Proposes an early-life RF exposure and neurodevelopment research protocol, including objective dosimetry …

Subject: Response to RFI HHS-OASH-2026-0397. Early-life electromagnetic field exposure and neurodevelopment: a pathophysiological hypothesis and a prospective cohort protocol. Perspective Physicians and researchers (healthcare professionals; research entity). Source: peer-reviewed research; the published protocol is attached. Observations from research This submission does not report human exposure-effect data; it presents a pathophysiological hypothesis and a protocol to test it [1]. We hypothesize that chronic exposure to anthropogenic electromagnetic radiation during the first 24 months of life, particularly during sleep, may act as a modulating cofactor in the pathogenesis of autism spectrum disorder (ASD). The hypothesized mechanisms are altered Ca2+/calmodulin signaling, mitochondrial oxidative stress, microglial activation and desynchronization of the mirror neuron system, consistent with the theoretical framework of Resonant Convergence [2]. Within this framework, Ion Cyclotron Resonance and thermomagnetic resonance are candidate transduction hypotheses, not yet validated. We explicitly acknowledge the constraints imposed by thermal noise [3]. The epidemiological objective is independent of the validation of these mechanisms: 1. Primary endpoint: continuous composite score (ESCS, CDI/MSEL, EEG mu rhythm 8-13 Hz). 2. Secondary exploratory endpoint: ASD diagnosis at 24 months (ADOS-2, ADI-R, DSM-5). Analyses use mixed-effects models and Firth regression, adjusted for socioeconomic status, screen time and parental health anxiety. Recommendation: prospective birth cohorts with objective exposure measurement. Knowledge gaps and exposure classification Prospective data on nighttime exposure during the first two years of life are lacking. Beyond SAR and power density, classification should account for low-frequency modulation, the ELF magnetic component, cumulative duration, time of day (sleep) and age of the exposed individual. Exposure assessment We propose integrating environmental RF/ELF measurements, source-proximity analysis, device inventories and wearable dosimetry, with objective verification of adherence to nighttime shielding. Children A differentiated assessment is needed. The 6-18 month window is critical for the maturation of the mirror neuron system and grey matter. During this phase, plasticity depends on calcium-dependent mechanisms and on the temporal precision of neuronal activity. Evidence below current limits In human cortical organoids, chronic RF exposure (800-2400 MHz) altered radial glia differentiation and induced the expression of ASD-associated genes via BET pathways. The effect was reversed by BET inhibition [4]. These are in vitro data, not directly extrapolable to humans, but they support the biological plausibility of the hypothesis. A preliminary study also observed EEG modulation with ELF fields of 20-30 microT at 1-4 Hz [5]. Research priorities Prospective pilot studies with continuous neurodevelopmental endpoints, followed by adequately powered confirmatory trials. We suggest that NIH fund pediatric cohorts with standardized dosimetry and common protocols for measuring infant exposure. Additional information Theoretical framework: [2]. Effects of ELF fields on ASD symptoms: [6]. Conflicts of interest: A. Greco is affiliated with the R&D Department of S.I.S.T.E.M.I. srl [field of activity]. [Funding: specify or declare none.] References [1] Garoli A, Greco A. Alpha Psychiatry 2026;27(4):53282. https://doi.org/10.31083/AP53282 [2] Greco A. Int J Mol Sci 2026;27:423. https://doi.org/10.3390/ijms27010423 [3] Adair R. Phys Rev A 1991;43:1039. https://doi.org/10.1103/physreva.43.1039 [4] Cakir B et al. Cell Rep 2025;44:116238. https://doi.org/10.1016/j.celrep.2025.116238 [5] Greco A. Transl Neurosci Res Rev 2019;2:38-52. https://doi.org/10.36959/817/524 [6] Pietramala K et al. Brain Sci 2024;14:1293. https://doi.org/10.3390/brainsci14121293