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Updated: Jan 15, 2026

Pharmacologic Induction of Epidermal Melanin and Protection Against Sunburn in a Humanized Mouse Model
Published on: September 7, 2013
Prolonged exposure to artificial light and carcinogenesis: A systematic review of oncostatic mechanisms associated
Gabriel Barboza1, Jêmina Oliveira1, Antônio Ferreira1
1Department of General Biology, Department of Medicine and Nursing, Federal University of Viçosa (UFV), Viçosa, Minas Gerais, Brazil.
Abstract:
Light pollution from widespread artificial illumination affects photosensitive organisms, including humans. Prolonged exposure to artificial light at night (ALAN), particularly blue light, is associated with melatonin suppression and circadian disruption, both implicated in carcinogenesis. This systematic review investigated the relationship between extended ALAN exposure and malignant neoplasms, identifying associated cancer types and biological mechanisms. A search was conducted in PubMed/Medline and Scopus using PRISMA guidelines. Original studies evaluating associations between ALAN, light pollution, or blue light and cancer in humans were included. Eighteen studies demonstrated a positive link between ALAN and breast cancer, with mechanisms involving interference in the cell cycle, DNA repair, oxidative stress, and activation of oncogenic pathways. Night-shift work correlated with increased breast cancer risk, reduced melatonin levels, and hormonal dysregulation. Exogenous melatonin showed oncostatic potential, reversing epigenetic changes induced by ALAN and reducing tumor burden. Melatonin suppression may promote tumor progression through circadian gene disruption and hormonal imbalance. While findings support a consistent link between ALAN exposure and oncogenesis-especially breast and prostate cancers-methodological variability and confounding factors, such as genetic predisposition and lifestyle, limit generalization. Further studies are needed to clarify mechanisms and explore preventive strategies, including light pollution control and melatonin-based interventions.
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