Chick edema disease, which is characterized by ascites and by pericardial, subcutaneous, and pulmonary edema, is caused in offsprings of hens exposed to dioxin-like action chemicals in their feed. This pathology is of ectodermal origin in the same way as the developmental deformities, particularly abnormalities observed in the field in most of the embryos or chicks that die during early development. One abnormality that has been correlated with concentrations of the above-mentioned substances in bird eggs is the crossed-bill syndrome found in North American cormorants (Phalacrocorax auritus).

The mechanism of action eliciting the shell thinning by DDE appears to be associated with inhibition of the enzyme Ca2+-ATPase in the eggshell gland. This action mode, studied in the laboratory, may be responsible for the effects observed in the field, such as the reduction of breeding success of several piscivorous and predator birds.

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