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Environmental Impacts on Reproductive Health and Fertility
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Book description

Many reproductive and developmental health problems are caused by exposure to chemicals that are widely dispersed in our environment. These problems include infertility, miscarriage, poor pregnancy outcomes, abnormal fetal development, early puberty, endometriosis, and diseases and cancers of reproductive organs. The compelling nature of the collective science has resulted in recognition of a new field of environmental reproductive health. Focusing on exposures to environmental contaminants, particularly during critical periods in development and their potential effects on all aspects of future reproductive life-course, this book provides the first comprehensive source of information bringing together the arguments that are spread out among various scientific disciplines in environmental health, clinical and public health fields. It provides a review of the science in key areas of the relationship between environmental contaminants and reproductive health outcomes, and recommendations on efforts toward prevention in clinical care and public policy.

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Contents

  • 9 - Environmental contaminants and effects on timing and progression of human pubertal development
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    Summary

    This is the introductory chapter of the book, which provides a review of the science in key areas of the relationship between environmental contaminants and reproductive and developmental health for students and practitioners in the fields of public health, environmental health and research, and medical and allied health professional training. Environmental reproductive health focuses on exposures to environmental contaminants, and their potential effects on all aspects of future reproductive health throughout the life course, including conception, fertility, pregnancy, child and adolescent development, and adult health. The book focuses on the role of/implications for/potential effects of exposure to endocrine-disrupting chemicals (EDCs) and subsequent reproductive and developmental outcomes. It brings together the core environmental health sciences that form a foundation of information from which to join with other disciplines and partners in related health, social, community, legal, and policy fields to explain the relationship between environmental contaminants and reproductive and developmental health.
  • 10 - Environmental contaminants and impacts on healthy and successful pregnancies
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    Summary

    This chapter reviews concepts of exposure and dose, identifies sources of contaminants, and describes the circumstances of human exposures. Occurrence of contaminants varies by setting and humans are exposed to multiple contaminants simultaneously or sequentially. Various processes act on contaminants to affect their ultimate fate and distribution within the body and the biologically effective dose relevant to the health outcome of concern. It is important to have information on sources of contaminants and the circumstances of exposure. The National Health and Nutrition Examination Survey (NHANES) contains multiple items relevant to contaminant exposure and dose. Human exposure and absorption of contaminants depend on properties of the contaminant and the medium in which it is present, as well as human activities, which change over the lifespan. The nature of reproductive system function and human development presents challenges to quantitative measurement of contaminant exposure and dose and subsequent study of health effects.
  • 11 - Environmental contaminants and reproductive and fertility effects in the male
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    Summary

    The ovarian hormones stimulate the development of the reproductive system, induce the development of secondary sexual characteristics, and promote a receptive endometrium for the growth and development of the proconceptus. The development of the ovary is dependent on local and endocrine factors that can be the target of endocrine disruptors. The T-shaped uterus seen in women exposed to diethylstilbestrol (DES) could represent a narrow and more branched structure, similar to the structure of the fallopian tube. Müllerian development is dependent on coordinated gene expression and hormone exposure. The genes that control normal patterning of the reproductive tract are beginning to be identified. The most important hormones regulating mammary gland development are estrogen and progesterone. During pregnancy and lactation, prolactin contributes to lobular differentiation and milk production. Estrogen and progesterone play a fundamental role during puberty to develop a normal adult breast.
  • 15 - Communicating with patients and the public about environmental exposures and reproductive risk
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    Summary

    This chapter discusses the key events occurring at different stages of development in the normal human male and how this impacts the reproductive function in adulthood. Development of the normal male reproductive system can be divided into five periods: fetal, neonatal, infancy/childhood, puberty, adulthood. Normal hormonal functioning of the fetal testis is essential for masculinization and for development of a male reproductive system. In neonatal male and female babies there is activation of the hypothalamic-pituitary axis and consequent increase in circulating levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH). During the neonatal period, Sertoli cells continue to proliferate and this is arguably the most important period in life in terms of the magnitude of increase in Sertoli cell numbers. Sertoli cells start expressing androgen receptor (AR) at the onset of puberty and this is considered one sign of maturation of these cells, as they terminally differentiate and cease proliferating.
  • 16 - Interpreting science in the policy context
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    Summary

    Epidemiologic studies and animal studies increasingly suggest that exposures to environmental chemicals, nutrition, physical factors, and other factors early in development have a role in susceptibility to disease in later life. The mammalian female reproductive system arises from the uniform paramesonephric duct, the müllerian duct. The major subtypes of epithelial ovarian cancer (EOC) show morphologic features that resemble those of the müllerian duct-derived epithelia of the reproductive tract. Exposure of the developing female reproductive tract to diethylstilbestrol (DES), either in vivo or in organ culture, repressed the expression of HOXA10 in the uterus and resulted in uterine metaplasia. Epigenetic change in the molecular program of cell differentiation in the affected tissues may be a common mechanism. Most regions of the mammalian genome exhibit little variability among individuals in tissue-specific DNA methylation levels. Future analyses of epigenetic imprints of genes explain the developmental origins of disease.
  • 17 - Conclusions – what does all this mean, and where are we going?
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    Summary

    This chapter focuses on the mechanisms by which environmental exposures can induce endocrine disruption. It highlights the mechanisms that play important roles in developmental programming. Endocrine-disrupting chemicals, which mimic the activity of endogenous hormones and activate receptors are termed agonists, whereas those that inhibit receptor activity are termed antagonists. During the perinatal period programming of the endocrine axis occurs, making this a vulnerable period of exposure to endogenous and exogenous stimuli. Among the endocrine-disrupting chemicals (EDCs), xenoestrogens have garnered a significant amount of attention due to the well-known effects of the xenoestrogen diethylstilbestrol (DES) in humans, and the identification of many other estrogenic anthropogenic chemicals. Metabolism plays a key role in maintaining hormone homeostasis. Endocrine-disrupting chemicals can disturb normal hormone homeostasis, which can have both direct and indirect effects on the reproductive function of both wildlife and human populations.

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