Bisphenol A and adiposity measures in peripubertal boys from the INMA-Granada cohort
2019; Elsevier BV; Volume: 173; Linguagem: Inglês
10.1016/j.envres.2019.03.045
ISSN1096-0953
AutoresVicente Mustieles, Maribel Casas, Patricia Ferrando-Marco, Olga Ocón‐Hernández, Iris Reina-Pérez, Andrea Rodríguez‐Carrillo, Fernando Vela-Soria, Rocío Pérez‐Lobato, Eva María Navarrete‐Muñoz, Carmen Freire, Nicolás Olea, Mariana F. Fernández,
Tópico(s)Effects and risks of endocrine disrupting chemicals
ResumoChildhood obesity is one of the most serious public health challenges of our times. Although an important body of experimental evidence highlights the obesogenic potential of endocrine disruptors such as bisphenol A (BPA), the epidemiological evidence remains inconclusive and limited. To assess associations between urinary BPA concentrations and several adiposity measures in peripubertal boys from the Environment and Childhood (INMA) cohort in Granada, Spain. BPA concentrations were determined in spot urine samples from 298 boys aged 9–11, and their weight, height, waist circumference, and percentage body fat mass were measured. Overweight/obesity was defined as BMI z-score ≥85th percentile and abdominal obesity as waist-to-height ratio (WHtR) ≥0.5. Associations were assessed using multivariable linear and logistic regression models. In adjusted models, each natural log-unit increase in urinary BPA concentrations was associated with higher BMI z-score (β = 0.22; 95%CI = 0.03, 0.41) and increased odds of overweight/obesity (OR = 1.46; 95%CI = 1.05, 2.05). Children with higher BPA concentrations had higher WHtR values (β = 0.007; 95%CI = −0.001, 0.015), and BPA was associated with a greater risk of abdominal obesity (OR = 1.45; 95%CI = 1.03, 2.06). No associations were found with % body fat mass. BPA may exert an obesogenic effect in peripubertal boys, potentially increasing the risk of overweight/obesity, especially abdominal obesity. However, these results should be interpreted with caution given the modest sample size and the possibilities of reverse causality and residual confounding by diet and lifestyle patterns.
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