| Autor: |
Forthun IH; Department of Clinical Science, University of Bergen, 5020 Bergen, Norway.; Children and Youth Clinic, Haukeland University Hospital, 5021 Bergen, Norway., Roelants M; Department of Public Health and Primary Care, Centre for Environment and Health KU Leuven, 3000 Leuven, Belgium., Knutsen HK; Department of Food Safety, Norwegian Institute of Public Health, 0213 Oslo, Norway.; Center for Sustainable Diets, Norwegian Institute of Public Health, 0213 Oslo, Norway., Haug LS; Department of Food Safety, Norwegian Institute of Public Health, 0213 Oslo, Norway.; Center for Sustainable Diets, Norwegian Institute of Public Health, 0213 Oslo, Norway., Iszatt N; Department of Food Safety, Norwegian Institute of Public Health, 0213 Oslo, Norway.; Center for Sustainable Diets, Norwegian Institute of Public Health, 0213 Oslo, Norway., Schell LM; Department of Epidemiology and Biostatistics, University at Albany, Albany, New York 12144, United States., Jugessur A; Centre for Fertility and Health, Norwegian Institute of Public Health, 0213 Oslo, Norway.; Department of Global Public Health and Primary Care, University of Bergen, 5020 Bergen, Norway., Bjerknes R; Department of Clinical Science, University of Bergen, 5020 Bergen, Norway.; Children and Youth Clinic, Haukeland University Hospital, 5021 Bergen, Norway., Oehme NB; Children and Youth Clinic, Haukeland University Hospital, 5021 Bergen, Norway., Madsen A; Medical Biochemistry and Pharmacology, Haukeland University Hospital, 5021 Bergen, Norway., Bruserud IS; Children and Youth Clinic, Haukeland University Hospital, 5021 Bergen, Norway., Juliusson PB; Department of Clinical Science, University of Bergen, 5020 Bergen, Norway.; Children and Youth Clinic, Haukeland University Hospital, 5021 Bergen, Norway.; Department of Health Registry Research and Development, Norwegian Institute of Public Health, 5808 Bergen, Norway. |
| Abstrakt: |
Per- and polyfluoroalkyl substances (PFAS) are widespread environmental contaminants with endocrine-disruptive properties. Their impact on puberty in boys is unclear. In this cross-sectional study, we investigated the association between PFAS exposure and pubertal timing in 300 Norwegian boys (9-16 years), enrolled in the Bergen Growth Study 2 during 2016. We measured 19 PFAS in serum samples and used objective pubertal markers, including ultrasound-measured testicular volume (USTV), Tanner staging of pubic hair development, and serum levels of testosterone, luteinizing hormone, and follicle-stimulating hormone. In addition to logistic regression of single pollutants and the sum of PFAS, Bayesian and elastic net regression were used to estimate the contribution of the individual PFAS. Higher levels of the sum of perfluorooctanesulfonic acid (PFOS), perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA), and perfluorohexanesulfonic acid (PFHxS) were associated with later pubertal onset according to USTV (age-adjusted odds ratio (AOR): 2.20, 95% confidence interval (CI): 1.29, 3.93) and testosterone level (AOR: 2.35, 95% CI: 1.34, 4.36). Bayesian modeling showed that higher levels of PFNA and PFHxS were associated with later pubertal onset by USTV, while higher levels of PFNA and perfluoroundecanoic acid (PFUnDA) were associated with later pubertal onset by testosterone level. Our findings indicate that certain PFAS were associated with delay in male pubertal onset. |
