liver were 20 μg/g for seleno-DL-methionine, 19 μg/g for seleno-L-methionine, and 9.9 μg/g for selenized yeast. In a second experiment, in which the basal diet was a commercial duck feed, survival after 2 weeks was 100% in ducklings fed 30 μg/g selenium as seleno-DL-methionine, seleno-L-methionine, or selenized yeast. Selenium concentrations in liver were similar for ducklings fed the 30-μg/g selenium diets as the DL or L forms of selenomethionine (27 and 25 μg/g), but lower for ducklings fed selenized yeast (13 μg/g). The greater toxicity of the L form of selenomethionine was probably related to the palatability or nutritional nature of the wheat-based diet used in experiment 1, but the exact reason for the difference between the DL and L forms is unknown. Biologically incorporated selenium, derived from high selenium wheat, was no more toxic than selenium derived from the two purified forms of selenomethionine, and the selenium in selenized yeast was not as toxic as that in the two forms of selenomethionine.

Archives of Environmental Contamination and Toxico↗

Comparison of the effects of seleno-Lmethionine, seleno-DL-methionine, and selenized yeast on reproduction of mallards

The toxicities of seleno- l -methionine, seleno- dl -methionine, and selenized yeast were compared. Ten pairs of mallards were fed a control diet and 15 pairs were fed diets containing 10 ppm selenium as seleno- dl -methionine, seleno- l -methionine, or selenized yeast. Hatching of fertile eggs was significantly lower for females fed 10 ppm selenium as seleno- dl -methionine (7.6%) and seleno- l -methionine (6.4%) than for controls (41.3%). Survival of ducklings was lower when their parents had been fed 10 ppm selenium as seleno- l -methionine (20.0%) than for controls (98.4%). The number of 6-day-old ducklings produced per female was significantly lower for mallards fed 10 ppm selenium as seleno- dl -methionine (0.47) or selenized yeast (2.67) than for controls (6.10), and was significantly lower for mallards fed seleno- l -methionine (0.13) than for mallards fed selenized yeast. The eighth eggs of females fed the dl or l forms of selenomethionine contained means of 9.2 and 8.9 ppm selenium, wet weight; these means were higher than the mean (6.6 ppm) for females fed selenized yeast. Among embryos that died at 7 days of age or older, the percentage of embryos that were deformed was 1.3% for controls, 24.6% for seleno- dl -methionine, 28.2% for seleno- l -methionine, and 11.0% for selenized yeast. The results suggested that seleno- dl -methionine and seleno- l -methionine were of similar toxicity and were both more toxic than selenium from selenized yeast.

Arkansas↗

Mercury poisoning in wildlife

Mercury is an intriguing contaminant because it has complex chemical properties, a wide range of harmful effects, and an infinite persistence in the environment. Die-offs of wildlife due to mercury have occurred in many countries, especially before mercury seed dressings were banned. Today, most mercury problems are associated with aquatic environments. Methylmercury, the most toxic chemical form, attacks many organ systems, but damage to the central nervous system is most severe. Harmful wet-weight concentrations of mercury, as methylmercury, in the tissues of adult birds and mammals range from about 8-30 ppm in the brain, 20-60 ppm in liver, 20-60 ppm in kidney, and 15-30 ppm in muscle. Young animals may be more sensitive.

Book chapter↗

Foreword

Explore the source record for details and available documents.

Book chapter↗

Selenium in birds

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Book chapter↗

Declines in organochlorines in eggs of red-breasted mergansers from Lake Michigan, 1977-78 versus 1990

From 1977–1978 to 1990, concentrations of polychlorinated biphenyls (PCBs) and most organochlorine pesticides declined in eggs of red-breasted mergansers ( Mergus serrator ) nesting on islands in northwestern Lake Michigan. Total PCBs decreased 60% (from 21 ppm in 1977–1978 to 8.5 ppm in 1990) and p,p ′-DDE decreased 66% (from 6.5 to 2.2 ppm). Dieldrin decreased only 16% (from 0.82 to 0.69 ppm). In 1990, 79.1% of incubated eggs hatched, which was not significantly different from the 83.5% that hatched in 1977–1978.

Environmental Monitoring and Assessment↗

Re-exposure of mallards to selenium after chronic exposure

Adult male mallards ( Anas platyrhynchos ) were fed a control diet or a diet containing 15 ppm selenium as seleno-D,L-methionine for 21 weeks. After this initial exposure, the mallards were fed untreated food for 12 weeks, then were re-exposed to selenium at 100 ppm for five weeks. During re-exposure to 100 ppm selenium, the birds that had previously been exposed to 15 ppm selenium and those that had not previously been exposed did not differ in percentage of mortality (14.7 and 14.3%), weight loss in survivors (39.3 and 41.2%), selenium concentrations in the livers of survivors (35 and 53 ppm, wet weight), or selenium concentrations in the livers of birds that died (35 and 40 ppm, respectively). When the data from the birds that had previously been exposed to 15 ppm selenium were combined with the data from the birds that had not previously been exposed, selenium concentrations in the livers of birds that had died on the 100-ppm selenium treatment (38 ppm) did not differ from the concentrations in the livers of birds that had survived (43 ppm).

Environmental Toxicology and Chemistry↗