Epigenetic Effects of Prenatal and Early Life Tobacco Smoke Exposure on AHRR Methylation
Publication Date : Aug-24-2026
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Abstract :
Prenatal tobacco smoke exposure is an important public health concern, particularly in settings where tobacco use and secondhand smoke (SHS) exposure remain widespread. This systematic review examined the relationship between prenatal tobacco exposure and DNA methylation changes, with emphasis on the aryl hydrocarbon receptor repressor (AHRR) gene, while also considering developmental outcomes and implications for high-exposure settings such as Indonesia. PubMed and Google Scholar were searched between January and June 2026, with the final search conducted on 14 June 2026. Studies published between 2005 and 2026 were eligible if they were English-language, peer-reviewed original research articles investigating prenatal tobacco exposure and offspring DNA methylation or relevant developmental outcomes. Studies from any country-income setting were eligible. Study selection followed predefined eligibility criteria and PRISMA 2020 guidelines. Three observational studies, including cohort and cross-sectional designs, were included. Direct evidence linking prenatal SHS exposure with AHRR methylation was limited. Most studies examined maternal active smoking during pregnancy and identified associations with altered offspring DNA methylation, including changes at tobacco-associated AHRR CpG sites. Prenatal SHS exposure was also associated with adverse neonatal outcomes, including lower birth weight. Findings were limited by the small number of eligible studies, observational designs, and limited representation of low- and middle-income countries. Current evidence suggests that prenatal tobacco exposure may contribute to epigenetic and developmental effects; however, further longitudinal research is needed, particularly in populations with high tobacco exposure burdens and in low- and middle-income countries where evidence remains limited.
