Abstract

Bisphenol A (BPA) is a recognized xenoestrogen, in that it possesses oestrogenic and anti-androgenic properties. These endocrine-disrupting effects of BPA at the estrogen receptor (ER) occur despite the very low affinity of BPA for the ERβ, which is 10,000 times lower than that of 17-β estradiol, and despite the European regulatory authorities stating that BPA is safe, at usual exposure concentrations, the use of BPA in baby drink bottles was banned in 2011. There exists conflicting evidence from human epidemiological studies as to its influence on adult male reproductive function, although animal data is more convincing. This mini-review will report on the limited epidemiological data from human studies relating early life exposure to BPA on adult male reproductive function. A long term follow-up study from Western Australia using a birth cohort, the Raine Study, demonstrated no adverse associations of antenatal exposure to BPA, and potentially a positive association with antenatal BPA exposure with sperm concentration and motility at 20 years of age, although recent scientific reports suggest traditional measures of BPA exposure may underestimate exposure levels, which makes data interpretation potentially flawed.

Highlights

  • Bisphenol A (BPA) is a widely used chemical which is ubiquitous within the environment, being present within plastics and epoxy resin

  • There have been many cross-sectional studies looking at linking assessment of reproductive function with current BPA exposure, such as timing of puberty and sperm counts, the purpose of this review was to determine if the exposures to BPA at a critical stage of development, the “masculinization programming window” may lead to a permanent perturbation in the hypothalamic-pituitary-gonadal axis

  • A major problem with animal studies of endocrine disrupting chemicals is that these chemicals are known to have potential different effects at different concentrations leading to difficulty in extrapolating animal effects to the human situation

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Summary

INTRODUCTION

Bisphenol A (BPA) is a widely used chemical which is ubiquitous within the environment, being present within plastics and epoxy resin. BPA at maternal serum concentrations may freely pass to the fetus across the placenta, leading to near-equivalent levels in fetal and maternal blood [7], measuring maternal circulating concentrations is a reasonable proxy for fetal exposure It has been assumed by many experts that sperm counts may have been diminishing over the last 30 years, this is hotly debated [18, 19], it is not disputed that the incidence of undescended testis, hypospadias and testicular cancer is increasing in some countries [20,21,22,23]. This mini-review will review the epidemiological studies of prenatal BPA exposure on human male reproductive function

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