Endocrine disruptor occur from low-dose exposure to exogenous hormones or hormonally active chemicals such as bisphenol A. These chemical can bind to receptors for other hormonally mediated processes. Furthermore, since endogenous hormones are already present in the body in biologically active concentrations, additional exposure to relatively small amounts of exogenous hormonally active substances can disrupt the proper functioning of the body's endocrine system. Thus, an endocrine disruptor can elicit adverse effects at much lower doses than a toxicity, acting through a different mechanism. The timing of exposure is also critical. Most critical stages of development occur in utero, where the fertilized egg
Endocrine disruptor BDE-47, affects the reproductive system and thyroid gland of female rats in doses of the order of those to which humans are exposed. Low concentrations of endocrine disruptors can also have synergistic effects in amphibians, but it is not clear that this is an effect mediated through the endocrine system. Critics have argued that data suggest that the amounts of chemicals in the environment are too low to cause an effect. A consensus statement by the Learning and Developmental Disabilities Initiative argued that "The very low-dose effects of endocrine disruptors cannot be predicted from high-dose studies, which contradicts the standard