Association of prenatal exposure to phthalates and synthetic phenols with pubertal development in three European cohorts.

Autor: Freire C; Department of Legal Medicine, Toxicology, and Physical Anthropology, School of Medicine, University of Granada, 18016, Granada, Spain; Instituto de Investigación Biosanitaria de Granada (ibs.GRANADA), 18012, Granada, Spain; CIBER of Epidemiology and Public Health (CIBERESP), Instituto de Salud Carlos III, 28029, Madrid, Spain. Electronic address: cfreire@ugr.es., Castiello F; Pediatric Unit, Germans Trias I Pujol University Hospital, 08916, Badalona, Spain., Babarro I; Faculty of Medicine and Nursing, University of the Basque Country (UPV/EU), 20014, Donostia/San Sebastián, Spain; Biogipuzkoa Health Research Institute, 20014, Donostia/San Sebastián, Spain., Anguita-Ruiz A; ISGlobal, 08036, Barcelona, Spain; CIBER of Physiopathology of Obesity and Nutrition (CIBEROBN), Instituto de Salud Carlos III, 28029, Madrid, Spain., Casas M; ISGlobal, 08036, Barcelona, Spain; Universitat Pompeu Fabra, 08005, Barcelona, Spain., Vrijheid M; CIBER of Epidemiology and Public Health (CIBERESP), Instituto de Salud Carlos III, 28029, Madrid, Spain; ISGlobal, 08036, Barcelona, Spain; Universitat Pompeu Fabra, 08005, Barcelona, Spain., Sarzo B; CIBER of Epidemiology and Public Health (CIBERESP), Instituto de Salud Carlos III, 28029, Madrid, Spain; Epidemiology and Environmental Health Joint Research Unit, FISABIO-Jaume I University-University of Valencia, 46020, Valencia, Spain., Beneito A; Epidemiology and Environmental Health Joint Research Unit, FISABIO-Jaume I University-University of Valencia, 46020, Valencia, Spain., Kadawathagedara M; Université Paris Cité and Université Sorbonne Paris Nord, Inserm, INRAE, 75004, Paris, France., Philippat C; University Grenoble Alpes, Inserm, U1209, CNRS UMR 5309, Team of Environmental Epidemiology Applied to Reproduction and Respiratory Health, Institute for Advanced Biosciences, 38000, Grenoble, France., Thomsen C; Department of Food Safety, Norwegian Institute of Public Health, 0456, Oslo, Norway., Sakhi AK; Department of Food Safety, Norwegian Institute of Public Health, 0456, Oslo, Norway., Lopez-Espinosa MJ; CIBER of Epidemiology and Public Health (CIBERESP), Instituto de Salud Carlos III, 28029, Madrid, Spain; Epidemiology and Environmental Health Joint Research Unit, FISABIO-Jaume I University-University of Valencia, 46020, Valencia, Spain; Department of Nursing, Faculty of Nursing and Chiropody, University of Valencia, 46010, Valencia, Spain.
Jazyk: angličtina
Zdroj: International journal of hygiene and environmental health [Int J Hyg Environ Health] 2024 Aug; Vol. 261, pp. 114418. Date of Electronic Publication: 2024 Jul 04.
DOI: 10.1016/j.ijheh.2024.114418
Abstrakt: Background: There is limited epidemiological evidence on the association of prenatal exposure to phthalates and synthetic phenols with altered pubertal timing.
Objective: To examine the association of prenatal exposure to phthalates, bisphenol A (BPA), parabens, benzophenone 3 (BP-3), and triclosan (TCS) with pubertal development in girls and boys from three European cohorts.
Methods: Urinary metabolites of six different phthalate diesters (DEP, DiBP, DnBP, BBzP, DEHP, and DiNP), BPA, methyl- (MePB), ethyl- (EtPB), propyl- (PrPB), and butyl-paraben (BuPB), BP-3, and TCS were quantified in one or two (1st and 3rd trimester) urine samples collected during pregnancy (1999-2008) from mothers in three birth cohorts: INMA (Spain), EDEN (France), and MoBa (Norway). Pubertal development of their children was assessed at a single visit at age 7-12 years (579 girls, 644 boys) using the parent-reported Pubertal Development Scale (PDS). Mixed-effect Poisson and g-computation and Bayesian Kernel Machine Regression (BKMR) were employed to examine associations of individual and combined prenatal chemical exposure, respectively, with the probability of overall pubertal onset, adrenarche, and gonadarche (stage 2+) in girls and boys. Effect modification by child body mass index (BMI) was also assessed.
Results: Maternal concentrations of the molar sum of DEHP and of DiNP metabolites were associated with a slightly higher probability of having started puberty in boys (relative risk, RR [95% CI] = 1.13 [0.98-1.30] and 1.20 [1.06-1.34], respectively, for a two-fold increase in concentrations), with a stronger association for DiNP in boys with overweight or obesity. In contrast, BPA, BuPB, EtPB, and PrPB were associated with a lower probability of pubertal onset, adrenarche, and/or gonadarche in all boys (e.g. overall puberty, BPA: RR [95% CI] = 0.93 [0.85-1.01] and BuPB: 0.95 [0.90-1.00], respectively), and the association with BPA was stronger in boys with underweight/normal weight. In girls, MEHP and BPA were associated with delayed gonadarche in those with underweight/normal weight (RR [95% CI] = 0.86 [0.77-0.95] and 0.90 [0.84-0.97], respectively). Most of these associations were trimester specific. However, the chemical mixture was not associated with any pubertal outcome in boys or girls.
Conclusions: Prenatal exposure to certain phthalates and synthetic phenols such as BPA may impact the pubertal development of boys, and weight status may modify this effect. BPA may also alter the pubertal development of girls.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2024 The Authors. Published by Elsevier GmbH.. All rights reserved.)
Databáze: MEDLINE
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