Table of Contents:
  • 1. What are environmental endocrine-disrupting chemicals (EDCs)?
  • 1.1 Introduction to EDCS
  • 1.2 Endocrine systems communicate with the environment
  • 1.3 Hormonal properties and mechanisms of EDCS
  • 1.3.1 Nuclear hormone receptors
  • 1.3.2 Membrane hormone receptors
  • 1.3.3 Steroidogenic enzymes
  • 1.4 Representative EDCs and their actions
  • 1.4.1 Industrial organohalogens (PCBs, PBDEs)
  • 1.4.2 Pesticides (DDT, methoxychlor)
  • 1.4.3 Phytoestrogens
  • 1.5 Summary and conclusions
  • 2. EDC exposures
  • 2.1 EDCs and wildlife
  • 2.1.1 Reproductive toxicity of EDCs in wildlife
  • 2.2 EDCs and humans
  • 2.2.1 Diethylstilbestrol (DES)
  • 2.2.2 PCBS
  • 2.2.3 Dioxins
  • 2.2.4 Low-dose human exposures: what is the evidence?
  • 2.3 Summary and conclusions
  • 3. EDCs and development
  • 3.1 Vulnerability of the developing fetus
  • 3.2 Fetal (developmental) basis of adult disease
  • 3.3 Critical developmental periods
  • 3.4 Key toxicological principles relevant to developmental exposures
  • 3.4.1 LOAEL/NOAEL
  • 3.4.2 Dose-response principles and why they do not apply to EDCs
  • 3.4.3 Low-dose effects of EDCs, lack of a threshold
  • 3.5 Summary and conclusions
  • 4. EDCs and the developing brain
  • 4.1 Hormones and brain sexual differentiation
  • 4.1.1 Hormones and neuronal survival and death
  • 4.2 EDCs and the perturbation of brain sexual differentiation
  • 4.2.1 Hypothalamic morphology
  • 4.2.2 Hypothalamic developmental apoptosis
  • 4.2.3 Neuronal phenotype
  • 4.3 EDCs and reproductive behaviors
  • 4.4 EDCs and non-reproductive behaviors
  • 4.4.1 Hormones and synaptic plasticity
  • 4.4.2 EDCs and neural plasticity
  • 4.4.3 EDC effects on the brain's dopamine neurons
  • 4.5 Summary and conclusions
  • 5. EDCs and neuroendocrine systems
  • 5.1 Neuroendocrine systems of the hypothalamus
  • 5.2 Reproductive neuroendocrine systems and perturbations by EDCs
  • 5.2.1 Background on GnRH neurons
  • 5.2.2 Sexual differentiation of the HPG axis
  • 5.2.3 Steroid hormone feedback and regulation of HPG function
  • 5.2.4 Disruption of GnRH neurons by EDCs
  • 5.2.4.1 In vitro evidence
  • 5.2.4.2 In vivo evidence
  • 5.2.4.3 Developmental EDC exposures and GnRH neurons
  • 5.2.5 EDCs, puberty, and the brain
  • 5.2.5.1 Disruption of puberty by environmental EDCs
  • 5.2.5.2 Kisspeptin neurons are potential targets for developmental EDCs
  • 5.3 Summary and conclusions
  • 6. Epigenetic effects of EDCS
  • 6.1 Molecular epigenetic mechanisms: an introduction
  • 6.2 Hormones and epigenetic change
  • 6.2.1 DNA methylation
  • 6.2.2 Histone modifications
  • 6.2.3 MicroRNAS
  • 6.3 Transgenerational epigenetic effects of EDCs
  • 6.3.1 Vinclozolin
  • 6.3.2 Bisphenol A
  • 6.3.3 Diethylstilbesterol (DES).
  • 6.3.4 Polychlorinated biphenyls (PCBs).
  • 6.3.5 Methoxychlor
  • 6.4 The importance of context in environmental epigenetics
  • 6.5 Summary and conclusions
  • 7. EDCs, the brain, and the future
  • 7.1 Can EDC effects be mitigated?
  • 7.2 What can we do to avoid EDC exposures?
  • 7.3 General conclusions
  • Acknowledgments
  • References
  • Author biographies.