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Archives of Environmental Contamination and Toxicology | 1993

Environmental contaminants in bald eagle eggs—1980–84—and further interpretations of relationships to productivity and shell thickness

Stanley N. Wiemeyer; Christine M. Bunck; Charles J. Stafford

Bald eagle (Haliaeetus leucocephalus) eggs were collected in 15 States in the United States in 1980–1984 and analyzed for organochlorine pesticides, polychlorinated biphenyls (PCBs), and mercury. Data were compared and combined with data from earlier studies to examine trends and refine relationships of contaminants to shell thickness and young production. Moderate shell thinning occurred in eggs from several States. The frequency of occurrence of detectable residues of several contaminants declined during 1969–84. DDE concentrations declined significantly in Wisconsin, Maine, and the Chesapeake Bay region. Some other contaminant residues declined, but usually not significantly. During 1980–84, DDE, PCB, and mercury concentrations were highest in eggs from Maine, whereas most contaminant concentrations were lowest in eggs from Arizona. DDE was most closely related to shell thickness and young production at sampled breeding areas. Fifteen percent shell thinning was associated with 16 μg/g DDE (wet weight) for eggs collected early in incubation. Young production was normal when eggs at sampled breeding areas contained < 3.6 μg/g DDE (wet weight), was nearly halved between 3.6 to 6.3 μg/g, and halved again when concentrations exceeded 6.3 μg/g. Several other contaminants were also associated with poor reproduction and eggshell thinning; however, their impact appeared to be secondary to that of DDE and was probably related to their high correlation with DDE. Data relating contaminant concentrations to mean 5-year production are applicable only to breeding areas where eggs are collected after failure to hatch, because such breeding areas are not representative of all nesting bald eagles in a given population.


Archives of Environmental Contamination and Toxicology | 1988

Organochlorine pesticides, polychlorinated biphenyls, and mercury in osprey eggs — 1970–79 — and their relationships to shell thinning and productivity

Stanley N. Wiemeyer; Christine M. Bunck; Alexander J. Krynitsky

Osprey (Pandion haliaetus) eggs were collected in 14 states in 1970–79 and analyzed for organochlorine pesticides, polychlorinated biphenyls (PCBs), and mercury. Moderate shell thinning occurred in eggs from several areas. DDE was detected in all eggs, PCBs in 99%, DDD in 96%, dieldrin in 52%, and other compounds less frequently. Concentrations of DDT and its metabolites declined in eggs from Cape May County, New Jersey between 1970–72 and 1978–79. Eggs from New Jersey in the early 1970s contained the highest concentrations of DDE. Dieldrin concentrations declined in eggs from the Potomac River, Maryland during 1971–77. Five different contaminants were significantly negatively correlated with shell thickness; DDE was most closely correlated. Ten percent shell thinning was associated with 2.0 ppm DDE, 15% with 4.2 ppm, and 20% with 8.7 ppm in eggs collected from randomly selected nests before egg loss. Shell thickness could not be accurately predicted from DDE concentrations in eggs collected after failure to hatch, presumably because the eggs with the thinnest shells had been broken and were unavailable for sampling. DDE was also significantly negatively correlated with brood size. Other contaminants did not appear to adversely affect shell thickness or reproductive success.


Journal of Wildlife Diseases | 1981

EFFECTS OF LEAD SHOT INGESTION ON δ-AMINOLEVULINIC ACID DEHYDRATASE ACTIVITY, HEMOGLOBIN CONCENTRATION, AND SERUM CHEMISTRY IN BALD EAGLES

David J. Hoffman; Oliver H. Pattee; Stanley N. Wiemeyer; Bernard M. Mulhern

Lead shot ingestion by bald eagles (Haliaeetus leucocephalus) is considered to be widespread and has been implicated in the death of eagles in nature. It was recently demonstrated under experimental conditions that ingestion of as few as 10 lead shot resulted in death within 12 to 20 days. In the present study hematological responses to lead toxicity including red blood cell ALAD activity, hemoglobin concentration and 23 different blood serum chemistries were examined in five captive bald eagles that were unsuitable for rehabilitation and release. Eagles were dosed by force-feeding with 10 lead shot; they were redosed if regurgitation occurred. Red blood cell ALAD activity was inhibited by nearly 80% within 24 hours when mean blood lead concentration had increased to 0.8 parts per million (ppm). By the end of 1 week there was a significant decrease (20-25%) in hematocrit and hemoglobin, and the mean blood lead concentration was over 3 ppm. Within as little as 1-2 weeks after dosing, significant elevations in serum creatinine and serum alanine aminotransferase occurred, as well as a significant decrease in the ratio of serum aspartic aminotransferase to serum alanine aminotransferase. The mean blood lead concentration was over 5 ppm by the end of 2 weeks. These changes in serum chemistry may be indicative of kidney and liver alterations.


Reviews of Environmental Contamination and Toxicology | 2004

Cyanide Hazards to Plants and Animals from Gold Mining and Related Water Issues

Ronald Eisler; Stanley N. Wiemeyer

Cyanide extraction of gold through milling of high-grade ores and heap leaching of low-grade ores requires cycling of millions of liters of alkaline water containing high concentrations of potentially toxic sodium cyanide (NaCN), free cyanide, and metal-cyanide complexes. Some milling operations result in tailings ponds of 150 ha and larger. Heap leach operations that spray or drip cyanide onto the flattened top of the ore heap require solution processing ponds of about 1 ha in surface area. Puddles of various sizes may occur on the top of heaps, where the highest concentrations of NaCN are found. Solution recovery channels are usually constructed at the base of leach heaps, some of which may be exposed. All these cyanide-containing water bodies are hazardous to wildlife, especially migratory waterfowl and bats, if not properly managed. Accidental spills of cyanide solutions into rivers and streams have produced massive kills of fish and other aquatic biota. Freshwater fish are the most cyanide-sensitive group of aquatic organisms tested, with high mortality documented at free cyanide concentrations >20 microg/L and adverse effects on swimming and reproduction at >5 microg/L. Exclusion from cyanide solutions or reductions of cyanide concentrations to nontoxic levels are the only certain methods of protecting terrestrial vertebrate wildlife from cyanide poisoning; a variety of exclusion/cyanide reduction techniques are presented and discussed. Additional research is recommended on (1) effects of low-level, long-term, cyanide intoxication in birds and mammals by oral and inhalation routes in the vicinity of high cyanide concentrations; (2) long-term effects of low concentrations of cyanide on aquatic biota; (3) adaptive resistance to cyanide; and (4) usefulness of various biochemical indicators of cyanide poisoning. To prevent flooding in mine open pits, and to enable earth moving on a large scale, it is often necessary to withdraw groundwater and use it for irrigation, discharge it to rapid infiltration basins, or, in some cases, discharge it to surface waters. Surface waters are diverted around surface mining operations. Adverse effects of groundwater drawdown include formation of sinkholes within 5 km of groundwater drawdown; reduced stream flows with reduced quantities of wate available for irrigation, stock watering, and domestic, mining and milling, and municipal uses; reduction or loss of vegetation cover for wildlife, with reduced carrying capacity for terrestrial wildlife; loss of aquatic habitat for native fishes and their prey; and disruption of Native American cultural traditions. Surface discharge of excess mine dewatering water and other waters to main waterways may contain excess quantities of arsenic, total dissolved solids, boron, copper, fluoride, and zinc. When mining operations cease, and the water pumps are dismantled, these large open pits may slowly fill with water, forming lakes. The water quality of pit lakes may present a variety of pressing environmental problems.


Journal of Wildlife Management | 1988

Environmental contaminants in California condors

Stanley N. Wiemeyer; J.M. Scott; M.P. Anderson; P.H. Bloom; Charles J. Stafford

Five wild California condors (Gymnogyps californianus) that died in 1980-86 were necropsied and tissues were analyzed for environmental contaminants. Three died of lead (Pb) poisoning, 1 presumably of cyanide (CN) poisoning, and 1 nestling of handling shock. Organochlorine concentrations were low in 4 condors that were analyzed for these contaminants. Blood samples from 14 wild and 14 captive condors were analyzed primarily for Pb. Five of 14 wild condors sampled had elevated (>0.70 ppm) concentrations of Pb in blood whereas Pb concentrations in all captive condors were low. Lead levels in individual birds often fluctuated over time. Lead exposure, especially poisoning, was a major factor affecting the wild California condor population during 1982-86. The probable source of Pb was bullet fragments in carrion on which condors were feeding. J. WILDL. MANAGE. 52(2):238-247 The wild population of California condors has been declining for many years (Koford 1953, Wilbur 1978, Snyder and Johnson 1985). In the winter of 1984-85 it declined from 15 to 9 individuals and 4 of 5 known breeding pairs were lost. Since 1985 1 wild California condor has died and the remaining 8 were placed in captivity to enhance the captive flock. Many causes have contributed to the decline of the condor although most are poorly documented (Wilbur 1978, Ogden 1983, Harlow et al. 1984). Some causes that appear to have contributed to the decline are shooting, loss of habitat, disturbance, inadequate food supply, and environmental contaminants. The role of contaminants in the decline of California condors has only been partially assessed (Kiff et al. 1979, Wiemeyer et al. 1983, 1986b). Contaminants such as 1,1-dichloro-2,2-bis(pchlorophenyl)ethylene (DDE); strychnine; sodium monofluoroacetate (Compound 1080); and Pb have been implicated in the condor decline but little corroborative evidence has been provided. The contaminant levels in potential condor food and in the tissues of turkey vultures (Cathartes aura) and common ravens (Corvus corax) that occur within the condor range were assessed in 1980-81 (Wiemeyer et al. 1986b). Wiemeyer et al. (1986b) determined that, in some cases, Pb concentrations in bones of turkey vultures and feathers of California condors were elevated above normal background levels. Elevated levels of organochlorines were also found in turkey vultures, but not in potential condor food. These findings prompted us to sample tissues and determine causes of mortality of all dead condors, and obtain blood samples from all condors captured for telemetry studies during 198286 or for use in captive flocks. Our objective was to identify contaminants that may have been involved in the decline of the condor population. For field assistance we gratefully acknowledge L. Andaloro, D. B. Barbour, D. A. Clendenen, J. Grantham, J. A. Hamber, S. B. Kimple, D. B. Ledig, V. J. Meretsky, J. C. Ogden, L. A. Riopelle, G. D. Sanders, H. A. Snyder, N. F. R. Snyder, and J. J. Woods of the Condor Research Center and veterinarians B. Gonzales of the Los Angeles Zoo; J. L. Allen, D. L. Janssen, and J. E. Oosterhuis of the San Diego Wild Animal Park; P. K. Ensley of the San Diego Zoo; and P. A. Gullett of the National Wildlife Health Center. N. J. Thomas provided analytical methods used at the National Wildlife Health Center. We thank S. H. Fritts, R. M. Jurek, H. R. Perry, J. E. Semberski, and M. G. Holmes for administrative support. We owe special thanks to the ranchers of Kern County who allowed us to trap California condors on their property. We thank J. Grantham, C. E. Grue, L. F. Kiff, O. H. Pattee, and S. R. Wilbur for reviewing the manuscript. The Idaho Cooperative Fish and Wildlife Research unit is funded and supported by Idaho Department of Fish and Game, University of Idaho, U.S. Fish and Wildlife Service, and the 1 Present address: Idaho Cooperative Fish and Wildlife Research Unit, College of Forestry, University of Idaho, Moscow, ID 83843.


Journal of Wildlife Diseases | 1986

ACUTE ORAL TOXICITY OF SODIUM CYANIDE IN BIRDS

Stanley N. Wiemeyer; Elwood F. Hill; James W. Carpenter; Alexander J. Krynitsky

Sensitivities of six avian species, black vulture (Coragyps atratus), American kestrel (Falco sparverius), Japanese quail (Coturnix japonica), domestic chicken (Gallus domesticus), eastern screech-owl (Otus asio), and European starling (Sturnus vulgaris), to acute poisoning by sodium cyanide (NaCN) were compared by single dose LD50s. Three species, domestic chickens, black vultures, and turkey vultures (Cathartes aura), were dosed with NaCN to determine cyanide residues in those that died and also in survivors, in addition to postmortem fate. Three flesh-eating species (black vulture, American kestrel, and eastern screech-owl; LD50s 4.0–8.6 mg/kg) were more sensitive to NaCN than three species (Japanese quail, domestic chicken, and European starling; LD50s 9.4–21 mg/kg) that fed predominantly on plant material. Elevated concentrations of cyanide were found in the blood of birds that died of cyanide poisoning; however, concentrations in birds that died overlapped those in survivors. Blood was superior to liver as the tissue of choice for detecting cyanide exposure. No gross pathological changes related to dosing were observed at necropsy.


Journal of Wildlife Diseases | 2003

Experimental lead poisoning in turkey vultures (Cathartes aura).

James W. Carpenter; Oliver H. Pattee; Steven H. Fritts; Barnett A. Rattner; Stanley N. Wiemeyer; J. Andrew Royle; Milton R. Smith

Lead-induced mortality appears to have been a major factor in the decline of the California condor (Gymnogyps californianus). We orally dosed turkey vultures (Cathartes aura) with BB-sized lead shot from January 1988 through July 1988 to determine physiologic response (delta-aminolevulinic acid dehydratase inhibition, erythrocyte protoporphyrin levels, anemia), diagnostic tissue lead concentrations (blood, liver, and kidney), and comparative sensitivity of this species. Two turkey vultures died and two became so intoxicated they were euthanized. Overall, responses of measured parameters were comparable to other species exposed to lead although there was considerable individual variation. Survival time (143–211 days), even with the large numbers of shot and constant redosing, was much longer than reported for other species of birds, suggesting considerable tolerance by turkey vultures to the deleterious effects of lead ingestion. Based on these observations, turkey vultures appear to be poor models for assessing the risk of lead poisoning to California condors or predicting their physiologic response.


Environmental Monitoring and Assessment | 1986

Environmental contaminants in surrogates, foods, and feathers of California condors (Gymnogyps californianus).

Stanley N. Wiemeyer; Ronald M. Jurek; John F. Moore

California condor (Gymnogyps californianus) foods and feathers, and turkey vultures (Cathartes aura), common ravens (Corvus corax), and their eggs were collected within the condor range to determine exposure of condors to environmental contaminants. Samples were analyzed for organochlorines and trace elements. Food items contained low concentrations of organochlorines and generally low concentrations of lead. DDE was detected in all vulture carcasses and nearly all raven carcasses at generally moderate concentrations. Other organochlorines occurred infrequently in carcasses and generally at low concentrations. Turkey vulture eggshells were 16% thinner than the pre-DDT mean; there was no change in shell thickness of raven eggs. Vulture eggs contained an average of 6.9 ppm DDE and two contained excessive concentrations of endrin. DDE concentrations were low in raven eggs. Residues of As, Cd, Cr, Cu, Fe, Hg, Ni, Se, Tl, and Zn in tissues of vultures and ravens appeared normal when compared with reference values for other species. Lead concentrations in bone of turkey vultures and feathers of condors appeared to be elevated above normal background concentrations in some cases. Current exposure of condors to organochlorines appears low; however, we are concerned about the excessive exposure of turkey vultures to organochlorines, possibly in Central America. Lead exposure to vultures and condors has occurred, but its significance to their populations is unknown.


Journal of Wildlife Diseases | 2006

LEAD POISONING IN CAPTIVE ANDEAN CONDORS (VULTUR GRYPHUS)

Oliver H. Pattee; James W. Carpenter; Steven H. Fritts; Barnett A. Rattner; Stanley N. Wiemeyer; J. Andrew Royle; Milton R. Smith

Elevated lead in the tissues of raptors, especially those that scavenge, is a common occurrence, and lead poisoning appears to be a significant problem in the ongoing recovery effort for California condors (Gymnogyps californianus). Elevated blood lead levels have been found in released birds, and a number of birds have died of lead poisoning. In earlier work, we dosed turkey vultures (Cathartes aura) with lead shot but found them to be a poor model for lead poisoning. In this study, we dosed four Andean condors (Vultur gryphus) with lead shot and found them to be quite sensitive, as two of the birds died and the other two exhibit signs of lead poisoning within 50 days. All lead-responsive parameters were affected, and regurgitation of dosed shot occurred only once. The response of the Andean condors appeared to mimic California condors, suggesting that once exposed to lead, the possibility of survival is poor. This is consistent with observations in the wild, where otherwise healthy birds exposed to metallic lead quickly succumb. At the very least, the release program has to maintain constant surveillance and an active lead monitoring program.


Estuaries | 1980

Residues of environmental pollutants and necropsy data for Eastern United States ospreys, 1964–1973

Stanley N. Wiemeyer; Thair G. Lamont; L.N. Locke

Thirty-three ospreys (Pandion haliaetus) that were found dead or moribund in the Eastern United States between 1964 and 1973 were necropsied. The brains and carcasses of 26 of these birds were analyzed for organochlorines. The livers of 18 and the kidneys of 7 were analyzed for selected metals. Most adults were recovered in April and May and most immatures were recovered in August through October. The adult sex ratio was highly unbalanced in favor of females. Major causes of mortality were impact injuries, emaciation, shooting, and respiratory infections. Of special interest were two birds with malignant tumors and one with steatitis. Many birds had undergone marked weight losses resulting in mobilization and redistribution of organochlorine residues. Organochlorines were detected in the birds at the following percentages: DDE 100%, PCB 96%, DDD 92%, dieldrin 88%, chlordanes (including nonachlors) 82%, DDT 65%, and heptachlor expoxide 38%. Organochlorine levels tended to be higher in adults than in immatures. One adult from South Carolina had a potentially dangerous level of dieldrin in its brain, which might have contributed to its death. Immature ospreys from Maryland had extremely elevated levels of copper in their livers compared with immatures from other areas and all adults. One immature from Maryland had an elevated level of arsenic in its liver, which might have contributed to its death. One adult from Florida that had died of impact injuries had potentially dangerous levels of mercury in both liver and kidney and slightly elevated levels of cadmium in these tissues. Additional birds appeared to have been exposed to contamination of the environment by arsenic and mercury. The levels of chromium, zinc, and lead in livers appeared normal.

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James W. Carpenter

United States Fish and Wildlife Service

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Oliver H. Pattee

United States Department of the Interior

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Alexander J. Krynitsky

United States Fish and Wildlife Service

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Christine M. Bunck

United States Fish and Wildlife Service

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John F. Miesner

United States Fish and Wildlife Service

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Barnett A. Rattner

Patuxent Wildlife Research Center

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David J. Hoffman

United States Fish and Wildlife Service

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Edward C. Murphy

University of Alaska Fairbanks

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Eugene Cromartie

United States Fish and Wildlife Service

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Peter L. Tuttle

United States Fish and Wildlife Service

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