{"id":"HHS-OASH-2026-0397-6338","number":"6338","name":"Alex Andreasen","organization":"","posted":"2026-10-28T04:00Z","received":"2026-10-21T04:00Z","body":"https://www.cell.com/cell-reports/fulltext/S2211-1247%2825%2901009-5\n\nThis study mentions autism like behaviour in animals exposed to EMF.\n\nAnd that ASD associated gene expression in cortical neurons and dendritic spine density seems to increase with RF exposure. Suggesting a link between autism development and RF exposure.\n\n\"...No major neurodevelopmental defect has been linked with RF exposure, mainly due to its relatively weak energy compared with X-rays or gamma rays.40 However, emerging evidence suggests that prolonged RF exposure may have subtle neurodevelopmental implications. Recent studies in animal models exposed chronically to RF have shown autism-like behaviors, raising concerns about the impact of RF on neurodevelopment.41 For instance, behavioral changes such as hyperactivity and cognitive deficits observed in animal models highlight the need for further exploration into the neurodevelopmental consequences of RF exposure in humans. Although decades’ worth of studies have reported a broad range of adverse impacts from RF on human health, RF-mediated dysregulation of human brain development has remained largely unknown. In this study, we showed the detrimental effects of RF exposure to cortical organoids.42\nThe perinatal period in neurogenesis encloses a distinctive window embodying diverse molecular and cellular processes required for proper development.5 Though prenatal brain development comprises high plasticity, it is vulnerable to internal and external perturbations. Thus, environmental insults, including chemicals, drugs, pollution, stress, and even prolonged ultrasound wave exposure, can permanently impact brain development and subsequent behavior.43,44 Our findings revealed that RF-exposed cortical neurons exhibited increases in ASD-associated gene expression and dendritic spine density, characteristics of patients on the autism spectrum.45 Furthermore, the parallels drawn from in utero RF exposure in animal models, which have demonstrated behavioral changes such as hyperactivity and memory deficits, underscore the relevance of our findings in a human context.41,46 These findings suggest a potential shared mechanism by which RF exposure may contribute to neurodevelopmental disorders across species. Altered morphology and transcriptome driven by RF exposure in hCOs further lead to aberrant and enhanced neuron firing. In fact, in utero RF exposure in mice models results in behavioral and cognitive changes such as hyperactivity and memory deficit.41 Notably, we showed that physical barrier protection or chemical treatment could attenuate the RF-induced damage during cortical organoid development.\nHere, we have thoroughly examined the effects of RF exposure and demonstrated RF-induced changes associated with ASD in the transcriptomics, morphology, and function of cortical neurons. This addition to the literature is particularly significant given that most studies have historically focused on genetic causes of ASD, while environmental factors, particularly RF exposure, have been understudied. By utilizing induced pluripotent stem cell (iPSC)-derived hCOs, our research offers insights that bridge the gap between animal models and human neurodevelopment. The use of human organoids enables us to detail the specific impacts of RF exposure on human neuronal cells, which may differ from findings observed in animal models.\nOur findings also point to the potential involvement of BET proteins in the regulation of neurodevelopmental pathways affected by RF treatment. We propose that BET proteins may be altered in RF-treated hCOs, similar to how they are affected in Rett syndrome model organoids with MeCP2 mutations.29 It remains to be determined whether BET proteins are significantly downregulated in RF-treated organoids. If so, the inhibition of BET proteins could serve as a therapeutic strategy to rescue delayed differentiation in these organoids. This interaction raises the question of whether RF exposure and BET regulation function in an epistatic relationship or operate independently\"","attachments":[],"attachment_inventory":true,"withheld":false,"source":"https://www.regulations.gov/comment/HHS-OASH-2026-0397-6338","tags":["child-development","sleep-cognition","policy-standards","research-evidence"],"source_hash":"ebe7753d313813b5804c17627bcdea5714b83a59e7d2e7c457b4d82a046b8145","slug":"child-development-comment-6338","classification":{"id":"HHS-OASH-2026-0397-6338","body_sha256":"e010cbd34e26a530c7baf7ff268e9d93e0656182dd5922fde12126a852ddd956","status":"ai_reviewed","primary_topic":"research","topics":[{"id":"research","evidence":"ed the detrimental effects of RF exposure to cortical organoids.42\nThe perinatal period in neurogenesis encloses a distinctive w"},{"id":"neurological","evidence":" models exposed chronically to RF have shown autism-like behaviors, raising concerns about the impact of RF on neurodevelopment.41 "},{"id":"mechanisms","evidence":"s also point to the potential involvement of BET proteins in the regulation of neurodevelopmental pathways affected by RF "},{"id":"reproductive","evidence":"ses required for proper development.5 Though prenatal brain development comprises high plasticity, it is vulnerable to internal and exte"}],"summary":"The commenter quotes research on RF exposure in cortical organoids and animal models, describing reported developmental and behavioral effects and proposed involvement of BET proteins.","reviewed_at":"2026-10-28T23:54:32Z","review_method":"Full comment-text review with exact source evidence; attachments not reviewed","review_source_sha256":"851e0cf0441527b9fac6388e9f916c439d2eb706d68d533d85b10e9d40c2c6c0","source_url":"https://rfsafe.net/hhs-comments/data/catalog.json","scope":"Original comment body; attachments excluded"},"forum_topics":["research","neurological","mechanisms","reproductive"],"primary_topic":"research","forum_title":"The commenter quotes research on RF exposure in cortical organoids and animal models, describing reported…"}