Human Exposure To Endocrine Disrupters And Semen Quality
Main Category: Urology / NephrologyAlso Included In: Fertility; Endocrinology; Men's health
Article Date: 03 May 2008 - 0:00 PDT
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UroToday.com - Male factor infertility is generally classified in terms of predisposing genetic (Klinefelter's syndrome, microdeletions of the Y-chromosome, CAG repeats, CFTR mutations), congenital (absence of vas deferens, cryptorchidism), medical (retrograde ejaculation, varicocele, primary testicular failure, hypogonadism, tumors), infectious (mumps- paramyxovirus, Chlamydia) or surgical factors (vasectomy, hernia repair, hydrocele repair, orchiopexy), however for a number of men idiopathic infertility is a frequent diagnosis. We propose that environmental factors, including exposure to endocrine disrupting chemicals, may be represented in this idiopathic category of diagnosis.
Endocrine disrupters are proposed to modulate or dysregulate the endogenous endocrine system via competitive or non-competitive binding at steroid hormone receptors, changes to synthesis, metabolism or transport of hormones or by changes in gene expression. Significant laboratory evidence supports endocrine disruption as a mechanism of action for several types of chemicals including polychlorinated biphenyls (PCBs), bisphenol A (BPA), 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), p,p'-DDE (p,p'-dichlorodiphenyl dichloroethylene)- the major breakdown product of DDT and mixtures such as pesticides. Though there is a relative paucity of population-based studies examining the effects of exposure to endocrine disrupters on human semen quality, it may be cautiously interpreted that endocrine disruption due to organochlorine exposures may be manifested as reduced sperm motility and morphology.
Consideration of an environmental etiology for male infertility has important clinical implications, particularly for semen analysis and the collection of patient information. The determination of sperm concentration, morphology, and motility remains the primary clinical approach to diagnose male infertility; however these assessments may be insufficient to detect molecular deficits that may be caused by environmental exposures. Routine assays to measure the capacity of sperm to undergo capacitation, acrosome reaction and sperm-egg binding are lacking. Development of assays to measure the interactions between sperm and egg may be limited by the restrictions on use of unfertilized human eggs. The promise of recombinant zona pellucidae glycoproteins and egg plasma membrane proteins as surrogates for human zonae and eggs may indeed be reflected in the development of more rigorous clinical assays for the determination of semen quality. These advances would refine our understanding of the subtle effects of endocrine disrupters and other environmental exposures on male infertility.
Urologists and reproductive endocrinologists should be encouraged to discuss environmental causes of infertility with their patients, including agricultural practices, exposures to pesticides, occupations related to the manufacture of chemicals, consumption of soy-products, Great Lakes fish and other dietary practices that may increase exposure to endocrine disrupters. These discussions may reveal modifiable changes in lifestyle or occupational safety practices that can mitigate some forms of idiopathic infertility. Within the infertility clinic, plastic-ware including culture dishes, tubes, semen collecting vials, pipette tips and other material that comes in contact with gametes should be single-use/disposable, and not subjected to conditions (heat, detergents) that would result in the degradation of plastic/polycarbonate products. Collection of environmental exposure data as part of infertility patient histories, particularly for clinics participating in research studies, would be invaluable to help ascertain the role of endocrine disrupters and other environmental factors in male infertility.
Written by Karen P. Phillips, PhD1,2,and Nongnuj Tanphaichitr, PhD3,4, as part of Beyond the Abstract on UroToday.com.
References
1 Faculty of Health Sciences, University of Ottawa, Ottawa, Ontario, Canada
2 Institute of Population Health, University of Ottawa, Ottawa, Ontario, Canada
3 Ottawa Health Research Institute, Ottawa Hospital, Ottawa, Ontario, Canada
4 Department of Biochemistry, Microbiology, and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario, Canada
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