Studies of the Chick Edema Disease

Flick, D. F.; Firestone, David; Ress, John; Allen, James

doi:10.3382/ps.0521637

Cited by 30 publications

(7 citation statements)

References 12 publications

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“…The dioxin-contaminated chicken embryos had brain, leg, and beak malformations and were smaller than uncontaminated embryos. Newly hatched chickens injected with dioxins as embryos were smaller than controls and had sparse and defective down formation (Flick et al, 1965(Flick et al, ,1973. The pathological changes we saw, particularly the slight growth depression, edema, and sparse down follicles, are consistent with the effects of dioxins seen in Flick's studies.…”

Section: Discussionsupporting

confidence: 84%

“…The edema was consistent with literature descriptions of chick edema disease (Sanger et al, 1958;Schmittle et al, 1958), the causative factor being identified as PCDDs (Flick et al, 1973). Three-day-old chickens treated with 1 or 10 ng TCDD/kg/d (i.e., about 50 ng/chick/d) for 3 wk suffered subcutaneous and pulmonary edema, distended abdomens, and increased peritoneal and pericardial fluid (Schwetz et al, 1973).…”

Section: Discussionsupporting

confidence: 82%

“…PCB contamination of double-crested cormorant embryos also results in subcutaneous edema, often without hydropericardium (G. Fox, personal communication). Earlier studies have indicated that domestic chicken embryos are very susceptible to dioxin contamination, exhibiting 80% mortality with 1.8 ng total dioxins per egg, and 100% mortality with 4.5 ng/egg (Flick et al, 1965(Flick et al, ,1973. The dioxin-contaminated chicken embryos had brain, leg, and beak malformations and were smaller than uncontaminated embryos.…”

Section: Discussionmentioning

confidence: 96%

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Dioxin contamination and growth and development in great blue heron embryos

Hart

Cheng

Whitehead³

et al. 1991

Journal of Toxicology and Environmental Health

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A great blue heron colony located near a pulp mill in British Columbia failed to fledge young in 1987, with a concurrent sharp increase in polychlorinated dibenzo-p-dioxin (PCDD) and polychlorinated dibenzofuran (PCDF) levels in their eggs. In 1988 we tested the hypothesis that the PCDD and PCDF contamination caused reproductive failure by increasing mortality of the heron embryos in ovo. Pairs of great blue heron eggs were collected from three British Columbia colonies with low, intermediate, and high levels of dioxin contamination: Nicomekl, Vancouver, and Crofton, respectively. One egg of each pair was incubated under laboratory conditions at the University of British Columbia (UBC) while the other egg was analyzed for PCDDs and PCDFs. All incubated eggs were fertile. All eggs from the Nicomekl colony hatched, while 13 of 14 eggs from Vancouver and 12 of 13 eggs from Crofton hatched. Subcutaneous edema was observed in 4 of 12 chicks from Crofton and 2 of 13 chicks from Vancouver. No edema was seen in the chicks from Nicomekl. There was a small, but significant, negative regression of plasma calcium concentration, yolk-free body weight, tibia length, wet, dry, and ash weight, beak length, and kidney and stomach weight of the hatched chicks on the tetrachlorodibenzo-p-dioxin (TCDD) level of the paired eggs. Fewer down follicles were present on the heads of TCDD-contaminated chicks. Hence while dioxins did not cause mortality of the heron embryos in ovo, the depression of growth and the presence of edema are suggestive that dioxins at the levels found in the environment have an adverse effect on the development of great blue heron embryos.

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Section: Discussionsupporting

confidence: 84%

Section: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 96%

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Dioxin contamination and growth and development in great blue heron embryos

Hart

Cheng

Whitehead³

et al. 1991

Journal of Toxicology and Environmental Health

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“…Although most of the PCDD and PCDF homologues in eggs were negatively correlated with reproductive variables, TCDD-EQs provided the highest correlations. Thus, reproductive failure in our study probably resulted from cumulative effects rather than from a single compound, as suggested in other studies (7,12,20,21). …”

Section: Methodssupporting

confidence: 58%

Effects of Polychlorinated Dibenzo-p-Dioxins and Dibenzofurans on Nesting Wood Ducks (Aix Sponsa) at Bayou Meto, Arkansas

White¹,

Hoffman²

1995

Environmental Health Perspectives

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Wood ducks (Aix sponsa) nesting along Bayou Meto downstream from a hazardous waste site in central Arkansas were contaminated with polychlorinated dibenzo-p-dioxins (PCDDs) and dibenzofurans (PCDFs). Residues in eggs, based on 2,3,7,8-tetrachlorodibenzo-p-dioxin equivalents (TCDD-EQ), ranged up to 611 parts per trillion (ppt), and egg arithmetic means were 90-fold higher at the site nearest the point source compared with a reference site. We monitored productivity of wood ducks in artificial nest boxes at three sites on the bayou and at a reference site on a separate drainage during [1988][1989][1990]. Productivity was suppressed (p<0.05) at the bayou sites compared with the reference site, and egg TCDD-EQs were inversely correlated (p < 0.001) with productivity in corresponding nests. The threshold range of toxicity, where reduced productivity was evident in wood ducks (based on TCDD-EQs), was > 20 to 50 ppt. Oxidative stress and teratogenic effects occurred in ducklings at the more contaminated nesting sites nearest the point source. These findings suggest that wood ducks may be more sensitive to PCDD and PCDF contamination than some other aquatic birds and could serve as an indicator species for monitoring biological impacts from these contaminants. Environ Health Perspect 1 03(Suppl 4): 37-39 (1995)

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“…A method was recently developed for the detection of low concentrations of TeDD in biological tissue,12 but an attempt to use this method in a monitoring program of the Environmental Protection Agency was not successfuL 15 Published information on the bioaccumulation of TCDD after long-term exposure is not available. Flick et al 16 found that the feeding of toxic fat contaminated with chlorinated dibenzodioxins resulted in pronounced cumulative toxicity in monkeys. Studies with single oral doses of C 14 -labeled 2,3,7 ,8-TCDD in rats indicate that half of the radioactive material was recovered within 21 days in the feces and only 13% in urine and 3% in expired air.…”

Section: Discussionmentioning

confidence: 98%

Epidemiology and Pathology of a Tetrachlorodibenzodioxin Poisoning Episode

Kimbrough¹,

Carter²,

Liddle³

et al. 1977

Archives of Environmental Health: An International Journal

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We describe epidemiological and laboratory investigation of a poisoning outbreak that involved three riding areas and killed fifty-seven horses, five colts, and numerous other animals. The outbreak was traced to the spraying of the areas with salvage oil contaminated with tetrachlorodibenzodioxin, trichlorophenol, and polychlorinated biphenyls. The contamination of the salvage oil resulted from the improper disposal of toxic industrial waste. In the tissues of the horses available for study, the most prominent lesion was a centrilobular fibrosis of the liver that arose in the wall of the central veins. This lesion resembled the chronic form of veno-occlusive disease of the liver in humans.

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Studies of the Chick Edema Disease

Cited by 30 publications

References 12 publications

Dioxin contamination and growth and development in great blue heron embryos

Dioxin contamination and growth and development in great blue heron embryos

Effects of Polychlorinated Dibenzo-p-Dioxins and Dibenzofurans on Nesting Wood Ducks (Aix Sponsa) at Bayou Meto, Arkansas

Epidemiology and Pathology of a Tetrachlorodibenzodioxin Poisoning Episode

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