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Prenatal and prepubertal exposures to organochlorine compounds and perfluoroalkyl substances and pubertal development at age 12: The PELAGIE cohort study.

Lola Menant,F. Rouget,Hélène Tillaut,C. Warembourg,Elke Rouxel,Fabrice Lainé,Éric Gaudreau,Sylvaine Cordier,R. Garlantézec,C. Monfort,C. Chevrier

Published 2025 in Environment International

ABSTRACT

BACKGROUND Emerging evidence suggests that prenatal and prepubertal exposure to organochlorine compounds (OCs) and perfluoroalkyl substances (PFASs) is associated with children's reproductive health. This study examines the potential impact of these exposures on pubertal development in 12-year-old children. METHODS Based on the French PELAGIE mother-child cohort, concentrations of OCs and PFASs were measured in cord blood (from 2003 to 2006) and in blood at age 12 (from 2016 to 2018). Medical staff assessed pubertal development (Tanner stages) at age 12, and girls self-reported age at menarche annually (ages 9-16). Associations between exposures and delayed or earlier pubertal development were analyzed using multinomial logistic and Cox regression models, adjusting for confounders, and using quantile g-computation for compound mixtures. RESULTS Among 502 children (250 girls, 252 boys; median age: 12.8 years), prenatal PFUdA exposure in girls was associated with delayed breast development [OR (95 %CI): 2.05 (1.03,4.06)]. In boys, prenatal PFHxS exposure was associated with reduced risk of earlier gonadal development [0.47 (0.26,0.83)], and β-HCH with reduced risks of both delayed [0.66 (0.43,0.99)] and earlier [0.69 (0.48,0.97)] pubic hair development. Prepubertal exposure in girls to HCB, PCBs, and PFASs was associated with increased risk of delayed breast development [e.g. , PFOA 2.53 (1.04,6.12)] and later age at menarche [e.g., ΣPCBs: HR 0.77 (0.61,0.97)]. In boys, prepubertal p,p'-DDE was associated with increased risk of earlier puberty [gonadal development: 1.77 (1.09,2.88); pubic hair growth: 1.56 (1.01,2.44)], while PCB-118 was associated with delayed development. Prepubertal PFASs were associated with reduced risk of earlier puberty [e.g., PFHxS-gonadal stages: 0.39 (0.20,0.75)]. In mixture analyses, no associations were observed with regards to prenatal exposure, but prepubertal exposure was associated with delayed pubertal development in girls. CONCLUSION Prenatal and prepubertal exposure to OCs and PFASs may alter pubertal development at age 12 in girls and boys, underscoring the need for further research.

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