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.

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 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.

In a rat experiment (n=59), a single 40-minute whole-body 28 GHz exposure at near-threshold WBA-SAR levels was evaluated under normal and heat conditions with restraint. After accounting for sham-related restraint stress, exposure was associated with increased serum-free corticosterone 1–3 days later, especially when rectal temperature rose by >1°C. Urinary catecholamines suggested an immediate inhibitory effect on stress response (notably noradrenaline), with heat amplifying effects and linking noradrenaline to tail surface temperature.