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Gary Heinz

Publications and source records attributed to Gary Heinz.

14 recordsLinked to original sources

Synthesis of maternal transfer of mercury in birds: Implications for altered toxicity risk

Maternal transfer is the predominant route of methylmercury (MeHg) exposure to offspring. We reviewed and synthesized published and unpublished data on maternal transfer of MeHg in birds. Using paired samples of females’ blood (n=564) and their eggs (n=1814) from 26 bird species in 6 taxonomic orders, we conducted a meta-analysis to evaluate whether maternal transfer of MeHg to eggs differed among species and caused differential toxicity risk to embryos. Total mercury (THg) concentrations in eggs increased with maternal blood THg concentrations; however, the proportion of THg transferred from females to their eggs differed among bird taxa and with maternal THg exposure. Specifically, a smaller proportion of maternal THg was transferred to eggs with increasing female THg concentrations. Additionally, the proportion of THg that was transferred to eggs at the same maternal blood THg concentration differed among taxonomic orders, with waterfowl (Anseriformes) transferring up to 382% more THg into their eggs than songbirds (Passeriformes). We provide equations to predict THg concentrations in eggs using female blood THg concentrations, and vice versa, which may help translate toxicity benchmarks across tissues and life stages. Our results indicate that toxicity risk of MeHg can vary among bird taxa due to differences in the maternal transfer of MeHg to offspring.

Environmental Science & Technology

A downstream voyage with mercury

Retrospective essay for the Bulletin of Environmental Contamination and Toxicology. As I look back on my paper, “Effects of Low Dietary Levels of Methyl Mercury on Mallard Reproduction,” published in 1974 in the Bulletin of Environmental Contamination and Toxicology, a thought sticks in my mind. I realize just how much my mercury research was not unlike a leaf in a stream, carried this way and that, sometimes stalled in an eddy, restarted, and carried downstream at a pace and path that was not completely under my control. I was hired in 1969 by the Patuxent Wildlife Research Center to study the effects of environmental pollutants on the behavior of wildlife. A colleague was conducting a study on the reproductive effects of methylmercury on mallards ( Anas platyrhynchos ), and he offered to give me some of the ducklings. I conducted a pilot study, testing how readily ducklings approached a tape-recorded maternal call. Sample sizes were small, but the results suggested that ducklings from mercury-treated parents behaved differently than controls. That’s how I got into mercury research—pretty much by chance.

Bulletin of Environmental Contamination and Toxico

Mercury in birds of San Francisco Bay-Delta, California: trophic pathways, bioaccumulation, and ecotoxicological risk to avian reproduction

San Francisco Bay Estuary in northern California has a legacy of mercury contamination, which could reduce the health and reproductive success of waterbirds in the estuary. The goal of this study was to use an integrated field and laboratory approach to evaluate the risks of mercury exposure to birds in the estuary. We examined mercury bioaccumulation, and other contaminants of concern, in five waterbird species that depend heavily on San Francisco Bay Estuary for foraging and breeding habitat: American avocets ( Recurvirostra americana ), black-necked stilts ( Himantopus mexicanus ), Forster’s terns ( Sterna forsteri ), Caspian terns ( Hydroprogne caspia ), and surf scoters ( Melanitta perspicillata ). These species have different foraging habitats and diets that represent three distinct foraging guilds within the estuary’s food web. In this report, we provide an integrated synthesis of the primary findings from this study and results are synthesized from 54 peer-reviewed publications generated to date with other unpublished results.

California

Ecotoxicology of mercury in fish and wildlife: Recent advances

A number of recent studies have documented subtle, yet potentially important effects of mercury on behavior, neurochemistry, and endocrine function in fish and wildlife at currently realistic levels of environmental exposure. Current levels of environmental methylmercury exposure are sufficient to cause significant biological impairment, both in individuals and in whole populations, in some ecosystems. Future toxicological studies on fish and wildlife will focus on linking biomarkers of methylmercury exposure and associated oxidative stress to effects on reproduction and population change; determining the genetic basis for mercury-related neurotoxic and other biological changes; determining the genetic basis for species differences in sensitivity to methylmercury; and linking toxic effects of methylmercury in individual animals to population-level changes.

Book chapter

Teratogenic efects of injected methylmercury on avian embryos

Controlled laboratory studies with game farm mallards ( Anas platyrhynchos ) and chickens ( Gallus gallus ) have demonstrated that methylmercury can cause teratogenic effects in birds, but studies with wild species of birds are lacking. To address this need, doses of methylmercury chloride were injected into the eggs of 25 species of birds, and the dead embryos and hatched chicks were examined for external deformities. When data for controls were summed across all 25 species tested and across all types of deformities, 24 individuals out of a total of 1,533 (a rate of 1.57%) exhibited at least one deformity. In contrast, when data for all of the mercury treatments and all 25 species were summed, 188 deformed individuals out of a total of 2,292 (8.20%) were found. Some deformities, such as lordosis and scoliosis (twisting of the spine), misshapen heads, shortening or twisting of the neck, and deformities of the wings, were seldom observed in controls but occurred in much greater frequency in Hg-treated individuals. Only 0.59% of individual control dead embryos and hatchlings exhibited multiple deformities versus 3.18% for Hg-dosed dead embryos and hatchlings. Methylmercury seems to have a widespread teratogenic potential across many species of birds.

Environmental Toxicology and Chemistry

Relating the ability of mallards to ingest high levels of sediment to potential contaminant exposure in waterfowl

When waterfowl feed from the bottom of bodies of water, they sometimes ingest sediments along with their food, and this sediment can be a major source of contaminants. Learning how much sediment waterfowl can consume in their diet and still maintain their health would be helpful in assessing potential threats from contaminants in sediment. In a controlled laboratory study the maximum tolerated percentage of sediment in the diet of mallards ( Anas platyrhynchos ) was measured. When fed a well‐balanced commercial avian diet, 50, 60, or 70% sediment in the diet on a dry‐weight basis did not cause weight loss over a two‐week period. Ducks fed this same commercial diet, but containing 80 or 90% sediment, lost 8.6 and 15.6% of their body weight, respectively, in the first week on those diets. After factoring in the ability of the mallards to sieve out some of the sediment from their diet before swallowing it, we concluded that the mallards could maintain their health even when approximately half of what they swallowed, on a dry‐weight basis, was sediment.

Environmental Toxicology and Chemistry

Reproduction in mallards exposed to dietary concentrations of methylmercury

The purpose of this experiment was to use mallards ( Anas platyrhynchos ) tested under controlled conditions to determine how much harm to reproduction resulted from various concentrations of mercury in eggs. Breeding pairs of mallards were fed a control diet or diets containing 1, 2, 4, or 8 μg/g mercury, as methylmercury chloride. Mean concentrations of mercury in eggs laid by parents fed 0, 1, 2, 4, or 8 μg/g mercury were 0.0, 1.6, 3.7, 5.9, and 14 μg/g mercury on a wet-weight basis. There were no signs of mercury poisoning in the adults, and fertility and hatching success of eggs were not affected by mercury. Survival of ducklings and the number of ducklings produced per female were reduced by the 4 and 8-μg/g dietary mercury treatments (that resulted in 5.9 and 14 μg/g mercury in their eggs, respectively). Ducklings from parents fed the various mercury diets were just as heavy as controls at hatching, but by 6 days of age ducklings whose parents had been fed 4 or 8 μg/g mercury weighed less than controls. Because we do not know if absorption of mercury from our diets would be the same as absorption from natural foods, the mercury concentrations we report in eggs may be more useful in extrapolating to possible harmful effects in nature than are the dietary levels we fed. We conclude that mallard reproduction does not appear to be particularly sensitive to methylmercury.

Ecotoxicology

Intraperitoneal injections as a possible means of generating varied levels of methylmercury in the eggs of birds in field studies

The ideal study of the effects of methylmercury on the reproductive success of a species of bird would be one in which eggs contained mercury concentrations ranging from controls to very heavily contaminated, all at the same site. Such a study cannot be realized at a mercury contaminated area or under laboratory conditions, but could be achieved by introducing methylmercury into breeding females and allowing them to deposit mercury in their eggs. Female mallards (Anas platyrhynchos) were intraperitoneally injected with solutions of methylmercury chloride dissolved in corn oil, propylene glycol, dimethyl sulfoxide, mineral oil, Olestra, Crisco, lard, hard paraffin, and a combination of hard and soft paraffin. In some cases, egg laying was delayed, either due to the solvent itself (in the case of Olestra, Crisco, and lard) or to the highest concentration of methylmercury chloride (500 &mu;g/g) in some of the solvents. Mercury in eggs ranged from a control level (< 0.1 &mu;g/g) to approximately 14 &mu;g/g on a wet weight basis, which more than covers the range of concentrations reported in wild bird eggs. Mercury concentrations in a series of eggs from the same female declined mostly due to excretion of mercury in prior eggs and not because of the length of time since the injection. Intraperitoneal injections hold promise in field studies where one would like to study the reproductive effects of a wide range of methylmercury levels in the eggs of a wild bird and under the natural conditions that exist in the field.

Environmental Toxicology and Chemistry

A nonlethal microsampling technique to monitor the effects of mercury on wild bird eggs

Methylmercury is the predominant chemical form of mercury reported in the eggs of wild birds, and the embryo is the most sensitive life stage to methylmercury toxicity. Protective guidelines have been based mainly on captive-breeding studies with chickens (Gallus gallus), mallards (Anas platyrhynchos), and ring-necked pheasants (Phasianus colchicus) or on field studies where whole eggs were collected and analyzed and the effects of the mercury were measured based on the reproductive success of the remaining eggs. However, both of these methods have limitations. As an alternative, we developed a technique that involves extracting a small sample of albumen from a live egg, sealing the egg, returning the egg to its nest to be naturally incubated by the parents, and then relating the hatching success of this microsampled egg to its mercury concentration. After first developing this technique in the laboratory using chicken and mallard eggs, we selected the laughing gull (Larus atricilla) and black-necked stilt (Himantopus mexicanus) as test subjects in the field. We found that 92% of the microsampled laughing gull eggs met our reproductive endpoint of survival to the beginning of hatching compared to 100% for the paired control eggs within the same nests. Microsampled black-necked stilt eggs exhibited 100% hatching success compared to 93% for the paired control eggs. Our results indicate that microsampling is an effective tool for nonlethally sampling mercury concentrations in eggs and, as such, can be used for monitoring sensitive species, as well as for improving studies that examine the effects of mercury on avian reproduction.

Environmental Toxicology and Chemistry

Overwinter survival of mallards fed selenium

Adult male mallards ( Anas platyrhynchos ) were fed diets supplemented with 0, 10, 20, 40, or 80 μg/g selenium in the form of selenomethionine. Mortality in each of these treatments was 0, 0, 25, 95, and 100%, respectively, during a 16-week exposure that started in November. After one week of treatment, body weights were significantly depressed by the 20, 40, and 80-μg/g selenium treatments, but not by 10 μg/g selenium. Four weeks after being returned to an untreated diet, the body weight of birds fed 20 μg/g selenium had increased to the point of being statistically inseparable from the weight of controls. Signs of selenium poisoning in the dead included severe emaciation, mottling of the liver, empty gizzard, and the presence of a yellowish fluid around some organs. Concentrations of selenium in blood were related to dietary treatments, but mortality was not clearly related to a threshold concentration of selenium in blood.

Archives of Environmental Contamination and Toxico

Selenium accumulation and elimination in mallards

Selenium accumulation and loss were measured in adult mallards ( Anas platyrhynchos ) fed selenomethionine during two experiments. In Experiment 1, both sexes were fed a diet containing 10 ppm selenium for 6 weeks, followed by 6 weeks on untreated feed. Selenium accumulation in liver and muscle of females was described by C=A(1−e −bt ). Concentrations of selenium were predicted to reach 95% of equilibrium faster in liver (7.8 days) than in muscle (81 days). The loss of selenium from liver and muscle of females was described by the exponential loss rate equation: C=Ae −bt , with half-times of 18.7 and 30.1 days, respectively. Males reached similar levels of selenium in liver and breast muscle as females and declined to similar levels once selenium treatment ended. In Experiment 2, females were fed increasing levels of selenium until some died. Survivors were switched to an untreated diet and selenium was measured in blood, liver, and breast muscle over 64 days. The same equation as in Experiment 1, C=Ae −bt , was used to describe the loss of selenium from blood and muscle. Halftimes were 9.8 and 23.9 days, respectively. For liver, the equation C C = A 1 e &#x2212; b 1 t + A 2 e &#x2212; b 2 t "> = A 1 e −b 1 t + A 2 e −b 2 t was used. Selenium initially decreased in liver by one-half in 3.3 days, with subsequent half-times of 3.9, 6.0, and 45.1 days.

Archives of Environmental Contamination and Toxico

Toxicity of organic and inorganic selenium to mallard ducklings

The toxicity of selenomethionine and sodium selenite to mallard ducklings ( Anas platyrhynchos ) was measured by feeding each form from hatching to six weeks of age at dietary concentrations of 0, 10, 20, 40, and 80 ppm selenium. At 80 ppm selenium, sodium selenite caused 97.5% mortality by six weeks and selenomethionine caused 100% mortality. At 40 ppm, these two forms of selenium caused 25 and 12.5% mortality. No mortality occurred at 10 or 20 ppm. Diets containing 20, 40, or 80 ppm selenium in both forms caused decreases in food consumption and growth. The only statistically significant effect of 10 ppm selenium was with sodium selenite, which resulted in larger livers than controls. Selenomethionine was more readily stored in the liver than sodium selenite at levels above 10 ppm selenium in the diet. Based on comparisons of residues of selenium in livers of surviving and dead ducklings, concentrations in the liver were not diagnostic of death due to selenium poisoning. Because both forms of selenium resulted in severe reductions in food consumption, selenium-induced starvation may have been related to duckling mortality. It was not clear whether either form of selenium at 10 ppm in the diet resulted in a leveling off of selenium concentrations in the liver within six weeks.

Archives of Environmental Contamination and Toxico

High PCB residues in birds from the Sheboygan River, Wisconsin

Organochlorine residues were measured in the carcasses and, in some cases, brains and stomach contents of four species of birds collected along the Sheboygan River, Wisconsin during the years 1976 to 1980. Polychlorinated biphenyls (PCBs) were high in all samples and were the contaminants of greatest concern. Carcass residues ranged from 23 to 218 ppm PCBs on a wet weight basis; these are levels associated with reproductive impairment in laboratory studies with some birds. Food items in the stomachs of collected birds contained from 12 to 58 ppm PCBs, indicating a heavy contamination of food sources. The brain of one bird contained 220 ppm PCBs, a level that is not in the lethal range but is very high. Birds feeding in the contaminated portions of the Sheboygan River may have been harmed by high PCB levels.

Wisconsin

Effects of dietary ABATE® on reproductive success, duckling survival, behavior, and clinical pathology in game-farm mallards

Forty-four pairs of game-farm mallards ( Anas platyrhynchos ) were fed ABATE ® 4E (temephos) to yield 0, 1, or 10 ppm ABATE ® beginning before the initiation of lay, and terminating when ducklings were 21 days of age. The mean interval between eggs laid was greater for hens fed 10 ppm ABATE ® than for controls. Clutch size, fertility, hatchability, nest attentiveness of incubating hens, and avoidance behavior of ducklings were not significantly affected by ABATE ® ingestion. The percentage survival of ducklings to 21 days of age was significantly lower in both treated groups than in controls, but brain acetylcholinesterase (AChE) activity was not inhibited in young which died before termination of the study. In 21-day-old ducklings, aspartate aminotransferase (AST) activity increased and plasma nonspecific cholinesterase (ChE) activity was inhibited by about 20% in both treatment groups, but there were no significant differences in brain AChE or plasma alanine aminotransferase (ALT) activities, or plasma uric acid concentration. Clinical chemistry values of adults were not affected. No ABATE ® , ABATE ® sulfoxide, or ABATE ® sulfone residues were found in eggs or tissue samples.

Archives of Environmental Contamination and Toxico