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Submits a cited infant-exposure research protocol and asks HHS to consider independent, adequately powered studies of neurodevelopment. Explicitly distinguishes a proposed study from proof of causation, describes measurement methods and candidate mechanisms, and notes observational design, confounding and limited statistical power. The attached paper has not been reviewed.

  • Research & federal duties: “ychiatry. 2026;27(4):53282. DOI: 10.31083/AP53282. This publication presents a prospective research protocol investigating whether electromagnetic radiation (EMR) exposure during the first 24 months of life m”
  • Children & vulnerable groups: “tocol investigating whether electromagnetic radiation (EMR) exposure during the first 24 months of life may influence neuro-developmental trajectories and Autism Spectrum Disorder (ASD) risk. Importantl”
  • Neurological symptoms & sleep: “netic radiation (EMR) exposure during the first 24 months of life may influence neuro-developmental trajectories and Autism Spectrum Disorder (ASD) risk. Importantly, this paper does not establish t”
  • Proposed biological mechanisms: “ identifies biological mechanisms that warrant further investigation, including voltage-gated calcium channels, intracellular calcium signaling, Ca²⁺/calmodulin pathways, mitochondrial metabolism, oxidative str”

Matched review of original text; attachments excluded. Review provenance

ORIGINAL COMMENT · UNEDITED TEXT
Scientific Article Submitted for HHS Review We respectfully submit the following peer-reviewed publication for consideration by the U.S. Department of Health and Human Services: Garoli A, Greco A. “Shielding the First 24 Postnatal Months of Life: A Proposal for a Prospective Cohort Study of Early-Life Electromagnetic Exposure and Autism Risk.” Alpha Psychiatry. 2026;27(4):53282. DOI: 10.31083/AP53282. This publication presents a prospective research protocol investigating whether electromagnetic radiation (EMR) exposure during the first 24 months of life may influence neuro-developmental trajectories and Autism Spectrum Disorder (ASD) risk. Importantly, this paper does not establish that EMR causes autism. It proposes a methodology for investigating the question prospectively. The authors propose following 1,000 full-term newborns for 24 months, comparing an EMR-reduced cohort (n=500) with a standard-exposure cohort (n=500). Exposure would be characterized through RF/ELF measurements, proximity analysis, device inventories and wearable dosimetry. Neurodevelopment would be evaluated using joint attention, language development and EEG mu-rhythm measures, with ASD diagnosis as a secondary exploratory endpoint. The article also identifies biological mechanisms that warrant further investigation, including voltage-gated calcium channels, intracellular calcium signaling, Ca²⁺/calmodulin pathways, mitochondrial metabolism, oxidative stress and neuronal synchronization. Ion Cyclotron Resonance (ICR) is presented as a candidate framework for understanding some of these interactions. The authors appropriately acknowledge that weak-field transduction and ICR mechanisms remain scientifically contested rather than established. The protocol is particularly relevant because it attempts to address a persistent challenge in EMR research: accurate exposure measurement. The proposed study incorporates environmental measurements, wearable dosimetry, shield-integrity monitoring, compliance records and repeated neuro-developmental assessments The authors also acknowledge significant limitations. Cohort allocation is observational rather than randomized, residual confounding may remain, and the proposed 1,000-participant study is underpowered to establish modest differences in ASD incidence. The study is therefore explicitly designed for exploratory signal detection and to generate data necessary for a larger confirmatory trial. We respectfully request that HHS review this publication and consider whether this hypothesis warrants independent, adequately powered, multi-center investigation. Future federal research could examine whether objectively measured RF/ELF exposure during infancy is associated with neuro-developmental differences; whether specific developmental windows are more sensitive; whether effects vary according to exposure characteristics; and whether genetic susceptibility, calcium signalling, mitochondrial function, oxidative stress or other biological pathways modify potential effects. Given the widespread exposure of children to electromagnetic fields, we believe these questions merit rigorous, independent scientific investigation. The objective should not be to presume that EMR either causes or does not cause neuro-developmental effects, but to establish the answer through appropriately designed prospective research.

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