The Influence of Environmental Exposure to Xenobiotics on the Genesis of Precocious Puberty

Abstract

Precocious puberty is characterised by the appearance of secondary sexual characteristics before the age of eight years in girls and nine years in boys and has become an increasingly relevant concern in child health. This review aimed to analyse the influence of environmental exposure to xenobiotics, particularly endocrine-disrupting chemicals, on the genesis of precocious puberty. The manuscript was structured as an integrative literature review, drawing on clinical, epidemiological and toxicological evidence concerning bisphenol A, phthalates, parabens, pesticides, perfluoroalkyl and polyfluoroalkyl substances, phytoestrogens and flame retardants. The reviewed literature indicates that these compounds may interfere with pubertal development through oestrogenic mimicry, antiandrogenic activity, altered steroidogenesis, changes in hormone bioavailability, non-genomic cellular signalling and epigenetic mechanisms. The hypothalamic-pituitary-gonadal axis, particularly the gonadotropin-releasing hormone and kisspeptin systems, appears to be especially vulnerable during prenatal life and early childhood, when neuroendocrine programming and detoxification pathways are still developing. The evidence discussed in the manuscript also suggests that exposure may occur through food packaging, household dust, cosmetics, agricultural residues, contaminated water and maternal transfer. Clinically, environmentally associated pubertal anticipation may involve premature thelarche, altered testicular development, accelerated bone maturation, reduced adult height potential and psychosocial vulnerability. The review further highlights the complexity of mixture effects, non-monotonic dose-response patterns and interactions with childhood obesity. Overall, the manuscript supports a cautious interpretation of the evidence and emphasises the need for preventive strategies that reduce avoidable childhood exposure while strengthening clinical surveillance and public-health regulation. The review therefore frames pubertal timing as a developmental outcome influenced by endocrine, environmental and social determinants rather than by a single exposure pathway.