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 narrative review proposes that low-intensity microwave/lower-frequency EMFs activate plasma membrane calcium channels in animals, increasing intracellular calcium and triggering downstream signaling including oxidative stress pathways. It further suggests that EMF actions in terrestrial multicellular plants are probably similar, with plant two-pore channels proposed as plausible mediators due to a comparable voltage sensor. The abstract describes briefly reviewed plant studies as consistent with this mechanism, but does not provide detailed exposure parameters or quantitative results.

This review discusses the comet assay and summarizes research on non-ionizing EMF exposure and DNA/chromosomal damage. It describes both positive and negative findings across studies, noting no consistent overall pattern for radiofrequency radiation (RFR). The authors nonetheless conclude that under certain exposure conditions RFR appears genotoxic and may affect DNA damage and repair, with evidence discussed as most applicable to exposures typical of cell phone use.