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Male Reproductive Toxicology: Environmental Exposures vs Reproductive Competence
Citation:
Klinefelter, G. Male Reproductive Toxicology: Environmental Exposures vs Reproductive Competence. Chapter 21, Mammlian Toxicology. John Wiley & Sons, Inc, Hoboken, NJ, 1:473-491, (2015).
Impact/Purpose:
EPA is very well represented by their collective chapter contributions in this upcoming book. This book is being put together by Dr. Abou-Donia, director of the Mammalian Toxicology Course (PHR 254)offered each fall in the Department of Pharmacology and Cancer Biology at Duke University Medical Center. The chapters in this book are taken from each contributor's course lecture. Thus, it is a more thorough 'lecture' than one has opportunity to present in the classrooom. It's an opportunity to put these lectures public domain to facilitate education to those unable to take the course.
Description:
Like the lecture this chapter begins with an overview of male reproductive biology and transitions into male reproductive toxicology. It ends with a brief discussion of the strengths and weaknesses in male reproductive toxicology and epidemiology today. This chapter is highly illustrative, featuring 16 figures to help clarify the discussions in the text. Subfertility is a world-wide problem, affecting as many as 10 million US couples. Of the —1.2 million couples actually examined, the male is the sole or partial cause of the problem 40% of the time (1). This is likely an underestimation of the real percentage linked to a male factor because of unsophisticated analyses of sperm quality. It has been estimated that 98% of male ‘subfertility’ cases result from compromised sperm quantity and/or quality while only 2% result from inadequate ejaculatory function (2). Over the past few decades, dozens of reports in the peer-reviewed literature have touted declines in semen quality in men, citing significant reductions in spem concentration (number/mi), total sperm count (number / ejaculate), semen volume, sperm motility, sperm morphology, etc. These published “trends” have been linked to exposure to environmental chemicals, most popularly known as endocrine disruptive chemicals (EDCs), chemicals that mimic or interfere with endocrine signaling. Moreover, it has been suggested that exposures to BOCs during reproductive development may be causally related to other effects including reproductive tract malformations such as hypospadias, cryptorchidism, and predisposition to testicular cancer or ejaculatory dysfunction (34). Collectively, these observed human phenotypes have been referred to as the testicular dysgenesis syndrome (TDS).