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Male infertility and the environment: A plethora of associations based on a paucity of meaningful data*
Citation:
KLINEFELTER, G. R. Male infertility and the environment: A plethora of associations based on a paucity of meaningful data*. Chapter 29, Marc Goldstein and Peter Schlegel (ed.), Surgical and Medical Management of Infertility. Cambridge University Press, New York, NY, , 253-261, (2013).
Impact/Purpose:
to research the speculation concerning environmental chemical exposures to men.
Description:
While speculation has run rampant for over a decade concerning the potential for environmental chemical exposures to compromise semen quality in men, there are really very few convincing examples of such a causal association, and these are not recent. The three most notable examples are lead, cadmium, and dibromochloropropane. In each case, the environmental exposures and effects observed in men were confirmed in animal toxicological studies. Data seemed to support a link between exposure to polychlorinated biphenyls (PCBs), which are no longer used, and reduced sperm quality in men, but this link was never confirmed in animals. Exposures to 'endocrine disruptive chemicals' such as the phthalates have failed to yield consistent trends in compromised semen quality in men and exposure data is often lacking. In general, epidemiology studies suffer from lack of consistent methodologies and adequate exposure data. Regardless, the reported increases in the incidence of phenotypes such as cryptorchidism, testicular cancer, hypospadias, and reduced sperm quality in certain populations of men have spurred a significant research effort in toxicology. The testicular dysgenesis syndrome (TDS) is based on the hypothesis that androgen deprivation during reproductive development of the male fetus results in the appearance of one or more of these phenotypes. In the laboratory, exposure of male offspring to sufficiently high levels of antiandrogens or phthalates during fetal development does indeed result in an array of abnormal phenotypes such as cryptorchidism, Sertoli cell-only tubules, Leydig cell hyperplasia, and epididymal agenesis. Unfortunately, sufficient single chemical low dose studies are lacking so the human relevance of these phenotypes remains in question. Importantly, the causal link between androgen deprivation and these phenotypes isunclear. Disclaimer: The research described in this article has been wholly funded and reviewed by the National Health and Environmental Effects Research Laboratory, Office of Research and Development, U.S. Environmental Protection Agency, and approved for publication. Approval does not signify that the contents reflect the views of the Agency nor does mention of trade names or commercial products constitute endorsement or recommendation for use.