Mack T. Finley

Uptake and retention of dietary cadmium in mallard ducks

Adult mallard ducks fed 0, 2, 20, or 200 ppm of cadmium chloride in the diet were sacrificed at 30-day intervals and tissues were analyzed for cadmium. No birds died during the study and body weights did not change. The liver and kidney accumulated the highest levels of cadmium. Tissue residues were significantly correlated in all treatment groups and residues increased with treatment level. Hematocrits and hemoglobin concentrations were normal in all groups throughout the study. Little cadmium accumulated in eggs of laying hens, but egg production was suppressed in the group fed 200 ppm.

Survival and reproductive success of black ducks fed methyl mercury

Abstract A diet containing 3 ppm mercury was fed to black ducks ( Anas rubripes ) for periods of 28 weeks during two consecutive breeding seasons. Clutch size, egg production, number of eggs incubated, hatchability and survival of ducklings were lower during both years in hens fed mercury. Reduced hatchability and poor duckling survival were the most harmful effects. During 2 years, 13 pairs of breeders fed mercury produced only 16 ducklings that survived 1 week compared with 73 ducklings from 13 pairs of controls. Mercury residues in eggs, embryos and ducklings averaged about 30% lower during the second breeding season compared with first year results. Third eggs laid by treated hens contained a mean of 6·14 and 3·86 ppm mercury during the first and second years. Whole embryos that failed to hatch contained means of 9·62 and 6·08 ppm mercury during the first and second years. Brains of dead ducklings contained between 3·25 and 6·98 ppm mercury and exhibited lesions characteristic of mercury poisoning. Relative tissue mercury levels for treated adult breeders were: feathers > liver > kidney > breast muscle > brain. Mercury levels in males and females did not differ.

Delta-aminolevulinic acid dehydratase enzyme activity in blood, brain, and liver of lead-dosed ducks

Abstract Mallard ducks were dosed with a single shotgun pellet (ca. 200 mg lead). After 1 month there was about 1 ppm lead in blood, 2.5 in liver, and 0.5 in brain. Lead-induced inhibition of δ-aminolevulinic acid dehydratase enzyme in blood and cerebellum was much greater than in cerebral hemisphere or liver and was strongly correlated with the lead concentration in these tissues. The cerebellar portion of the brain was more sensitive to δ-aminolevulinic acid dehydratase enzyme inhibition by lead than were the other tissues examined. There was also a greater increase in the glial cell marker enzyme, butyrylcholinesterase, in cerebellum than in cerebral hemisphere, suggesting that nonregenerating neuronal cells were destroyed by lead and replaced by glial cells in that portion of the brain. Even partial loss of cerebellar tissue is severely debilitating in waterfowl, because functions critical to survival such as visual, auditory, motor, and reflex responses are integrated at this brain center.

Histopathologic effects of dietary cadmium on kidneys and testes of mallard ducks.

Mallard ducks fed 2, 20, or 200 ppm cadmium chloride were sacrificed at 30, 60, and 90 d. No mortality occured during the study and body weights remained unchanged. Kidney weights of the 200-ppm group were significantly greater after 60 and 90 d than those of controls; also, testis weights were significantly lower after 90 d. Kidneys of ducks fed 2 and 20 ppm cadmium were relatively unaffected; however, slight to severe kidney lesions were found in the 200-ppm group after 60 d of treatment. No significant lesions were found in mallard testes after feeding 2 ppm cadmium in the diet, and only a few birds in the 20-ppm group showed slight to moderate gonad alterations. After 90 d of treatment, however, testes of males fed 200 ppm had atrophied and the spermatogenic process had ceased. This study should provide important information for the interpretation of cadmium levels found in kidneys and testes of wild ducks.

Influence of laying on lead accumulation in bone of mallard ducks

Paired mallard ducks (Anas platyrhynchos) were given No. 4 lead shot, and bone lead concentrations were compared in drakes and in laying and nonlaying hens. Lead accumulation was significantly greater in bones with a high medullary content (femur and sternum) compared with bones with a lower medullary content (ulna-radius or wingbones). In dosed groups, hens always contained higher bone lead residues than drakes. After dosage with one shot (approximately 200 mg lead), lead in femurs of laying hens averaged 488.4 ppm compared with 113.6 ppm in nonlaying hens. Femurs of drakes averaged 9.4 ppm lead. Dosage with the second lead shot did not result in further accumulation of bone lead in hens, but increased bone lead concentrations threefold in drakes, suggesting that saturation levels for bone lead had already been reached in the hens after ingestion of one shot. There was no demonstrable relationship between egg production and bone lead residues. The high lead residues, found in medullary bones of laying hens indicate that sex and physiological condition are major factors influencing lead absorption by bone.

Delta-aminolevulinic acid dehydratase: inhibition in ducks dosed with lead shot.

Abstract Lead concentration in blood and erythrocyte δ-aminolevulinic acid dehydratase (ALAD) activity was measured in mallard ducks dosed with one all-lead shot or one lead-iron combination shot. For 2 weeks after dosage, lead in blood of ducks given an all-lead shot was fourfold higher than in those dosed with lead-iron shot. At 3 and 4 weeks, the differences in lead residues were directly proportional to lead content of the shots. ALAD activities measured at these intervals were inversely correlated (P

Sublethal effects of chronic lead ingestion in mallard ducks

Mallard drakes (Anas platyrhynchos) fed 1, 5, or 25 ppm lead nitrate were bled and sacrificed at 3-wk intervals. No mortality occurred, and the pathologic lesions usually associated with lead poisoning were not found. Changes in hematocrit and hemoglobin concentration did not occur. After 3-wk ducks fed 25 ppm lead exhibited a 40% inhibition of blood delta-aminolevulinic acid dehydratase activity that persisted through 12 wk exposure. After 12 wk treatment similar enzyme inhibition was present in the ducks fed 5 ppm lead. At 3 wk there was a small accumulation of lead (less than 1 ppm) in the liver and kidneys of ducks fed 25ppm lead; no further increases occurred throughout the exposure. No significant accumulation of lead occurred the the tibiae or wing bones. Groups of ducks fed 5 and 25 ppm diets for 12 wk were placed on clean feed and examined through a 12 wk posttreatment period. After 3 wk on clean diet delta-aminolevulinic acid dehydratase activity and lead concentrations in the blood had returned to pretreatment levels. Even though lead concentrations in the blood, soft organs and bone were low, a highly significant negative correlation between blood lead and blood enzyme activity was obtained. This enzyme bioassay should provide a sensitive and precise estimate for monitoring lead in the blood for waterflow.

TOXICITY OF EXPERIMENTAL LEAD-IRON SHOT VERSUS COMMERCIAL LEAD SHOT IN MALLARDS

The toxicity of an experimental lead-iron shot containing 38.1 percent lead was compared with commercial lead shot in mallard ducks (Anas platyrhynchos) fed corn for 14 weeks. Significantly higher mortality occurred in ducks dosed with commercial lead shot compared to ducks given lead-iron shot containing comparable amounts of lead. Loss of body weight was indicative of the difference in toxicity of the 2 types of shot. Mortality was dose related in ducks given commercial lead shot; one #8 shot (73 mg lead) caused 35 percent mortality with higher amounts of lead causing 80 to 100 percent mortality. Ingestion of up to 2 #4 lead-iron shot (111 mg lead) caused no significant weight loss and only 5 per- cent mortality. However, ducks dosed with 5 lead-iron shot suffered 45 percent mortality and those given 16 shot 50 percent mortality. J. WILDL. MANAGE. 42(1):32-39 Lead poisoning from ingested lead shot is still a major cause of mortality in water- fowl. A recent survey showed that the inci- dence of lead shot in gizzards ranged from 1.3 to 29.1 percent (White and Stendell 1977). They also reported a significant posi- tive correlation between frequency of lead shot in gizzards and lead residues in wing- bones. Considerable efforts are being made to develop nontoxic substitutes for lead shot. Toxicity studies using several types of shot have shown that lead-induced mor- tality is in proportion to the amount of lead present in the shot (Irby et al. 1967, Grandy

Reproduction and residue accumulation in black ducks fed toxaphene

Three sets of 15 pairs of black ducks (Anas rubripes) were given 0, 10, or 50 ppm toxaphene in a dry mash diet for a period of 19 months, which included two breeding seasons. Survival of adults was not affected, but the weights of treated males were depressed during the summer months. Egg production, fertility, hatchability, eggshell thickness, growth, and survival of young did not vary with toxaphene ingestion in either breeding season. However, the mean number of days required to complete a clutch was lower in birds fed toxaphene than in birds on the control diet. Clutches of hens fed 50 ppm toxaphene showed improved hatching success in the second year of the study.Carcass wet-weight (70% moisture) residues in adults and the young birds averaged from 50 to 100% of the dietary concentration (7% moisture); egg residues showed a similar trend. Carcass residues did not reflect those found in the livers or brains of the adults, which seldom exceeded 0.5 ppm. Toxaphene residues were found in the brain of only one 10 ppm bird, but were present in nearly all of the 50 ppm birds. Toxaphene residues were present in the liver all all birds ingesting toxaphene.