Marina Vafeiadi1, Theano Roumeliotaki2, Antonis Myridakis3, Georgia Chalkiadaki2, Eleni Fthenou2, Eirini Dermitzaki4, Marianna Karachaliou2, Katerina Sarri2, Maria Vassilaki2, Euripides G Stephanou3, Manolis Kogevinas5, Leda Chatzi2. 1. Department of Social Medicine, Faculty of Medicine, University of Crete, Heraklion, Greece. Electronic address: m.vafeiadi@med.uoc.gr. 2. Department of Social Medicine, Faculty of Medicine, University of Crete, Heraklion, Greece. 3. Environmental Chemical Processes Laboratory (ECPL), Department of Chemistry, University of Crete, Heraklion, Greece. 4. Department of Clinical Chemistry, School of Medicine, University of Crete, Heraklion, Crete, Greece. 5. Centre for Research in Environmental Epidemiology (CREAL), Barcelona, Spain; Hospital del Mar Research Institute (IMIM), Barcelona, Spain; CIBER Epidemiología y Salud Pública (CIBERESP), Barcelona, Spain.
Abstract
BACKGROUND: Bisphenol A (BPA) is a chemical used extensively worldwide in the manufacture of plastic polymers. The environmental obesogen hypothesis suggests that early life exposure to endocrine disrupting chemicals such as BPA may increase the risk for wt gain later in childhood but few prospective epidemiological studies have investigated this relationship. OBJECTIVES: We examined the association of early life BPA exposure with offspring obesity and cardiometabolic risk factors in 500 mother-child pairs from the RHEA pregnancy cohort in Crete, Greece. METHODS: BPA concentrations were measured in spot urine samples collected at the 1st trimester of pregnancy) and from children at 2.5 and 4 years of age. We measured birth wt, body mass index (BMI) from 6 months to 4 years of age, waist circumference, skinfold thickness, blood pressure, serum lipids, C-reactive protein, and adipokines at 4 years of age. BMI growth trajectories from birth to 4 years were estimated by mixed effects models with fractional polynomials of age. Adjusted associations were obtained via multivariable regression analyses. RESULTS: The prevalence of overweight/obesity was 9% at 2, 13% at 3% and 17% at 4 years of age. Geometric mean BPA concentrations were 1.2μg/g creatinine±7.9 in 1st trimester, 5.1μg/g±13.3 in 2.5 years and 1.9μg/g±4.9 in 4 years. After confounder adjustment, each 10-fold increase in BPA at 4 years was associated with a higher BMI z-score (adj. β=0.2; 95% CI: 0.01, 0.4), waist circumference (adj. β=1.2; 95% CI: 0.1, 2.2) and sum of skinfold thickness (adj. β=3.7mm; 95% CI: 0.7, 6.7) at 4 years. Prenatal BPA was negatively associated with BMI and adiposity measures in girls and positively in boys. We found no associations of early life exposure to BPA with other offspring cardiometabolic risk factors. CONCLUSIONS: Prenatal BPA exposure was not consistently associated with offspring growth and adiposity measures but higher early childhood BPA was associated with excess child adiposity.
BACKGROUND:Bisphenol A (BPA) is a chemical used extensively worldwide in the manufacture of plastic polymers. The environmental obesogen hypothesis suggests that early life exposure to endocrine disrupting chemicals such as BPA may increase the risk for wt gain later in childhood but few prospective epidemiological studies have investigated this relationship. OBJECTIVES: We examined the association of early life BPA exposure with offspring obesity and cardiometabolic risk factors in 500 mother-child pairs from the RHEA pregnancy cohort in Crete, Greece. METHODS:BPA concentrations were measured in spot urine samples collected at the 1st trimester of pregnancy) and from children at 2.5 and 4 years of age. We measured birth wt, body mass index (BMI) from 6 months to 4 years of age, waist circumference, skinfold thickness, blood pressure, serum lipids, C-reactive protein, and adipokines at 4 years of age. BMI growth trajectories from birth to 4 years were estimated by mixed effects models with fractional polynomials of age. Adjusted associations were obtained via multivariable regression analyses. RESULTS: The prevalence of overweight/obesity was 9% at 2, 13% at 3% and 17% at 4 years of age. Geometric mean BPA concentrations were 1.2μg/g creatinine±7.9 in 1st trimester, 5.1μg/g±13.3 in 2.5 years and 1.9μg/g±4.9 in 4 years. After confounder adjustment, each 10-fold increase in BPA at 4 years was associated with a higher BMI z-score (adj. β=0.2; 95% CI: 0.01, 0.4), waist circumference (adj. β=1.2; 95% CI: 0.1, 2.2) and sum of skinfold thickness (adj. β=3.7mm; 95% CI: 0.7, 6.7) at 4 years. Prenatal BPA was negatively associated with BMI and adiposity measures in girls and positively in boys. We found no associations of early life exposure to BPA with other offspring cardiometabolic risk factors. CONCLUSIONS: Prenatal BPA exposure was not consistently associated with offspring growth and adiposity measures but higher early childhood BPA was associated with excess child adiposity.
Authors: Beverly S Rubin; Maneesha Paranjpe; Tracey DaFonte; Cheryl Schaeberle; Ana M Soto; Martin Obin; Andrew S Greenberg Journal: Reprod Toxicol Date: 2016-08-02 Impact factor: 3.143
Authors: Luke Montrose; Vasantha Padmanabhan; Jaclyn M Goodrich; Steven E Domino; Marjorie C Treadwell; John D Meeker; Deborah J Watkins; Dana C Dolinoy Journal: Epigenetics Date: 2018-04-18 Impact factor: 4.528
Authors: Chalana M Sol; Susana Santos; Liesbeth Duijts; Alexandros G Asimakopoulos; Maria-Pilar Martinez-Moral; Kurunthachalam Kannan; Vincent W V Jaddoe; Leonardo Trasande Journal: Environ Int Date: 2020-09-01 Impact factor: 9.621
Authors: Sarah Zulkifli; Amirah Abdul Rahman; Siti Hamimah Sheikh Abdul Kadir; Noor Shafina Mohd Nor Journal: Eur J Pediatr Date: 2021-04-24 Impact factor: 3.183
Authors: Joseph M Braun; Nan Li; Tye E Arbuckle; Linda Dodds; Isabelle Massarelli; William D Fraser; Bruce P Lanphear; Gina Muckle Journal: Environ Res Date: 2019-02-26 Impact factor: 6.498