Environmental heat exposure and female pubertal timing: biological plausibility, emerging evidence and research priorities

Over the past century, female pubertal timing has progressively advanced and this trend cannot be fully explained by genetic factors, childhood obesity, endocrine-disrupting chemicals, air pollution or other established risk factors alone, thereby providing a rationale for investigating additional environmental exposures. As climate change increases the frequency and intensity of heat waves worldwide, chronic thermal stress may represent a potential contributor to earlier pubertal timing that warrants further investigation. This narrative review integrates current evidence on heat exposure and neuroendocrine regulation to propose a biological framework linking prolonged heat-wave exposure to earlier female pubertal timing. Available evidence suggests that thermal stress may influence pubertal timing through multiple converging pathways, including activation of the hypothalamic–pituitary–adrenal axis, metabolic alterations involving insulin and IGF-1, sleep disruption with reduced melatonin secretion and, more speculatively, modulation of hypothalamic KNDy neurons involved in both thermoregulation and reproductive control. To date, it is important to note that the proposed relationship between heat exposure and earlier pubertal timing remains a biologically plausible hypothesis supported primarily by indirect epidemiological and mechanistic evidence, as direct evidence of causality in humans is lacking. Because children living in socioeconomically disadvantaged environments often experience greater exposure to extreme heat, climate-related endocrine effects may also contribute to widening health inequalities. Clarifying this relationship could expand current understanding of climate-sensitive pediatric endocrine health and inform future epidemiological research as well as public health strategies aimed at protecting children from the long-term consequences of rising global temperatures