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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., (Copyright (c) 2010 SETAC.)

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 microg/g mercury, as methylmercury chloride. Mean concentrations of mercury in eggs laid by parents fed 0, 1, 2, 4, or 8 microg/g mercury were 0.0, 1.6, 3.7, 5.9, and 14 microg/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-microg/g dietary mercury treatments (that resulted in 5.9 and 14 microg/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 microg/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.

We measured halogenated organic contaminants (HOCs) [polybrominated diphenyl ethers (PBDEs), polychlorinated biphenyls (PCBs), and dichloro-diphenyl-trichloroethane (DDT)] and P450 [e.g., ethoxyresorufin-O-dealkylase (EROD)] stress in livers from Caspian tern (Hydroprogne caspia) adults and Forster's tern (Sterna forsteri) adults and chicks in San Francisco Bay (SFB). Penta BDEs and tetra PBDEs composed 46-66% of SigmaPBDE in terns. PCB homologues di, tri, penta, hexa, and hepta composed 93-95% of SigmaPCBs and p'p-DDE composed 82-98% of all SigmaDDTs. We found similar concentrations of SigmaPBDEs [mean micrograms per gram wet weight (ww) +/- standard error = 0.4 +/- 0.1], SigmaPCBs (5.9 +/- 1.6), and SigmaDDTs (0.6 +/- 0.1) among species, sexes, and regions. However, concentrations were higher in Forster's tern adults than chicks (SigmaPBDEs = 0.4 +/- 0.1 and 0.1 +/- 0.1; SigmaPCBs = 7.08 +/- 2.4 and 2.4 +/- 1.4; SigmaDDTs = 0.5 +/- 0.1 and 0.1 +/- 0.1; respectively), and there was a nonsignificant trend of elevated SigmaPBDEs and SigmaPCBs for adult Forster's terns in the Central South Bay and Lower South Bay portions of SFB. Combined Forster's tern and Caspian tern SigmaDDTs bioaccumulated similarly to selenium, but not mercury, and there was a nonsignificant but positive trend for SigmaPBDEs and SigmaPCBs bioaccumulation with mercury. P450 protein activity was higher in adult Forster's terns than Caspian terns, higher in Central South Bay than in Lower South Bay, and higher in adult Forster's terns than in chicks.

Measurements of Hg concentrations in avian eggs can be used to predict possible harm to reproduction, but it is not always possible to sample eggs. When eggs cannot be sampled, some substitute tissue, such as female blood, the diet of the breeding female, or down feathers of hatchlings, must be used. When female mallards (Anas platyrhynchos) were fed diets containing methylmercury chloride, the concentration of Hg in a sample of their blood was closely correlated with the concentration of Hg in the egg they laid the day they were bled (r2 = 0.88; p < 0.001). Even when the blood sample was taken more than two weeks after an egg was laid, there was a strong correlation between Hg concentrations in female blood and eggs (r2 = 0.67; p < 0.0002). When we plotted the dietary concentrations of Hg we fed to the egg-laying females against the concentrations of Hg in their eggs, the r2 value was 0.96 (p < 0.0001). When the concentrations of Hg in the down feathers of newly hatched ducklings were plotted against Hg in the whole ducklings, the r2 value was 0.99 (p < 0.0003). Although measuring Hg in eggs may be the most direct way of predicting possible embryotoxicity, our findings demonstrate that measuring Hg in the diet of breeding birds, in the blood of egg-laying females, or in down feathers of hatchlings all can be used to estimate what concentration of Hg may have been in the egg., (Copyright 2009 SETAC.)

We injected doses of methylmercury into the air cells of eggs of 26 species of birds and examined the dose-response curves of embryo survival. For 23 species we had adequate data to calculate the median lethal concentration (LC(50)). Based on the dose-response curves and LC(50)s, we ranked species according to their sensitivity to injected methylmercury. Although the previously published embryotoxic threshold of mercury in game farm mallards (Anas platyrhynchos) has been used as a default value to protect wild species of birds, we found that, relative to other species, mallard embryos are not very sensitive to injected methylmercury; their LC(50 )was 1.79 microg/g mercury on a wet-weight basis. Other species we categorized as also exhibiting relatively low sensitivity to injected methylmercury (their LC(50)s were 1 microg/g mercury or higher) were the hooded merganser (Lophodytes cucullatus), lesser scaup (Aythya affinis), Canada goose (Branta canadensis), double-crested cormorant (Phalacrocorax auritus), and laughing gull (Larus atricilla). Species we categorized as having medium sensitivity (their LC(50)s were greater than 0.25 microg/g mercury but less than 1 microg/g mercury) were the clapper rail (Rallus longirostris), sandhill crane (Grus canadensis), ring-necked pheasant (Phasianus colchicus), chicken (Gallus gallus), common grackle (Quiscalus quiscula), tree swallow (Tachycineta bicolor), herring gull (Larus argentatus), common tern (Sterna hirundo), royal tern (Sterna maxima), Caspian tern (Sterna caspia), great egret (Ardea alba), brown pelican (Pelecanus occidentalis), and anhinga (Anhinga anhinga). Species we categorized as exhibiting high sensitivity (their LC(50)s were less than 0.25 microg/g mercury) were the American kestrel (Falco sparverius), osprey (Pandion haliaetus), white ibis (Eudocimus albus), snowy egret (Egretta thula), and tri-colored heron (Egretta tricolor). For mallards, chickens, and ring-necked pheasants (all species for which we could compare the toxicity of our injected methylmercury with that of published reports where methylmercury was fed to breeding adults and was deposited into the egg by the mother), we found the injected mercury to be more toxic than the same amount of mercury deposited naturally by the mother. The rank order of sensitivity of these same three species to methylmercury was, however, the same whether the methylmercury was injected or maternally deposited in the egg (i.e., the ring-necked pheasant was more sensitive than the chicken, which was more sensitive than the mallard). It is important to note that the dose-response curves and LC(50)s derived from our egg injections are useful for ranking the sensitivities of various species but are not identical to the LC(50)s that would be observed if the mother bird had put the same concentrations of mercury into her eggs; the LC(50)s of maternally deposited methylmercury would be higher.

The U.S. Army Corps of Engineers conducted a water drawdown on Navigation Pool 8 of the Upper Mississippi River during the summers of 2001 and 2002 to increase aquatic vegetation production and thereby improve fish and wildlife habitat. Flooding of previously dried wetlands, however, may increase the rate of mercury methylation and make mercury more available to terrestrial vertebrates that feed in aquatic environments. Our objective was to determine if mercury, other elements, and organochlorine contaminants were more available to vertebrates following the 2001 drawdown. Tree swallow (Tachycineta bicolor) eggs and nestlings were collected at two sites on Pool 8 and a nearby Reference site in 2000 (pre-2001 drawdown), 2001 (pre-2001 drawdown) and 2002 (post-2001 drawdown) and tissues were analyzed for mercury, other elements, and organochlorine contaminants. Bioindicator measurements of genetic damage, oxidative stress, ethoxyresorufin-O-dealkylase activity, and the ratio of liver to nestling mass were also measured in nestlings at all sites and all years. Based on a multivariate analysis, the 2001 drawdown of Pool 8 did not influence element concentrations, organochlorine concentrations, or bioindicator response. Concentrations of inorganic and organochlorine contaminants in tree swallow eggs and nestlings were not at toxic levels. Hatching success did not differ among years and was comparable to the nationwide average.

Lead poisoning of waterfowl has been reported for decades in the Coeur d'Alene River Basin (CDARB) in Idaho as a result of the ingestion of lead-contaminated sediments. This study was conducted to determine whether the addition of phosphoric acid to sediments would reduce the bioavailability and toxicity of lead to mallards (Anas platyrhynchos) as related to adverse hematological effects and altered plasma chemistries. Mallards received diets containing 12% clean sediment (controls) or 12% sediment from three different CDARB sites containing 4520, 5390, or 6990 microg/g lead (dw) with or without phosphoric acid amendment. Blood lead concentrations were significantly higher in all CDARB treatment groups and ranged from geometric mean values of 5.0 microg/g for the first two sites to 6.2 microg/g for the third site. With amendments, all blood lead concentrations became 41% to 64% lower. Red blood cell ALAD activity was depressed by 90% or more with lead-contaminated sediment from all sites and did not differ with amended diets. Free erythrocyte protoporphyrin (FEP) concentrations were elevated by contaminated sediment from all sites. Amendment decreased the elevations in FEP by as much as 80%. Hematocrit values and hemoglobin concentrations were lower for all lead site sediments by as much as 30% for site 3. Plasma enzyme activities for ALT, CK, and LDH-L were elevated by as much as 2.2-fold, and plasma creatinine concentration was 1.7-fold higher for site 3 sediment. Amendments restored hematocrit, hemoglobin, and plasma enzyme activities so that they did not differ from controls. Although amendments of phosphorus substantially reduced the bioavailability of lead and alleviated many of the adverse hematological effects, lead concentrations in the blood of mallards fed the amended sediments were still above those believed to be harmful to waterfowl under the present conditions.

In recent years, high concentrations of mercury have been found in wading birds in Florida, USA. Great egret (Ardea alba) chicks (2 weeks old) were dosed orally daily with the equivalent of 0, 0.5, or 5 microg/g Hg as methylmercury chloride in the diet for up to 12 weeks. Weakness of the legs or paralysis occurred in all high-dosed birds. Geometric mean blood Hg concentrations were 0.17, 10.3, and 78.5 microg/g (wet wt), respectively. Mercury concentrations for organs (microg/g wet wt), including brain (0.22, 3.4, and 35, respectively), liver (0.34, 15.1, 138, respectively), and kidney (0.28, 8.1, and 120, respectively), increased in a dose-dependent manner. Total glutathione (GSH) peroxidase activity was significantly lower in the plasma, brain, liver, and kidney of the high-dosed group. Plasma aspartate aminotransferase activity increased with mercury treatment, whereas lactate dehydrogenase activity decreased. Four other plasma chemistries were decreased significantly in the high-dosed group and included uric acid, total protein, albumin, and inorganic phosphorus. Lipid peroxidation increased in liver (low and high dose) and brain (high dose). Tissue changes in concentrations of reduced thiols included decreased total thiols and protein-bound thiols in liver, decreased protein-bound thiols in kidney, and increased GSH in kidney and brain. Activities of GSH S-transferase and oxidized glutathione reductase increased in liver. In kidney, GSH S-transferase and glucose-6-phosphate dehydrogenase activities increased with mercury dose. These findings, including apparent compensatory changes, are compared to other Hg studies where oxidative stress was reported in egrets, herons, and diving ducks in the field and mallards in the laboratory.

Day-old mallard (Anas platyryhnchos) ducklings received either a clean sediment (24%) supplemented control diet, Coeur d'Alene River Basin, Idaho (CDARB) sediment (3449 microg/g lead) supplemented diets at 12% or 24%, or a positive control diet (24% clean sediment with equivalent lead acetate to the 24% CDARB diet) for 6 weeks. The 12% CDARB diet resulted in a geometric mean concentration of 396 ppb (WW) brain lead with decreased brain protein and ATP concentrations but increased oxidized glutathione (GSSG) relative to the control diet. The 24% CDARB diet resulted in a concentration of 485 ppb brain lead with lower brain weight and ATP concentration than controls but higher concentrations of reduced glutathione (GSH) and calcium. Lead acetate accumulated twice as well as CDARB derived lead and resulted in histopathological lesions of the brain. With a combination of a suboptimal diet and 24% CDARB, brain lead concentration was higher (594 ppb) than with 24% CDARB in the standard diet, histopathological lesions became apparent and GSH was higher than suboptimal diet controls.

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 134.8 microg/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 0.80 microg/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 0.36-1.18 microgMeHg/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.

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 Se-related 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 black-necked 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.

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 microg/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.

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.

Wood ducks (Aix sponsa) nesting along Bayou Meto downstream from a hazardous waste site in central Arkansas were contaminated with polychlorinated dibenzo-p-dioxins (PCDDs) and dibenzofurans (PCDFs). Residues in eggs, based on 2,3,7,8-tetrachlorodibenzo-p-dioxin equivalents (TCDD-EQ), ranged up to 611 parts per trillion (ppt), and egg arithmetic means were 90-fold higher at the site nearest the point source compared with a reference site. We monitored productivity of wood ducks in artificial nest boxes at three sites on the bayou and at a reference site on a separate drainage during 1988-1990. Productivity was suppressed (p < 0.05) at the bayou sites compared with the reference site, and egg TCDD-EQs were inversely correlated (p < 0.001) with productivity in corresponding nests. The threshold range of toxicity, where reduced productivity was evident in wood ducks (based on TCDD-EQs), was > 20 to 50 ppt. Oxidative stress and teratogenic effects occurred in ducklings at the more contaminated nesting sites nearest the point source. These findings suggest that wood ducks may be more sensitive to PCDD and PCDF contamination than some other aquatic birds and could serve as an indicator species for monitoring biological impacts from these contaminants.

High concentrations of arsenic (As) and selenium (Se) have been found in aquatic food chains associated with irrigation drainwater. Total biomass of invertebrates, a major source of protein for wild ducklings, may vary in environments that are contaminated with selenium. Day-old mallard (Anas platyrhynchos) ducklings received an untreated diet (controls) containing 22% protein or diets containing 15 ppm Se (as selenomethionine), 60 ppm Se, 200 ppm As (as sodium arsenate), 15 ppm Se with 200 ppm As, or 60 ppm Se with 200 ppm As. In a concurrent experiment, the same sequence was repeated with a protein-restricted (7%) but isocaloric diet. After 4 weeks, blood and tissue samples were collected for biochemical and histological examination. With 22% protein and 60 ppm Se in the diet, duckling survival and growth was reduced and livers had histopathological lesions. Arsenic alone caused some reduction in growth. Antagonistic interactive effects occurred between As and Se, including complete to partial alleviation of the following Se effects: mortality, impaired growth, hepatic lesions and lipid peroxidation, and altered glutathione and thiol status. With 7% protein, survival and growth of controls was less than that with 22% protein, Se (60 ppm) caused 100% mortality, and As (200 ppm) caused mortality, decreased growth, and liver histopathology. These findings suggest the potential for antagonistic effects of Se and As on duckling survival, growth, and physiology with adequate dietary protein but more severe toxicological effects when dietary protein is diminished.

Die-offs of waterfowl have occurred in the Coeur d'Alene River system in northern Idaho since at least the early 1900's. We investigated causes of mortality and lead and cadmium contamination of 46 tundra swans (Cygnus columbianus) from 1987 to 1989; an additional 22 swans found dead in 1990 were not examined. We necropsied 43 of the 46 birds found from 1987 to 1989; 38 of these were from the Coeur d'Alene River system, which has been contaminated with mining and smelting wastes for a century, and the other 5 were from a nearby, relatively uncontaminated area. Of the 36 livers of swans from the contaminated area that were analyzed, 32 contained lethal levels of lead (6 to 40 micrograms/g, wet weight) and all birds exhibited several symptoms of lead poisoning, notably enlarged gall bladders containing viscous, dark-green bile. Only 13% of the lead-poisoned birds (10% when data were included from other studies of swans in the area) contained shot, compared to 95% of lead-poisoning swans in studies outside northern Idaho. Lead concentrations in blood samples from 16 apparently healthy swans (0.5 to 2.3 micrograms/g, and 4 lead-poisoned birds found moribund (1.3 to 9.6 micrograms/g) indicating that tundra swans accumulated high levels of lead from ingestion of sediment that contained up to 8,700 micrograms/g of lead and plants that contained up to 400 micrograms/g. The swans spend only a few weeks in the area staging during the spring migration. The five tundra swans from the uncontaminated area had low levels of lead and essentially no symptoms of lead poisoning.(ABSTRACT TRUNCATED AT 250 WORDS)

Severe gross and microscopic lesions and other changes were found in adult aquatic birds and in embryos from Kesterson Reservoir (a portion of Kesterson National Wildlife Refuge), Merced County, Calif., during 1984. Adult birds from that area were emaciated, had subacute to extensive chronic hepatic lesions, and had excess fluid and fibrin in the peritoneal cavity. Biochemical changes in their livers included elevated glycogen and non-protein-bound sulfhydryl concentrations and glutathione peroxidase activity but lowered protein, total sulfhydryl, and protein-bound sulfhydryl concentrations. Congenital malformations observed grossly in embryos were often multiple and included anophthalmia, microphthalmia, abnormal beaks, amelia, micromelia, ectrodactyly, and hydrocephaly. Mean concentrations of selenium in livers (94.4 ppm, dry weight) and kidneys (96.6 ppm) of birds collected at the Kesterson ponds were about 10 times those found at a nearby control area (8.3 and 12.2 ppm). We conclude that selenium present in the agricultural drainage water supplied to the Kesterson ponds accumulated in the food chain of aquatic birds to toxic concentrations and caused the lesion and other changes observed.