Published December 1995 | Version v1
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Sigmoidal response model for radiation risk

Creators

  • 1. Kinki Univ., Higashi-Osaka, Osaka (Japan). Atomic Energy Research Inst.

Description

From epidemiologic studies, we find no measurable increase in the incidences of birth defects and cancer after low-level exposure to radiation. Based on modern understanding of the molecular basis of teratogenesis and cancer, I attempt to explain thresholds observed in atomic bomb survivors, radium painters, uranium workers and patients injected with Thorotrast. Teratogenic injury induced by doses below threshold will be completely eliminated as a result of altruistic death (apoptosis) of injured cells. Various lines of evidence obtained show that oncomutations produced in cancerous cells after exposure to radiation are of spontaneous origin and that ionizing radiation acts not as an oncomutation inducer but as a tumor promoter by induction of chronic wound-healing activity. The tissue damage induced by radiation has to be repaired by cell growth and this creates opportunity for clonal expansion of a spontaneously occurring preneoplastic cell. If the wound-healing error model is correct, there must be a threshold dose range of radiation giving no increase in cancer risk. (author)

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Part of:
Modeling of biological effects and risks of radiation exposure

Additional details

Publishing Information

Imprint Title
Modeling of biological effects and risks of radiation exposure
Imprint Pagination
254 p.
Journal Page Range
p. 54-69
Report number
NIRS-M--106

Conference

Title
26. National Institute of Radiological Sciences symposium
Dates
8-9 Dec 1994
Place
Chiba (Japan)

Optional Information