ECEESPE2025 Poster Presentations Environmental Endocrinology (20 abstracts)
Exposure to per- and polyfluoroalkyl substances during fetal development and risk of testicular germ cell cancer in adult life
Cecilie Uldbjerg 1,2 , Youn-Hee Lim 3,4 , Astrid Beck 1,2 , Jørgen Petersen 1,2,5 , Karina Sørensen 6 , David Kristensen 1,2,7 , Panu Rantakokko 8 , Brent Coull 9 , Christian Lindh 10 , Niels Skakkebaek 1,2,11 , Russ Hauser 12 , Elvira Bräuner 1,2 , Lærke Priskorn 1,2 & Anders Juul 1,2,11
1Department of Growth and Reproduction, Copenhagen University Hospital- Rigshospitalet, University of Copenhagen, Denmark, Copenhagen, Denmark; 2International Centre for Research and Research Training in Endocrine Disruption of Male Reproduction and Child Health (EDMaRC), Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark; 3Section of Environmental Health, Department of Public Health, University of Copenhagen, Copenhagen, Denmark; 4Department of Preventive Medicine, Seoul National University College of Medicine, Seoul, South Korea; 5Section of Biostatistics, Department of Public Health, University of Copenhagen, Copenhagen, Denmark; 6Danish National Biobank, Statens Serum Institut, Copenhagen, Denmark; 7Roskilde University, Department of Science and Environment, Roskilde, Denmark; 8Department of Health Security, Finnish Institute for Health and Welfare, Kuopio, Finland; 9Department of Biostatistics, T. H. Chan School of Public Health, Harvard University, Boston, United States; 10Division of Occupational and Environmental Medicine, Department of Laboratory Medicine, Lund University, Lund, Sweden; 11Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark; 12Department of Environmental Health, T. H. Chan School of Public Health, Harvard University, Boston, United States
JOINT1275
Background: Testicular germ cell cancer (TGCC) originates in fetal life, and exposure to environmental chemicals during fetal development may play a role. However, reliable epidemiological data are lacking due to the long latency between fetal exposure and disease onset, and challenges in accurate exposure assessment. Per- and polyfluoroalkyl substances (PFAS) can act as endocrine disruptors during fetal life with potential effects on reproductive health. We investigated the association between exposure to PFAS during fetal development and risk of TGCC in adult life.
Methods: We conducted a nested case-control study of 549 mother-son pairs (103 TGCC cases, 446 matched controls) using prospectively collected data. The sample population included more than 100, 000 pregnant women with biobanked serum samples collected between 1985-1995, a period before PFAS restrictions and thus of high exposure potential. Sons of these women diagnosed with TGCC were identified from the Danish Cancer Registry until 2023. Concentrations of eight PFAS were quantified in maternal serum by liquid chromatography tandem mass spectrometry. Associations of individual PFAS and their mixtures with risk of TGCC were estimated through stratified Cox regression and quantile g-computation models.
Results: In main analyses, no strong or statistically significant associations were observed between individual PFAS and TGCC risk. However, hazard ratios (HR) for sulfonic acids (e. g., PFOS, PFHxS, PFHpS) generally suggested higher TGCC risks, whereas carboxylic acids tended to be associated with lower risks. Mixture analyses supported this opposing pattern, showing slightly higher TGCC risk for the JOINT effect of sulfonic acids (HR 1. 13, 95% CI: 0. 89; 1. 44) and lower risk for carboxylic acids (HR 0. 72, 95% CI: 0. 51; 1. 02). Stratified analyses by TGCC histological subtype demonstrated consistent differences, with generally positive associations for seminomas, in contrast to generally inverse associations for nonseminomas. For PFOS, a quartile increase in concentrations was associated with a higher seminoma risk (HR 1. 31, 95% CI: 0. 98; 1. 76).
Conclusions: Our study, using biobanked maternal serum collected decades prior to diagnosis, provides no robust evidence linking PFAS exposure during fetal development to TGCC risk in adult life. However, indications that sulfonic acids may have an adverse effect compared to carboxylic acids were observed. The generally weak associations may reflect the limited sample size or the complexity in identifying specific chemicals during fetal development as risk factors for TGCC in epidemiological studies. Further research is needed to clarify whether other environmental chemicals, possibly as mixtures, may contribute to the development of TGCC.
Volume 110
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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