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6 postsExposure to hexavalent chromium and 1800 MHz electromagnetic radiation can synergistically induce intracellular DNA damage in mouse embryonic fibroblasts
This PubMed-listed in vitro study tested whether 1800 MHz RF-EMF exposure can modify chemically induced DNA damage in mouse embryonic fibroblasts under standardized, non-thermal conditions. The authors report RF-EMF alone did not produce detectable DNA damage and did not significantly increase damage from hydrogen peroxide, 4-nitroquinoline-1-oxide, or cadmium. However, co-exposure with hexavalent chromium (Cr(VI)) was reported to synergistically increase DNA damage in the comet assay, which the authors interpret as possible selective exacerbation of Cr(VI)-induced genotoxicity requiring further investigation.
Negative Controls That Matter
RF Safe argues that “no effect” findings in some RF exposure studies should be interpreted as meaningful negative controls rather than as evidence that RF has no biological effects. The post presents RF Safe’s “S4–Mito–Spin” framework, claiming certain skin cell types (fibroblasts and keratinocytes) are predicted to be relatively resistant to non-thermal RF effects, so null results in these cells can be consistent with the model. It cites in-vitro studies at 3.5 GHz (5G-modulated) reporting no changes in ROS measures, stress responses, or UV-B DNA repair kinetics under specified SAR conditions, and frames these nulls as boundary conditions rather than a general safety conclusion.
Exposure to hexavalent chromium and 1800 MHz electromagnetic radiation can synergistically induce intracellular DNA damage in mouse embryonic fibroblasts
This in vitro study tested whether 1800 MHz RF-EMF modifies chemically induced DNA damage in mouse embryonic fibroblasts under non-thermal exposure conditions. RF-EMF alone did not produce detectable DNA damage and did not significantly enhance damage from hydrogen peroxide, 4NQO, or cadmium. In contrast, co-exposure with hexavalent chromium (Cr(VI)) was reported to synergistically increase DNA damage, suggesting a selective co-genotoxic interaction under specific chemical conditions.
Effects of Simultaneous In-Vitro Exposure to 5G-Modulated 3.5 GHz and GSM-Modulated 1.8 GHz Radio-Frequency Electromagnetic Fields on Neuronal Network Electrical Activity and Cellular Stress in Skin Fibroblast Cells
This in-vitro study exposed primary cortical neurons and human immortalized skin fibroblasts to simultaneous 5G-modulated 3.5 GHz and GSM-modulated 1.8 GHz RF-EMF at SARs of 1 or 4 W/kg. It reports no significant changes in neuronal network firing/bursting activity and no alteration of mitochondrial ROS in fibroblasts. Stress-related signaling readouts showed only minor, threshold-level variations without a consistent pattern, and no HSF1 activation was observed. Overall, the authors conclude there is no strong evidence of biological effects under these exposure conditions.
5G-exposed human skin cells do not respond with altered gene expression and methylation profiles
This in vitro study exposed human skin cells (fibroblasts and keratinocytes) to 5G-band electromagnetic fields for 2 hours and 48 hours using a fully blinded design. Exposures were up to ten times permissible limits, with sham exposure as a negative control and UV exposure as a positive control. The study reports that observed gene expression and DNA methylation differences were minor and consistent with random variation, supporting no detectable EMF-related effect under the tested conditions.
Skin Fibroblasts from Individuals Self-Diagnosed as Electrosensitive Reveal Two Distinct Subsets with Delayed Nucleoshuttling of the ATM Protein in Common
This study reports on 26 adults self-diagnosed with electromagnetic hypersensitivity (EHS) who provided skin biopsies to generate primary fibroblast lines. The authors describe two EHS subsets based on questionnaire and DNA damage-related measures, and report delayed ATM nucleoshuttling after X-ray exposure in all samples, interpreted as impaired DNA repair signaling. They propose a molecular model linking EHS to ATM pathway dysfunction and suggest this could relate to increased cancer risk or accelerated aging.