The following comments were submitted for Nuclear Information & Resource Service on March 18, 2005. These comments consider an International Commission on Radiological Protection (ICRP) draft document which discusses the connections between low-doses of radiation and cancer induction. The document title is “Low-Dose Extrapolation of Radiation-Related Cancer Risk” and can be found at http://www.icrp.org/docs/Low-dose_TG_rept_for_web.pdf For further info, contact NIRS: www.nirs.org; 301-270-6477 or email@example.com
Thank you for the opportunity to comment on this report. It is to be commended for recognizing the damage radiation is capable of–what many in the public interest community have contended for years. ICRP’s recognition of the extent and depth of radiation damage, the shortcomings of current methods of damage assessment and the realization that new scientific studies are finding results that overturn currently used protection assumptions are a welcome change from industry and government denials.
However, certain conclusions in this report do not address the dangers it reveals. To acknowledge that these damaging phenomena exist and not account for them in radiation risk is negligent at best. If “risk” assessment of radiation damage is not able to account for these newly recognized, paradigm-shifting effects, such as the bystander effect and genomic instability, we need a method of protection that will. We challenge the ICRP to take this next step.
ICRP contends that epidemiological studies are not statistically powerful enough to tell us about the lowest doses of radiation. I would contend that, while this may be true to a degree, there are other factors that prevent assessment at this level such as inadequate or completely wrong dose reconstruction, error in assumptions regarding the radionuclides in question and other assumptions made before the studies even begin that could cloud the result.
To ICRP’s credit, they recognize that cancers in this dose range may be numerous even while they contend epidemiology studies aren’t sensitive enough to see them. ICRP contends that lack of evidence doesn’t mean the phenomena doesn’t exist.
The ICRP says that epidemiological data does not point to a threshold, although these studies are most likely not statistically powerful enough to settle this question, either. They also recognize that synergistic affects may be present.
Perhaps most importantly, ICRP finally recognizes that a DDREF is not appropriate in many cases where for many years, radiation protection bodies and regulators assumed it to be representative. Since the Hiroshima/Nagasaki disease studies are the basis for many of the above assumptions, the ICRP is challenging their status as the paradigm for low dose assessment, which is a welcome change. The public interest community agrees with many of these points and believes that this recognition of the scientific evidence is long over due.
Where the epidemiological studies fall short, cell studies can offer insight; namely a look into what damage comes from the lowest doses of radiation. With cells, there is no dose lower than a single track of radiation. So the question becomes, how low is low? While a track delivered to a cell can impart quite a large dose, that dose to the whole body would be considered negligible. Is it?
ICRP says evidence shows that radiation damage is fundamentally different from endogenous system “damage”. The clustered and/or closely spaced nature of radiation damage makes it more difficult to repair, leaving non-repairs or misrepairs. This type of damage occurs at even low doses of radiation. Repair mechanisms are not always accurate and there is strong evidence that there is no lower dose of radiation at which accuracy of repair is 100%. Additionally, the ends of the DSBs from radiation exposure are damaged in such a way as to not lend themselves to proper connection or repair; whereas naturally occurring double strand breaks leave a “clean” end—one that can undergo an expected reaction or repair.
Radiation also damages the base of DNA in clusters that could not only be difficult to repair but could inhibit further repair and cause further DSBs. In general, one type of damage may influence the repair of another type of damage. DSB may occur below the ionization threshold energies. Additionally, studies show radiation exposure can cause further radiosensitivity in certain instances. Cells with severe defects are often eliminated by the cell cycle, but cells with minor damage may slip through the elimination process and continue on to form tumors.
ICRP recognizes the existence of genomic instability and bystander effect and recognizes that they come from both high and low LET radiations. These effects negate the previous assumption that only radiation crossing the nucleus of a cell is able to impart damage. ICRP says the linear dose response is based on this assumption. If that is true, then this standard is no longer protective enough. These phenomena may be of significance to the transgenerational effects of radiation because available evidence suggests that instability induced in parental germ cells shows up in their offspring. There is further evidence that this instability could lead to “increased susceptibility to the induction of tumors in the offspring”. To reiterate, this instability is transmissible between generations.
ICRP mentions adaptive response, concluding that since the mechanism by which it occurs is still unknown, judging its effect on radiation risk is difficult. But the relevance of adaptive response to a real-world exposure scenario is highly suspect. The “priming” dose necessary for subsequent “benefit” assumes foreknowledge of an accident, or dirty bomb; who will be where and what kind of exposure they will have. This is a ridiculous situation by any measure, not at all representative of real life; nor does it speak to low doses over long time periods, as we will see with permanent radioactive contamination. Adaptive response also seems to happen within a specific period of time after the priming dose. Again, this does not match real life. Adaptive response is not seen across all cell types, a fact recognized by ICRP. So while it is an interesting scientific pursuit, studying adaptive response is probably not relevant to most exposures, including routine releases.
As with epidemiological evidence, the current cellular biological evidence points to no threshold of dose.
ICRP also present a laundry list: a recognition of all the uncertainties in risk analysis including uncertainties regarding DDREF, natural variation due to sex or genetic differences, dose reconstruction errors and misdiagnosis.
The ICRP’s evidence and conclusions must be repeated back to them, so that they may better understand the layperson’s reaction to this evidence. The layperson will look at the confirmed link between radiation and cancer, the strong indication that radiation can not only lead to more radiosensitivity, but also some very frightening effects across generations (the transgenerational effects of parental germ cells mentioned) and they will ask for protection of the most sensitive members of the population. They will look at the lack of evidence of a threshold dose and evidence of repair inaccuracy at even the slightest doses to the cell and conclude, not in error, that there is NO safe radiation dose. In fact, NIRS and many members of the lay public and scientific communities have long seen in the data what ICRP is just now recognizing. And as the population grows more radiosensitive due to various exposures allowed by the ICRP, there will be fewer and fewer able to live disease free. In the end, this price is too high to pay. If ICRP is unwilling to protect the most sensitive now, how will we protect them when their numbers grow? ICRP says it isn’t enough to recognize that an effect exists, we must know the mechanism for its action. But how much damage will be done between what we know and what science discovers? If the wave of a tsunami is bearing down on a town, the person who stops to ask where it came from will get swept into the sea. Knowing that gene instability, a precursor to cancer and other diseases, comes from radiation exposure should be enough to spring into action to protect the public. While asking the question “how” is necessary and an interesting scientific inquiry, we disagree that this is needed for protection. This is, perhaps, the difference between scientific sensibilities and common sense.
The ICRP makes some disturbing assumptions about “risk” and what the public is willing to accept. But we are not just talking about the risk of dying today. With radiation we are talking about the mortality and morbidity of our children; the increased radiosensitivity of them, their decreased ability to fend off disease. We are talking about a weakening of the gene pool. Therefore, radiation exposure is wholly unique, not like driving a car or weighing the risks of a plane crash, but actually damaging our future survival in a way that very well may not be reversible. These risks cannot be compared. When we step into a vehicle and accept that risk, we have NOT tacitly agreed by default to radiation exposure. ICRP should not make any statement that presumes this. ICRP states “It is highly likely that there will always be uncertainty about low-dose risk, and that we will have to come to terms with that uncertainty.” I would disagree that the way to do this is through risk because this method apparently does NOT allow for what we know.
With the current recognition of scientific evidence, all the potential shortcomings and some truly frightening transgenerational phenomena in cell studies, ICRP should reevaluate its 2005 recommendations and err in favor of caution. Even with as many warning signs as science presents, many trumpeted by the public for decades, ICRP says they still cannot determine the result of some of these phenomena on radiation risk. Let me submit that if the risk estimates will not accommodate effects such as bystander and genomic instability, that we abandon the concept of risk estimates in favor of the precautionary principle or some other mechanism that protects those among us who may already be radiosensitive, unborn, genetically damaged, etc.