Is exposure to endocrine disrupting compounds during fetal/post-natal development affecting the reproductive...

Concerns have been raised about the potential adverse effects on reproductive health and immune status of farm animals following exposure to a range of natural and synthetic environmental compounds that disrupt normal hormonal actions. These compounds range from natural plant oestrogens (e.g. genistein, coumesterol) and mycoestrogens (e.g. Aflatoxins, zearalenone) to growth promoting pharmaceuticals (e.g. trenbolone acetate, melengastrol acetate) to chemicals spread in water, sewage sludge or the atmosphere such as detergents and surfactants (e.g. octylphenol, nonylphenol), plastics (e.g. bisphenol-A, phthalates), pesticides (e.g. methoxychlor, dieldrin, DDT) and industrial chemicals (e.g. PCB, TCDD). These compounds are commonly termed 'endocrine disrupting compounds' (EDCs) or 'endocrine disruptors' due to their ability to act as either hormone agonists or antagonists or the ability to disrupt hormone synthesis, storage or metabolism. A similar group of compounds are called 'immunotoxicants' and are thought to affect the immune system mainly by disrupting B and T cell homeostasis. As more studies are performed it is becoming clear that many compounds can directly or indirectly affect both the endocrine and immune systems. The susceptibility of target tissues is related to the stage of development, the cumulative exposure dose and the immune status of the individual. While some of the effects of the EDCs on the endocrine and immune systems are quite distinct, many are subtle and identifying the causative agent from the vast array of environmental challenges including EDCs, nutrition, temperature, etc. can be problematic. Identifying the causative agent is confounded by the possibility that effects that are observed in the adult may be due to exposure to EDCs during fetal life. This has major implications for the determination of universal end-point measurements to assess exposure to EDCs in farm animals.