Evaluating Phthalates and Bisphenol in Foods: Risks for Precocious Puberty and Early-Onset Obesity

Abstract

Recent scientific results indicate that diet is the primary source of exposure to endocrine-disrupting chemicals (EDCs) due to their use in food processing, pesticides, fertilizers, and migration from packaging to food, particularly in plastic or canned foods. Although EDCs are not listed on nutrition labels, their migration from packaging to food could inadvertently lead to food contamination, affecting individuals by inhalation, ingestion, and direct contact. The aim of our narrative review is to investigate the role of phthalates and bisphenol A (BPA) in foods, assessing their risks for precocious puberty (PP) and early-onset obesity, which are two clinical entities that are often associated and that share common pathogenetic mechanisms. The diverse outcomes observed across different studies highlight the complexity of phthalates and BPA effects on the human body, both in terms of early puberty, particularly in girls, and obesity with its metabolic disruptions. Moreover, obesity, which is independently linked to early puberty, might confound the relationship between exposure to these EDCs and pubertal timing. Given the potential public health implications, it is crucial to adopt a precautionary approach, minimizing exposure to these EDCs, especially in vulnerable populations such as children.

Keywords: adolescents; bisphenol; children; foods; obesity; pediatrics; phthalates; precocious puberty.

Figure 1

Flowchart of criteria for study selection.

Figure 2

The interaction between diet, phthalates, and bisphenols with precocious puberty and early onset of obesity. Created by Biorender.com®. DEHP = Di(2-ethylhexyl) phthalate; DEP = diethyl phthalate, DiDP = diisodecyl phthalate; DiNP = diisononyl phthalate; HHWM = high-molecular-weight phthalates; HPA = hypothalamic-pituitary-adrenal; LHWM = low-molecular-weight phthalates; PPARSs = Peroxisome proliferator-activated receptors.