Factors affecting the toxicity of methylmercury injected into eggs.

We developed a standardized protocol for comparing the sensitivities of the embryos of different bird species to methylmercury when methylmercury was injected into their eggs. During the course of developing this protocol, we investigated the effects of various factors on the toxicity of the injected methylmercury. Most of our experiments were done with chicken (Gallus domesticus), mallard (Anas platyrhynchos), and ring-necked pheasant (Phasianus colchicus) eggs, all of which were purchased in large numbers from game farms. A smaller amount of work was done with double-crested cormorant (Phalacrocorax auritus) eggs collected from the wild. Several solvents were tested, and corn oil at a rate of 1 microl/g egg contents was selected for the final standardized protocol because it had minimal toxicity to embryos and because methylmercury dissolved in corn oil yielded a dose-response curve in a range of egg concentrations that was similar to the range that causes reproductive impairment when the mother deposits methylmercury into her own eggs. The embryonic stage at which eggs were injected with corn oil altered mercury toxicity; at early stages, the corn oil itself was toxic. Therefore, in the final protocol we standardized the time of injection to occur when each species reached the morphologic equivalent of a 3-day-old chicken embryo. Although solvents can be injected directly into the albumen of an egg, high embryo mortality can occur in the solvent controls because of the formation of air bubbles in the albumen. Our final protocol used corn oil injections into the air cell, which are easier and safer than albumen injections. Most of the methylmercury, when dissolved in corn oil, injected into the air cell passes through the inner shell membrane and into the egg albumen. Most commercial incubators incubate eggs in trays with the air cell end of the egg pointing upward, but we discovered that mercury-induced mortality was too great when eggs were held in this orientation. In addition, some species of bird eggs require incubation on their sides with the eggs being rolled 180 degrees for them to develop normally. Therefore, we adopted a procedure of incubating the eggs of all species on their sides and rolling them 180 degrees every hour. Little has been published about the conditions of temperature, humidity, and the movements to which eggs of wild birds need to be subjected for them to hatch optimally under artificial incubation. Not unexpectedly, hatching success in an artificial incubator is generally less than what natural incubation by the parents can achieve. However, the survival of control embryos of most wild bird species was good (generally > or = 80%) up to within 1 or 2 days of hatching when we incubated the eggs at 37.5 degrees C (or 37.6 degrees C for gallinaceous species) at a relative humidity that resulted in an approximate 15% to 16% loss in egg weight by the end of incubation and by incubating the eggs on their sides and rolling them 180 degrees /h. To improve statistical comparisons, we used survival through 90% of incubation as our measurement to compare survival of controls with survival of eggs injected with graded concentrations of mercury.

Embryotoxic thresholds of mercury: estimates from individual mallard eggs.

Eighty pairs of mallards ( Anas platyrhynchos) were fed an uncontaminated diet until each female had laid 15 eggs. After each female had laid her 15th egg, the pair was randomly assigned to a control diet or diets containing 5, 10, or 20 microg/g mercury as methylmercury until she had laid a second set of 15 eggs. There were 20 pairs in each group. After the second set of 15 eggs, the pair was returned to an uncontaminated diet, and the female was permitted to lay another 30 eggs. For those pairs fed the mercury diets, the even-numbered eggs were incubated and the odd-numbered eggs were saved for possible mercury analysis. Mercury in the even-numbered eggs was estimated as the average of what was in the neighboring odd-numbered eggs. Neurological signs of methylmercury poisoning were observed in ducklings that hatched from eggs containing as little as 2.3 microg/g estimated mercury on a wet-weight basis, and deformities were seen in embryos from eggs containing about 1 microg/g estimated mercury. Although embryo mortality was seen in eggs estimated to contain as little as 0.74 microg/g mercury, there were considerable differences in the sensitivity of mallard embryos, especially from different parents, with some embryos surviving as much as 30 or more microg/g mercury in the egg.

Lead shot toxicity to passerines.

This study evaluated the toxicity of a single size 7.5 lead shot to passerines. No mortalities or signs of plumbism were observed in dosed cowbirds (Molothrus ater) fed a commercial diet, but when given a more natural diet, three of 10 dosed birds died within 1 day. For all survivors from which shot were recovered, all but one excreted the shot within 24 h of dosing, whereas, the dead birds retained their shot. Shot erosion was significantly greater (P < 0.05) when weathered shot were ingested compared to new shot, and the greatest erosion was observed in those birds that died (2.2-9.7%). Blood lead concentrations of birds dosed with new shot were not significantly different (P = 0.14) from those of birds exposed to weathered shot. Liver lead concentrations of birds that died ranged from 71 to 137 ppm, dry weight. Despite the short amount of time the shot was retained, songbirds may absorb sufficient lead to compromise their survival.

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 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.

Developmental toxicity of lead-contaminated sediment in Canada geese (Branta canadensis).

Sediment ingestion has recently been identified as an important exposure route for toxicants in waterfowl. The effects of lead-contaminated sediment from the Coeur d'Alene River Basin (CDARB) in Idaho on posthatching development of Canada geese (Branta canadensis) were examined for 6 wk. Day-old goslings received either untreated control diet, clean sediment (48%) supplemented control diet, or CDARB sediment (3449 microg/g lead) supplemented diets at 12%, 24%, or 48%. The 12% CDARB diet resulted in a geometric mean blood lead concentration of 0.68 ppm (ww), with over 90% depression of red blood cell ALAD activity and over fourfold elevation of free erythrocyte protoporphyrin concentration. The 24% CDARB diet resulted in blood lead of 1.61 ppm with decreased hematocrit, hemoglobin, and plasma protein in addition to the effects just described. The 48% CDARB diet resulted in blood lead of 2.52 ppm with 22% mortality, decreased growth, and elevated plasma lactate dehydrogenase-L (LDH-L) activity. In this group the liver lead concentration was 6.57 ppm (ww), with twofold increases in hepatic lipid peroxidation (thiobarbituric acid-reactive substances, TBARS) and in reduced glutathione concentration; associated effects included elevated glutathione reductase activity but lower protein-bound thiols concentration and glucose-6-phosphate dehydrogenase (G-6-PDH) activity. The kidney lead concentration in this group was 14.93 ppm with subacute renal tubular nephrosis in one of the surviving goslings. Three other geese in this treatment group exhibited calcified areas of marrow, and one of these displayed severe chronic fibrosing pancreatitis. Lead from CDARB sediment accumulated less readily in gosling blood and tissues than reported in ducklings but at given concentrations was generally more toxic to goslings. Many of these effects were similar to those reported in wild geese and mallards within the Coeur d'Alene River Basin.

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) mist-netted 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.

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 microgram/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 microgram/g of lead in the blood and 28 microgram/g in the liver (wet-weight basis) and 1,660 microgram/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 microgram/g for mallards fed 24% lead-contaminated sediment and 16 microgram/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 microgram/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 microgram/g) than in the commercial diet (13 microgram/g).

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.

Comparison of the effects of seleno-L-methionine, 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.

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 micrograms/g selenium as seleno-L-methionine (36%) than for ducklings fed 30 micrograms/g selenium as seleno-DL-methionine (100%) or 30 micrograms/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 micrograms/g selenium as seleno-DL-methionine (12 micrograms/g, wet weight), seleno-L-methionine (11 micrograms/g), and high selenium wheat (11 micrograms/g), but was lower when the selenium came from selenized yeast (6.2 micrograms/g). When fed 30 micrograms/g selenium from the various sources, the selenium concentrations in liver were 20 micrograms/g for seleno-DL-methionine, 19 micrograms/g for seleno-L-methionine, and 9.9 micrograms/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 micrograms/g selenium as seleno-DL-methionine, seleno-L-methionine, or selenized yeast. Selenium concentrations in liver were similar for ducklings fed the 30-micrograms/g selenium diets as the DL or L forms of selenomethionine (27 and 25 micrograms/g), but lower for ducklings fed selenized yeast (13 micrograms/g).(ABSTRACT TRUNCATED AT 250 WORDS)

Declines in organochlorines in eggs of red-breasted mergansers from Lake Michigan, 1977-1978 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.

Reproduction of mallards following overwinter exposure to selenium.

Forty pairs of mallards (Anas platyrhynchos) were fed 15 ppm selenium as selenomethionine for about 21 weeks during winter. Twenty pairs served as controls. At the end of 21 weeks, which coincided with the onset of the reproductive season, selenium treatment was ended. Four birds died while on selenium treatment. Treated females lost weight, and their egg-laying was delayed. Hatching success of some of the first eggs laid by selenium-treated females was lower than that of controls, and a few of these early eggs contained deformed embryos, but, after a period of about two weeks off the selenium-treated diet, reproductive success returned to a level comparable with that of controls. The return to normal reproductive success was the result of a corresponding decrease in selenium concentrations in eggs once selenium treatment ended.

Subchronic hepatotoxicity of selenomethionine ingestion in mallard ducks.

Two-year-old male mallards (Anas platyrhynchos) received a control diet (0.2 ppm Se) or diets containing 1, 2, 4, 8, 16, or 32 ppm Se as selenomethionine for 14 wk. Se accumulated readily in the liver in a dose-dependent manner, reaching a mean concentration of 29 ppm (wet weight) in the 32 ppm group. Dietary Se of 2 ppm or greater increased plasma glutathione peroxidase activity. Mortality (10%) and histopathological effects, including bile duct hyperplasia and hemosiderin pigmentation of the liver and spleen, occurred in the 32 ppm group. These histopathological effects were accompanied by lower hemoglobin concentrations (16 and 32 ppm groups) and hematocrit (32 ppm group), and elevated plasma alkaline phosphatase activity (32 ppm group) indicative of cholestatic liver injury. Other manifestations of hepatotoxicity included significant linear dose responses for hepatic oxidized glutathione (GSSG) concentrations and ratio of GSSG to reduced glutathione (GSH). Means for both of these responses differed from controls in groups receiving 8-32 ppm Se. Mean hepatic GSH and malondialdehyde (a measure of lipid peroxidation) concentrations were significantly elevated in the 16 and 32 ppm groups. Subchronic effects of selenomethionine, which occurs in vegetation, are of particular interest with respect to the health of wild aquatic birds in seleniferous locations.

Contaminants in American alligator eggs from Lake Apopka, Lake Griffin, and Lake Okeechobee, Florida.

Residues of organochlorine pesticides, polychlorinated biphenyls (PCBs), and 16 elements were measured in American alligator (Alligator mississippiensis) eggs collected in 1984 from Lakes Apopka, Griffin, and Okeechobee in central and south Florida. Organochlorine pesticides were highest in eggs from Lake Apopka. None of the elements appeared to be present at harmful concentrations in eggs from any of the lakes. A larger sample of eggs was collected in 1985, but only from Lakes Griffin, a lake where eggs were relatively clean, and Apopka, where eggs were most contaminated. In 1985, hatching success of artificially incubated eggs was lower for Lake Apopka, and several organochlorine pesticides were higher than in eggs from Lake Griffin. However, within Lake Apopka, higher levels of pesticides in chemically analyzed eggs were not associated with reduced hatching success of the remaining eggs in the clutch. Therefore, it did not appear that any of the pesticides we measured were responsible for the reduced hatching success of Lake Apopka eggs.

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. Half-times were 9.8 and 23.9 days, respectively. For liver, the equation C = A1e-b1t + A2e-b2t 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.

Hepatic glutathione metabolism and lipid peroxidation in response to excess dietary selenomethionine and selenite in mallard ducklings.

Studies were conducted with mallard (Anas platyrhynchos) ducklings to determine the effects of excess dietary selenium (Se) on hepatic glutathione concentration and associated enzymes, and lipid peroxidation. Day-old ducklings were fed 0.1, 10, 20, or 40 ppm Se as seleno-DL-methionine or sodium selenite for 6 wk. Selenium from selenomethionine accumulated in a dose-dependent manner in the liver, resulting in a decrease in the concentration of hepatic-reduced glutathione (GSH) and total hepatic thiols (SH). These effects were accompanied by a dose-dependent increase in the ratio of oxidized glutathione (GSSG) to GSH, and an increase in malondialdehyde concentration as evidence of lipid peroxidation. Hepatic and plasma GSH peroxidase activity was initially elevated at 10 ppm Se as selenomethionine, whereas GSSG reductase activity was elevated at higher dietary concentrations of Se. Selenium from sodium selenite accumulated in the liver to an apparent maximum at 10 ppm in the diet, resulting in an increase in hepatic GSH and GSSG accompanied by a small decrease in total hepatic SH. Sodium selenite resulted in an increase in hepatic GSSG reductase activity at 10 ppm and in plasma GSSG reductase activity at 40 ppm. A small increase in lipid peroxidation occurred at 40 ppm. These findings indicate that excess dietary Se as selenomethionine has a more pronounced effect on hepatic glutathione metabolism and lipid peroxidation in ducklings than does selenite, which may be related to the pattern of accumulation. Effects of Se as selenite appear to be less pronounced in ducklings than reported in laboratory rodents. The effects of selenomethionine, which occurs in vegetation, are of particular interest with respect to the health of wild aquatic birds in seleniferous locations.

Embryotoxic and teratogenic effects of selenium in the diet of mallards.

Mallards (Anas platyrhynchos) were fed a control diet, diets containing 1, 5, 10, or 25 ppm Se as sodium selenite, or a diet containing 10 ppm Se as seleno-DL-methionine in the first of two experiments. Selenium at 10 ppm as selenomethionine or 25 ppm as sodium selenite caused a 40-44% decrease in the total number of eggs that hatched compared to controls. Selenium at 25 ppm (sodium selenite) resulted in a 19% decrease in mean embryonic weight at 18 d of incubation, accompanied by a 6% decrease in crown-rump length. Ten parts per million Se as selenomethionine was more teratogenic than sodium selenite at 25 ppm. Selenomethionine (10 ppm Se) resulted in an incidence of 13.1% malformations that were often multiple, whereas sodium selenite (10 and 25 ppm Se) resulted in 3.6 and 4.2% malformations. The teratogenicity of selenomethionine was confirmed in a second experiment in which mallards received 1, 2, 4, 8, or 16 ppm Se as selenomethionine, resulting in 0.9, 0.5, 1.4, 6.8, and 67.9% malformations, respectively. These malformations included hydrocephaly, microphthalmia, lower bill defects, and foot defects with ectrodactyly. Both forms of selenium increased the incidence of edema and stunted embryonic growth. Selenomethionine (10 ppm Se) resulted in a significant increase of approximately 40% in plasma glutathione peroxidase activity and a 70% increase in sorbitol dehydrogenase activity (indicative of hepatotoxicity) in hatchlings. Sodium selenite (25 ppm Se) resulted in fourfold elevation in plasma uric acid concentration, indicative of renal alteration. Selenomethionine accumulated much better in eggs than did sodium selenite. These findings indicate that selenomethionine is considerably more teratogenic and generally more embryotoxic than sodium selenite, probably due to higher uptake of selenomethionine.

Mercury accumulation in mallards fed methylmercury with or without added DDE.

Adult female mallards (Anas platyrhynchos) were fed a control diet or diets containing 1 ppm methylmercury chloride, 5 ppm methylmercury chloride, 1 ppm methylmercury chloride plus 5 ppm DDE, or 5 ppm methylmercury chloride plus 5 ppm DDE. The presence of DDE in the diet did not affect retention of mercury in breast muscle or eggs. There was a good correlation between the levels of mercury in the breast muscle of females and their eggs, and this correlation was unaffected by the presence of DDE in the diet. This correlation suggests that one could predict mercury levels in female mallards in the field when only eggs have been collected and vice versa.