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.

This RF Safe commentary argues that HHS, under Secretary Robert F. Kennedy Jr., was correct to remove FDA webpages that gave broad assurances that cell phone radiation is “not dangerous.” It claims blanket safety messaging is scientifically indefensible given animal toxicology findings (notably the U.S. National Toxicology Program studies), a WHO-commissioned systematic review of animal cancer studies (Mevissen et al., 2025), and references to federal court findings. The piece frames the change as a precautionary, science-based correction rather than an anti-science move.

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.

RF Safe presents the “S4-Mito-Spin” framework as a hypothesis aiming to unify proposed non-thermal biological effects reported in some EMF studies (e.g., oxidative stress, DNA damage, fertility effects, and tumors in animal models). The article describes a multi-mechanism model involving voltage-gated channel forced oscillation, mitochondrial/NOX amplification to reactive oxygen species bursts, and radical-pair/spin-state effects, with a novel “density-gated” concept to explain tissue-specific and inconsistent findings. It also suggests the framework could connect EMF hazards with therapeutic uses, citing FDA-approved RF devices such as TheraBionic as an example of RF modulation of biology.

This review/technical note discusses whether chronic EMF exposure, mainly from mobile phones and wireless devices, should be reconsidered as a possible risk factor for oral cancer/OSCC. It highlights biological plausibility and reports from pilot cytogenetic and laboratory studies, plus limited epidemiological observations, suggesting increased micronucleus formation and altered stress responses in buccal mucosal cells among long-term users. The authors emphasize that a direct causal link to OSCC is not established and call for more comprehensive research.

This rat study assessed 30-day 2600 MHz EMF exposure effects on kidney tissue and DNA damage in blood lymphocytes, with an EMF+quercetin group included. Kidney histopathology and immunohistochemistry were reported as similar across groups, and oxidative stress markers did not significantly change. The EMF-only group showed significant DNA damage in lymphocytes by Comet assay.

This animal study used Drosophila knockout lines to examine whether visual (Rh1) versus non-visual (Rh7) opsins contribute to blue-light-associated neural damage. Flies were continuously exposed to 488 nm blue light from egg deposition to 20 days, and brain DNA damage and vacuolisation were assessed. The study reports greater DNA damage and neurodegeneration markers in Rh1 knockout flies than in wild-type or Rh7 knockout flies, and concludes Rh1 is a predominant mediator of blue-light-induced neurotoxicity in the fly CNS.

This narrative review discusses proposed non-thermal mechanisms by which chronic, low-intensity RF-EMR from ubiquitous wireless sources may affect male reproductive health. It highlights oxidative stress, mitochondrial dysfunction, impaired testosterone synthesis/steroidogenesis, and declines in sperm quality as reported outcomes. The authors argue that current SAR/thermal-based guidelines may not capture these endpoints and call for updated standards and precautionary measures.

This review summarizes studies reporting radiofrequency radiation (RFR)-associated changes in gene expression across biological systems. Reported affected genes relate to cellular stress responses, oxidative processes, apoptosis, DNA damage detection/repair, protein repair, and neural function regulation. The authors highlight reported gene expression effects at or below 0.4 W/kg SAR and argue this challenges current guideline assumptions, while noting that not all studies find significant effects.

This review discusses epidemiological and mechanistic reports linking EMF exposure with oxidative stress and disease risk, and introduces an Electromagnetic Pathogenesis (EMP) conceptual model. The model proposes that non-ionizing EMFs increase mitochondrial electron leakage via electron tunneling, raising free radical production and oxidative stress. The authors argue oxidative stress is a primary mechanism connecting EMF exposure to cancer, cardiovascular, neurodevelopmental/neurodegenerative diseases, and behavioral/reproductive effects, and suggest reducing exposure may lower risk.

This animal study examined whether prenatal exposure to 3.5 GHz radiofrequency radiation (2 hours/day) affects male reproductive outcomes later in life. Male rat offspring assessed at 12 months showed multiple adverse testicular and cellular findings in exposed groups versus sham controls, including impaired spermatogenesis markers, increased abnormal sperm morphology, increased DNA damage, and increased apoptosis, with full-gestation exposure generally most pronounced. The authors interpret the results as evidence of persistent reproductive toxicity from prenatal exposure and call for further mechanistic work and precautionary actions.

This review discusses recent studies on microwave and RF exposure and their reported impacts on molecular and cytogenetic materials. It states there is growing evidence that RF exposure can induce DNA damage at levels considered safe by current standards, and cites newly reported genetic alterations in rat cancers after lifetime low-level RF exposure. The article concludes that these findings challenge existing exposure guidelines and support reconsideration of regulatory limits.

This randomized controlled animal study examined chronic 35.5 GHz millimeter wave exposure in male Wistar rats (2 hours/day for 60 days) compared with control and sham groups. The exposed group showed reduced sperm count and viability along with testicular histopathological changes. Oxidative stress markers shifted toward increased lipid peroxidation and reduced antioxidant defenses, and comet assay results indicated increased DNA damage.

This scoping review and evidence map (PRISMA-ScR) summarizes over 500 studies on RF-EMF exposure and genotoxicity across in vitro, in vivo, and epidemiological research. The authors report a higher proportion of significant DNA damage findings in in vivo and epidemiological studies than in vitro studies, with DNA base damage commonly reported under real-world/pulsed/GSM talk-mode conditions and longer exposures. They conclude that DNA damage has been observed at exposure levels below ICNIRP limits and recommend precautionary measures and updates to guidelines to address potential non-thermal effects.

This in vitro study exposed yeast suspensions to 2.45 GHz near-field microwave radiation at 2 cm and 4 cm for 20 or 60 minutes. It reports oxidative-stress-related changes (reduced antioxidant activity with increased membrane permeability) after 20 minutes at 2 cm, an effect not reproduced by conventional heating. The study also reports a trend toward increased DNA damage under both exposure conditions and mild membrane permeability changes after 60 minutes at 4 cm.

This narrative review discusses biological mechanisms and reported health effects of anthropogenic extremely low frequency (ELF) and wireless communication (WC) electromagnetic fields. It highlights oxidative stress and DNA damage as key mechanistic endpoints and proposes an IFO-VGIC pathway linking EMF exposure to ROS overproduction and cellular dysfunction. The authors interpret the broader literature as indicating risks (e.g., cancer, infertility, EHS) even below current exposure limits and advocate precautionary policy measures, including stricter limits and a 5G moratorium.

This animal study examined short- and long-term 700 MHz (lower-band 5G) radiofrequency exposure in female Wistar rats, comparing control, sham, and exposed groups. It reports no DNA damage and no change in estrous cycle length, but increased ovarian oxidative stress markers in exposed animals. Long-term exposure was associated with ovarian histopathological alterations, while estradiol and progesterone stayed within normal ranges and testosterone increased slightly but significantly.

This National Toxicology Program technical report describes 900 MHz whole-body RFR exposures (GSM and CDMA) in male and female Sprague Dawley rats from in utero through up to 2 years. The report concludes clear evidence of carcinogenic activity in males for both modulations based on malignant schwannoma of the heart, with malignant glioma of the brain also reported as related to exposure. In females, the report concludes equivocal evidence of carcinogenic activity for both modulations based on selected tumor outcomes, and genetic toxicology findings were mixed with some comet assay increases/equivocal results but negative micronucleus assays.

This review discusses the comet assay and summarizes research on non-ionizing EMF exposure and DNA/chromosomal damage. It describes both positive and negative findings across studies, noting no consistent overall pattern for radiofrequency radiation (RFR). The authors nonetheless conclude that under certain exposure conditions RFR appears genotoxic and may affect DNA damage and repair, with evidence discussed as most applicable to exposures typical of cell phone use.