The most compelling case linking a specific suite of adverse biological effects such as embryonic and chick mortality, edema, growth retardation, and deformities (notably crossed bills) to residues of dioxin-like compounds can be made for piscivorous birds (e.g., herring gulls, Forster's terns, double-crested cormorants, and Caspian terns). In the Great Lakes, USA, deformities in aquatic birds were found to be similar to deformities induced in offspring of farm-raised chickens exposed to PCDDs and PCDFs in feed. However, it has been shown that most (>90%) of the TEQ found in the eggs of cormorants and terns in the Great Lakes is accounted for by planar PCBs, rather than PCDDs/Fs, which accounted for between 2% and 9% of the toxic equivalents.
Studies of European cormorants in Dutch field-collected eggs found that in ovo exposure to PCDDs and PCDFs may explain reduced reproductive success, but postnatal exposure and parental behavior may also be contributing factors. In fact, recent work has shown that in ovo exposure to dioxins can lead to grossly asymmetric development of avian brains - a phenomenon seen in field-collected great blue herons, cormorants, and eagles, as well as laboratory chickens.
Laboratory studies have shown other bird species to be susceptible to PCDD and PCDF exposure; however, LD50 values and biological responses vary widely among bird species. Studies involving chickens and pheasants suggest that, in general, birds display decreased egg production, embryotoxicity, and cardiovascular malformations. At least one study suggested that chickens may be more sensitive to dioxins and PCBs than wild birds, indicating that care should be taken when extrapolating ecotoxicity data between wild and domestic bird species.
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