Environmental factors shaping atopic dermatitis: Lessons from longitudinal cohort studies

Atopic dermatitis (AD) is a prevalent chronic inflammatory skin disease arising from a multifaceted interplay between genetic susceptibility and environmental exposures. Longitudinal cohort studies have been instrumental in elucidating the contribution of environmental factors to both the onset and persistence of AD. This review synthesizes evidence from such studies to delineate key environmental determinants across various domains. Early-life exposures, including delivery mode and antibiotic exposure, modulate microbial composition and function, thereby influencing immune development and predisposing individuals to AD. Both outdoor and indoor air pollutants, such as particulate matter and volatile organic compounds, have been shown to impair skin barrier integrity and dysregulate immune responses, facilitating the initiation and progression of AD. Nutritional factors, encompassing maternal and infant dietary patterns, shape gut microbiota and metabolite profiles and systemic immune activity, further modulating AD risk. Moreover, psychological stress during the prenatal and postnatal periods has been associated with alterations in immune function and epigenetic programming, which may heighten susceptibility to AD. Environmental influences also appear to vary by AD phenotype and trajectory, underscoring the need for individualized prevention strategies. Advances in exposome research, encompassing both external and internal environmental components, have enhanced mechanistic understanding and facilitated the identification of candidate biomarkers. Collectively, current evidence supports the notion that early-life environmental exposures act not as isolated determinants but in concert with genetic, microbial, and immunologic factors to shape AD pathogenesis. A comprehensive framework integrating exposomics and multiomics may ultimately inform the development of targeted preventive and therapeutic strategies for children with AD.