This PubMed-listed paper argues that the U.S. regulatory framework for radiofrequency radiation (RFR) from wireless technologies is outdated, lacks adequate oversight and enforcement, and has not been meaningfully updated since 1996. It contends that FCC exposure limits focus on short-term, high-intensity effects and do not address long-term, low-intensity exposures, with insufficient safeguards for children, pregnancy, and other vulnerable groups. The authors also discuss alleged regulatory capture, gaps in monitoring and compliance, and propose reforms including independent research, updated safety limits, and stronger pre- and post-market surveillance.

This RF Safe article argues that the main barrier to addressing radiofrequency radiation (RFR) and other non-native EMFs is structural policy and governance failure rather than a lack of scientific evidence. It cites the 2021 D.C. Circuit decision in Environmental Health Trust et al. v. FCC as criticism of the FCC’s rationale for keeping 1996 RF exposure limits, and it points to the Radiation Control for Health and Safety Act of 1968 as a mandate for HHS to run a research-backed radiation control program. The piece also references the U.S. National Toxicology Program’s animal findings and frames the lack of further NTP RF studies as a policy shortcoming, while promoting an “S4 MITO spin” mechanistic framework and a proposed “Clean Ether Act.”

RF Safe presents “S4 MITO spin” as a proposed mechanistic framework arguing that peer-reviewed evidence can be unified to explain reported biological effects from radiofrequency radiation (RFR) and other non-native EMFs. The post highlights animal studies (notably NTP and Ramazzini) as showing carcinogenic “signals” and emphasizes non-linear dose–response patterns, asserting relevance to regulatory exposure limits. It frames the model as empirically grounded and testable, while acknowledging it is not a complete theory of all EMF effects.

RF Safe argues that radiofrequency radiation (especially pulsed or modulated signals with low-frequency components) can alter local membrane potentials at nanometer scales where voltage-gated ion channel S4 sensors operate. It claims these shifts could change ion channel gating in immune cells, altering calcium and proton signaling, increasing oxidative stress, and promoting innate immune activation that may contribute to autoimmune-like inflammation. The piece presents a mechanistic causal chain and highlights heart and nerve tissue as potentially more susceptible due to high ion-channel density and mitochondrial content, but does not present new study data in the provided text.

This animal study examined whether paternal exposure to 4.9 GHz (5G) radiofrequency radiation affects male offspring in C57BL/6 mice. It reports increased anxiety-like behavior and reduced sperm quality in adult F1 males from exposed fathers, alongside reported LRGUK hypermethylation and reduced LRGUK expression in testes. The abstract reports no significant effects on depression-like behavior, learning/memory, or fertility across F1–F2 generations.

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 compares two epidemiologic studies of radio-frequency radiation (RFR) exposure among military personnel with overlapping patient groups. One study reported a statistically significant increase in cancer among exposed individuals, while the other did not, which the review attributes to a smaller sample size. The review highlights similar cancer patterns across both studies, including a high proportion of hematolymphoid cancers and earlier onset among exposed individuals, and interprets these similarities as evidence of carcinogenic effects.

This paper presents a mixed-method study protocol examining electromagnetic hypersensitivity (EHS) in relation to mobile phone radiofrequency radiation exposure among undergraduate students. The quantitative component aims to identify predictors of EHS using a biopsychosocial model, while the qualitative component explores individual experiences through in-depth interviews. The abstract provides study design details and sample size but does not report study results.

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.