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 animal study tested whether short-term 28 GHz (5G-band) millimeter-wave exposure modifies doxorubicin-induced cardiotoxicity in male rats and whether vitamin C mitigates effects. Co-exposure to 28 GHz EMR was reported to worsen several indices of DOX-related cardiac injury (including CAT reduction, increased BAX expression, and QT prolongation), while vitamin C provided partial attenuation. The authors emphasize that results are limited to a short-duration preclinical model and that human relevance remains preliminary.

RF Safe argues for a “toxicity-based” interpretation of EMF/EMR exposure, claiming there are plausible biological mechanisms by which EMFs could cause symptoms rather than merely correlate with them. It highlights proposed pathways involving voltage-gated ion channels, oxidative stress/ROS (including mitochondrial effects), and radical-pair/cryptochrome mechanisms. The piece advocates a precautionary approach that treats non-native EMR as an environmental toxicant and calls for exposure minimization and alternative technologies, while noting that quantitative risk at everyday exposure levels remains debated.

This magazine article reviews the Japan-Korea "NTP Lite" RF animal toxicity collaboration and its relationship to prior NTP (2018) and Ramazzini Institute reports of RF-associated tumors in male rats. It notes NTP Lite used a single whole-body SAR of 4 W/kg and completed a two-year exposure phase in 2022, but final reporting is delayed with histopathology and genotoxicity work ongoing. The author highlights protocol harmonization across labs while raising concerns about unexplained animal deaths and physiological differences in exposed groups, and frames the broader evidence as supportive of RF-related cancer risk in laboratory animals.

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 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 PRISMA-adherent systematic review searched PubMed, Scopus, and the Cochrane Library for studies (2017–2024) on physiological or behavioral responses to EMF exposure, emphasizing studies reporting harmful or concerning effects. Across 24 included studies (human non-randomized, in vitro, and animal), the review reports negative biological effects including oxidative stress, inflammation, genotoxicity, cardiovascular and fertility-related outcomes, neuronal activity changes, and plant photosynthesis impacts. The authors report that most studies had moderate to high risk of bias and therefore the overall certainty of evidence was lower, and they highlight major gaps in long-term human evidence and exposure standardization.

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 animal experiment exposed adult male rats to 6 GHz RF-EMR (0.065 W/kg) for 4 hours/day over 42 days and compared them with sham controls. The exposed group showed higher comet assay genotoxicity metrics, though not statistically significant, and more prominent liver histopathological changes (e.g., portal inflammation and congestion). The authors conclude that 6 GHz exposure can cause histopathological and DNA-level changes in rat liver tissue under the studied conditions.

This in vitro study exposed BV2 mouse microglial cells to 3.5 GHz EMF for 2 hours and reports reduced cell growth and increased apoptosis alongside oxidative stress and signaling changes. The authors report that ROS generation and activation of JNK-1/2 and p38 MAPK were key events in the observed cytotoxicity. Polydeoxyribonucleotide (PDRN) reportedly reduced several EMF-associated cytotoxicity markers, suggesting a potential mitigating effect under the tested conditions.