Paragraphs 251 and 673 discuss the possibility of cataract as a stochastic effect, referring to the animal experiments in which radiation cataract was suppressed by inhibition of epithelial cell division. These experiments imply the cause of radiation cataract is not the cell death, but they do not evidence the effect on the clinical level is stochastic.
Lens opacity could be explained by damage to single epithelial cells, and the opacity will expand with cell division if the damaged cell continues to produce abnormal lens fibers. If a small number of damaged cells could develop into cataract, those cells have to acquire growth advantage or opaque fibers deteriorate normal fibers in some way. However, there is no supporting evidence for those mechanisms. While disrupted alignment of lens fibers possibly develop into cataract, those changes do not last long unless the dose is quite high (Holsclaw DS et al. Exp Eye Res 48, 385-398, 1989.). Eventually expansion of the opacity should be limited as long as majority of the epithelial cells remain undamaged.
Therefore, even if the micro-opacity is a stochastic event, it is thought to develop into clinically-significant cataract only after a certain level of exposure. This is similar to mental retardation due to in-utero exposure, in which the decrease in IQ is stochastic, but there is a threshold for the clinically-significant retardation.
In this context, epidemiological studies reviewed in this report include both clinical and subclinical effects, and the trend is not necessarily consistent. Careful re-evaluation of each study and in-depth analyses are desired to establish the dose response for the “clinically-significant” changes. At least compilation of the authors’ lines is not enough.