Analysis of global DNA methylation changes in human keratinocytes immediately following exposure to a 900 MHz...

The increasing use of nonionizing radiofrequency electromagnetic fields (RF-EMFs) in a wide range of technologies necessitates studies to further understanding of biological effects from exposures to such forms of electromagnetic fields. While previous studies have described mechanisms for cellular changes occurring following exposure to low-intensity RF-EMFs, the role of molecular epigenetics has not been thoroughly investigated. Specifically unresolved is the effect of RF-EMFs on deoxyribonucleic acid (DNA) methylation, which is a powerful epigenetic process, used by cells to regulate gene expression. DNA methylation is dynamic and can be rapidly triggered in response to external stimuli such as exposure to RF-EMFs. In the present study, we performed a global analysis of DNA methylation patterns in human keratinocytes exposed to 900 MHz RF-EMFs for 1 h at a low dose rate (estimated mean specific absorption rate (SAR) < 10 mW/kg). We used a custom system to allow stable exposure of cell cultures to RF-EMFs under biologically relevant conditions (37 °C, 5% CO₂ , 95% humidity). We performed whole genome bisulfite sequencing directly following RF-EMF exposure to examine the immediate changes in DNA methylation patterns and identify early differentially methylated genes in RF-EMF-exposed keratinocytes. By correlating global gene expression to whole genome bisulfite sequencing, we identified six common targets that were both differentially methylated and differentially expressed in response to RF-EMF exposure. The results highlight a potential epigenetic role in the cellular response to RF-EMFs. Particularly, the six identified targets may potentially be developed as epigenetic biomarkers for immediate responses to RF-EMF exposure. Bioelectromagnetics. 1-13, © 2023 Bioelectromagnetics Society. This article has been contributed to by U.S. Government employees and their work is in the public domain in the USA.