Abstract
There is general agreement that ionizing radiation is the best understood of the common environmental causes of cancer. Although the mechanisms by which radiation damage to tissue leads to cancer are not known precisely, a considerable body of radiobiological theory has evolved, providing valuable guidelines for the analysis of observational data. The existence in man of a cancer risk from ionizing radiation is well established. It appears to affect all or nearly all tissues in which cancer commonly occurs. It is the nature of this risk that now excites our interest, including 1) the relative sensitivities of various tissues to the carcinogenic effects of ionizing radiation, 2) the influence of sex, age at exposure, hormonal status and other host factors at the time of exposure, and the influence of cancer risk factors other than radiation, on the carcinogenic response to radiation, 3) the distribution over time following exposure of the excess cancer risk from radiation, and 4) the influence of various dimensions of exposure, including dose, radiation quality (linear energy transfer, or LET), and fractionation and protraction of dose. These factors are not unrelated, particularly the dimensions of exposure, but it is the cancer risk from low-dose, low-LET radiation that is of most concern for public policy, and about which there is the most controversy.
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© 1981 Plenum Press, New York
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Land, C.E. (1981). Biological Models in Epidemiology: Radiation Carcinogenesis. In: Berg, G.G., Maillie, H.D. (eds) Measurement of Risks. Environmental Science Research, vol 21. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-4052-2_5
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DOI: https://doi.org/10.1007/978-1-4684-4052-2_5
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