ALBERT

Notes: Abstract Snapping turtles (Chelydra serpentina) were collected from a brackish-water and a nearly freshwater area in the contaminated Hackensack Meadowlands of New Jersey and an uncontaminated freshwater area in Maryland to determine the effects of environmental contaminants on a resident wetland species. No turtles were observed or caught in the Meadowlands at two trapping sites that were the most heavily contaminated by metals. Snapping turtles from the brackish-water area had an unusually low lipid content of body fat and reduced growth compared to turtles from the fresh-water areas in New Jersey and Maryland. Despite the serious metal contamination of the Hackensack Meadowlands, the metal content of kidneys and livers from New Jersey turtles was low and not greatly different from that of the Maryland turtles. Organochlorine pesticide concentrations in body fat were generally low at all three study areas. Polychlorinated biphenyls (PCBs) concentrations in fat were highest in male turtles from the New Jersey brackish-water area. Analysis of blood for amino-levulinic acid dehydratase, albumin, glucose, hemoglobin, osmolality, packed cell volume, total protein, triglycerides, and uric acid failed to reveal any differences among groups that would indicate physiological impairment related to contaminants.

Notes: Abstract. Between 1983 and 1986 the National Wildlife Health Center (NWHC) conducted a nationwide study of lead poisoning of waterfowl from federal and state refuges. This survey was done to assist in identifying zones with lead-poisoning problems. One thousand forty one moribund or dead waterfowl were collected and examined. The presence or absence of 13 gross lesions selected as indicators of lead poisoning and three lesions indicating body condition was recorded. Lead-poisoning diagnoses were based on the finding of at least 6–8 ppm (wet weight) lead in the liver and either lead shot in the gizzard content or at least one convincing gross lesion indicative of lead poisoning. Four hundred twenty-one of these waterfowl were diagnosed as lead poisoned. The NWHC survey provided a comprehensive basis for estimating the sensitivities, specificities, and likelihood ratios of the gross lesions of lead poisoning and the associated hepatic lead concentrations for several species of waterfowl. Some of the 13 defined gross lesions were more common than others; frequencies ranged from 3% to 80% in the 421 lead-poisoned waterfowl. The most reliable indicators of lead poisoning were impactions of the upper alimentary tract, submandibular edema, myocardial necrosis, and biliary discoloration of the liver. Each of the 13 lesions occurred more frequently in the lead-poisoned birds, but each of the lesions also occurred in waterfowl that died of other causes. The number of lead shot present in a bird's gizzard was only weakly correlated with its hepatic lead concentration; however, this weak correlation may have been adequate to account for differences in hepatic lead concentrations among species, once the weights of the species were taken into account. Although lead-poisoned ducks tended to have higher hepatic mean lead concentrations than did lead-poisoned geese or swans, the differences were probably a result of a greater dose of shot per body weight than to kinetic differences between species. Hepatic lead concentrations were independent of age and sex. Ninety-five percent of waterfowl diagnosed as lead poisoned had hepatic lead concentrations of at least 38 ppm dry weight (10 ppm wet weight). Fewer than 1% of the waterfowl that died of other causes had a concentration that high. This fifth percentile, of 38 ppm dry weight (10 ppm wet weight), is a defensible criterion for identifying lead-poisoned waterfowl when interpreting hepatic lead concentrations in the absence of pathological observations.

Notes: Abstract 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.

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

Notes: Abstract For the 1983 nesting season, Forster's tern (Sterna forsteri) reproductive success was significantly impaired on organochlorine contaminated Green Bay, Lake Michigan compared to a relatively uncontaminated inland location at Lake Poygan, Wisconsin. Compared with tern eggs from Lake Poygan, eggs from Green Bay had significantly higher median concentrations of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), other polychlorinated dibenzo-p-dioxins (PCDDs), total polychlorinated biphenyls (PCBs), total (three congeners) non-ortho, ortho' PCBs, five individual PCB congeners known to induce aryl hydrocarbon hydroxylase (AHH) and several other organochlorine contaminants. Conversions of analytical concentrations of TCDD and PCB congeners based on relative AHH induction potencies allowed for estimation of total 2,3,7,8-TCDD equivalents. Two PCB congeners, 2,3,3′,4,4′- and 3,3′,4,4′,5-pentachlorobiphenyl (PeCB) accounted for more than 90% of the median estimated TCDD equivalents at both Green Bay and Lake Poygan. The median estimated TCDD equivalents were almost 11-fold higher in tern eggs from Green Bay than in eggs from Lake Poygan (2175 and 201 pg/g). The hatching success of Green Bay sibling eggs from nests where eggs were collected for contaminant analyses was 75% lower at Green Bay than at Lake Poygan. Hatchability of eggs taken from other nests and artificially incubated was about 50% lower for Green Bay than for Lake Poygan. Among hatchlings from laboratory incubation, those from Green Bay weighed approximately 20% less and had a mean liver weight to body weight ratio 26% greater than those from Lake Poygan. In both field and laboratory, mean minimum incubation periods were significantly longer for eggs from Green Bay compared to Lake Poygan (8.25 and 4.58 days, respectively). Mean minimum incubation time for Green Bay eggs in the field was 4.37 days longer than in the laboratory. Hatchability was greatly improved when Green Bay eggs were incubated by Lake Poygan adults in an egg-exchange experiment, but was sharply decreased in Lake Poygan eggs incubated in Green Bay nests. Nest abandonment and egg disappearance were substantial at Green Bay but nil at Lake Poygan. Thus, not only factors intrinsic to the egg, but also extrinsic factors (parental attentiveness), impaired reproductive outcome at Green Bay. The epidemiological evidence from this study strongly suggested that contaminants were a causal factor. AHH-active PCB congeners (intrinsic effects) and PCBs in general (extrinsic effects) appeared to be the only contaminants at the concentrations measured in eggs, capable of producing the effects that were observed at Green Bay.

Notes: Abstract. 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 (38μg/g) than in the commercial diet (13 μg/g).