Hereditary effects of ionizing radiation have traditionally been framed through a stringent mutation-to-disease model: parental germ cell exposure, irreversible chromosomal abnormalities or nuclear DNA mutations, transmission, and attributable hereditary disease. This framework remains essential, and human studies have not established radiation-attributable hereditary diseases after parental preconception exposure. Advances in genomic and other omics technologies, however, reveal a wider spectrum of molecular and cellular changes in offspring, whose clinical significance may be absent, indirect, or uncertain. These include quantitative changes in DNA abundance, such as mitochondrial DNA copy number, as well as signals detected by epigenomic, transcriptomic, and metabolic approaches. We adapt a four-layer evidentiary framework for environmental health communication that separates biological or genomic signals, intergenerational persistence, health-related phenotypes, and attributable hereditary diseases as evidence categories rather than an inevitable causal sequence. Communicators should identify the relevant layer, describe the evidence source and uncertainty, state what a finding does and does not support, and connect it to proportionate action.
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Fukunaga et al. (2026) studied this question.
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