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Environmental contaminants and endocrine health
Environmental Contaminants and Endocrine Health focuses specifically on contaminants with hormonal disrupting activities. The book provides insights into the multiple effects of endocrine-disrupting chemicals (EDCs) and their mechanism of action (MoA) on metabolism, reproduction and the multiple physiological roles of the endocannabinoid system which has recently been indicated as new target. The content systematically covers EDC sources and effects, EDCs as sources of disease and health impairment in laboratory models, EDCs as the cause of disease and health impairment in humans and wild species, and the removal of hazardous pollutants from wastewaters to highlight intervention, mitigation and adaptation for reduced threat.
Intro -- Environmental Contaminants and Endocrine Health -- Copyright -- Dedication -- Contents -- Contributors -- Foreword -- Preface -- Acknowledgments -- Chapter 1: Endocrine-disrupting chemical sources and effects -- Chapter 1.1: Endocrine system -- 1. Fundamentals of hormones -- 1.1. Hormone classes -- 1.1.1. Lipid-derived hormones -- Steroid hormones -- Eicosanoids -- 1.1.2. Amino acid-derived hormones -- 1.1.3. Peptide hormones -- 1.2. Hormone receptors: Nuclear and membrane receptors -- 1.2.1. The nuclear receptor superfamily -- 1.2.2. Transmembrane receptors -- 1.3. Hormone transport, peripheral metabolism, and clearance -- 1.3.1. Hormone transport, binding proteins, and the role of the circulatory system -- 1.3.2. Peripheral hormone metabolism and clearance -- 2. Vertebrate endocrine physiology: Organs, axes, and hormones -- 2.1. Hypothalamic-pituitary-gonadal (HPG) axis -- 2.1.1. The hypothalamus and GnRH -- 2.1.2. The anterior pituitary and gonadotropins -- 2.1.3. The gonads, estrogens, androgens, and progestogens -- 2.2. The adrenal glands and associated hormones and systems -- 2.2.1. Overview of adrenal hormones -- Corticosteroids: Glucocorticoids and mineralocorticoids -- Catecholamines -- Adrenal androgens -- 2.2.2. Adrenal gland morphology -- 2.2.3. Regulation of adrenal hormone secretion -- The hypothalamic-pituitary-adrenal (HPA) axis -- The renin-angiotensin-aldosterone system (RAAS) -- 2.3. The hypothalamic-pituitary-thyroid (HPT) axis -- 2.3.1. The hypothalamus and thyrotropin-releasing hormone (TRH) -- 2.3.2. Anterior pituitary gland and thyrotropin (TSH) -- 2.3.3. Thyroid gland and thyroid hormones -- 2.4. The somatotropic axis -- 2.5. Metabolic and nutritional endocrinology -- 2.5.1. Hormonal control of feeding and digestion -- 2.5.2. Hormonal control of nutrient and energy balance -- 2.5.3. Adipose tissue endocrinology.
2.5.4. Peroxisome proliferator-activated receptors -- 2.6. Other vertebrate hormones and glands -- References -- Further reading -- Chapter 1.2: Endocrine-disrupting chemicals (EDCs) in environmental matrices and human bodily fluids -- 1. Introduction -- 2. Endocrine-disrupting chemicals (EDCs) -- 3. EDCs sources, exposure and presence in tissues and body fluids -- 4. Plastics -- 4.1. Plastics as EDCs -- 4.2. Emerging chemical alternatives and the constantly changing landscape -- 5. Pesticides -- 6. Flame retardants -- 7. Poly- and perfluoroalkyl substances (PFASs) -- 8. Polychlorinated biphenyls (PCBs) -- 9. Sunscreen -- 10. Conclusion -- References -- Chapter 1.3: In vitro-, ecological-, murine, and human models for examining the effects of EDCs -- 1. Summary -- 2. In vitro models for examining the effects of EDCs -- 3. Ecological models for examining the effects of EDCs -- 4. Murine models for examining the effects of EDCs -- 5. Human models for examining the effects of EDCs -- 6. Overview -- References -- Chapter 1.4: Endocrine-disrupting chemicals and their mode of action: The case of nuclear receptors and the evolution of ... -- 1. Introduction -- 2. Evolution and nuclear receptors: A conceptual framework -- 3. Endocrine disruption via nuclear receptors -- 4. Conclusions -- References -- Chapter 1.5: EDCs impacts on human populations. Addressing multiple chemicals in human exposure and epidemiological studies -- 1. Background -- 1.1. How are we exposed? -- 1.2. What is a mixture? -- 1.3. How do we assess exposure to mixtures? -- 1.4. What is biomonitoring? -- 1.5. What are resulting data? -- 1.6. How are exposure mixtures linked to health? -- 2. Assessing chemical mixtures in a birth cohort study: A simulated example -- 2.1. Simulation data -- 2.2. Exposure continuum mapping (ECM) -- 2.3. Stage 1: Exposure characterization with ECM.
2.4. Estimation of joint health effects -- 2.5. Results -- 3. Conclusions -- References -- Chapter 2: Endocrine-disrupting chemicals as source of disease and health impairment in laboratory models -- Chapter 2.1: EDCs: Focus on metabolic alteration of mammalian and nonmammalian models -- 1. Introduction -- 2. Approaches used to investigate the adverse actions of EDCs on the liver function -- 2.1. Histological and histopathological evaluation of liver injury -- 2.2. Glycogen storage assessment through histological staining -- 2.3. Immunohistochemistry investigation of liver biomarkers -- 2.4. Apoptosis -- 2.5. Fourier-transform infrared spectroscopy hepatic characterization -- 2.6. Targeted or total mRNA transcriptomics analysis -- 2.7. RT-qPCR assessment of liver transcripts levels -- 2.8. Quantification of protein levels by Western blot -- 2.9. Hepatic proteomics analysis -- 2.10. Metabolomics approach to study EDCs-induced liver alterations -- 3. Hepatic metabolism alteration in nonmammalian model species: A 5-year survey -- 3.1. Teleost liver metabolism alterations -- 3.1.1. Bisphenols exposure -- Bisphenol A -- Bisphenols other than BPA -- 3.1.2. Phthalates exposure -- 3.1.3. Perfluoroalkylated substances (PFAs) exposure -- 3.1.4. Glyphosate exposure -- 3.2. Metabolic alterations in amphibians -- 3.2.1. Plasticizer exposure -- 3.2.2. PFOA exposure -- 3.2.3. Glyphosate exposure -- 4. Hepatic metabolism alteration in mammalian species: A 5-year survey -- 4.1. Bisphenols exposure -- 4.2. Phthalates exposure -- 4.3. Perfluoroalkylated substances (PFAs) exposure -- 4.4. Glyphosate exposure -- 5. Conclusions -- References -- Chapter 2.2: EDCs: Focus on reproductive alterations in mammalian and nonmammalian models -- 1. Introduction -- 2. Reproductive toxicity outcomes in nonmammalian and mammalian species: A 5-year survey.
2.1. Reproductive toxicity in teleost -- 2.1.1. Exposure to BPA -- Outcomes on male reproduction -- Outcomes in female reproduction -- 2.1.2. Exposure to bisphenol analogs other than BPA -- Outcomes in male reproduction -- Outcomes in female reproduction -- 2.1.3. Exposure to phthalates -- Outcomes in male reproduction -- Outcomes in female reproduction -- 2.1.4. Exposure to perfluoroalkylated substances (PFASs) -- 2.2. Reproductive toxicity in amphibian models -- 2.2.1. Toxicity of pesticides and herbicides -- 2.2.2. Toxicity of phthalates and analogs -- 2.3. Reproductive toxicity in mammalian models -- 2.3.1. BPA, a recognized threat to reproduction in mammals -- Outcomes in male reproduction -- Outcomes in female reproduction -- 2.3.2. Exposure to BPA alternatives: An emerging threat to mammalian reproduction -- 2.3.3. Phthalates, recognized threats for mammalian reproduction -- Outcomes in male reproduction -- Outcomes in female reproduction -- 2.3.4. PFASs, emerging threat for reproduction in mammals -- Outcomes in male reproduction -- Outcomes in female reproduction -- 3. Are microplastics deleterious for reproduction in mammals? -- 4. Conclusion -- References -- Chapter 2.3: The EDCs as epigenetic disruptors: Implications for development and health -- 1. Introduction to epigenetics -- 1.1. The epigenetic marks -- 1.1.1. DNA methylation -- 1.1.2. Histone modifications -- 1.1.3. Noncoding RNAs -- 1.2. Inheritance of epigenetic marks -- 2. Interference of EDCs with the epigenetic dynamics -- 3. The impact of epigenetic effects triggered by EDCs on health conditions -- 3.1. Development and differentiation -- 3.2. Metabolic disorders -- 3.3. Reproductive disorders -- 3.4. Neuroendocrine system and behavior -- 3.5. Heart function and cardiovascular system -- 4. Concluding remarks -- References.
Chapter 2.4: Endocrine disrupting chemicals induce the epigenetic transgenerational inheritance of disease -- 1. Introduction -- 2. Molecular epigenetic mechanisms -- 3. Epigenetic transgenerational inheritance -- 4. Developmental etiology of epigenetic transgenerational inheritance -- 5. Germline epimutations -- 6. Transgenerational gene expression changes -- 7. Conclusion -- Acknowledgments -- References -- Chapter 2.5: Endocrine disruption persistence through development and across generations can be mediated by environmental ... -- 1. Introduction -- 2. Environmental perturbation of genome organization as DIPE mediator -- 3. How do HEC perturbations determine the phenotypic manifestations of DIPE? -- 4. How are HEC perturbations propagated? -- 5. How are HEC perturbations originated? -- 5.1. Preconception exposure and gamete perturbations -- 5.2. Preconception exposure and F1 HEC perturbation -- 5.3. Preconception exposure and F1 endocrine disruption putatively driven by HEC perturbations -- 6. Concluding remarks -- References -- Chapter 2.6: Alterations of the endocannabinoid system by endocrine-disrupting chemicals: Effects on metabolism and repro ... -- 1. The endocannabinoid system -- 1.1. Endocannabinoids -- 1.2. Endocannabinoid receptors -- 1.3. Enzymatic machinery -- 1.3.1. Anabolic enzymes -- 1.3.2. Catabolic enzymes -- 2. Endocannabinoid system, endocrine-disrupting chemicals, and hepatic metabolism -- 2.1. Hepatic endocannabinoid system -- 2.2. Endocrine-disrupting chemicals and hepatic endocannabinoid system -- 2.2.1. Plastic polymers and plasticizers -- 2.2.2. Polybrominated compounds -- 2.2.3. Pesticides -- 2.2.4. Parabens -- 3. Endocannabinoid system, endocrine-disrupting chemicals, and reproduction -- 3.1. Gonadal endocannabinoid system -- 3.2. Endocrine-disrupting chemicals and gonadal endocannabinoid system -- 3.2.1. Surfactants.
edited by Oliana Carnevali, Gary Hardiman.
Includes bibliographical references and index.