Brown pelican: Population status, reproductive success, and organochlorine residues in Louisiana, 1971-1976
No abstract available.
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A group of 16 mallard hens ( Anas platyrhynchos ), that had been given feed containing 40 ppm of p,p' -DDE for 96 days, laid eggs with shells averaging about 15%–20% thinner than those of ten control birds during and up to 42 days after treatment. In eight of the treated birds killed at that time, whole-body DDE residues averaged 33.1 ppm (wet weight). The other eight treated birds and ten controls were kept through the winter with no additional DDE exposure and penned separately five days for individual egg collection about three weeks after laying began in spring. At that time (nearly 11 months after DDE feeding had stopped), the treated birds laid eggs with shells averaging 7.4% thinner than control eggshells (significant at P≤0.05) and their whole-body DDE residues averaged 9.6 ppm (wet weight). Variations in eggshell thickness and DDE residues were considerable among treated birds. However, regression analysis showed moderate negative correlations (r=−0.51 to −0.62) between eggshell thickness and DDE residues in whole bodies and eggs, and strong positive correlations (r=0.73 and 0.91) between DDE residues in whole bodies and in eggs.
3-Chloro-4-methyl benzamine HCl (DRC-1339), an avian toxicant, was fed to five species of birds for periods up to 120 days. The 30-day LC 50 of uniformly treated feed for starlings was 4.7 ppm and the 90-day LC 50 was 1.0 ppm. The 28-day LC 50 for coturnix was 18 ppm. The 30-day LC 50 for pigeons was less than 100 ppm. Pheasants fed diets containing 2% DRC-1339 baits diluted to a rate of 286 ppm of DRC-1339 died within 22 days. Bobwhite quail fed similar diets suffered some mortality at levels as low as 2.9 ppm, but most survived 10 times this dosage level for the 120-day test period. Application of the Kenaga “Index of Chronicity,” resulted in the conclusion that DRC-1339 was cumulatively toxic to birds. Reproduction in coturnix was adversely affected by treatments at 10 ppm of DRC-1339 and above. Reproduction in pigeons was adversely affected by a treatment of 25 ppm. In coturnix, DRC-1339 caused an increased incidence of egg breakage and decreased both egg and live chick production. In pigeons, DRC-1339 caused an increase in the proportion of infertile eggs. Reproductive ability of first generation offspring was not affected when parent coturnix and pigeons were fed DRC-1339. These data emphasize the need for care in the use of DRC-1339. The bait should be used only as registered and care exercised in storage and disposal of unused baits to avoid poisoning of nontarget species.
Captive black ducks ( anas rubripes ) were fed dietary DDE [1,1-dichloro-2,2- bis ( p -chlorophenyl)ethylene] at 10 ppm (dry weight; about 2 ppm on a natural diet basis) for 2 breeding seasons, then untreated feed for 2 succeeding years. Residues of DDE in the carcasses of adults declined 90% during the 2-year clean-up period. Following 2 years of dietary DDE, mean residues in eggs reached 64.9 ppm. Even after 2 years on clean feed, DDE residues in the eggs averaged 6.2 ppm or 9.5% of the mean DDE level reached after 2 years on treated feed. Shells of eggs from treated hens were about 20% thinner than shells of eggs from controls. Stoppage of DDE dosage resulted in progressively thicker shells, yet even after 2 years on untreated feed hens laid eggs with shells about 10% thinner than control hens. After DDE was removed from the diet, DDE residues in the eggs decreased, shell thickness increased, and reproductive success improved. Hens previously exposed to DDE, but then fed clean feed for 2 years, still produced significantly fewer surviving ducklings than did control hens.
Wild-trapped starlings ( Sturnus vulgaris ) were fed concentrations of Morsodren (2, 4, and 8 ppm), DDE or Aroclor 1254 (5, 25, and 100 ppm), or malathion (8, 35, and 160 ppm) that were found to be sublethal in pen-reared Coturnix quail fed these amounts for 12 weeks. Plasma enzymes had to be measured earlier than planned in starlings fed Morsodren (at three weeks) or the organochlorine compounds (at seven weeks) because of unexpected, subsequent mortality. Variations in enzyme response were greater in wild than in pen-reared birds, but not enough to mask the toxicant-induced changes in enzyme activity. Cholinesterase activities decreased in birds fed Morsodren or malathion, and increased in those fed the organochlorine compounds. Lactate dehydrogenase activities increased two-fold in starlings fed Morsodren and two- to four-fold in those fed the organochlorine compounds, but only 50% in those fed malathion. Further examination of enzyme profiles showed that creatine kinase and aspartate aminotransferase activities increased two-to four-fold in birds fed Morsodren or the organochlorine compounds but not at all in those fed malathion. Thus the classes of environmental contaminants fed to starlings could be easily distinguished by these enzymatic parameters. Evaluation of enzymatic profiles appears to be a potentially valuable technique to monitor the presence of toxicants in wild populations, especially if used to complement standard chemical residue analyses. Here the residue analyses showed, after three weeks feeding, that mercury in the carcasses reflected the concentrations fed daily, whereas accumulation in the livers was two- to four-fold greater. After seven weeks feeding, liver residues of either organochlorine compound were about three-fold higher than the concentrations fed daily. However, four times as much DDE as Aroclor 1254 had accumulated in the carcasses.
Blood samples were taken for two successive years from canvasback ducks trapped in the Chesapeake Bay. The first winter (1972–1973) five plasma enzymes known to respond to organochlorine poisoning were examined. Abnormal enzyme elevations suggested that 20% of the population sampled (23/115 ducks) might contain organochlorine contaminants, but no residue analyses were performed. The second winter (1974) two of the same enzymes, aspartate aminotransferase and lactate dehydrogenase, and a third enzyme known to be specifically inhibited by lead, delta-aminolevulinic acid dehydratase, were assayed in 95 blood samples. Blood residues of organochlorine compounds and of lead were determined in representative samples, and the correlations between residue levels and enzyme changes were examined. The enzyme bioassays in 1974 indicated that lead was a more prevalent environmental contaminant than organochlorine compounds in canvasback ducks; 17% of the blood samples had less than one-half of the normal delta-aminolevulinic acid dehydratase activity, but only 11% exhibited abnormal aspartate aminotransferase or lactate dehydrogenase activities. These findings were confirmed by residue analyses that demonstrated lead concentrations four times higher than background levels, but only relatively low organochlorine concentrations. There was a highly significant inverse correlation between delta-aminolevulinic acid dehydratase activity and blood lead concentrations (P<0.01), and a weaker but significant correlation between plasma aspartate aminotransferase activity and blood PCB concentrations (P<0.05). It was apparent that delta-aminolevulinic acid dehydratase activity in the blood provided a sensitive and precise estimate of lead contamination in waterfowl. In canvasback ducks 200 ppb of lead in the blood caused a 75% decrease in delta-aminolevulinic acid dehydratase activity, a magnitude of enzyme inhibition that disturbs heme synthesis and is regarded as detrimental in humans.
Patterns of mortality and inhibition of brain and plasma ChE in birds treated with ChE inhibitors were studied in an attempt to determine the validity of using ChE activity as a monitoring and diagnostic technique. Analysis of brain ChE activity proved to be reliable for diagnosing and monitoring effects of selected ChE inhibitors in birds. Brain ChE inhibition exceeding 20% indicated exposure, and inhibition greater than 50% was sufficient for diagnosing cause of death. Individuals that died from dietary exposure to parathion or carbofuran had brain ChE activities below 55% of normal; although individuals could survive with brain ChE activity lower than 50%. Problems associated with collection, storage, and analysis of tissues for ChE activity are discussed.
Experiments involving dietary toxicity and residue relationships of DDT, dieldrin, and endrin were conducted with short-tailed shrews. Dietary concentrations of DDT dissolved in vegetable oils were usually more toxic than diets containing comparable amounts of powdered DDT. Younger shrews, particularly females, were more tolerant of powdered DDT than older animals; yet, there were no conspicuous age differences in toxicity of DDT dissolved in oils. In comparison to other mammals, short-tailed shrews are not unusually sensitive to DDT, dieldrin, or endrin on the basis of two-week feeding tests. The influence of age and sex on toxicity of DDT, endrin, and dieldrin was sometimes more important than body weight. Of those shrews of the same age and sex that were fed the same dietary dosage, heavier shrews were more tolerant than lighter individuals; and, heavier shrews tended to lose a greater percentage of body weight before death. There was a range of 15 to 105 DDT equivalents in brains of shrews dying on dietary dosages of DDT. Six shrews fed a high level of DDT seemed to have unusual metabolite capabilities and died with apparent lethal levels of DDD in their brains. Levels of dieldrin in brains of shrews that died on a dietary dosage of dieldrin ranged from 3.7 to 12.6 ppm. In the rates of gain and loss experiments where shrews were given diets containing 400 ppm DDT or 50 ppm dieldrin up to 17 days, high residues were noted in tissues of shrews after two weeks on a contaminated diet and a few died at that time. After shrews were placed on clean food, it was determined that >50% of the dieldrin residues in carcass and brain were lost in <2 weeks. Males and females fed DDT for 17 days lost >50% of residues of DDT and metabolites in brains after 2 weeks on clean food; males lost nearly 50% of residues in carcasses after two weeks on clean food compared with a loss of only 11% in females.
Metals are released into aquatic systems from many sources, often at sublethal concentrations. The effects of sublethal concentrations of metals on fish are not entirely understood. The objective of this study was to determine the hematological and biochemical effects of a range of copper concentrations (6.4, 16.0, 26.9 ??g Cu/L) on rainbow trout (Oncorhynchus mykiss) over a prolonged period of time. Trout were exposed to copper, and, at intervals of 3, 7, 14, and 21 days, selected parameters were evaluated. Hemoglobin, hematocrit, plasma glucose, and plasma cortisol levels were elevated in trout exposed to 26.9 ??g Cu/L at day 3 and then returned to levels comparable to control fish. Plasma protein and lactate levels were not significantly altered in trout from any copper treatment. Hepatic copper concentration and hepatic metallothionein mRNA expression were consistently elevated in trout exposed to 26.9 ??g Cu/L. Both of these parameters stabilized by day 3, with only hepatic copper concentration showing a further increase at day 21. Hepatic copper concentration and hepatic metallothionein mRNA expression appear to be robust indicators of copper exposure. Most blood-based parameters evaluated appear to be associated with a transitory, nonspecific stress response. The return of elevated hematological and biochemical parameters to control levels after 3 days and thestabilization of hepatic metallothionein mRNA expression and copper concentration over a similar time period suggested acclimation to dissolved copper at 26.9 ??g/L. Further analysis of the data on blood-based parameters indicated that certain parameters (hemoglobin, hematocrit, plasma glucose, plasma cortisol) may be useful in field monitoring.
Over the past decade, destruction and degradation of wetland habitat has contributed to the decline of wading bird colonies on the Atlantic Coast. In 1998, an initial assessment of the possible contribution of metal pollution to declining heron populations in Chesapeake and Delaware Bays was conducted. Study sites included two heronries in industrialized locations (Pea Patch Island, DE and Baltimore Harbor, MD), and a reference site (Holland Island) remotely located in the southern Chesapeake Bay. Concentrations of 19 metals, metalloids, and trace elements were examined in blood and breast feathers of 14-16 day old nestling black-crowned night-herons. Metal concentrations in blood were low and showed few site differences, though mercury was elevated at Pea Patch Island as compared to other sites. In feathers, metal concentrations appeared to be in the low to moderate range at all sites, though limited data exist for interpreting pollutant concentrations in feathers of nestling wading birds. Where differences were detected, concentrations at Pea Patch Island were consistently greater than those at Baltimore Harbor and Holland Island. Feathers collected at Pea Patch Island had significantly greater concentrations of aluminum, barium, iron, lead, magnesium, and manganese, but were generally found to be within the range of concentrations detected in other nestling birds, where that information was available. Based on these results, metal pollution does not appear to be an immediate threat to BCNH colonies at these two locations, though future monitoring of some elements (Pb, Mn, and Al) may be warranted.
Methylmercury has been suspected as a cause of impaired reproduction in wild birds, but the confounding effects of other environmental stressors has made it difficult to determine how much mercury in the eggs of these wild species is harmful. Even when a sample egg can be collected from the nest of a wild bird and the mercury concentration in that egg compared to the laboratory-derived thresholds for reproductive impairment, additional information on the mercury levels in other eggs from that nest would be helpful in determining whether harmful levels of mercury were present in the clutch. The measurement of mercury levels in chorioallantoic membranes offers a possible way to estimate how much mercury was in a chick that hatched from an egg, and also in the whole fresh egg itself. While an embryo is developing, wastes are collected in a sac called the chorioallantoic membranes, which often remain inside the eggshell and can be collected for contaminant analysis. We fed methylmercury to captive mallards to generate a broad range of mercury levels in eggs, allowed the eggs to hatch normally, and then compared mercury concentrations in the hatchling versus the chorioallantoic membranes left behind in the eggshell. When the data from eggs laid by mercury- treated females were expressed as common logarithms, a linear equation was created by which the concentration of mercury in a duckling could be predicted from the concentration of mercury in the chorioallantoic membranes from the same egg. Therefore, if it were not possible to collect a sample egg from a clutch of wild bird eggs, the collection of the chorioallantoic membranes could be substituted, and the mercury predicted to be in the chick or whole egg could be compared to the thresholds of mercury that have been shown to cause harm in controlled feeding studies with pheasants, chickens, and mallards.
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No abstract available.
The objective of our study was to determine the efficiency with which lake trout retain DDT from their natural food. Our estimate of DDT assimilation efficiency would represent the most realistic estimate, to date, for use in risk assessment models.
No abstract available.