|Year : 2016 | Volume
| Issue : 3 | Page : 117-121
What can we tell people about the health effects of radiation exposure?
Anthony D Wrixon
Castellezgasse 25/2/6, 1020 Vienna, Austria
|Date of Web Publication||30-Nov-2016|
Anthony D Wrixon
Castellezgasse 25/2/6, 1020 Vienna
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Wrixon AD. What can we tell people about the health effects of radiation exposure?. Radiat Prot Environ 2016;39:117-21
| Introduction|| |
What can we tell people about the health effects of radiation exposure? This has long been a troubling question. However, it is a question that those involved in radiation protection need to be able to answer in a way that it is both understandable by nonprofessionals but scientifically correct. It inevitably arises following a major nuclear accident, but may arise in connection with any particular exposure situation whether occupational, public, or medical. When the concern is with exposure of a population, collective effective dose is generally used as a surrogate for the risk that that population runs. And thus, the trite answer to the question that is then sometimes given is that the number of health effects (i.e., primarily cancers) in the exposed population is derived by multiplying the collective effective dose by the risk factor given, for example, in Publication 103 of the International Commission on Radiological Protection (ICRP) (Since 1928, ICRP has developed, maintained, and elaborated the International System of Radiological Protection used worldwide as the common basis for radiological protection standards, legislation, guidelines, programmes: and practice.) (i.e., of the order of 5%/Sv). Similarly, the risk that an individual is understood to run would be given by his or her effective dose also multiplied by this risk factor. But this would imply, among other things, that these numbers are independent of the magnitude of individual dose or doses involved. But is this really the case? Does, for example, an effective dose of 10 µSv to each individual in a population of 100 million lead to the same number of health effects as an effective dose of 100 mSv to each individual in a population of a 10,000? Both result in a collective effective dose of 1000 mSv. Where is the evidence for this?
Most people involved in radiation protection are aware of some of the assumptions made in the derivation of the ICRP risk factors–extrapolation of epidemiological information obtained at moderate or high doses, the transfer of data across populations with very different diets and cancer incidence, the averaging over sex and age, and the projection over a lifetime. Even then, the temptation to use collective effective dose without further qualification to determine the number of health effects arose following the Chernobyl accident in 1986 and, more recently, the Fukushima-Daiichi accident in 2011, both of which resulted in very low doses to very large populations remote from the accident sites. That those outside the field of protection may do this is understandable, but, that there should be those within the field who do it, is not; they forget that effective dose and its collective counterpart are quantities derived for protection purposes and protection purposes only. They ignore the ICRP warning  that it is inappropriate to use collective effective dose in assessing actual risk, and that “in particular, the calculation of the number of cancer deaths based on collective effective doses from trivial individual doses should be avoided.” Correspondingly, the actual risk to individuals in that population or the probability that a particular cancer was caused by the exposure should not be obtained from a simple consideration of the effective dose to an individual.
The naivety that leads to this lies in a failure to recognize the boundary between true scientific knowledge and scientifically based, but still unproven, inferences. The latter are necessary for taking decisions relating to the protection of workers, members of the public and patients. Their use to imply factual consequences, for example, in communicating the consequences of nuclear accidents is misleading and can cause unnecessary concern.
For the radiation protectionist, a large part of the problem is due to his or her familiarity with the recommendations of ICRP and regulatory requirements derived from them and a lack of familiarity with the underlying science, as reflected particularly in publications of the United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR was established in 1955 by the UN General Assembly in response to widespread concerns about the effects of radiation on human health and the environment. Over the decades, it has evolved to become the world authority on global levels and effects of ionizing radiation. It neither addresses the benefits or economics of radiation technology nor does it set protection policy, these being within the mandate of other international bodies.), or even the annexes of the ICRP recommendations (e.g., Annex A of ICRP Publication 103). In essence, the line between science and its application has become blurred. Radiation protection is not “pure science”; it is based on science but also relies on assumptions that are necessary for the application of scientific knowledge to real-life issues.
This article is intended to assist those who may need to respond to questions about the health impact of a particular exposure scenario. It draws heavily on the annex of a report of UNSCEAR, prepared at the request of the UN General Assembly, which addresses the philosophical differences between the information obtained by proper application of scientific method and the inferences that are made based on that information.
| Scientific Knowledge|| |
Knowledge of the health effects of radiation exposure has steadily increased ever since the discovery of X-rays and radium-226 at the end of the 19th century. Early on, the main concern was with those effects that occurred in the short term following high exposures, i.e., the so-called “deterministic effects”, examples of which are acute radiation syndrome, skin burns, epilation–loss of hair–and sterility. Indeed, protection standards were initially based on the prevention of such effects. We now know that deterministic effects are caused by extensive cell death or cell malfunctioning and, as such, are characterized by a threshold, generally at a high dose (i.e., above 1 Sv) that must be exceeded before the health effect occurs and by an increase in the severity of the health effect with increasing dose. The threshold for a particular deterministic effect to occur varies somewhat from individual to individual and according to the circumstances, but will certainly occur if the dose is high enough. For instance, the threshold for skin burns is above acute doses of 5–10 Gy that for temporary hair loss is around 4 Gy. Nowadays, knowing the exposure situation (i.e., the dose that has been received), with expert clinical judgment, we can relatively easily attribute such a deterministic effect in an individual to the exposure that has been received. We can also predict with reasonable confidence the evolution of deterministic effects in an individual who has been subjected to a high accidental exposure significantly above the relevant threshold.
Over time, the focus of protection shifted to those health effects that occurred in populations in the long term following exposures that included moderate effective doses (say, above 100 mSv), such as the radium dial painters, patients exposed for various medical reasons, and the survivors of the atomic bombings in Japan (i.e., the so-called “stochastic effects”). These effects occur either in the exposed individual (solid cancers and leukemia) or, it is supposed, in their descendants (heritable diseases), although the primary interest now is in cancer induction in the exposed individual (The major problem in the decades immediately following the Second World War was believed to be heritable effects. However, heritable effects were subsequently shown to be of secondary importance in comparison with cancer induction). We know that these effects are initiated by the modification of the genetic material of cells in such a way that the cells survive. These effects are statistical in nature–they occur in only a small fraction of those exposed–and, as a consequence, to study their occurrence, it is necessary to have recourse to statistical techniques, i.e., epidemiological studies, in which the number of a particular health effect in the exposed population is compared with that in a similar but unexposed population.
There are two main types of epidemiological study used to investigate the increased frequency of stochastic effects–cohort and case–control. In a cohort study, individuals are selected on the basis of their exposure and then the frequency of occurrence of health effects is observed over a period of time. In a case–control study, the individuals are selected on the basis of observed health effects and then their exposure is determined. A third type, geographical correlation studies, often termed “ecological studies”, involve the use of disease rates based on data aggregated over geographical areas and these are compared with aggregated data on the levels of exposure to a noxious agent. The possibilities for bias and confounding in this third type of study are well known and they cannot be used to evaluate convincingly causal relationships. Cohen provides an example of a geographical correlation study purporting to show that radon in homes is not a hazard to health. However, in contrast, the results of a number of independent case–control studies ,, indicate the risk associated with radon in homes in a consistent manner. Moreover, it is this consistency that provides the confidence that a causal relationship exists between radon exposure and the risk of lung cancer. Confidence is further strengthened when dose–response gradients are apparent.
Even so, any result from such studies is subject to uncertainty, which, for a given population size, as the dose becomes lower, makes it increasingly difficult to discern a genuine increase in the frequency of a health effect due to radiation exposure relative to the baseline frequency of the disease. This uncertainty is a purely statistical matter, but there are other uncertainties associated with epidemiological studies–inherent biases in the method used and inability to account for all confounding factors. And then, there are the uncertainties associated with extending the observations of increased frequency of disease that can be attributed to radiation exposure over the entire lifetime of the studied population and with applying the results to other populations with different habits, diets, and exposure to other hazards. Even so, using plausible assumptions, the UNSCEAR has estimated excess lifetime mortality (averaged over both sexes and all ages in the population) for five specific populations to be: (a) For all solid cancers combined, 0.36%–0.77% for an acute dose of 0.1 Gy and 4.3%–7.2% for an acute dose of 1 Gy and (b) for leukaemia, 0.03%–0.05% for an acute dose of 0.1 Gy and 0.6%–1.0% for an acute dose of 1 Gy. The statistical uncertainty of the estimates was assumed to be of the order of a factor of 2, and lower bounds of the confidence interval included 0. Our confidence in these values is such that we would expect them to be reproduced in any future epidemiological study of a large population exposed to moderate doses, with uncertainty dependent on the size of the population and dose received. This also means that we should be able to predict the number of cancers in a population exposed to moderate doses and, correspondingly, the risk to an individual exposed to a moderate dose.
On the other hand, the UNSCEAR has not estimated excess lifetime mortality for populations exposed to low and very low effective doses, i.e., below 100 mGy, since there is no solid epidemiological, and therefore scientific, basis for doing so. If there were a risk of health effects in a population exposed at these levels, it would normally be masked by the high background incidence of cancer (i.e., it would be within the statistical “noise”).
Unlike the situation with cancers, no epidemiological study of human populations has ever indicated any increase in heritable disease that can be attributed to radiation exposure irrespective of the magnitude of the dose received. That such health consequences may occur is however indicated by theory–the fact that radiation can damage the DNA within cells–and has been demonstrated by studies of animals exposed to high doses. For human populations, however, any increase would be masked by the background of genetic defects, which is of the order of a few percent of live births–again, the increase would be masked by the statistical noise. Nevertheless, the data from animal experiments have led to the development of models to infer the risk of heritable effects in humans and the UNSCEAR has expressed this as 0.41%–0.64% of the baseline rate per gray of parental irradiation in the next generation. However, this risk cannot be unequivocally verified or, for that matter, refuted at present.
| Application of Science|| |
In radiation protection, we are mostly concerned about low and very low doses–generally below an effective dose of 100 mSv–so, this is a region where we need to make judgments about health effects to establish protection standards. We simply cannot say that we do not have sufficient scientific information. Judgments need to be made on the basis of the scientific information that we do have.
The main problem is the shape of the dose–response relationship below doses above which stochastic health effects have been observed in exposed populations (i.e., generally below effective doses around 100 mSv and above). A number of possible relationships have been proposed, several having their proponents and being scientifically reasonable. Some suggest a threshold below which there are no stochastic effects; others suggest even a beneficial effect at very low doses.Neither is beyond the realms of possibility. The idea that radiation of natural origin could be beneficial for health goes back to the first half of the last century; even these days, spas exist in some countries where people can receive some exposure to radon as part of their treatment or therapy.,
The ICRP, however, has adopted a linear dose–effect relationship, without threshold (the implication is that, in principle, any exposure however small entails some risk of unwanted consequences). What this means is that the gradient of the curve (the risk per unit dose) does not vary with the magnitude of the dose. This is a useful assumption in that it enabled the ICRP to confirm or establish its effective dose limits on the basis of acceptability of risk. This relationship also underpins the concept of collective effective dose (In principle, if the risks of deleterious effects of radiation exposure increase linearly with dose and there is no threshold, the sum of the doses received by all of the people exposed from a particular source should give a measure of the detriment associated with that source. It is on that basis that the ICRP, many years ago, established the concept of “collective dose”). Hence, the assumption is a pragmatic one, but it has not been scientifically confirmed. As the ICRP states: “although there are recognized exceptions, for the purposes of radiological protection the commission judges that the weight of evidence on fundamental cellular processes coupled with dose–response data supports the view that in the low dose range, below about 100 mSv, it is scientifically plausible to assume that the incidence of cancer or heritable effects will rise in direct proportion to an increase in the equivalent dose in the relevant organs and tissues.”
| So What Should We Say to People About the Health Consequences of Low- and Very Low-Dose Exposure?|| |
If the dose had been close to the 100 mSv level, it would be reasonable to say that the risk is unlikely to be significantly different from the risk that would arise somewhat above that dose. However, if the dose had been much lower, all that can be said based on science is that, if there were a risk, the health effect would be too small to be discernible from the normal incidence of that health effect. This is not downplaying the health effects of radiation exposure; it simply expresses the possibility of a health consequence and at the same time, puts that consequence into some perspective with the overall hazards of life. It also avoids exaggeration of the risk which “could lead quite unnecessarily to a panic reaction by the public about possible health effects and to erroneous decisions by the authorities” (a criticism of exaggerated claims of the consequences of the Chernobyl accident).
The Fukushima-Daiichi nuclear accident, like that at Chernobyl, led to the release to the environment of substantial quantities of iodine-131 and two radioisotopes of cesium–cesium-134 and cesium-137–resulting in doses to members of the public over a large area of the country, and even further afield. The following is quoted from the UNSCEAR assessment of levels and effects of the Fukushima-Daiichi accident  and provides us with an example of a well-formulated statement of the consequences of low- and very-low radiation exposure:
“The doses to the general public, both those incurred during the first year and estimated for their lifetimes, are generally low or very low. No discernible increased incidence of radiation-related health effects are expected among exposed members of the public or their descendants. The most important health effect is on mental and social well-being, related to the enormous impact of the earthquake, tsunami and nuclear accident, and the fear and stigma related to the perceived risk of exposure to ionizing radiation. Effects such as depression and post-traumatic stress symptoms have already been reported. Estimation of the occurrence and severity of such health effects are outside the committee's remit.”
“For adults in Fukushima Prefecture, the committee estimates average lifetime effective doses to be of the order of 10 mSv or less, and first-year doses to be one third to one half of that. While risk models by inference suggest increased cancer risk, cancers induced by radiation are indistinguishable at present from other cancers. Thus, a discernible increase in cancer incidence in this population that could be attributed to radiation exposure from the accident is not expected. An increased risk of thyroid cancer in particular can be inferred for infants and children. The number of infants that may have received thyroid doses of 100 mGy is not known with confidence; cases exceeding the norm are estimated by model calculations only, and in practice they are difficult to verify by measurement.”
| Rules of Thumb|| |
The following is a summary of the points made in this article based on the relevant UNSCEAR report:
- A deterministic effect in an individual can be attributed to radiation exposure if the exposure is above the relevant threshold and differential pathological diagnosis that eliminated possible alternative causes is achievable
- Following an acute radiation exposure significantly above a threshold for a deterministic effect, the evolution of that effect can be predicted with confidence
- An increased incidence of cancer in a population exposed to effective doses above about 100 mSv can be attributed to radiation exposure through epidemiological analysis, provided that, among other things, the increased frequency of cases of the stochastic effect is sufficient to overcome the inherent statistical and other uncertainties; however, a particular cancer in an individual cannot be attributed to radiation exposure even if that individual received a dose above 100 mSv
- An increased risk of cancer in a population can be predicted if each individual had received an effective dose above 100 mSv
- No heritable disease in a human population can at present be attributed to radiation exposure, irrespective of dose, but it is reasonable to assume that there is a risk of such disease from radiation exposure, albeit of less significance than the risk of cancer induction
- The number of health effects occurring in a population exposed to low- and very-low effective doses (i.e., well below 100 mSv) cannot be calculated scientifically from the risk factors given by the ICRP or UNSCEAR
| References|| |
ICRP. The 2007 Recommendations of the International Commission on Radiological Protection, Publication 103. Oxford, New York: Pergamon Press; 2007.
UNSCEAR. Effects of Ionizing Radiation. Volume I: Report to the General Assembly, Scientific Annexes A and B. UNSCEAR 2006 Report. United Nations Scientific Committee on the Effects of Atomic Radiation. United Nations Sales Publication E.08.IX.6. United Nations, New York; 2008.
UNSCEAR. Effects of Ionizing Radiation. Volume II: Report to the General Assembly, Scientific Annexes C, D and E. UNSCEAR 2006 Report. United Nations Scientific Committee on the Effects of Atomic Radiation. United Nations Sales Publication E.09.IX.5. United Nations, New York; 2009.
UNSCEAR. Sources, Effects and Risks of Ionizing Radiation. Volume I: Report to the General Assembly, Scientific Annex A. UNSCEAR 2012 Report. United Nations Scientific Committee on the Effects of Atomic Radiation. United Nations Sales Publication E.16.IX.1. United Nations, New York; 2015.
ICRP. The history of ICRP and the evolution of its policies. Published in ICRP publication 109. Ann. ICRP 39 (1), 75-69; 2009.
Cohen BL. Relationship between exposure to radon and various types of cancer. Health Phys 1993;65(5):529-31.
Darby S, Hill D, Auvinen A, Barros-Dios JM, Baysson H, Bochicchio F, et al.
Radon in homes and risk of lung cancer: Collaborative analysis of individual data from 13 European case-control studies. BMJ 2005;330:223.
Lubin JH, Wang ZY, Boice JD Jr., Xu ZY, Blot WJ, De Wang L, et al.
Risk of lung cancer and residential radon in China: Pooled results of two studies. Int J Cancer 2004;109:132-7.
Krewski D, Lubin JH, Zielinski JM, Alavanja M, Catalan VS, Field RW, et al.
A combined analysis of North American case-control studies of residential radon and lung cancer. J Toxicol Environ Health A 2006;69:533-97.
UNSCEAR. Report of the United Nations Scientific Committee on the Effects of Atomic Radiation 2010. Fifty-seventh Session, Includes Scientific Report: Summary of Low-dose Radiation Effects on Health. UNSCEAR 2010 Report. United Nations Scientific Committee on the Effects of Atomic Radiation. UNSCEAR 2010 Report: United Nations Sales Publication M.II.IX.4. United Nations, New York; 2011.
UNSCEAR. Hereditary Effects of Radiation. UNSCEAR 2001 Report. United Nations Scientific Committee on the Effects of Atomic Radiation, 2001 Report to the General Assembly, with Scientific Annex. United Nations Sales Publication E.01.IX.2. United Nations, New York; 2001.
Tubiana M, Aurengo A, Averbeck D, Masse R. Recent reports on the effect of low doses of ionizing radiation and its dose-effect relationship. Radiat Environ Biophys 2006;44:245-51.
Doss M. Evidence supporting radiation hormesis in atomic bomb survivor cancer mortality data. Dose Response 2012;10:584-92.
ICRP. Recommendations of the ICRP. ICRP publication 26. Ann. ICRP 1 (3), 1977.
Balonov MI. On protecting the inexperienced reader from Chernobyl myths. J Radiol Prot 2012;32:181-9.
UNSCEAR. Sources, Effects and Risks of Ionizing Radiation. Volume I Scientific Annex A. Levels and Effects of Radiation Exposure due to the Nuclear Accident after the 2011 Great East-Japan Earthquake and Tsunami, UNSCEAR 2013 Report. United Nations Scientific Committee on the Effects of Atomic Radiation. United Nations Sales Publication E.14.IX.1. United Nations, New York; 2014.