Richard C. Miller

The potential radiation hazards associated with routine screening mammography, in terms of breast cancer induction, are discussed in the context of the potential benefits. The very low energy X-rays used in screening mammography (26-30 kVp) are expected to be more hazardous, per unit dose, than high-energy X- or γ-rays, such as those to which A-bomb survivors (from which radiation risk estimates are derived) were exposed. Based on in vitro studies using oncogenic transformation and chromosome aberration end-points, as well as theoretical estimates, it seems likely that low doses of low-energy X-rays produce an increased risk per unit dose (compared with high energy photons) of about a factor of 2. Because of the low doses involved in screening mammography, the benefit-risk ratio for older women would still be expected to be large, though for younger women the increase in the estimated radiation risk suggests a somewhat later age than currently recommended--by about 5-10 years--at which to commence routine breast screening.

Both cell lethality and neoplastic transformation were assessed for C3H10Tl/2 cells exposed to neutrons with energies from 0.040 to 13.7 MeV. Monoene

Synchronised populations of mouse C3H/10T-1/2 cells were obtained by a stringent mitotic dislodgment procedure. Mitotic cells rapidly attach and progress sequentially through the cell cycle. Irradiation (3 Gy of X rays) was carried out at intervals from 0 to 18 h after initiating cell cycle progression of the mitotic cells. Oncogenic transformation was enhanced 10-fold over cells irradiated soon after replating (G1 and S phases) for cells in a near 2 h period corresponding to cells in G2 phase but not in mitosis. The cell surviving fraction had a 2-1/2-fold variation with resistant peaks corresponding to the late G1 and late S phases. These findings provide experimental support for the hypothesis initiated by Rossi and Kellerer and developed by Brenner and Hall to explain the LET dependent inverse dose rate effect for oncogenic transformation.

Considerable evidence has recently accumulated, both in vivo and in vitro, to suggest that neutrons at low dose rates, or in multiple fractions, have an enhanced effectiveness for inducing neoplastic transformation. A consistent pattern has emerged as to the dependence of the effect on dose, dose rate, and radiation type. A consistent model of the phenomenon as a function of dose, dose rate, and radiation type is presented. The approach, first suggested by Rossi, is that cells are extra sensitive in part of their cycle. Then an acute exposure of cycling cells to high-LET radiation results in some fraction of the sensitive cells receiving large depositions of energy--greater than required for the effect. If the exposure is protracted, a larger proportion of sensitive cells will be exposed, but to smaller numbers of energy depositions--still enough, however, to produce the effect. The model produces results consistent with all available data on enhancement of neoplastic transformation in the C3H 10T1/2 system by protraction or fractionation at medium or high LET. Implications for radiation protection and the radon problem are discussed.