NCRP 52nd Annual Meeting, Meeting The Needs of the Nation for Radiation Protection
Abstract
Questions for David J. Brenner, Nolan Hertel, Jerry W. Hiatt, Kathryn A. Higley, and Michael Weber Q: How does epigenetics play a role in estimating radiation-induced risk? D. Brenner: I can give you a simple answer, and that is that we don't know. We don't know how much genetics plays a role in radiation-induced cancer risks, and we know even less about how epigenetics affects radiation-induced cancer risks. It wouldn't surprise me if epigenetics played a significant role. Q: Bystander effects can be both protective and detrimental. How does this influence support for the LNT (linear no-threshold) model? D. Brenner: The questioner is quite right: bystander effects can be killing effects, which at low doses would be protective, as well as mutagenic which might increase cancer risks. Which of those wins is something that we don’t know in the context of radiation-induced cancer. The other part of the answer is that we don't know if bystander effects are in any way significant in the radiation-induced cancer context. So we neither know whether bystander effects are going to reduce cancer risks or increase cancer risks, or even whether they are relevant to radiation-induced cancer risks. We've worked on bystander effects for quite a long time, and it's a bit disappointing to say that's as much as we know - or don't know. Q: Can you comment about the effect of dose rate on radiation risk? D. Brenner: Dose rate was on my list of topics right at the beginning of my talk that I said…
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