Cancer risk from low-level radiation

BL Cohen - American Journal of Roentgenology, 2002 - Am Roentgen Ray Soc
BL Cohen
American Journal of Roentgenology, 2002Am Roentgen Ray Soc
Cohen and thermal processes occur roughly a million times per day in each of the trillions of
cells in our bodies, but only about one per cell per day remains unrepaired and survives as
long-term mutations; it is these mutations that are normally responsible for human cancers.
The DNA damage from radiation is, on average, more severe than damage from chemicals
or thermal processes. However, a dose of 0.1 Sv (10 rem), which is near the upper limit of
lowlevel radiation, is estimated to cause only 0.004 long-term mutations per cell [2, 3], a …
Cohen and thermal processes occur roughly a million times per day in each of the trillions of cells in our bodies, but only about one per cell per day remains unrepaired and survives as long-term mutations; it is these mutations that are normally responsible for human cancers. The DNA damage from radiation is, on average, more severe than damage from chemicals or thermal processes. However, a dose of 0.1 Sv (10 rem), which is near the upper limit of lowlevel radiation, is estimated to cause only 0.004 long-term mutations per cell [2, 3], a trivial addition to the one mutation per cell per day resulting from natural processes. Taking all this into account, it is evident that cancer-initiating events are not the controlling factor in determining the dose–response relationship for radiation in the low-level radiation region, as was assumed in the linear no-threshold theory. The principal effect of radiation is in modifying the biologic defense mechanisms, rather than in providing initiating events.
Am Roentgen Ray Soc