The choice of an animal model is ultimately crucial to toxicological testing. If one does not use the appropriate model for the chemical and endpoint being studied, then the test results may not really provide the appropriate toxicological information. There are three basic types of animal models: sentinel models, screening models, and mechanistic models, Each of these models has specific needs and requirements, some of which overlap, some of which are distinctly different. Therefore, some animal models are more appropriate for evaluating the effects of some chemicals than are other animal models. This article will present the argument that the chicken embryo is especially appropriate as an animal model for studying the mechanism of the developmental toxicological effects of the polyhalogenated aromatic hydrocarbons (PHAHs).
The PHAHs are a group of toxicologically related compounds including, in part, the polychlorinated dibenzodioxins, dibenzofurans and biphenyls. The chicken (Gallus gallus) embryo is relatively sensitive to the toxicological effects of the PHAHs being approximately two orders of magnitude more sensitive than the mature bird. The chicken embryo has been used to demonstrate general toxicological effects (i.e. the LD50), immunotoxicity, cardiovascular toxicity, teratogenicity, hepatotoxicity and neurotoxicity. Many of these effects, or analogous effects, have also been observed in mammals and fish. Thus, most animals appear to respond to the PHAHs with a similar toxicological profile, indicating that many of the biomarkers used for the PHAHs are valid across a number of species, including the chicken. Furthermore, the chicken embryo is relatively inexpensive to use for toxicity testing. In addition, all effects detected are due to direct effects on the embryo and are not complicated by maternal interactions. In short, for sensitivity, ease of use, cost and applicability of results to other animals, the chicken embryo is an excellent animal model for evaluation of the mechanism underlying the developmental toxicological effects of the PHAHs.