Polychlorinated Biphenyls Influence on Hatchability ,

Briggs, D. M.; Harris, Jonathan

doi:10.3382/ps.0521291

Cited by 15 publications

(6 citation statements)

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“…After biphenyl withdrawal, hatchability of eggs laid by the pullets fed Aroclors 1232, 1242 and 1248 showed signs of improvement in Period 2, which consequently resulted in a significant period difference (P < 0.01). The results with Aroclors 1232, 1242 and 1248 agree with those of ; those of Aroclor 1242 agree with those of Briggs and Harris (1973) and Britton and Huston (1973); those of Aroclor 1248 agree with those of Scott et al (1971). Conversely, the results obtained with Aroclor 1254 do not agree with those of Lillie et al (1974).…”

Section: Hatchabilitysupporting

confidence: 90%

Toxicity of Certain Polychlorinated and Polybrominated Biphenyls on Reproductive Efficiency of Caged Chickens

et al. 1975

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The biphenyls tested with caged White Leghorn pullets were polychlorinated biphenyl (PCBs) Aroclors 1232, 1242, 1248, 1254 and 1016 and polybrominated biphenyl (PBB) PBP-6 at the 5, 10 and 20 p.p.m. levels. These pollutants exerted no adverse effects on egg production, egg weight, egg shell thickness, feed consumption, adult body weight changes, livability and fertility after 8 weeks of biphenyl feeding, irrespective of biphenyl level or compound. Hatchability of fertile eggs as a result of biphenyl feeding was significantly affected by 10 or 20 p.p.m. and by three PCB compounds (Aroclors 1232, 1242, 1248). The hatchability (%) of eggs laid by pullets fed 10 and 20 p.p.m. declined to 78 and 45, respectively, for Aroclor 1232, 48 and 5 for Aroclor 1242 and 40 and 5 for Aroclor 1248 after 6 weeks of biphenyl feeding, as compared with 90 for the control group. The most common embryonic abnormality was edema in the neck and rump areas. Biphenyl supplementation in the maternal diet also caused a shift in the peak pattern of embryonic death. Progeny growth as a result of biphenyl in the maternal diet was significantly depressed by 10 or 20 p.p.m. and by Aroclors 1242 and 1248. The level of the three PCBs found to be toxic to chickens appears to lie somewhere between 5 and 10 p.p.m.

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Section: Hatchabilitysupporting

confidence: 90%

Toxicity of Certain Polychlorinated and Polybrominated Biphenyls on Reproductive Efficiency of Caged Chickens

et al. 1975

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“…Bi-weekly embryo mortality results appear in Figure 1. There were no consistent significant differences in fertility of eggs from pullets fed the PCBs and controls throughout the study, agreeing with other reports (Dahlgren and Linder, 1971;Briggs and Harris, 1973;Britton and Huston, 1973;Lillie et al, 1974). The 74.0, 54.7, and 59.2 percent average mortalities in embryos of eggs from pullets fed 2,4,5,3',4'-pentachlorobiphenyl, Aroclor 1242, and Aroclor 1254, respectively, were significantly higher (p. < .001) than the 12.2 percent mortality in embryos of eggs from control pullets and mortality in eggs from pullets fed the other three purified components.…”

Section: Resultssupporting

confidence: 92%

“…Biochem. Pheasants (Dahlgren and Linder, 1971), quail (Hill et al, 1974), and chickens (Scott et al, 1971;Briggs and Harris, 1973;Britton and Huston, 1973;Lillie et al, 1974) all exhibit decreased reproductive performance when PCB's are consumed. 37: 1197-1207.…”

Section: Introductionmentioning

confidence: 99%

Effects of Purified Polychlorinated Biphenyl Analogs on Chicken Reproduction

Hansen

1975

Poultry Science

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Polychlorinated biphenyl (PCB) compounds were administered in the diet to White Leghorm pullets for 10 weeks. Average embryonic mortality in eggs from pullets fed Aroclor 1242, Aroclor 1254 and 2,4,5,3',4',-pentachloro-biphenyl was 54.7, 59.2 and 74.0 percent, respectively, which was significantly high (p less than .001) compared to controls; however, these three feeds were shown qualitatively to have dibenzodioxin contamination. Degree of chlorination of PCB analogs may not infer that they are toxic, but rather, the position of substitution may be the factor that determines the toxicity to developing embryos.

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“…Embryos from leghorn hens fed Aroclor 1242 developed hearts with ridges on the exterior of the right ventricle in contrast to the controls (Briggs and Harris, 1973). In egg injection studies, Cheung et al (1981) found that TCDD caused a dose-related increase in the incidence of all types of cardiovascular malformations.…”

Section: Biologymentioning

confidence: 92%

“…The susceptibility of avian embryos to these chick-edema active compounds was documented through egg injection studies (McLaughlin et al, 1963;Flick et al, 1965b;Verrett, 1970;Carlson and Duby, 1973) and through adult feeding and reproduction studies (Scott et al, 1971;Britton and Huston, 1973;Briggs and Harris, 1973;Platonow and Reinhart, 1973;Tumasonis et al, 1973;Bush et al, 1974;Cecil et al, 1974). The effects consistently noted in these studies included reduced hatchability, embryotoxicity, and teratogenesis.…”

Section: Theory and Factsmentioning

confidence: 95%

Great lakes embryo mortality, edema, and deformities syndrome (GLEMEDS) in colonial fish‐eating birds: Similarity to chick‐edema disease

Gilbertson¹,

Kubiak

Ludwig³

et al. 1991

Journal of Toxicology and Environmental Health

342

150

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Several species of colonial fish-eating birds nesting in the Great Lakes basin, including herring gulls, common terns and double-crested cormorants, have exhibited chronic impairment of reproduction. In addition to eggshell thinning caused by high levels of DDT and metabolites, the reproductive impairment is characterized by high embryonic and chick mortality, edema, growth retardation, and deformities, hence the name Great Lakes embryo mortality, edema, and deformities syndrome (GLEMEDS). The hypothesis has been advanced that GLEMEDS in colonial fish-eating birds resembles chick-edema disease of poultry and has been caused by exposure to chick-edema active compounds that have a common mode of action through the cytochrome P-448 system. Detailed evidence has been collected from the following three groups of studies on herring gulls in the lower Great Lakes during the early 1970s; Forster's terns in Green Bay, Wisconsin in 1983; and double-crested cormorants and Caspian terns in various locations in the upper Great Lakes from 1986 onwards. It has proved difficult to establish not only the onset of the disease in the various species at various locations but also the period in which chick-edema active compounds were released. Anecdotal evidence suggested that serious egg mortality in Lake Ontario herring gulls first occurred in 1966, through the signs of chick-edema disease were not looked for until 1974. Only indirect evidence is available on the date of the release of one of the presumed causal agents, 2,3,7,8-tetrachlorodibenzo-p-dioxin, but highest levels may have occurred in the early to mid 1960s. More reliable data show that the onset of the improvement of reproduction of Lake Ontario herring gulls coincided with the declines in organochlorine compounds and particularly 2,3,7,8-TCDD and PCB. Similarly, information on the onset of the disease and exposures in the Forster's tern and double-crested cormorants in Green Bay is uncertain but bird banders did not observe deformities until the 1970s, which corresponds with the onset of high levels of PCB. If the disappearance of the Caspian tern from Saginaw Bay in the mid 1960s corresponds with the onset of GLEMEDS at that location, then there is a close temporal relationship to the onset of high PCB levels. Chick-edema disease is difficult to diagnose because there is no specific lesion, but rather there is a suite of lesions.(ABSTRACT TRUNCATED AT 400 WORDS)

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Polychlorinated Biphenyls Influence on Hatchability ,

Cited by 15 publications

References 0 publications

Toxicity of Certain Polychlorinated and Polybrominated Biphenyls on Reproductive Efficiency of Caged Chickens

Toxicity of Certain Polychlorinated and Polybrominated Biphenyls on Reproductive Efficiency of Caged Chickens

Effects of Purified Polychlorinated Biphenyl Analogs on Chicken Reproduction

Great lakes embryo mortality, edema, and deformities syndrome (GLEMEDS) in colonial fish‐eating birds: Similarity to chick‐edema disease

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