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Analyses of the Life Span Study (LSS) of Japanese atomic bombing survivors have routinely incorporated corrections for additive classical measurement errors using regression calibration. Recently, several studies reported that the efficiency of the simulation-extrapolation method (SIMEX) is slightly more accurate than the simple regression calibration method (RCAL). In the present paper, the SIMEX and RCAL methods have been used to address errors in atomic bomb survivor dosimetry on solid cancer and leukaemia mortality risk estimates. For instance, it is shown that using the SIMEX method, the ERR/Gy is increased by an amount of about 29 % for all solid cancer deaths using a linear model compared to the RCAL method, and the corrected EAR 10(-4) person-years at 1 Gy (the linear terms) is decreased by about 8 %, while the corrected quadratic term (EAR 10(-4) person-years/Gy(2)) is increased by about 65 % for leukaemia deaths based on a linear-quadratic model. The results with SIMEX method are slightly higher than published values. The observed differences were probably due to the fact that with the RCAL method the dosimetric data were partially corrected, while all doses were considered with the SIMEX method. Therefore, one should be careful when comparing the estimated risks and it may be useful to use several correction techniques in order to obtain a range of corrected estimates, rather than to rely on a single technique. This work will enable to improve the risk estimates derived from LSS data, and help to make more reliable the development of radiation protection standards.

Chronic myeloid leukemia (CML) invites biologically based radiation risk modeling because CML is simultaneously well-understood, homogeneous and prevalent. CML is known to be caused by a translocation involving the ABL and BCR genes, almost all CML patients have the BCR-ABL translocation, and CML is prevalent enough that its induction is unequivocally detected among Hiroshima A-bomb survivors. In a previous paper, a linear-quadratic-exponential (LQE) dose-response model was used to estimate the lifetime excess risk of CML in the limit of low doses of gamma-rays, R gamma. This estimate assumed that BCR-ABL translocation dose-response curves in stem cells for both neutrons and gamma-rays, differ only by a common proportionality constant from dicentric aberration dose-response curves in lymphocytes. In the present paper we challenge this assumption by predicting the BCR-ABL dose response. The predictions are based on the biophysical theory of dual radiation action (TDRA) as it applies to recent BCR-to-ABL distance data in G0 human lymphocytes; this data shows BCR and ABL geometric distributions that are not uniform and not independent, with close association of the two genes in some cells. The analysis speaks against the previous proportionality assumption. We compute 11 plausible LQE estimates of R gamma, 2 based on the proportionality assumption and 9 based on TDRA predictions. For each estimate of R gamma we also compute an associated estimate of the number of CML target cells, N; the biological basis of the LQE model allows us to form such estimates. Consistency between N and hematological considerations provides a plausibility check of the risk estimates. Within the group of estimates investigated, the most plausible lifetime excess risk estimates tend to lie near R gamma = 0.01 Gy-1, substantially higher than risk estimates based on the proportionality assumption.