Yolk sac edema

Hatchability was reduced at 226 and 302 ng/kg egg, with greatest mortality at the sac-fry stage. In all TCDD groups, sac fry that died developed subcutaneous yolk-sac edema. There were no deaths at egg concentrations of 34 ng/kg and some deaths at 55 ng/kg... 

Fish-specific TEFs of halogenated diphenyl ethers have been low also in a rainbow trout early life stage mortality bioassay [85]. Halogenated diphenyl ethers were inactive in this bioassay, whereas polyhalogenated dibenzo-p-dio-xins, dibenzofurans, and biphenyls reduced growth and produced yolk sac edema and craniofacial malformations. PCDEs 71, 77, 102, 118, and 126 and PBDEs 47,85, and 99 were analyzed in this bio assay. 

Incardona et al. (2005) affirm that embryos of fishes exposed to wheathered ANS oil and to mixtiues of PAHs developed a pericardium syndrome, yolk sac edema, reduction in the craniumfacial structure and body axis defects. Many of the defects were induced by individual exposition to the tricyclic aromatic hydrocarbons that is one the most abundant class between the wheathered ANS oil, causing secondaiy impacts in the cardiac fimction of the embryo, coincident with the development of the cardiac conduction system. 

A 1963 report of embryotoxic and teratogenic effects of Aroclor 1242 anticipated the later findings of PCBs as environmental pollutants by five years. When McLaughlin et al. injected the Aroclor into the yolk sacs of 20 fertilized eggs prior to incubation, only one chick hatched--and it died within two days (ref. 140). Embryos examined showed beak deformities, edema and a retarded growth pattern. 

Tuvikene (1995) reports that eggs of fishes contaminated with anthracene, after exposition to ultraviolet radiation, presented alterations in the development such as edema, malfunction of the yolk sac and deformities in the eyes. According to Tilghman Hall and Oris (1991), PAHs, specifically anthracene, can be transferred by the mother to her offspring. 

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