An RF Safe article presents a personal narrative and hypothesis that “non-native EMFs” act as “entropic waste” that could disrupt early embryonic neurodevelopment (neurulation), potentially contributing to neural-tube defects and later neurodevelopmental outcomes such as autism/ADHD. The author links a family tragedy to this hypothesis and argues for reducing wireless exposure as a precaution. The post cites several studies/reports (e.g., Farrell 1997, Aldad 2012, NTP 2018, WHO SR4A 2025) but does not provide detailed methods or evidence appraisal within the excerpt.

This RF Safe article argues that a critical embryonic window during neural tube formation (around days 21–28 post-conception) may link neural tube defects and a “major subset” of autism/ADHD-like traits, and it suggests electromagnetic fields could be a contributing factor. The author connects a personal story about a child’s death from a neural tube defect with claims about chick-embryo research reporting increased neural-tube malformations under weak electromagnetic fields. The piece also references developmental biology literature to support the broader idea that early embryogenesis/neurulation can influence later neurodevelopment, while presenting a speculative bioelectric/ion-channel mechanism.

RF Safe argues that a single biological mechanism explains widespread harm to children from modern wireless signals (cell phones, Wi‑Fi, 5G, DECT), emphasizing that these signals are “pulsed and modulated.” The post claims that “animal proof” is now high-certainty and references “WHO 2025 GRADE-rated systematic reviews,” linking EMF exposure to rare cancers in young people, declining sperm counts, and childhood autoimmune/neurodevelopmental disorders. The excerpt provided does not include citations or details sufficient to verify these claims.

This review argues that EMF exposure is associated in the literature with several adverse central nervous system outcomes, including blood-brain barrier disruption, oxidative stress, neurotransmitter changes, cognitive effects, and neurodevelopmental impacts. It reports that evidence on EMFs and brain tumors is conflicting, while noting WHO’s classification of radiofrequency EMFs as possibly carcinogenic to humans. The authors highlight prenatal and childhood periods as potentially more vulnerable and call for more standardized long-term and mechanistic research to guide public health policy.

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 and in vitro study examined non-thermal 900 MHz RF-EMF exposure during prenatal and postnatal development at 0.08 and 0.4 W/kg SAR. The authors report changes consistent with altered neurodevelopment, including reduced BDNF, reduced in vivo cell proliferation, and disrupted synaptic balance in rat pup brain regions. In vitro, exposed neural stem cells showed increased apoptosis and DNA double-strand breaks and shifts in cell populations toward glial lineages. The authors conclude that regulatory-level 900 MHz exposure can disrupt key neurodevelopmental processes in rodents.

This prospective cohort study followed 105 neonates/infants for one year and measured household RF-EMF using a selective radiation meter, categorizing exposure into tertiles. Higher household RF-EMF exposure was associated with lower ASQ-3 neurodevelopmental scores, particularly in motor and problem-solving domains, and higher odds of monitor/refer classifications for fine motor and problem-solving. The abstract notes these associations persisted after adjustment for low birth weight, though exposure was measured at a single time point and key confounders (e.g., prenatal phone use, parental interaction) were not assessed.