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.

RF Safe argues that celebrity-branded mobile services (citing reported plans for “Beast Mobile” and the announced “Trump Mobile”) could normalize near-body, all-day phone use—especially among children—and therefore carry ethical responsibility for scaled RF exposure. The piece cites legal and scientific developments (including the 2021 Environmental Health Trust v. FCC decision, the U.S. NTP animal studies, and a WHO-commissioned systematic review) to claim the evidence base has “moved decisively” toward concern about long-term RF-EMF effects. It also promotes a proposed mechanistic framework ("S4–Mito–Spin") and suggests shifting indoor connectivity toward Li‑Fi (IEEE 802.11bb) as a harm-reduction approach.

This RF Safe article argues that it is no longer accurate to claim there is no mechanism or no evidence of harm from RF exposure below current limits. It presents a proposed biological framework involving voltage-gated ion channels, oxidative stress pathways, and radical-pair (spin-dependent) chemistry, and cites animal studies (NTP and Ramazzini) and other literature as supporting evidence. The piece frames the remaining uncertainty as the magnitude of human risk rather than whether a hazard exists.

An RF Safe article argues that, as of 2025, evidence is “decisive” that man-made radiofrequency (RF) fields can cause cancer and other biological harm, and that non-thermal mechanisms are now established. It cites animal studies (including NTP and Ramazzini), a 2025 WHO-commissioned systematic review (as described by the author), and proposed mechanisms involving voltage-gated ion channels, oxidative stress, and radical-pair/spin chemistry. The piece calls for updated safety standards that consider modulation and tissue vulnerability, while stating it is “not a call for panic.”

RF Safe argues that animal evidence for RF-related carcinogenicity is now strong and should not be dismissed, citing the NTP (2018) and Ramazzini (2018) lifetime rodent studies as showing statistically significant increases in the same rare tumor types (heart schwannomas and brain gliomas). The post further claims that effects occurred at relatively low whole-body SAR levels and references additional mechanistic hypotheses (e.g., VGCC-related models and radical-pair/spin effects) and a reported human ultrasound observation of acute non-thermal changes. These points are presented as supporting a shift away from a “thermal-only” interpretation, but the item is advocacy/commentary and does not provide full methodological details in the excerpt.

This RF Safe article argues that the “strongest” RF-EMF literature supports concern about cancer-related findings, emphasizing non-monotonic dose–response patterns in the U.S. National Toxicology Program (NTP) rat study and citing additional analyses and animal studies. It reports that FDA evaluations have downplayed the human relevance of NTP results due to high exposures and inconsistencies, and counters that some effects may occur at lower exposure levels than commonly claimed. The piece also references the Ramazzini Institute rat study as supportive evidence at lower whole-body SARs and mentions a 2024 PLOS ONE paper analyzing Ramazzini tumors, but provides limited detail in the excerpt.

RF Safe argues that findings it describes as “high-certainty” from WHO-commissioned systematic reviews show RF-EMF causes malignant heart Schwannomas and brain gliomas in rodents and reduces male fertility. The post proposes a unifying non-thermal mechanism—the “S4-mitochondria axis”—suggesting RF-EMF interacts with the voltage-sensing S4 helix of voltage-gated ion channels (VGICs) and is amplified by mitochondrial density. It concludes that the combination of animal evidence and a proposed mechanism supports precautionary revisions to exposure guidelines and more mechanistic research.

This RF Safe article argues that U.S. radiofrequency (RF) exposure policy is outdated, emphasizing that FCC limits adopted in 1996 are based on preventing tissue heating and do not address alleged non-thermal biological effects. It claims responsibility for protecting public health from electronic product radiation was effectively ceded from health agencies to the FCC, and that Section 704 of the Telecommunications Act limits local governments from opposing wireless infrastructure on health grounds if FCC limits are met. The piece cites epidemiology, cell studies, and animal studies (notably the U.S. National Toxicology Program and the Ramazzini Institute) to argue that evidence has accumulated and regulation should be updated, but it presents these points in an advocacy framing rather than as a balanced review.

RF Safe argues that an FDA-authorized therapeutic radiofrequency device (TheraBionic P1) demonstrates biologically meaningful “non-thermal” RF effects, and contrasts this with consumer wireless regulation that it says is based primarily on heating (SAR) limits set in 1996. The post frames this as a regulatory and legal gap, citing the Radiation Control for Health and Safety Act and Telecommunications Act Section 704 as factors limiting local and public-health oversight. It also references several epidemiology and animal studies (e.g., Interphone, Hardell, CERENAT, IARC 2011 classification, and the U.S. NTP rodent studies) to support the claim that non-thermal effects and health risks warrant stronger scrutiny, though the article’s presentation is advocacy-oriented.

RF Safe argues that non-native RF-EMF affects biology primarily through voltage-gated ion channels (VGICs), proposing an “Ion Forced Oscillation” model in which pulsed RF signal components influence the S4 voltage sensor and downstream cellular signaling. The post frames electromagnetic hypersensitivity (EHS) as a continuum of individual sensitivity thresholds to a proposed VGIC → mitochondrial ROS → immune activation cascade, rather than a distinct condition. It cites multiple external studies and reviews (including a WHO-commissioned animal review) to support a mechanistic narrative linking RF exposure to oxidative stress, inflammation, and certain tumor findings in rodents, but the article itself is a mechanistic/interpretive argument rather than original research.

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 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 systematic review evaluated RF EMF exposure and cancer outcomes in experimental animals, including chronic cancer bioassays and tumor-promotion designs. Across 52 included studies, the authors report high certainty of evidence for increased malignant heart schwannomas and gliomas in male rats, and moderate certainty for increased risks of several other tumor types. Many other organ systems showed no or minimal evidence of carcinogenic effects, and the authors note challenges in translating animal findings to human risk assessment due to exposure and mechanistic uncertainties.

This paper presents a meta-analysis of 11 peer-reviewed epidemiologic studies examining long-term (>=10 years) cell phone use with laterality analyses. It reports that long-term use is associated with an approximately doubled risk of an ipsilateral brain tumor. The abstract states statistical significance for glioma and acoustic neuroma, but not for meningioma.