Prenatal exposure to phenols and benzophenones in relation to markers of male reproductive function in adulthood

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Introduction: Environmental exposure during fetal life may disrupt testicular development. In humans, a limited number of studies have investigated whether these adverse effects persist into adulthood. Using data from a prospective, population-based birth cohort study, The Copenhagen Mother-Child cohort, the objective was to assess if there is an association between fetal exposure to selected phenols and benzophenones and markers of testicular function in adult men. Methods: Pregnant women were recruited in 1997–2001. Their sons were examined clinically at 18-20 years of age, with focus on adult markers of reproductive function (anogenital distance (AGD), semen quality and reproductive hormones). In total, 101 18–20-year-old men were included, whose mothers during pregnancy had a serum sample drawn and analyzed for bisphenol A (BPA) and seven other simple phenols, as well as six benzophenones. To investigate the association between chemical levels (in tertiles, T1-T3) in relation to markers of reproductive function, univariate and multiple linear regression analyses were performed. Results: In fully adjusted analyses, increased levels of luteinizing hormone (LH) were observed with higher fetal exposure to BPA (percentage difference (95%CI)) (T2: 12% (-8%,36%) and T3: 33% (10%,62%), compared to T1) and benzophenone-3 (BP-3) (T2: 21% (-2%,49%), T3: 18% (-4%,45%)), while no clear association was seen to total testosterone (TT). Higher levels of BPA and BP-3 were associated with a lower TT/LH ratio, although only significant for BPA (p-trend=0.01). No associations were seen to AGD or markers of semen quality. Conclusion: In conclusion, high exposure to BPA and BP-3 was associated with a compensated reduced Leydig cell function but no other changes in markers of reproductive health. As maternal levels of BPA and BP-3 were not correlated, separate effects may be at play. Larger studies on long-term reproductive consequences of prenatal exposures are warranted to validate our findings.

OriginalsprogEngelsk
Artikelnummer1071761
TidsskriftFrontiers in Endocrinology
Vol/bind13
ISSN1664-2392
DOI
StatusUdgivet - 2022

Bibliografisk note

Funding Information:
This study was supported by Innovation Fund Denmark (IFD 8056-00005B), Centre on Endocrine Disruptors, Danish Environmental Protection Agency (MST-611-00012), “Oda og Hans Svenningsens Fond” (F-22451-08), “Fabrikant Vilhelm Pedersen og Hustrus Legat” (NNF15OC0017642), “Fonden til Lægevidenskabens Fremme” (17-L-0297), Academy of Finland, Sigrid Juselius Foundation, Kirsten and Freddy Johansen Fund, and Turku University Hospital Special Governmental Fund.

Publisher Copyright:
Copyright © 2022 Holmboe, Scheutz Henriksen, Frederiksen, Andersson, Priskorn, Jørgensen, Juul, Toppari, Skakkebæk and Main.

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