Ambient Air Pollution, Polycyclic Aromatic Hydrocarbons, and Pubertal Development: A Critical Review of Emerging Evidence
TL;DR
Air pollution may alter pubertal timing through endocrine-disrupting mechanisms, with PAHs representing a plausible mechanistic pathway and longitudinal cohorts, pollutant mixture analyses, and male populations suggested.
Abstract
Puberty is a sensitive period of endocrine development with lifelong implications for cardiometabolic and reproductive health. This review evaluates evidence linking ambient air pollution and polycyclic aromatic hydrocarbons (PAHs) to pubertal development. Studies suggest that associations between air pollution and pubertal timing depend on pollutant composition, exposure timing, and exposure intensity. Component-level analyses of PM2.5 implicate organic matter (OM) and sulfate fractions in associations with earlier menarche and precocious puberty, with OM enriched in combustion-derived PAHs. In contrast, high chronic PM2.5 exposure has also been associated with delayed menarche in heavily polluted settings. Biomarker studies further support biological plausibility, associating PAH exposure to earlier breast development and disruption of hypothalamic kisspeptin–GnRH signaling. Evidence suggests that air pollution may alter pubertal timing through endocrine-disrupting mechanisms, with PAHs representing a plausible mechanistic pathway. Future studies should prioritize longitudinal cohorts, pollutant mixture analyses, and male populations.