Abstract

Environmental chemicals have long been known to be a threat due to their ability to interact with physiological systems in vertebrates, including endocrine systems. These “hormone mimics” that have adverse effects are termed endocrine-disrupting chemicals (EDCs). These EDCs emanate from a variety of sources, often being developed for specific needs, such as those used as pesticides, herbicides, or industrial and domestic applications. The characteristics of EDCs differ vastly in terms of life-cycle in the environment, chemical and pharmacological characteristics of the parent compounds and their metabolites, and even in physiological target(s). In birds, the potential for adverse effects of EDCs was first realized with the thinning of eggs in bald eagles, with a dramatic in loss of viable chicks and population level impact. However, effects from exposure to EDCs in birds can be highly variable, with differences associated with species sensitivity, timing of exposure, extent of exposure, and reproductive strategies; precocial species are extremely vulnerable during embryonic development whereas altricial species appear to remain more transiently sensitive throughout their lifetime. The primary endocrine systems impacted by EDCs are the reproductive, thyroid, and stress axes. However, there are a number of other physiological impacts observed in metabolic, cardiac, and immune systems as well as hematological effects associated with some chemicals. Domestic and wild birds come in contact with a vast array of these chemicals in their environment, and both are often exposed to complex combinations. The interactions of EDCs with endocrine systems occur through a variety of mechanisms, including binding to receptors, interference with enzyme systems, modulation of transmitters, and impacting growth factors. Because of unique characteristics of birds, it is important to consider both toxicological and endocrine effects, as many of these EDCs have toxicological effects at higher exposures. Predictive tools to predict risk have focused on activation of the aryl hydrocarbon receptor (AhR) in comparison to the known effect of dioxin. A more recent approach produces an Adverse Outcomes Pathway, which provides an effective framework to encompass mechanisms through to ecological impacts. Major classes of EDCs will be reviewed in this chapter, along with specific effects on birds in the context of vulnerable species, breeding strategies, and lifetime effects of exposure to EDCs.

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