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Report No. 080 - Induction of Thyroid Cancer by Ionizing Radiation (1985) This is a members only link.

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The purpose of this Report is to evaluate the potential of exposure to x and gamma external radiation and/or to internally deposited radionuclides to induce thyroid cancer in humans. Any such effort is necessarily subject to the constraint of limited data, and this is particularly true for radionuclides deposited in the thyroid. What human data exist relate primarily to exposure to external x irradiation or, to a much lesser degree, to internally deposited I-131. In spite of such limitations, practical protection procedures require a quantitative assessment of the potential of radiation exposure to induce human thyroid cancer. That potential is most often expressed in terms of the risk of developing radiation induced thyroid cancer. To develop risk estimates, it is necessary to examine the reports and assumptions from existing human and non-human studies. However, the transfer of inferences from animal studies to humans is perilous. In addition, large gaps in the existing data, the low incidence of thyroid cancer, and the small size of populations available for study make risk derivations uncertain. At best, the potential of radiation exposures to cause human thyroid cancer can only be approximated. This Report makes use of such data as are available to develop average risk estimates for combined populations over various ranges of radiation dose to the thyroid. The estimates are not intended and should not be used for application to individuals. Their use in any circumstances requires understanding and careful consideration of their limitations and must include evaluation of a large number of often ill-defined factors such as type and amount of exposure, time since exposure, and differences of sex, age and heredity. Since most available data on the induction of cancer by radiation are obtained from populations that received relatively large exposures, extrapolation to lower dose levels is often necessary. However, large exposures often cause cell death which can influence the incidence of observed carcinogenesis. For this reason, the dose ranges used for the calculation of risk are confined to situations in which human thyroidal carcinogenesis has been demonstrated and for which cell killing is not thought to be a serious limiting factor.
Scientific Committee:
H. R. Maxon. Chairman

D.V. Becker
S.A. Book
C.R. Buncher
S.R. Thomas
E.L. Saenger, Advisor
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