Northern Prairie Wildlife Research Center
Like some of the earlier studies, several subsequent studies (Quortrup and Shillinger 1941; Jordan and Bellrose 1950; Rosen and Bankowski 1960) did not stress the loss of body weight that is characteristic of chronic lead poisoning in waterfowl. Bellrose (1964) reported that waterfowl starving because of lead poisoning weighed about 50% of normal, but Trainer and Hunt (1965) found no correlation between the body weights of swans with more than 100 lead pellets in their gizzards and swans with 10 or fewer pellets.
Generally, captive waterfowl that die of chronic lead poisoning lose from 40 to 60% of their body weight before death; they also lose a greater percentage of body weight during mild weather than during cold weather. On the other hand, captive waterfowl that die of acute lead poisoning may lose relatively little weight before death. W.L. Anderson (1975) also found a direct correlation between body weight and number of lead pellets in gizzards of wild ducks that had died of acute lead poisoning. Sanderson and Irwin (1976: Table 16) reported that 8 of 20 male game-farm mallards on a diet of corn and dosed with five No. 4 lead pellets on 1 July died of acute lead poisoning an average of 7.6 days later after losing 20.5 percent of their body weight. The 12 remaining ducks died of chronic lead poisoning an average of 20.7 days after dosing and had lost 47.6 percent of their body weight. Waterfowl in the wild, we assume, would follow patterns similar to those of captive waterfowl.
Reports vary concerning the effects of lead poisoning on the appetites of waterfowl, and the topic merits further investigation. Early workers (Phillips and Lincoln 1930; Shillinger and Cottam 1937; Quortrup and Shillinger 1941; Adler 1942) indicated that lead-poisoned waterfowl showed no decrease and sometimes showed an increase in appetite. Beer and Stanley (1965) found that many birds that had died of lead poisoning had eaten shortly before death. Other investigators, however, have reported that lead poisoning causes a loss of appetite and that a decreased intake of food is one of the earliest external symptoms in lead-poisoned birds. Jordan and Bellrose (1951) found that captive mallards not dosed with lead but fed only the amount of food eaten by paired ducks dosed with lead showed weight loss and other symptoms that were similar to those shown by the lead-poisoned ducks. Irby et al. (1967) reported that ducks decreased their consumption of corn for 1-3 weeks after dosing with lead. During the second half of the experiment (the second month), however, the surviving dosed ducks ate as much or more corn than did their controls. Irwin et al. (1974) found that adult game-farm mallards dosed with lead and fed corn had reduced appetites but that dosed ducks fed an "adequate" diet (among other components, the adequate diet contained 19.2 percent protein compared with 8.8 percent protein in corn) showed no loss of appetite. Sanderson and Irwin (1976:63) did not measure food consumption in their studies; however, they noted decreased consumption of corn in ducks dosed with lead. In some instances, they found that shortly before ducks died of lead poisoning, their appetite for corn returned.
Quortrup and Shillinger (1941) reported that distention of the proventriculus and esophagus occurs because food cannot pass the gizzard. In one group of 70 captive mallards, Sanderson and Irwin (1976:63, Table 62) found that only 1 bird of 17 that died of lead poisoning from 4 to 8 days after dosing with lead had food in the digestive tract; none of the 17 showed impaction. In the same group of 70 ducks, among those that died from 9 through 39 days after dosing, 7 (10.0 percent) had corn in the esophagus and 2 (2.9 percent) had the esophagus impacted with corn; 26 (37.1 percent) had corn in the proventriculus and 7 (10.0 percent) had the proventriculus impacted with corn; 53 (75.7 percent) had corn present in the gizzard and 1 (1.4 percent) had the gizzard impacted with corn.
In spite of several clinical symptoms for lead poisoning in waterfowl, researchers cannot always be certain that an individual bird has died of or is suffering from lead poisoning. Many symptoms are seen only at necropsy. Recently, however, several diagnostic techniques, some of which can be used with live birds, have been described.
Although no individual relationship has been found between the amount of lead shot in a gizzard and lead residues in wing bones, a significant correlation between the two occurs on a population basis (White and Stendell 1977:472). The amount of lead in gizzards of mallards and pintails was closely related to the amount of lead in their wing bones as reported by the U.S. Fish and Wildlife Service (1978) and by W.L. Anderson (1975) for lesser scaups at Rice Lake, Illinois. Lead appears almost immediately in the wing bones after lead shot are ingested by birds. Thus, ducks that have expelled eroded pellets from their digestive tracts show an absence of gizzard lead but retain lead residue in their wing bones.
Wing bones (radii-ulnae) collected at random from 4,190 ducks during the National Waterfowl Wing Survey in 1972 and 1973 were analyzed for lead by the WARF Institute of Madison, Wisconsin, for the U.S. Fish and Wildlife Service (Stendell et al. 1979). Bones of adults contained concentrations of lead about twice as high as concentrations found in juveniles. Lead levels were highest in the Atlantic Flyway, at moderate levels in the Mississippi and Pacific flyways, and lowest in the Central Flyway.
A bimodal distribution of lead was found in most of the immature mallards with wing bones containing lead; the higher levels were believed to be the result of shot ingestion. About one-third of the wings analyzed from immature mallards had high levels of lead: 37.5 percent in the Mississippi Flyway, 36.6 percent in the Pacific Flyway, and 21.2 percent in the Central Flyway (Stendell et al. 1979). Moreover, these birds were only a few months old and had been exposed to heavily hunted areas for 4 months at most. Elevated lead levels ranged from 8.5 to 82.3 ppm, with a mean of 24.4 ± 17.3, and were found in samples from various states.
When penned year-old mallards were dosed with one No. 4 lead pellet, concentrations of lead in the wing bones of laying hens proved to be more than 4 times higher than levels found in the wing bones of nonlaying hens (Finley and Dieter 1978). Apparently the mobilization of calcium for egg laying increased the absorption of lead from the blood stream. In a similar but earlier experiment, Finley et al. (1976) found high levels of lead deposition in skeletons of laying hens; these levels may have resulted from calcium mobilization from bones during eggshell formation. According to Stendell et al. (1979), the lead content of bones is similar in males and females outside of the breeding season.
Blood samples have been used to determine the extent of lead toxicosis in waterfowl populations. The level of blood lead considered toxic but sublethal is 0.5 ppm, and the U.S. Fish and Wildlife Service recently established ≥0.2 ppm as a level above background levels. As demonstrated by Dieter (1979) in an examination of blood from 400 canvasbacks from Chesapeake Bay and the Upper Mississippi River, 1974-1978, symptoms of lead toxicity began to appear at 0.2 ppm. At levels of 0.5 ppm and higher (average 0.58 ppm), 12 percent of the canvasbacks showed significant depression of delta-aminolevulinic acid dehydratase (ALAD) enzyme activity. A reduction of ALAD enzyme activity in the brain causes cerebellar damage (Dieter and Finley 1979). Biochemical lesions in the brain precede such external symptoms of lead poisoning as wing droop and vent staining.
The level of protoporphyrin (PP) in the blood has also been used to determine levels of lead toxicosis in waterfowl. Roscoe et al. (1979) found that PP levels exceeding 40 ppm indicate lead poisoning; at 500 ppm an impairment of motor functions occurs. Motor functions of the nervous system correlate and control muscular activity. PP is important because it is a precursor to hemoglobin and because PP increases in the blood of lead-poisoned waterfowl, thereby indirectly indicating the amount of lead in the blood.
Anderson and Havera (1985) evaluated three methods of determining lead poisoning in Illinois waterfowl: (1) lead in blood, (2) PP in blood, and (3) ingested lead pellets in gizzards. They concluded that the lead level in blood was the most sensitive indicator of toxicosis, the PP level was less so, and the presence of ingested lead pellets was least likely to indicate the degree of exposure to lead. They found that 8.1 percent of the blood samples from 1,135 mallard in 4 areas in Illinois had lead levels of ≥0.5 ppm. Of blood samples from 864 Canada geese at 3 locations, 6.5 percent had ≥0.5 ppm lead levels. Fifteen (5.7 percent) of the blood samples from 264 canvasbacks collected in March from the Keokuk Pool on the Mississippi River had ≥0.5 ppm lead.
Analysis of the liver and other organs
A number of studies have used the analysis of heavy metals in the livers of waterfowl as a measure of exposure to lead. Adrian and Stevens (1979) emphasized the importance of using liver samples that are oven-dried to a constant weight; wet weights were found to produce sizeable errors.
In dead and moribund lesser scaup collected at Rice Lake, Illinois, W.L. Anderson (1975:267) found means of 47 and 43 ppm (wet weight) lead in livers of males and females, respectively; 62 and 77 ppm (wet weight) in kidneys; and 34 and 55 ppm (wet weight) in wing bones. He reported a high correlation between lead in the livers and lead in the wing bones of female scaup.
An analysis of Canada geese, victims of lead poisoning in eastern Colorado, disclosed an average lead level of 102 ppm in livers, 125 ppm in kidneys, and 41 ppm (dry weight) in wing bones (Szymczak and Adrian 1978: 301). A high correlation between the lead concentration in the liver and the concentration in the kidneys of the same specimens was reported.
Scanlon et al. (1980) examined waterfowl taken by Maryland hunters and compared the number of birds with ≥10 ppm lead in their livers (dry weight) and the presence or absence of ingested shot. They found that 28.8 percent of the waterfowl with shot in the gizzards had ≥10 ppm lead in their livers but that 16.2 percent of the birds without lead in their gizzards had equally high levels of lead in their livers. Of 613 specimens representing 14 species, 18.8 percent had liver lead of ≥10 ppm.
At Catahoula Lake and Lacassine National Wildlife Refuge, Louisiana, 1,110 dead and incapacitated waterfowl were collected for liver analysis and shot ingestion (Shealy et al. 1982). A level of 6.0 ppm wet weight or 20.0 ppm dry weight was used to indicate lead toxicosis. Of the entire sample, 74.8 percent had liver lead at those levels or higher. Lead toxicosis, as determined by levels of lead in livers, was distributed among species as follows: pintails, 82.2 percent; mallards, 80.0 percent; snow geese, 77.2 percent; whitefronted geese, 68.6 percent; and canvasbacks, 52.4 percent. The ingestion of lead shot among species was comparable: 75.0 percent of the pintails, 68.3 percent of the mallards, 76.9 percent of the snow geese, 71.0 percent of the white-fronted geese, and 60.9 percent of the canvasbacks contained ingested lead pellets. The average number of pellets ingested for pintails was 3.9; for mallards, 4.2; for snow geese, 2.0; and for white-fronted geese, 5.4 (Zwank et al. 1985).
The effect of lead poisoning on the size of certain internal organs may differ according to species and the stage of toxicosis and its nature - acute or chronic. Several investigators (Coburn et al. 1951; Jordan and Bellrose 1951; Locke and Bagley 1967; and Bates et al. 1968) found smaller-than-average livers, kidneys, hearts, and spleens in waterfowl suffering from lead poisoning. In contrast, Chupp and Dalke (1964) reported large livers in swans that died from lead poisoning from mine wastes in Idaho. Adler (1944) also reported enlarged kidneys, spleens, and livers in 4 wild lead-poisoned Canada geese in Wisconsin.
Sanderson and Irwin (1976) agreed that lead toxicosis results in a reduction of liver size. They also pointed out that the effect of lead on the liver of ducks is confounded "by the effects of seasons and their differing influences on the total rate of food consumption and on the relative rates of food consumption by the sexes, the average postdosing survival time, diet, and the lead-induced results of anorexia" (p. 30A). They also found that "the mean weights of livers of most dosed ducks were heavier than livers of undosed controls." They had no explanation for the heavy livers in dosed ducks, but they also found (p. 62) that the mean weights of livers, spleens, and testes of lead-dosed ducks that survived to the end of the experiment were significantly heavier than the mean weights of these organs for all lead-dosed ducks that died during the experiment.
Locke et al. (1966) found that acid-fast inclusion bodies in the proximal convoluted tubules of the kidneys can be used as presumptive evidence of lead poisoning in mallards, but this technique does not work for Canada geese (Locke et al. 1967).
Barrett and Karstad (1971) reported that erythrocytes from lead-poisoned Canada geese and mallards subjected to blue-ultraviolet light showed red fluorescence. This quick and simple technique can be used on live birds and is as reliable as some of the more conventional techniques.
One of the common characteristics of lead-poisoned waterfowl is severe anemia (Beer and Stanley 1965). The main sources of this anemia are probably the production of defective red cells and the impaired release of red cells (Bates et al. 1968). Hemosiderosis commonly occurs in kidneys, livers, and spleens of lead-poisoned waterfowl.
Calcium versenate (Ca EDTA) injected intraveously is diagnostic for heavy metals. If a live, lead-poisoned bird is injected with Ca EDTA, the symptoms do not reappear for about 48 hours (Rosen and Bankowski 1960). Several intraperitoneal injections of Ca EDTA in a solution of 6.6 percent cause lead-poisoned ducks to regain their appetites and to recover (Wobeser 1969).
For a discussion of several other methods of diagnosing lead poisoning in waterfowl, see Forbes and Sanderson (1978:256-260).