Science and trans-science in radiation risk assessment: Child cancer around the nuclear fuel reprocessing plant at Sellafield, U.K.

The Science o f the Total Environment, 53 (1986) 201--216 Elsevier Science Publishers B.V., Amsterdam -- Printed in The Netherlands

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SCIENCE AND TRANS-SCIENCE IN RADIATION RISK ASSESSMENT: CHILD CANCER AROUND THE NUCLEAR FUEL REPROCESSING PLANT AT SELLAFIELD, U.K.

DAVID CROUCH

Science Policy Research Unit, University of Sussex, Falmer, Brighton BN1 9RF (United Kingdom) (Received February 21st, 1986;accepted March 20th, 1986)

ABSTRACT The assessment of health risks to the population from radionuclides in the environm e n t is a complex and as yet incomplete science: biogeochemical mechanisms of environmental transfer and concentration are poorly understood; models of radionuclide metabolism rely largely on inconclusive and contradictory experiments with animals, and the principles by which results may be extrapolated to humans are unknown; uncertainties in the dosimetry of alpha-emitters in children and the foetus are acute; and chronic doubt persists over the magnitude of low-level dose--response for radiation carcinogenesis. To deny uncertainties of this nature is to court public distrust of scientific risk assessment; public confidence in nuclear power technologies might be strengthened through a more open discussion of the technical difficulties involved. These problems are described with reference to the assessment of cancer risks at a large nuclear facility in the north of England. The extent of uncertainties in a recent radiological risk assessment are found to be such that, should scientific concern persist over the exceptional incidence of child cancer in the locality, greater consideration should be given to a reappraisal of the risk calculation.

INTRODUCTION

Policy analysts concerned with the safety and regulation of large-scale technologies are becoming increasingly aware of significant problems associated with the scope and limits of quantitative technological risk assessment [1]. Demands for precise quantification are often unrealistic; the complexity of the risks and the nature and extent of uncertainties in their technical specification may prohibit a fully scientific response. Such difficulties can be characterized in Alvin Weinberg's apt terminology as trans-scientific [2]. In principle they refer to questions of fact and can be formulated in terms of existing scientific methods and procedures, but they are in practice unresolvable in these terms alone. An example would be the dose--response for

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202 radiation carcinogenesis in mice: exact knowledge of this relationship would require so many mice as to make its empirical determination impracticable. When trans-scientific problems underlie an important policy choice, differences in scientific opinion can be greatly magnified as scientists' competence and motives come under close public scrutiny. A consequence of controversies of this nature is that it becomes particularly difficult to distinguish the scientific w o o d for the political trees. In his analysis of transscience, Weinberg noted that procedures for the establishment of consensus within the scientific c o m m u n i t y can conflict with those by which political consensus is achieved in democratic society: scientific consensus is based upon a high degree of tacit judgement and expertise that is difficult to make explicit in a public forum. It is reasonable, therefore, to infer that in so far as public policy involves trans-scientific rather than scientific issues, the role of scientists in contributing to the formulation of such policies should be different from their role when the issues can be resolved by science unambiguously

[2]. This paper examines the role of quantitative risk assessment in radiological protection. Though its conclusions are intended to be general, it focuses on the recent controversy over the possible raised incidence of child cancer around the large nuclear fuel reprocessing plant at Sellafield in the north of England. Late in 1983 epidemiological data were reported indicating a "bullse y e " pattern of cancer incidence in the under 15 population around Sellafield, centering on the nearby coastal village of Seascale [3]. An official inquiry was immediately announced under the guidance of an Independent Advisory Group chaired by Sir Douglas Black. A number of complementary epidemiological studies were prepared for the inquiry, together with a detailed radiological risk assessment by the National Radiological Protection Board (NRPB) [4]. The inquiry found that the incidence of lymphatic leukaemia amongst children under 10 years of age living in Seascale since the late 1960s was 10 times the national average. According to the NRPB, however, the levels of radioactivity discharged from the Sellafield plant were far too "low to account for the observed incidence; it found that predicted and observed values differed by between 2 and 3 orders of magnitude. Largely on this basis, the inquiry concluded that there was no evidence of any general health risk near the plant [5]. The publication of the Black Report, however, has not resolved the controversy, which has since received close attention in the scientific press. As a result, the interpretation of the statistics has been usefully clarified and some significant errors have been revealed [6, 7]. With regard to radiological risk assessment, there has been some speculation over whether the Sellafield plant could have been the cause of the observed leukaemia incidence [8-10]. By means of a critical review of recent literature, this paper aims to examine the extent of scientific uncertainties in radiological risk assessment, and to ask h o w in the light of such considerations satisfactory, consensual protection policies might best be pursued.

203 TECHNICAL UNCERTAINTIES IN THE NRPB RISK ASSESSMENT

The considerable fundamental research effort in radiological protection suggests that the scientific basis for confidence in radiological risk assessment is n o t complete; the assumption on which all quantitative risk assessment is based -- the status of which I wish to appraise -- is that it is adequate. On the basis of this assumption, the NRPB has attempted to evaluate from measured environmental levels of radioactivity, and reported effluent discharges, the risk to seven cohorts of 175 children born in Seascale village at 5-year intervals since 1945. The metabolic and dosimetric models employed were substantially those recommended by the International Commission on Radiological Protection (ICRP) [ 11]. Individual difficulties with the models were treated separately in appendices to the report; thus the risk assessment was given without an error bar and w i t h o u t consideration of the likely uncertainty in the result owing to different effects in combination [4]. It would be mistaken, however, to infer that there was no scope for judgement or subjective evaluation in the NRPB's work. Inevitably, gaps remain in our knowledge of the biological and environmental behaviour of radioactive chemicals, some more significant than others. Since it is generally assumed that a greater margin of uncertainty surrounds the behaviour of the long-lived, alpha-emitting isotopes in the actinide series [5], I shall concentrate largely on these.

Behaviour of radionuclides in the environment In order to assess the intake of radionuclides by the population it was necessary to know both the concentrations of radioactivity in environmental materials and the pathways by which the population might have been exposed. The NRPB recognized the paucity of monitoring data at Sellafield: the first year for which comprehensive data on environmental concentrations were available was 1978. Thus the concentrations of most of the radionuclides prior to the mid-1970s had to be estimated from reported levels of yearly effluent discharged from the plant [4]. F o r caesium isotopes and other radionuclides t h a t remain in the water phase, concentrations are closely related to current discharges. There is no such clarity over the distribution of the actinides, however, since they are known to bind rapidly to sediments [12]. As a result, concentrations in marine foods and sediments may be significantly affected by discharges in past years. Just what proportion of actinides in the coastal environment comes from current discharges and h o w much from accumulations in the sea bed is u n k n o w n [ 1 3 ] . The physical and biochemical processes that govern the mobilization and biological availability of the actinides are just beginning to De recognized [14, 15]. Taylor has reviewed the evidence to 1982 and has found large fluctuations in environmental concentrations over time, location, and species of marine fauna bearing no obvious relation to yearly discharge [16]. Hunt has calculated that concentrations of plutonium and americium from the plant in environmental materials may be related to discharges over a period of between 1 and

204 8 years; annual variations in discharge levels and in the dispersion and dilution of sediments prevent establishment of the environmental equilibrium necessary to make an accurate assessment of this relationship [17]. Further uncertainties surround the resuspension of contaminated sediments in seaspray. That this exposure pathway might be significant was first considered only at the Windscale Inquiry in 1977 [18], so monitoring data are recent. Their implications are only n o w becoming apparent: in late 1983 Sir Edward Pochin and his colleagues at the NRPB were n o t aware of any risk estimation yet performed for this pathway of exposure [19]. Scientists at the Atomic Energy Authority have measured the actinide content of seaspray in Cumbria, finding that the concentration of actinides in air is directly proportional to that in local sediment. The americium content of the spray is many thousand times that of contaminated water free of sediment, pointing to some u n k n o w n b u t potentially significant mechanism of concentration in the surf [20]. The magnitude of scientific uncertainty over the significance of these environmental mechanisms for radiological protection emerged in June 1985 when it was reported that ecologists were perplexed at the large variations in levels of radioactivity found in plants and animals around Sellafield, two orders of magnitude greater than in familiar biological processes; this poses problems for sampling methods and raises questions about protection standards based on average levels of contamination [21]. The results of much of this work remain unobtainable, reportedly because of the worry that the findings will undermine current safety standards [22]. Measurements of beta-emitters in the Seascale population indicate levels of contamination lower than would be expected on the basis of the available environmental monitoring data [23]. However, local human data on the actinides are meagre. Autopsy studies of plutonium in British adults report significantly increased concentrations in six subjects from West Cumbria [24]. In short, estimates of population exposure via environmental pathways are largely hypothetical. Hamilton has remarked that it is unwise to rely upon the o u t p u t of existing models to safeguard people from ionizing radiation in the marine environment; the problems demand research of a fundamental nature [25]. Account has also to be taken of variations in individual habits and behaviour. The NRPB found that these were likely to be most significant in the case of children exhibiting the p h e n o m e n o n of p i c a - - the deliberate ingestion of non-edible material -- and in the handling of contaminated objects on the beach [4]. Metabolism of radionuclides

Once figures for the intake had been chosen, the NRPB had to make estimates of the passage and distribution throughout the b o d y of radioactivity in the lung and gut. The metabolic models and parameters used in

205 this part of the calculation were essentially those recommended by the ICRP [11]. As chapter 9 of ICRP Publication No. 30 makes clear, the lack of knowledge a b o u t metabolism represents the largest factor of uncertainty in most estimates of dose. Many of the metabolic parameters are based on experiments in animals. It is a well-recognized principle of environmental toxicology that results obtained in animal experiments are n o t necessarily translatable directly to human populations [26]. No measurements have been made on humans of the uptake of plutonium or americium through the wall of the gastrointestinal (GI) tract [27]. In animal experiments the fraction of plutonium absorbed into the blood from the gut varies by several orders of magnitude according to the species of experimental animal; complicating factors include the period of fasting before exposure, the rate of ingestion, and diet [15, 27, 28]. The experimental determination of absorption factors is hampered by the high concentrations of plutonium needed to obtain measurable levels of uptake [ 29]. Similar problems are experienced with respect to models of inhalation. There have been a few long-term studies of particle retention in the human lung, b u t there are insufficient human data on the relative fractions of particles retained in the conducting airways and lymph nodes from which to estimate clearance from these sites by mechanical transport [30]. Laboratory studies on animals are contradictory: those on rats put the latter at no more than 1%, while those on dogs indicate that it could be 15% [30]. Moreover, the high lung deposits of toxic dusts often used to facilitate estimates may cause effects interfering with clearance which would not occur at permissible levels of exposure [ 3 1 ] . Associated with the existing human data there are usually large uncertainties attached to direct measurements of actinides in the lung, reflected in the observed variability in repeated measurements taken on the same individual [32]. Fry, Bailey and James have found considerable diversity in the particle clearance rates of a small group of individuals, leading to differences of a factor of 4 or more in committed dose equivalent to the lung tissue after inhalation of a long-lived radionuclide [33]. In a study of an individual worker exposed to airborne plutonium, Ramsden, Bains and Fraser have reported the lung burden to be a factor of 4 less than that calculated from the ICRP model [34]. Further uncertainties surround this model: the clearance pathways for insoluble particles in the upper respiratory tract are defined arbitrarily [ 35]. ICRP assumes that 40% of the pulmonary deposit is cleared via the conducting airways with a half-time of one day [ 1 1 ] . Bailey, Fry and James have found no evidence for such a rapid clearance mechanism [ 3 6 ] . Newton, Taylor and Eakins report retention half-times for plutonium and americium oxide in the lung of a single worker up to 30 times higher than those assumed by ICRP. Furthermore, far less material was cleared via the trachea into the GI tract than would be predicted by the ICRP model. As a result, they conclude that the ICRP's clearance model can grossly underestimate the long-term irradiation of systemic sites [ 3 7 ] .

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Finally, ICRP estimates are intended for the protection of workers occupationally exposed to pure forms of radioactive chemicals. Most of its metabolic data for GI transfer of the actinides are based on animal experiments in which high concentrations of inorganic forms of radionuclides are injected directly into the stomach in a single dose [27]. In the environment, however, radionuclides are usually in the form of chemical c o m p o u n d s with organic materials. Cooper and Harrison have identified several complexing agents in foodstuffs which lead to elevated gut absorption of plutonium in rats [29]. In experiments on fasted animals, Larsen et al. report strong evidence that the value of the human gut transfer factor is 5 -- 10 times higher than that used by the NRPB [4], and there is evidence of an inferential nature suggesting that it might be higher by more than 2 orders of magnitude [15]. Uncertainties over the effect of chemical form also complicate the understanding of particle clearance mechanisms in the lung [ 33, 38 ]. The NRPB have recently recognized some of these uncertainties [39]. The need to subordinate their detailed treatment to the pursuit of a risk calculation is succinctly expressed in ICRP Publication No. 30: "The function describing uptake and retention of radionuclides in a body tissue following its ingestion or inhalation may be very complex and therefore it is convenient to describe the transfer of radionuclides within the body by simple models which facilitate calculation." [ 11 ] (Emphasis added. )

Dosimetry in radiosensitive tissue Once a figure for the amount of radioactivity in the body tissues had been chosen, together with its retention time, it was necessary to decide on the dose to radiosensitive tissue. In the ICRP model carcinogenic effects are assumed to be directly related to dose, that is, to the energy deposited by radiation per unit mass of irradiated tissue. In terms of.the likely mechanisms of radiation carcinogenesis, however, the mass of tissue is of very little significance. It could be argued that there are more cells at risk in a larger body and therefore, in contrast to dose, cancer risk will increase with mass [40]. These kinds of considerations are particularly important for densely ionizing radiations: at the cellular level, alpha-particle dose averaged throughout the tissue may be considered biologically almost meaningless [41]. This problem arose in the context of the 'hot particle' debate in the early 1970s. As a result it is now generally assumed that the risk of cancer of the lung is proportional to the dose averaged over the entire organ [42]. The h o t particle debate, however, refuses to lie down. Doubts remain over the irradiation of the lymph nodes, which may be sensitive to leukaemia induction by alpha radiation [43, 44]. When insoluble material is inhaled, a very high concentration of radioactivity can be found in the lymph nodes [45]. This is particularly relevant because Seascale cancers were predominantly cancers of the lymphatic system. The related leukaemia risk cannot be calculated because the location of sensitive cells is n o t known. In experiments on animals lymphatic leukaemia has not been induced in the lungs of

207 dogs or mice, but it has in rats [43]. Sir Edward Pochin of the NRPB has remarked in this regard: "I d o n ' t k n o w w h e t h e r w e are closer to the dog, lymph node behaviour." [43]

t h e m o u s e , or t h e rat in

terms of

Similar considerations relate to the induction of leukaemia in the red bone marrow (RBM). It is n o t k n o w n which are the sensitive cells in the marrow, though it is generally assumed that the haematopoetic stem cells are likely targets for leukaemogenesis [4]. In its risk assessment the NRPB assumed these to be evenly distributed through the RBM. There is a body of evidence, however, to indicate that the stem cells are n o t uniformly or randomly distributed [46]. They have been found to be in greater concentration near the bone surface, which is where a bone surface-seeking radionuclide such as plutonium lodges in the skeleton. The situation is complex because the lymphatic cells are likely to be nearer the centre of the marrow. On the other hand, it is possible that their leukaemogenicity increases with proximity to the bone [47]. After the Black inquiry, a confidential meeting of government scientists recognized that these considerations may have caused the calculation of bone marrow dose from the actinides to have been underestimated [48]. Doctor M.C. Thorne of ICRP has put the possible errors due to RBM microdosimetry at no more than an order of magnitude [49]. Others have stressed our relative ignorance of the biological effects of alpha radiation (see below), and the decision by the NRPB to average the dose throughout organ tissue is a reflection of this uncertainty.

Risk models for children pr Predicting the effect of ionizing radiation on children is " a biological minefield" [50]. Parameters in the metabolic and physiological models taken to be constant for adults are generally recognized to be age-dependent in children. The NRPB has made an a t t e m p t to m o d i f y the standard ICRP models in order to calculate doses to young people [51] ; i t is the only example of its kind. Furthermore, the modifications are somewhat rudimentary. The model only takes into account changes in physiology, that is, in body dimensions and mass. Consequently it only relates to the modified dosimetry of radionuclides within a growing body, and thus the points made above apply in even greater measure to this model. As a result, it assumes that the distribution and retention models recommended by ICRP for adult workers, and the corresponding parameters, are also appropriate for young people. This approximation is inevitable because the metabolism of radionuclides in children is known in just a few cases; the NRPB made provision for the age-specific metabolic behaviour of only tritium, carbon, sulphur, and iodine

[4].

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Apart from these elements and the case of the foetus (see below), unmodified ICRP models and parameters were employed throughout the main part of the NRPB calculation, and it was on the basis of these that the expected Seascale leukaemia deaths were computed. The problems of age-specificity were postponed until the latter part of the report in which the sensitivity of the calculation to different metabolic factors was given a summary examination. Its conclusion was that none of the factors examined had a substantial effect on the analysis. It is in the appendices to the calculation, however, that the full extent of the "minefield" becomes apparent. The discussion of the RBM dose in children relies at best on a handful of animal experiments. The treatment of the age-dependence of inhalation, lung deposition, and clearance of particles of different sizes is entirely mathematical and lacking supportive empirical material. The dependence on age of the gastrointestinal absorption of radionuclides is empirically the best documented, b u t it is confronted by the problems described above; in evaluating the absorption of actinides in newborn animals extrapolation of the animal data to uptake in the human is particularly tenuous [27]. Since the Black inquiry the NRPB has accepted that its dosimetric model for the skeleton may n o t be appropriate for young persons, and it reports that a modified version is being developed [39]. One problem in reviewing these particular aspects of the calculation is that many of the relevant models were prepared by the NRPB itself. They were unique, mostly very recent, and a significant proportion were unpublished. Thus there is no other reference point from which to explore alternative estimates of the risk. In the case of doses to the foetus this problem is most acute. Prior to the Black inquiry there simply were no estimates of foetal radiation risk from radionuclides in the mother. There are no generally accepted methods for calculating the doses to foetal organs from maternal intakes of radionuclides and so several ad hoc methods were developed for the report [4]. The foetal model for plutonium was published 2 months before the risk assessment itself [52]. As in the child model described above, this model is of necessity preoccupied with changes in physiology during gestation rather than with metabolic behaviour. Thus the fractional distribution of plutonium in the organs of the foetus is taken to be the same as that in the mother. Transfer of actinides from mother to child is based entirely on experiments in animals: as the authors of the model remark, reliance on animal evidence is much greater in the development of foetal than of adult metabolic models, and extreme care is needed in the extrapolation from animals to man. They also question whether the conventional concept of dose has any meaning when applied to the foetus: it seems unlikely that committed effective dose equivalent, which is the quantity recommended for adult members of the population, is an appropriate criterion for the estimate of risks to the foetus [ 52]. The uncertainties described above are so broad and uncharted that it is almost impossible to give even a rough indication of their magnitude, or the specific sites at which they are likely to be most significant. The only

209 quantification of this kind relates to the possible increased absorption of radionuclides through the gut wall of the new-born child. Increased absorption is t h o u g h t to be due to intestinal permeability to gamma globulins (large protein molecules) in milk, from which passive i m m u n i t y is acquired [27]. The NRPB has recognized that GI absorption rates of actinides in neonatal rats and hamsters are much higher than in adults, and has recommended an absorption factor for humans in the first few m o n t h s of life 20 times greater than the adult value [27]. In piglets, however, Sullivan and Gorham have reported the GI absorption of plutonium-238 nitrate to be 1000 times the value in adult swine [53]. They also f o u n d t h a t a substantial fraction of the plutonium incorporated in early life remained in the liver and skeleton for a prolonged period: after 1 year 8% still remained in the skeleton of the piglet, in contrast with 0.1% in the rat. Owing to similarities in skeletal development, retention of actinides in the liver, and life-span, the authors concluded that GI absorption and retention of actinides in young humans may more closely resemble that in pigs than that in rats or hamsters. In conclusion, ICRP Publication No. 30 states clearly: "The Commission does n o t r e c o m m e n d the use of the data and the models described in this report to estimate committed dose equivalent to members of a population, for example from radionuclides in the environment, by adjusting solely on the basis of differences in mass of organs or magnitude of intake." [ 11 ]

Yet because of the uncertainties in the underlying science, this is precisely what the NRPB was in large measure forced to do.

The dose--response relationship Once an estimate of the dose to sensitive tissue in the children had been made, the NRPB had to decide on the likely biological effect that would result. There are two major components of radiation dose, each of which can be expected to provoke widely different biological effects. Low linear-energytransfer (LET) radiation (beta and gamma) is sparsely ionizing, and therefore results in far less tissue damage per unit dose than high LET radiations {neutrons and alpha-particles). There are few reliable human data on the magnitude of radiation effects at low dose levels, thus risk estimates in the chronic low-dose range are made by extrapolating from higher doses and higher rates of exposure. It is c o m m o n l y assumed that a linear extrapolation is realistic, and may possibly overestimate the risk at low doses from low LET radiation [54]. A factor is then introduced to account for the higher relative biological effectiveness (RBE) of high LET dose. In the Sellafield risk assessment the NRPB adopted an RBE of 20 to extrapolate from low to high LET radiation [4]. The relation of dose to biological response in radiation carcinogenesis continues to provoke controversy; some believe current risk estimates to be too low [55, 56], some too high [57], and yet others believe that small

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doses of radiation are positively beneficial [ 5 8 ] . The response of the NRPB to this problem has been to point out that, according to its risk calculation, the dose from natural background radiation is so much larger than that from Sellafield that any significant increase in the risk factors employed in the calculation would imply a leukaemia incidence due to background absurdly high in view of its average incidence nationwide [59, 6 0 ] . The risk factors and RBE chosen by the NRPB led to a prediction that background radiation is responsible for about 15% of the total incidence of child leukaemia from all sources [4]. The view that only a small proportion of human cancers is caused by background radiation is supported by a number of large-scale epidemiological studies which have failed to find any correlation between background radiation levels and cancer incidence. In a comprehensive review of this literature, however, Archer has suggested that studies which have n o t found any obvious relationship may be misleading in that they have minimized the carcinogenic role of naturally occuring high LET radioactivity [61]. Because regional differences in the low LET (gamma) c o m p o n e n t of the background appear n o t to be large enough to account for the observed variations in biological effect, he has postulated that the high~ LET c o m p o n e n t might be the most important factor in background radiation carcinogenesis. In support of this claim, his own epidemiological findings indicate a strong correlation between high LET background radiation and a number of human cancers [62]. The implication is that existing evidence on background radiation and cancer is not incompatible with significantly raised risk factors for high LET radiation carcinogenesis. Uncertainties over alpha dose--response at low dose levels are n o t confined to discussions of background radiation. Of the limited human data, the largest and most thoroughly analyzed irradiated population consists of survivors of the A-bomb explosions at Hiroshima and Nagasaki. A recent re,evaluation of this data by the Lawrence Livermore Laboratory, however, has shown that t h e high LET radiation dose to this population m a y have been grossly overestimated [63]. This study has provoked a vigorous new debate over the adequacy of accepted radiation risk factors [64]. If correct, a major consequence is the virtual disappearance o f nearly all the useful high LET data for human carcinogenesis; studies on other human populations are equally ambiguous and have received far less critical attention [65, 66]. There is a considerable b o d y of laboratory studies that indicate possible supra-linearity in alpha dose--response at low doses, implying that a linear interpolation for high LET radiation m a y involve an underestimate of the risk [66--68]. It would also appear that fractionated or protracted exposure to alpha radiation at low doses induces a greater response than a single exposure resulting in the same dose; there is no satisfactory explanation for this finding [68]. Furthermore, it is now well established for numerous tissues and for different animal species that the RBE of alpha radiation depends also on the biology of the target tissue [68]. Such considerations

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have led Coggle to remark that the current accumulation o f evidence in this area of cancer biology serves only to illuminate our ignorance [66]. With regard to dose -- response for low LET radiation, the evidence is also inconclusive; extrapolating from their.work on diagnostic X-ray exposure in utero, Stewart and Kneale have calculated that up to 70% of child leukaemia may be due to background radiation [69]. Once uncertainties of this order are recognized, discussion of Sellafield radiation dose in relation to natural background becomes largely incidental, and the controversy over dose -response at both high and low LET takes on a crucial significance. The deep divisions within the scientific c o m m u n i t y over different approaches to the estimation of risk factors are well illustrated by the stormy history of the BEIR-III Report [ 7 0 ] . There is a similar debate within the NRPB itself. Whilst senior members of the Board long associated with the ICRP defend a radiobiological approach to risk assessment [ 7 1 ] , the late G.W. Dolphin voiced an opinion that, judging from the current knowledge of radiation carcinogenesis and by its progress in the last 20 or 30 years, it will be many more decades before an acceptable theory is evolved relating risk of cancer to radiation dose; in the meantime this relationship can only be derived, if at all, from the epidemiology of human populations [72]. In a similar vein, the late J.A. Reissland succinctly expressed the trans-scientific nature of radiological risk assessment: "Since there is judgement as well as technical evaluation from the data, it is inevitable that there will be dissent from the values put forward. There is no evidence to disprove the ICRP risk factors, however, neither is there any evidence to verify them." [73]

DISCUSSION AND CONCLUSIONS

The scientific basis for confidence in radiological risk assessment is seriously lacking. This conclusion is consistent with the growing consensus amongst policy analysts that the risks of nuclear technologies are par excellence a tran~scientific issue [1]. It also resolves the apparent paradox (noted elsewhere [8] ) that, according to radiological risk assessment, should further cases of child leukaemia occur in Seascale village the less likely would be any connection with radiation from the SeUafield plant. To recognize this fact is not, however, to suggest that the NRPB's calculations are incompetent or flawed: in itself, their trans-scientific nature does not imply that the NRPB achieved anything less than the best evaluation of the radiation risk possible in the circumstances [74]. Rather it is to accept that in order to bridge the gaps in its knowledge it had to employ a significant a m o u n t of subjective expert judgement, as opposed to simply following the logic of an ineluctable mathematical rationality. In response to criticism of the risk assessment, and speculation that Sellafield could have been the cause of the observed leukaemia incidence,

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the Director of the NRPB has stated: "We have sought diligently f o r plausible sources o f e r r o r o f this magnitude and failed t o f i n d t h e m . We are o p e n t o a n y sensible suggestion." [ 5 9 ]

The ritual claim by responsible organizations to an attainment of perfect technical control in radiological risk assessment has been noted elsewhere [75] ; in the face of the extensive uncertainties outlined above, however, it is disingenuous to maintain that such precision is achievable. There is growing public reluctance to accept the pronouncements of official bodies responsible for radiologicai protection, the more so if they come shrouded in a mist of scientific jargon and rhetoric. The public, however, cannot be expected to share the experience, skill, and expertise of organisations such as the NRPB in assessing radiation risks, and this gap in understanding serves as a basis for anxiety and intransigence. When an issue transcends science and impinges on society, public worries can easily be exploited by interested parties owing to obvious uncertainties in the risk estimates. Indeed, that the NRPB's treatment of acknowledged uncertainties was post hoc and piecemeal, rather than formal and systematic, is a notable deficiency in the calculation; the approach makes the magnitude of combined errors in the final risk estimate impossible to determine. In an interesting paper [76], Prof. M.G. Morgan has listed various strategies open to risk analysts for dealing with scientific uncertainty: (1) Perform a single-value-best-estimate analysis and ignore the uncertainty. (2) Perform a single-value-best-estimate analysis, then acknowledge the uncertainty, perform various sensitivity calculations, and provide a qualitative and/or quantitative discussion of the uncertainty. (3) Estimate some coefficient of uncertainty (such as the standard deviation) for each important model coefficient, and then use analytical procedures to propagate this uncertainty through the analysis. (4) Characterize uncertain coefficients as subjective probability distributions and then propagate this uncertainty through the analysis, usually through the use of stochastic simulation. (5) Treat some coefficients parametrically, performing the analysis for a variety of plausible values of each of these coefficients. (6) Perform order-of-magnitude analysis which does not produce unique "answers" but rather estimates based on the range of possible answers. The analytical strategy appropriate for a given risk analysis depends on the a m o u n t of associated uncertainty; the strategies are listed above in order of increasing problem uncertainty. As Morgan notes, far too much risk assessm e n t that is done as single-value-best-estimate analysis should be done as probabilistic analysis. The NRPB adopted strategy 2. Some of the uncertainties outlined above, however, such as the effects of individual biological and behavioural variability, warrant treatment of type 5 or 6. Morgan has developed a software system to facilitate such analyses. Uncertainties over the functional form of a model are much harder to deal

213 with in this way. An exploratory approach, changing the model around to learn what matters and what doesn't, and order-of-magnitude arguments that do the same thing, are about the best that could be h o p e d for. The overiding object of these approaches, however, would be to explicitly identify assumptions and operations and to present results in a clear, open manner which allows others to easily verify, use, modify, and extend the analysis. Risk assessments meeting such criteria might provide a framework for discussion between conflicting parties in a less adversarial and more consensual environment, since all parties would find it easier to understand the implications of alternative model formulations and assumptions. In conclusion, there can be no d o u b t that rigorous, quantitative risk assessments performed by organizations endowed with the requisite training and experience are an essential part of industrial regulation and standardsetting. Without a secure social basis for confidence in radiological risk assessment, however, it is unlikely that consensus over nuclear power technology can be achieved. Thus the radiological protection profession should seek to elicit public approval and trust through a more frank discussion of the difficulties involved in its work. As the director of the NRPB remarked in 1984: "We must be neither blandly reassuring nor deliberately alarmist." [77] It is likely that greater public alarm is caused by retrospective admissions of important uncertainties than if they are stated clearly at the outset.

ACKNOWLEDGEMENTS I would like to thank Andrew Barry, Diana Hicks, Steve Lax, Gordon MacKerron, Erik Millstone, and Nigel Minchin for valuable criticism of the manuscript, and Erik Millstone for encouragement and supervision of the research.

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