Interactive effects of selenium, methionine, and dietary protein on survival, growth, and physiology in mallard ducklings.

Concentrations of over 100 ppm (100 mg/kg) selenium (Se) have been found in aquatic food chains associated with irrigation drainwater. Both quantity and composition of dietary protein for wild ducklings may vary in selenium-contaminated environments. Day-old mallard (Anas platyrhynchos) ducklings received one of the following diets containing 22% protein: unsupplemented (controls), 15 ppm Se (as selenomethionine), 60 ppm Se, methionine supplemented, 15 ppm Se with methionine supplement, or 60 ppm Se with methionine supplement. In a second concurrent experiment the above sequence was repeated with a protein-restricted (11%) but isocaloric diet. In a third concurrent experiment all ducklings received 44% protein with 0, 15, or 60 ppm Se added. After 4 weeks, blood and tissue samples were collected for biochemical and histological examination. With 22% protein and 60 ppm Se in the diet, duckling survival and growth was reduced and histopathological lesions of the liver occurred. Antagonistic interactive effects occurred between supplementary methionine and Se, including complete to partial alleviation of the following Se effects by methionine: mortality, hepatic lesions, and altered glutathione and thiol status. With 11% protein, growth of controls was less than that with 22% protein, Se (60 ppm) caused 100% mortality, and methionine supplementation, although protective afforded less protection than it did with 22% protein. With 44% protein, ducklings experienced physiological stress, and Se was more toxic than with methionine-supplemented 22% protein. These findings suggest the potential for antagonistic effects of Se, methionine, and protein on duckling survival and physiology.

Interactive effects of arsenate, selenium, and dietary protein on survival, growth, and physiology in mallard ducklings.

High concentrations of arsenic (As) and selenium (Se) have been found in aquatic food chains associated with irrigation drainwater. Total biomass of invertebrates, a major source of protein for wild ducklings, may vary in environments that are contaminated with selenium. Day-old mallard (Anas platyrhynchos) ducklings received an untreated diet (controls) containing 22% protein or diets containing 15 ppm Se (as selenomethionine), 60 ppm Se, 200 ppm As (as sodium arsenate), 15 ppm Se with 200 ppm As, or 60 ppm Se with 200 ppm As. In a concurrent experiment, the same sequence was repeated with a protein-restricted (7%) but isocaloric diet. After 4 weeks, blood and tissue samples were collected for biochemical and histological examination. With 22% protein and 60 ppm Se in the diet, duckling survival and growth was reduced and livers had histopathological lesions. Arsenic alone caused some reduction in growth. Antagonistic interactive effects occurred between As and Se, including complete to partial alleviation of the following Se effects: mortality, impaired growth, hepatic lesions and lipid peroxidation, and altered glutathione and thiol status. With 7% protein, survival and growth of controls was less than that with 22% protein, Se (60 ppm) caused 100% mortality, and As (200 ppm) caused mortality, decreased growth, and liver histopathology. These findings suggest the potential for antagonistic effects of Se and As on duckling survival, growth, and physiology with adequate dietary protein but more severe toxicological effects when dietary protein is diminished.

Interactive effects of boron, selenium, and dietary protein on survival, growth, and physiology in mallard ducklings.

High concentrations of boron (B) and selenium (Se) have been found in aquatic food chains associated with irrigation drainwater. Total biomass of invertebrates, a major source of protein for wild ducklings, is sometimes diminished in agricultural drainwater ponds contaminated with Se and B. Day-old mallard (Anas platyrhynchos) ducklings received an untreated diet (controls) containing 22% protein or diets containing 15 ppm (microgram/g) Se (as selenomethionine), 60 ppm Se, 1,000 ppm B (as boric acid), 15 ppm Se with 1,000 ppm B, or 60 ppm Se with 1,000 ppm B. In a concurrent experiment, the above sequence was repeated with a protein-restricted (7%) but isocaloric diet. After four weeks, blood and tissue samples were collected for biochemical and histological examination. With 22% protein and 60 ppm Se in the diet, duckling survival and growth was reduced and histopathological lesions of the liver occurred. Boron alone caused some reduction in growth. Several interactive effects occurred between B and Se, including further reduction in growth, and increases in plasma glutathione reductase activity, hematocrit, hemoglobin and plasma protein concentrations. With 7% protein, the growth of controls was less than that with 22% protein, 60 ppm Se caused 100% mortality, and growth effects of 15 ppm Se and 1,000 ppm B alone were more pronounced than with 22% protein. Selenium accumulation increased in the liver with 7% protein. Interactive effects were greater for Se and B with 7% protein than with 22% protein and included significant mortality and enhanced accumulation of Se in the liver. These findings suggest the potential for more severe toxicological effects of Se and B independently and interactively on duckling survival and development when dietary protein is diminished.

A survey of Pb, Cu, Zn, Cd, Cr, As, and Se in earthworms and soil from diverse sites.

Earthworms and soils were collected from 20 diverse sites in Maryland, Pennsylvania, and Virginia, and were analyzed for Pb, Cu, Zn, Cd, Cr, As, and Se. Correlation coefficients relating concentrations of the elements in earthworms to concentrations in soil were low (-0.20

The incidence and gene frequency of ataxia-telangiectasia in the United States.

Ataxia-telangiectasia (A-T) is an autosomal recessive neurological syndrome of considerable interest because homozygotes are highly predisposed to cancer. Vigorous casefinding in the United States in 1970-72 and 1980-84 identified 231 white, 29 black, and three Oriental A-T cases that provide information about the incidence and gene frequency of A-T. White patients identified in this study were born at the rate of 3.0 per million live births in the U.S. in the years 1965-69. The highest observed incidence was in the state of Michigan for 1965-69, where identified white A-T patients were born at the rate of 11.3 per million births. Based on the incidence data, the minimum frequency of a single hypothetical A-T gene in the U.S. white population was estimated to be .0017. Pedigree analysis, which estimates the gene frequency from the proportion of affected close blood relatives of homozygous probands, estimated the most likely gene frequency to be .007 on the assumption that A-T is a single homogeneous genetic syndrome, with 95% confidence limits of .0012-.02. Given that complementation analysis has demonstrated the genetic heterogeneity of A-T, the A-T heterozygote frequency will probably fall between 0.68% and 7.7%, with 2.8% being the most likely estimate.

Mortality and cancer incidence in 263 patients with ataxia-telangiectasia.

Mortality and cancer incidence were measured retrospectively in 263 ataxia-telangiectasia (A-T) homozygotes. For white and black A-T patients, respectively, all-cause mortality was 50 and 147 times higher than expected based on U.S. mortality rates. There were 52 primary cancers, representing a 61-fold cancer excess for white probands and a 184-fold excess for black probands. The cancer excess was most pronounced for lymphoma, with 252- and 750-fold excesses observed for whites and blacks, respectively. All the age-specific mortality and cancer incidence rates for blacks exceeded those for whites, and overall mortality was 3.0 times higher for black probands than for whites (P less than .001), whereas cancer incidence was 2.2 times higher (P less than .06). Among the white A-T patients, 36% of those who had died had lived at least until 20 years of age, and 33% of those still living were at least 20 years old.

Pesticide, PCB, and lead residues and necropsy data for bald eagles from 32 states-1978-81.

In 1978-81, 293 bald eagles (Haliaeetus leucocephalus) from 32 states were necropsied and analyzed for organochlorine pesticides, polychlorinated biphenyls (PCB), and lead residues. DDE was found in all carcasses; PCB, DDD, trans-nonachlor, dieldrin and oxychlordane were next in order of percent frequency of detection. The median levels of DDE and PCB have declined when compared with previous collections. Five specimens contained high levels of dieldrin in their brains which may have contributed to their deaths. Seventeen eagles contained liver lead residues greater than 10 ppm and probably died of lead poisoning. Trauma and shooting are the most common causes of death.

DDE residues in young wood ducks (Aix sponsa) near a former DDT manufacturing plant.

Breast muscle DDE residues were as high as 5.8 ppm wet-weight basis and 280 ppm lipid-weight basis in young wood ducks (Aix sponsa) collected on Wheeler National Wildlife Refuge near a former DDT manufacturing plant in northern Alabama. The average DDE residue in wood ducks collected nearest the plant was 46 times background levels 74 km from the plant.

Organochlorine residues and shell thicknesses in eggs of the clapper rail, common gallinule, purple gallinule, and limpkin (class Aves), eastern and southern United States, 1972-74.

Organochlorine residues and shell thicknesses were surveyed in eggs of the clapper rail (Rallus longirostris), purple gallinule (Porphyrula martinica), common gallinule (Gallinula chloropas), and limpkin (Aramus guarauna) from the eastern and southern United States. Clapper rail eggs were collected during 1972-73 in New Jersey, Virginia, and South Carolina. During 1973-74, gallinule eggs were collected in Florida, South Carolina, and Louisiana, and limpkin eggs were collected in Florida. Egg contents were analyzed for residues of organochlorine pesticides, including DDT, TDE, DDE, dieldrin, mirex, heptachlor epoxide, oxychlordane, cis-chlordane (and/or trans-nonachlor), cis-nonachlor, hexachlorobenzene (HCB), toxaphene, and endrin, and for polychlorinated biphenyls (PCBs). Shell thicknesses of recent eggs of these species were compared with archival eggs that had been collected before 1947. With the exception of the limpkin, the majority of eggs analyzed contained residues of p,p'-DDE and PCBs. Geometric means ranged from 0.10 ppm to 1.3 ppm. Small amounts (less than 1.0 ppm) of mirex, dieldrin, cis-chlordane (and/or trans-nonachlor), TDE, and DDT were detected in a few eggs. No evidence of eggshell thinning was found for any of the species studied. DDE residues in clapper rail eggs were higher in New Jersey and Virginia than in South Carolina.

DDT contamination at Wheeler National Wildlife Refuge.

Disposal of industrial waste resulted in massive DDT contamination at Wheeler National Wildlife Refuge, Alabama. Nearly a decade after the cessation of DDT manufacturing at the facility responsible, concentrations of DDT residues in the local fauna are still high enough to suggest avian reproductive impairment and mortality. Populations of fish-eating birds are low, endangered species are being exposed, and muscle lipids of game birds contain up to 6900 parts of DDT (isomers and metabolites) per million.

Organochlorine pesticide, PCB, and PBB residues and necropsy data for bald eagles from 29 states--1975-77.

During 1975-77, 168 bald eagles (Haliaeetus leucocephalus) found moribund or dead in 29 states were analyzed for organochlorine pesticides and polychlorinated biphenyls (PCBs); 32 specimens from 13 states were analyzed for polybrominated biphenyls (PBBs). PCBs were present in 166 bald eagle carcasses and DDE was found in 165. TDE and dieldrin were identified in 137 samples, trans-nonachlor in 118, and oxychlordane in 90. Brains of five eagles contained possible lethal levels of dieldrin, and two eagles possibly died of endrin poisoning. Nine eagle livers, analyzed because of suspected lead poisoning, contained high levels of lead. Twenty percent of the eagles died from shooting, the most common cause of death; this cause of death, however, has declined.

Residues of organochlorine pesticides and polychlorinated biphenyls and autopsy data for bald eagles, 1973-74.

Eighty-six bald eagles found sick or dead during 1973-74 in 24 States were analyzed for organochlorine compounds. DDE was detected in all caracasses; polychlorinated biphenyls (PCB's) were found in all but two. Seventy-five carcasses contained TDE and/or dieldrin. Four eagles had possibly lethal levels of dieldrin in the brain. Bald eagles continue to retain high residue levels of organochlorine pollutants. Illegal shooting remained the most common cause of death but accounted for a smaller percentage of the mortalities than in the two previous biennial collections.

Residues of organochlorine pesticides and polychlorinated biphenyls and autopsy data for bald eagles, 1971-72.

Thirty-seven bald eagles found sick or dead in 18 States during 1971-72 were analyzed for organochlorine pesticides and polychlorinated biphenyls (PCB's). DDE and PCB's were detected in all bald eagle carcasses; 30 carcasses contained DDD and 28 contained dieldrin. Four eagles contained possibly lethal levels of dieldrin and nine eagles had been poisoned by thallium. Autopsies revealed that illegal shooting was the most common cause of mortality. Since 1964 when data were first collected, 8 of the 17 eagles obtained from Maryland, Virginia, South Carolina, and Florida possibly died from dieldrin poisoning; all four specimens from Maryland and Virginia were from the Chesapeake Bay Tidewater area.