Combined extraction-cleanup column chromatographic procedure for determination of dicofol in avian eggs.

Dicofol in avian eggs was completely oxidized to dichlorobenzophenone (DCBP) when a hexane Soxhlet extraction procedure was used. This degradation did not occur with other avian tissues (muscle and liver). For this reason, a combined extraction-cleanup column chromatographic procedure, without added heat, was developed for the determination of dicofol in avian eggs. Homogenized subsamples of eggs were mixed with sodium sulfate, and the mixture was added as the top layer on a column prepacked with Florisil. The dicofol and other compounds of interest were then eluted with ethyl ether-hexane. The extracts, relatively free from lipids, were quantitated on a gas chromatograph equipped with a 63Ni electron-capture detector and a methyl silicone capillary column. Recoveries from chicken eggs, fortified with dicofol and other DDT-related compounds, averaged 96%. Analysis of eggs of eastern screech-owls, fed a meat diet containing 10 ppm technical Kelthane, showed that both dicofol and DCBP were present. Results were confirmed by gas chromatography/mass spectrometry. This method is rapid and reliable, involves a minimum of sample handling, and is well suited for high volume determination of dicofol in eggs and other avian tissues.

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.

Gas-liquid chromatographic and gas-liquid chromatographic-mass spectrometric determination of fenvalerate and permethrin residues in grasshoppers and duck tissue samples.

A procedure is described for determining fenvalerate and permethrin residues in grasshoppers and duck tissues. Samples are Soxhlet-extracted with hexane and cleaned up by gel permeation chromatography with an in-line alumina column. Samples are analyzed by gas-liquid chromatography with electron capture detection, and confirmed by gas-liquid chromatography-mass spectrometry. The average recovery from fortified tissues was 97%.

Effects of DDE and PCB (Aroclor 1260) on experimentally poisoned female little brown bats (Myotis lucifugus): lethal brain concentrations.

Adult female little brown bats (Myotis lucifugus) were collected in a church attic in North East, Cecil County, Md. Mealworms (Tenebrio molitor) containing organochlorine pollutants were fed to the bats as follows: 5 bats were dosed at 480 ppm DDE, 12 at 150 ppm DDE, 5 at 1000 ppm polychlorinated biphenyl (PCB; Aroclor 1260), and 12 at 15 ppm PCB. Seven other bats were fed untreated mealworms. The objective was to elevate brain levels of DDE and PCB to lethality and measure these concentrations. During 40 d of dosage, one DDE-dosed bat and two PCB-dosed bats died after exhibiting the prolonged tremor that characterizes organochlorine poisoning. After dosage, surviving bats were starved to elevate brain levels of toxicants, and three additional DDE-dosed bats had tremors before dying. The mean brain concentration of DDE diagnostic of death was estimated as 603 ppm, range 540-670 ppm. This mean is 16-18% higher than means for Mexican free-tailed bats (Tadarida brasiliensis) and common grackles (Quiscalus quiscula), and may indicate less sensitivity. Lethal brain concentrations of Aroclor 1260 were 1300 and 1500 ppm. Such values appear to be higher than values (Aroclor 1254) for brown-headed cowbirds (Molothrus ater). During starvation, DDE-dosed bats lost weight about 24% faster than controls. If smaller amounts of stored DDE cause increases in metabolic rates of nonfeeding bats, as during hibernation or migration, the result could be premature energy depletion and increased mortality.

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.

Gas-liquid chromatographic determination of kepone in field-collected avian tissues and eggs.

A procedure is described for determining Kepone (decachlorooctahydro-1,3,4-metheno-2H-cyclobuta [cd] pentalene-2-one) residues in avian egg, liver, and tissue. Samples were extracted with benzene-isopropanol, and the extract was cleaned up with fuming H2SO4-concentrated H2SO4. Kepone was separated from organochlorine pesticides and polychlorinated biphenyls on a Florisil column and analyzed by electron capture gas-liquid chromatography (GLC). The average recovery from spiked tissues was 86%. The analyses performed on 14 bald eagle carcasses and livers, 3 bald eagle eggs, and 14 osprey eggs show measurable levels which indicate that Kepone accumulates in the tissues of fish-eating birds. Residues were confirmed by GLC-mass spectrometry.

Ruptured-yolk peritonitis and organochlorine residues in a royal tern.

Ruptured-yolk peritonitis was responsible for the death of a royal tern. Lodgment of eggs in the oviduct was probably due to reverse peristalsis brought about by breakage of the thin-shelled eggs and secondary bacterial infection. The thin shells were apparently not related to the low levels of DDE and other organochlorine pollutants found in tissues and egg contents.