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Risk estimates for fast neutrons and implications for radiation protection
International Congress Series 1236 (2002) 3 – 12
Risk estimates for fast neutrons and implications for radiation protection Albrecht M. Kellerer * Radiobiological Institute, University of Munich, Schillerstraße 42, 80336 Munich, Germany
Abstract The risks of low neutron doses are of increasing interest with regard to exposures in aviation, in the transport of nuclear fuel, or even in an accident as that in Tokaimura. In the absence of epidemiological information, the neutron risk coefficient is currently taken to be the product of two uncertain low-dose extrapolations, nominal risk coefficient for the photons and presumed maximum relative biological effectiveness of the neutrons. An approach is presented here that avoids the lowdose extrapolations and invokes, instead, the product of the excess risk from epidemiological observations at an intermediate reference dose of g-rays—here taken to be 1 Gy—and the assumed value, R1, of the neutron RBE against this reference dose. With R1 between 20 and 50 the solid, the cancer mortality data of the A-bomb survivors provide an excess relative risk (ERR) for the neutrons between 8 and 16/Gy. This result is converted into a risk coefficient in terms of the lifetime attributable risk (LAR) relative to the neutron effective dose as defined by ICRP. The result is at high neutron energies somewhat in excess of the current ICRP nominal risk factor, while it agrees with ICRP for the degraded fast neutron spectra that are of major pragmatic interest. The so-called Hiroshima neutron discrepancy will not influence the neutron risk estimate because any remaining uncertainty of the neutron doses in Hiroshima is minor at the reference dose of 1 Gy. D 2002 Elsevier Science B.V. All rights reserved. Keywords: Neutrons; RBE; Risk coefficient; Solid cancers; A-bomb survivors; Effective dose; Ambient dose equivalent
1. Introduction Neutrons are known to be far more effective than g-rays, particularly in small doses. However, this knowledge was derived exclusively from cell studies or animal experiments. No late effects from neutrons have been observed in man. *
Corresponding author. Tel.: +49-89-5996-818; fax: +49-89-5996-840. E-mail address: [email protected] (A.M. Kellerer).
0531-5131/02 D 2002 Elsevier Science B.V. All rights reserved. PII: S 0 5 3 1 - 5 1 3 1 ( 0 1 ) 0 0 7 6 1 - 0
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A.M. Kellerer / International Congress Series 1236 (2002) 3–12
On the basis of the former A-bomb dosimetry system, TD65 [1], it has been argued that much of the excess cancer rate in Hiroshima was due to neutrons [2,3]. However, this assumption led to a re-examination of the A-bomb dosimetry and then to the current dosimetry system, DS86 [4], which specified much lower neutron doses than the earlier system, TD65. It was then concluded, perhaps prematurely, that any effect contributed by the neutrons would be minor and that no direct information on the neutron risks could be derived from the A-bomb data.
2. The familiar estimation procedure In the absence of epidemiological evidence, it was realized that the neutron risk estimates would have to be derived by combining information on the effects of g-rays, with the radiobiological knowledge on the relative biological effectiveness of the neutrons. While there are (as will be seen) different approaches, a seemingly straightforward but somewhat problematic procedure was adopted. In this approach, a maximum RBE of the neutrons, RBEmax, is inferred from the experiments and is multiplied into the risk coefficient, a, for g-rays: an ¼ RBEmax a:
ð1Þ
This procedure has the serious weakness to be based not just on one extrapolation but actually on a product of two extrapolated numbers, RBEmax and a. This involves considerable uncertainty, permits widely different conclusions, and thus, invites fruitless controversy. A consideration of the numerical values can illustrate the problem. For the maximum RBE, RBEmax, the values that range from at least 10 to 100 have been quoted. For the photon risk coefficient, a typical lifetime attributable cancer risk estimate is 0.1/Gy. However, ICRP invokes a reduction factor of 2 and obtains 0.05/Gy [5]. Others, for example the United Nations Committee UNSCEAR [6], have considered a reduction factor between 2 and 10, which involves photon risk estimates down to 0.01/Gy. The resulting options are sufficiently broad to make the result almost meaningless. The pessimist’s view is then: an ¼ RBEmax a ¼ 100 0:1=Sv ¼ 10=Gy
ð2Þ
while the optimist might choose: an ¼ RBEmax a ¼ 10 0:01=Sv ¼ 0:1=Gy:
ð3Þ
Less extreme assessments lie somewhere in between, and the ICRP radiation-weighting factor for the neutrons [5] reflects such a balanced view. However, it is clear that any inference will remain judgmental. The issue would be academic if the neutrons were irrelevant to radiation protection, however, they are of increasing concern. Half of the effective dose in air travel is from neutrons, and the radiation exposure of the aircrews is a topic of growing interest, as well as the neutron exposures from the handling or transport of spent nuclear fuel. In Germany,
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this latter issue has in fact become a very hot political item. Extravagant claims of high neutron risks have contributed to the problem. In short, there are good reasons to ask whether there is a better way to deduce the risk factor for neutrons.
3. A more direct approach The diagram in Fig. 1 explains an alternative and simpler procedure that can replace the familiar approach [7]. All experimental evidence suggests that the dose relation is linear for neutrons. For grays, most radiobiological studies show upward curved dose relations as indicated in the diagram in terms of excess relative risk (ERR) although no curvature is seen in the solid cancer data of the A-bomb survivors. Thus, the effect of larger g-ray doses is fairly well known, while the initial slope of the g-ray curve is somewhat uncertain. However, there is no need to invoke the shape of the g-ray curve at low doses. It is sufficient to consider the rather well-defined g-ray effect at an intermediate reference dose D1, e.g., D1 = 1 Gy. One then requires the RBE of the neutrons against this fairly high reference dose. Let this RBE be termed as R1. It can be more reliably determined in animal experiments than the elusive low-dose extrapolation RBEmax. Experiments on the induction of non-lethal and lethal tumors in rats suggest R1 = 50 [8,9], and experiments on life shortening in mice suggest values closer to R1 = 20 [10,11]. Which of these values is more representative for late neutron effects in man is uncertain, but it appears reasonable to assume that the most plausible value lies in the range 20 –50.
Fig. 1. Schematic diagram of the dose dependence of the excess relative risk after an acute g-exposure and the dependence for fast neutrons that is inferred in terms of the relative biological effectiveness, R1, of the neutrons against the reference g-ray dose D1 = 1 Gy. The grey area covers the g-ray dependence to indicate the uncertainty at low doses. It brackets all possible dependencies from a simple linear dose relation with the reference slope c = ERR1/D1 (DDREF = 1) to a linear – quadratic dependence with the initial slope, a, six times smaller than the reference slope (DDREF = 6).
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If the excess relative risk ERR1 due to the acute g-ray dose D1 is known from an epidemiological study, then the risk coefficient for the neutrons, an, is the product of the reference slope, c = ERR1/D1, for the g-rays and the assumed neutron RBE, R1: an ¼ R1 c
0
reference slope0 for the c rays : c ¼ ERR1 =D1 :
ð4Þ
4. Application to the solid cancer mortality of the A-bomb survivors The A-bomb data are the major basis of g-ray risk estimates. In the familiar treatment, the neutrons are accounted for roughly in terms of a weighted dose, and the reference slope for the g-rays is determined by the ERR at the weighted dose of 1 Gy [12 – 14]. The neutron risk coefficient is then readily obtained by multiplication with R1. In reality, the issue is somewhat more complex because it is a premature conclusion that the A-bomb data are more or less representative for g-rays only. The neutron contribution to the absorbed dose is small, only about 11 mGy in a 1-Gy total absorbed dose [4]. However, if, for example, R1 is 35, then 30 mGy of neutrons have the same effect as 1 Gy of g-rays, and 11 mGy have 35% of the effect of 1 Gy of g-rays [7,15]. A detailed analysis can quantify the neutron contribution to the observed solid cancer excess mortality of the A-bomb survivors [16]. Consider first the conventional analysis. It assigns an RBE of w = 10 to the neutrons and makes reference to the colon dose. Both choices are inadequate. w = 10 is a very low weight factor to represent the neutron RBE, and reference to the colon, which is the deepest lying organ, is a poor choice because the organ-averaged neutron dose is actually twice as large as the colon dose [7]. It is not
Fig. 2. Dose dependence for solid cancer mortality according to the A-bomb data (1950 – 1990) and the conventional treatment in terms of a weighting factor, w = 10, and reference to the colon dose [16]. The inferred small effect contribution by the neutrons is indicated by the narrow shaded band. The dots and standard errors represent the fit to individual dose categories.
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surprising that these biased assumptions suggest a very small neutron contribution to the observed effect represented by the narrow dark shaded band in Fig. 2. The explicit analysis refers to the organ-averaged dose and considers RBE values, R1, between 20 and 50. With these more realistic assumptions, the effect attribution to neutrons is, of course, considerably larger. The result is given in Fig. 3. As shown for R1 = 35, the neutron contribution is now fairly substantial. For R1 = 50, it would be still somewhat larger, and it is important to note that the effect attributable to the g-rays is correspondingly smaller. Taking into account these considerations, it is now fairly simple to derive the neutron risk coefficient in its dependence on the assumed neutron RBE, R1. Fig. 4 gives the result in terms of the ERR for solid cancer mortality [7]. The coefficient increases with the assumed neutron RBE, but this increase is somewhat less than proportional because a higher attribution to the neutrons somewhat reduces the effect attribution to 1 Gy of grays. This is also represented in Fig. 4. The main conclusion is that the uncertainty of the neutron risk coefficient has reasonably narrowed down to about a factor of 2, which is a notable improvement in comparison to the factor of 100 that was mentioned at the outset. In fact, if one considers the doubtful reduction factor DDREF for the photons, one might be tempted to say that the risk coefficient for the neutrons is less uncertain than the risk coefficient for the photons. One widely discussed uncertainty with regard to neutrons is, of course, the possibility of a revision of the Hiroshima neutron doses. Since the publication of DS86, there have been indications that DS86 underestimates the neutron doses at larger distances, i.e., at low
Fig. 3. Dose dependence for solid cancer mortality according to the A-bomb data (1950 – 1990) and the explicit analysis in terms of an assumed RBE of the neutrons, R1, against 1 Gy of g-rays and reference to the organaveraged dose [16]. The inferred larger effect contribution by the neutrons is indicated by the shaded band for R1 = 35 (the two other solid lines indicate the cases R1 = 20 or 50).
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Fig. 4. The risk factor, an, for fast neutrons in terms of the excess relative risk, ERR/Gy, for solid cancer mortality [7]. The excess relative risk (ERR) is here taken to be an average for the age at exposure and the attained age model (see text). The lower curve represents the inferred reference slope, i.e., ERR from 1 Gy g-rays. The values are given in their dependence on the assumed neutron RBE, R1, versus the acute g-ray dose 1 Gy. The grey band represents the 95% confidence interval in the fit to the solid cancer mortality data.
doses. An NAS Committee [15] has published an interim report that suggests—on the basis of the determination of fast neutron fluence through Ni-63 measurements in Hiroshima copper samples [17]—that the current dosimetry revision will lead to much smaller changes in the neutron doses than had been indicated by the thermal neutron activation measurements [18]. Some correction may be required at low doses, but at a total dose of 1 Gy—and this is the reference dose in the present analysis—the DS86 doses are not going to change much. The present results are therefore essentially independent of the current dosimetry revision.
5. Comparison to the ICRP nominal risk coefficient A central issue in the current discussion on neutron risk—with considerable impact on the practice of radiation protection—is, of course, the validity of the ICRP nominal risk coefficient if applied to neutrons. The ICRP risk coefficient [5] is expressed not in terms of
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the excess relative risk, ERR, but in terms of the lifetime attributable risk. One must therefore translate the ERR in the diagram for the risk coefficient into the lifetime attributable risk, LAR. In line with the conventions adopted by ICRP, one obtains for a working population [19]: LAR ¼ 0:11ERR:
ð5Þ
The values ERR/Gy = 8 and ERR/Gy = 16 that result (according to Fig. 4) to the neutron RBE of R1 = 20 and R1 = 50 correspond then to LAR/Gy = 0.9 and LAR/Gy = 1.8. ICRP gives the nominal solid cancer fatality risk coefficient 0.036/Sv for the occupational exposure [5]. Its radiation-weighting factor for neutrons has a maximal value around wR = 22 for fission energy neutrons [5]. Naively, one would use this factor to convert the risk estimate in terms of Sv to the risk estimate in terms of Gy, and this would provide the value: LAR=Gy ¼ 22 LAR=Sv ¼ 22 0:036 ¼ 0:8:
ð6Þ
The values 0.9 –1.8/Gy that result for the plausible range of neutron RBEs would then exceed the ICRP nominal risk coefficient. However, this numerical exercise would be erroneous. ICRP defines the neutron effective dose not as the product of the weighting factor, wR, and the neutron absorbed dose, i.e., the neutron tissue kerma. Instead, it applies the weighting factor to the mixture of the neutron and the g-ray dose that is caused by the neutrons incident on the human body [5]. This makes a substantial difference because at the most effective and most prevalent neutron energies, there is a considerable g-ray fraction [20] as shown in the diagram of Fig. 5. The ICRP radiation-weighting factor must, therefore, not be seen as representing a true neutron RBE. It represents an RBE of a mixed g-ray and neutron radiation. Once this difference is realized, it is fairly straightforward to derive the risk estimate for the unit neutron effective dose by summing the risk estimates for the g-ray and for the neutron component.
Fig. 5. The genuine neutron fraction, Fn, of the organ-weighted absorbed dose from a (anterior – posterior) neutron exposure (left ordinate – solid curve [20]) and the radiation-weighting factor, wR, (right ordinate – dashed curve [5]) in their dependence on neutron energy, En.
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Fig. 6. Lifetime solid cancer fatality risk (LAR/Sv) relative to the neutron effective dose for a working population. The values are given in their dependence on neutron energy, En. The solid curve results with R1 = 35. The grey band represents the possible values that result for R1 between 20 and 50. The assumed RBE values between 20 and 50 refer to the energy range 0.2 – 1 MeV where the neutrons are most effective. Outside this region, the values LAR/Sv need to be seen as conservative. For a population of all ages, roughly the same values are obtained in terms of the attained age model, while the age at exposure model provides values that are higher by a factor of 1.6. The current ICRP nominal risk coefficients are included for comparison as a dotted line (0.036/Sv, working population) and a dashed line (0.045/Sv, population of all ages).
Fig. 6 gives the result in terms of the shaded band. The values correspond to the assumed neutron RBE values between 20 and 50, which are realistic for the energy range 0.2– 1 MeV where the neutrons are most effective. Outside this energy range, the RBE values are lower, which makes the results conservative where the solid line is drawn lightly. It is seen that the present analysis provides a risk estimate for solid cancer mortality that slightly exceeds the ICRP nominal risk coefficient. The estimate agrees with the ICRP
Fig. 7. Lifetime attributable risk (LAR*/Sv) relative to the ambient dose equivalent of the neutrons (H*) in its dependence on neutron energy, En. The diagram is—apart from the difference between LAR/Sv and LAR*/Sv— analogous to Fig. 6.
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value for the fairly low energies that are of particular importance in moderated neutron spectra since they are typical for an occupational exposure or for a population exposure due to an accident as that in Tokaimura. The numerical risk estimates ought to be seen as guidelines and not as precise predictions. Any of the differences between the results that are obtained here and the current ICRP nominal risk coefficient are thus not very significant. An additional factor makes the difference even less essential. This is the fact that the neutron effective dose is, in practice, monitored in terms of the ambient dose equivalent, H* [21]. This operational quantity overestimates the effective dose at most neutron energies [22]. The ICRP risk coefficient is therefore (as shown in Fig. 7) strongly conservative against the risk coefficient of the neutrons relative to H*.
6. Conclusion The neutron risk coefficient that is derived from typical neutron RBE values and from the reliably known effect of larger doses on the A-bomb survivors is in remarkable agreement with the current ICRP nominal risk coefficient. Its numerical value is independent of the still somewhat controversial issue of the reduction factor DDREF for the photons, and it is also unlikely to be substantially affected by the outcome of the current revision of the A-bomb dosimetry. This conclusion is important since it may reduce some of the apprehension that has recently arisen with regard to neutron exposures from the handling and transport of nuclear fuel or from exposure in aviation. There are of course implications on risk modelling for g-rays. As has been suggested here, if the neutrons have had a higher contribution to the effects among the A-bomb survivors than previously assumed, the effect attribution to the g-rays is somewhat reduced. However, this is a separate issue and needs separate consideration.
References [1] R.C. Milton, T. Shohoji, Tentative 1965 radiation dose (TD65) estimation for atomic bomb survivors, ABCC Report TR, Radiation Research Effects Foundation, Hiroshima, 1968, pp. 1 – 68. [2] H.H. Rossi, A.M. Kellerer, The validity of risk estimates of leukemia incidence based on Japanese data, Radiat. Res. 58 (1974) 131 – 140. [3] H.H. Rossi, C.W. Mays, Leukemia risk from neutrons, Health Phys. 34 (1978) 353 – 360. [4] W.C. Roesch (Ed.), US – Japan Joint Reassessment of Atomic Bomb Radiation Dosimetry in Hiroshima and Nagasaki, vols. 1 and 2 RERF, Hiroshima, 1987. [5] International Commission on Radiological Protection, The 1990 recommendations of the International Commission on Radiological Protection, ICRP Publication 60, Ann. ICRP 21 (1 – 3) Pergamon, Oxford, 1991. [6] UNSCEAR, Sources and Effects of Ionizing Radiation, Report to the General Assembly, United Nations, New York, 1988, p. 39. [7] A.M. Kellerer, L. Walsh, Risk estimation for fast neutrons with regard to solid cancer (2001), submitted for publication. [8] J. Lafuma, D. Chmelevsky, J. Chameaud, M. Morin, R. Masse, A.M. Kellerer, Lung carcinomas in Sprague – Dawley rats after exposure to low doses of radon daughters, fission neutrons, or g-rays, Radiat. Res. 118 (1989) 230 – 245.
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[9] C. Wolf, J. Lafuma, R. Masse, M. Morin, A.M. Kellerer, Neutron RBE for tumors with high lethality in Sprague – Dawley rats, Radiat. Res., 2000. [10] B.A. Carnes, D. Grahn, J.F. Thomson, Dose – response modeling of life in a retrospective analysis of the combined data from the Janus program at Argonne National Laboratory, Radiat. Res. 119 (1989) 39 – 56. [11] V. Covelli, M. Coppola, V. Di Majo, S. Rebessi, B. Bassini, Tumor induction and life shortening in BC3F1 female mice at low doses of fast neutrons and X-rays, Radiat. Res. 113 (1989) 362 – 374. [12] D.A. Pierce, Y. Shimizu, D.L. Preston, M. Vaeth, K. Mabuchi, Studies of the mortality of atomic bomb survivors: report 12. Part I. Cancer, Radiat. Res. 146 (1996) 1 – 27. [13] D.E. Thompson, K. Mabuchi, E. Ron, M. Soda, M. Tokunaga, S. Ochikubo, S. Sugimoto, T. Ikeda, M. Terasaki, S. Izumi, D.L. Preston, Cancer incidence in atomic bomb survivors: Part II. Solid tumors, 1958 – 1987, Radiat. Res. 137 (1994) 17 – 67. [14] UNSCEAR, Sources and Effects of Ionizing Radiation, Annex I, Epidemiological Evaluation of RadiationInduced Cancer, vol. 2, United Nations, New York, 2000, pp. 297 – 450. [15] NAS/NRC, Status of the dosimetry for the Radiation Effects Research Foundation (DS86), Report of the Committee on Dosimetry for RERF, National Academy Press, Washington, DC, USA, 2001 (in press, available at http://www.nap.edu/catalog/10103.html). [16] A.M. Kellerer, L. Walsh, Risk coefficient for g-rays with regard to solid cancer, Technical Report, SBILMU-216/6.2001. [17] W. Ru¨hm, K. Knie, G. Rugel, A.A. Marchetti, T. Faestermann, C. Wallner, J.E. McAninch, T. Straume, G. Korschinek, Accelerator mass spectrometry of 63NI at the Munich tandem laboratory for estimating fast neutron fluences from the Hiroshima atomic bomb, Health Phys. 79 (2000) 358 – 364. [18] T. Straume, S.D. Egbert, W.A. Woolson, R.C. Finkle, P.W. Kubik, H.E. Grove, P. Sharma, M. Hoshi, Neutron discrepancies in the DS86 dosimetry system, Health Phys. 63 (1992) 421 – 426. [19] A.M. Kellerer, L. Walsh, On the Conversion of Solid Cancer ERR into Lifetime Attributable Risk, Technical Report, SBI-LMU-214/4.2001. [20] G. Dietze, B.R.L. Siebert, Photon and neutron dose contributions and mean quality factors in phantom of different size irradiated by monoenergetic neutrons, Radiat. Res. 140 (1994) 130 – 133. [21] International Commission on Radiation Units and Measurements (ICRU), Quantities and Units in Radiation Protection Dosimetry, Report 51, 1993. [22] ICRP Publication 74, Conversion Coefficients for Use in Radiological Protection Against External Radiation, vol. 26, no. 3/4, Pergamon, 1996.
Risk estimates for fast neutrons and implications for radiation protection Albrecht M. Kellerer * Radiobiological Institute, University of Munich, Schillerstraße 42, 80336 Munich, Germany
Abstract The risks of low neutron doses are of increasing interest with regard to exposures in aviation, in the transport of nuclear fuel, or even in an accident as that in Tokaimura. In the absence of epidemiological information, the neutron risk coefficient is currently taken to be the product of two uncertain low-dose extrapolations, nominal risk coefficient for the photons and presumed maximum relative biological effectiveness of the neutrons. An approach is presented here that avoids the lowdose extrapolations and invokes, instead, the product of the excess risk from epidemiological observations at an intermediate reference dose of g-rays—here taken to be 1 Gy—and the assumed value, R1, of the neutron RBE against this reference dose. With R1 between 20 and 50 the solid, the cancer mortality data of the A-bomb survivors provide an excess relative risk (ERR) for the neutrons between 8 and 16/Gy. This result is converted into a risk coefficient in terms of the lifetime attributable risk (LAR) relative to the neutron effective dose as defined by ICRP. The result is at high neutron energies somewhat in excess of the current ICRP nominal risk factor, while it agrees with ICRP for the degraded fast neutron spectra that are of major pragmatic interest. The so-called Hiroshima neutron discrepancy will not influence the neutron risk estimate because any remaining uncertainty of the neutron doses in Hiroshima is minor at the reference dose of 1 Gy. D 2002 Elsevier Science B.V. All rights reserved. Keywords: Neutrons; RBE; Risk coefficient; Solid cancers; A-bomb survivors; Effective dose; Ambient dose equivalent
1. Introduction Neutrons are known to be far more effective than g-rays, particularly in small doses. However, this knowledge was derived exclusively from cell studies or animal experiments. No late effects from neutrons have been observed in man. *
Corresponding author. Tel.: +49-89-5996-818; fax: +49-89-5996-840. E-mail address: [email protected] (A.M. Kellerer).
0531-5131/02 D 2002 Elsevier Science B.V. All rights reserved. PII: S 0 5 3 1 - 5 1 3 1 ( 0 1 ) 0 0 7 6 1 - 0
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A.M. Kellerer / International Congress Series 1236 (2002) 3–12
On the basis of the former A-bomb dosimetry system, TD65 [1], it has been argued that much of the excess cancer rate in Hiroshima was due to neutrons [2,3]. However, this assumption led to a re-examination of the A-bomb dosimetry and then to the current dosimetry system, DS86 [4], which specified much lower neutron doses than the earlier system, TD65. It was then concluded, perhaps prematurely, that any effect contributed by the neutrons would be minor and that no direct information on the neutron risks could be derived from the A-bomb data.
2. The familiar estimation procedure In the absence of epidemiological evidence, it was realized that the neutron risk estimates would have to be derived by combining information on the effects of g-rays, with the radiobiological knowledge on the relative biological effectiveness of the neutrons. While there are (as will be seen) different approaches, a seemingly straightforward but somewhat problematic procedure was adopted. In this approach, a maximum RBE of the neutrons, RBEmax, is inferred from the experiments and is multiplied into the risk coefficient, a, for g-rays: an ¼ RBEmax a:
ð1Þ
This procedure has the serious weakness to be based not just on one extrapolation but actually on a product of two extrapolated numbers, RBEmax and a. This involves considerable uncertainty, permits widely different conclusions, and thus, invites fruitless controversy. A consideration of the numerical values can illustrate the problem. For the maximum RBE, RBEmax, the values that range from at least 10 to 100 have been quoted. For the photon risk coefficient, a typical lifetime attributable cancer risk estimate is 0.1/Gy. However, ICRP invokes a reduction factor of 2 and obtains 0.05/Gy [5]. Others, for example the United Nations Committee UNSCEAR [6], have considered a reduction factor between 2 and 10, which involves photon risk estimates down to 0.01/Gy. The resulting options are sufficiently broad to make the result almost meaningless. The pessimist’s view is then: an ¼ RBEmax a ¼ 100 0:1=Sv ¼ 10=Gy
ð2Þ
while the optimist might choose: an ¼ RBEmax a ¼ 10 0:01=Sv ¼ 0:1=Gy:
ð3Þ
Less extreme assessments lie somewhere in between, and the ICRP radiation-weighting factor for the neutrons [5] reflects such a balanced view. However, it is clear that any inference will remain judgmental. The issue would be academic if the neutrons were irrelevant to radiation protection, however, they are of increasing concern. Half of the effective dose in air travel is from neutrons, and the radiation exposure of the aircrews is a topic of growing interest, as well as the neutron exposures from the handling or transport of spent nuclear fuel. In Germany,
A.M. Kellerer / International Congress Series 1236 (2002) 3–12
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this latter issue has in fact become a very hot political item. Extravagant claims of high neutron risks have contributed to the problem. In short, there are good reasons to ask whether there is a better way to deduce the risk factor for neutrons.
3. A more direct approach The diagram in Fig. 1 explains an alternative and simpler procedure that can replace the familiar approach [7]. All experimental evidence suggests that the dose relation is linear for neutrons. For grays, most radiobiological studies show upward curved dose relations as indicated in the diagram in terms of excess relative risk (ERR) although no curvature is seen in the solid cancer data of the A-bomb survivors. Thus, the effect of larger g-ray doses is fairly well known, while the initial slope of the g-ray curve is somewhat uncertain. However, there is no need to invoke the shape of the g-ray curve at low doses. It is sufficient to consider the rather well-defined g-ray effect at an intermediate reference dose D1, e.g., D1 = 1 Gy. One then requires the RBE of the neutrons against this fairly high reference dose. Let this RBE be termed as R1. It can be more reliably determined in animal experiments than the elusive low-dose extrapolation RBEmax. Experiments on the induction of non-lethal and lethal tumors in rats suggest R1 = 50 [8,9], and experiments on life shortening in mice suggest values closer to R1 = 20 [10,11]. Which of these values is more representative for late neutron effects in man is uncertain, but it appears reasonable to assume that the most plausible value lies in the range 20 –50.
Fig. 1. Schematic diagram of the dose dependence of the excess relative risk after an acute g-exposure and the dependence for fast neutrons that is inferred in terms of the relative biological effectiveness, R1, of the neutrons against the reference g-ray dose D1 = 1 Gy. The grey area covers the g-ray dependence to indicate the uncertainty at low doses. It brackets all possible dependencies from a simple linear dose relation with the reference slope c = ERR1/D1 (DDREF = 1) to a linear – quadratic dependence with the initial slope, a, six times smaller than the reference slope (DDREF = 6).
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If the excess relative risk ERR1 due to the acute g-ray dose D1 is known from an epidemiological study, then the risk coefficient for the neutrons, an, is the product of the reference slope, c = ERR1/D1, for the g-rays and the assumed neutron RBE, R1: an ¼ R1 c
0
reference slope0 for the c rays : c ¼ ERR1 =D1 :
ð4Þ
4. Application to the solid cancer mortality of the A-bomb survivors The A-bomb data are the major basis of g-ray risk estimates. In the familiar treatment, the neutrons are accounted for roughly in terms of a weighted dose, and the reference slope for the g-rays is determined by the ERR at the weighted dose of 1 Gy [12 – 14]. The neutron risk coefficient is then readily obtained by multiplication with R1. In reality, the issue is somewhat more complex because it is a premature conclusion that the A-bomb data are more or less representative for g-rays only. The neutron contribution to the absorbed dose is small, only about 11 mGy in a 1-Gy total absorbed dose [4]. However, if, for example, R1 is 35, then 30 mGy of neutrons have the same effect as 1 Gy of g-rays, and 11 mGy have 35% of the effect of 1 Gy of g-rays [7,15]. A detailed analysis can quantify the neutron contribution to the observed solid cancer excess mortality of the A-bomb survivors [16]. Consider first the conventional analysis. It assigns an RBE of w = 10 to the neutrons and makes reference to the colon dose. Both choices are inadequate. w = 10 is a very low weight factor to represent the neutron RBE, and reference to the colon, which is the deepest lying organ, is a poor choice because the organ-averaged neutron dose is actually twice as large as the colon dose [7]. It is not
Fig. 2. Dose dependence for solid cancer mortality according to the A-bomb data (1950 – 1990) and the conventional treatment in terms of a weighting factor, w = 10, and reference to the colon dose [16]. The inferred small effect contribution by the neutrons is indicated by the narrow shaded band. The dots and standard errors represent the fit to individual dose categories.
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surprising that these biased assumptions suggest a very small neutron contribution to the observed effect represented by the narrow dark shaded band in Fig. 2. The explicit analysis refers to the organ-averaged dose and considers RBE values, R1, between 20 and 50. With these more realistic assumptions, the effect attribution to neutrons is, of course, considerably larger. The result is given in Fig. 3. As shown for R1 = 35, the neutron contribution is now fairly substantial. For R1 = 50, it would be still somewhat larger, and it is important to note that the effect attributable to the g-rays is correspondingly smaller. Taking into account these considerations, it is now fairly simple to derive the neutron risk coefficient in its dependence on the assumed neutron RBE, R1. Fig. 4 gives the result in terms of the ERR for solid cancer mortality [7]. The coefficient increases with the assumed neutron RBE, but this increase is somewhat less than proportional because a higher attribution to the neutrons somewhat reduces the effect attribution to 1 Gy of grays. This is also represented in Fig. 4. The main conclusion is that the uncertainty of the neutron risk coefficient has reasonably narrowed down to about a factor of 2, which is a notable improvement in comparison to the factor of 100 that was mentioned at the outset. In fact, if one considers the doubtful reduction factor DDREF for the photons, one might be tempted to say that the risk coefficient for the neutrons is less uncertain than the risk coefficient for the photons. One widely discussed uncertainty with regard to neutrons is, of course, the possibility of a revision of the Hiroshima neutron doses. Since the publication of DS86, there have been indications that DS86 underestimates the neutron doses at larger distances, i.e., at low
Fig. 3. Dose dependence for solid cancer mortality according to the A-bomb data (1950 – 1990) and the explicit analysis in terms of an assumed RBE of the neutrons, R1, against 1 Gy of g-rays and reference to the organaveraged dose [16]. The inferred larger effect contribution by the neutrons is indicated by the shaded band for R1 = 35 (the two other solid lines indicate the cases R1 = 20 or 50).
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Fig. 4. The risk factor, an, for fast neutrons in terms of the excess relative risk, ERR/Gy, for solid cancer mortality [7]. The excess relative risk (ERR) is here taken to be an average for the age at exposure and the attained age model (see text). The lower curve represents the inferred reference slope, i.e., ERR from 1 Gy g-rays. The values are given in their dependence on the assumed neutron RBE, R1, versus the acute g-ray dose 1 Gy. The grey band represents the 95% confidence interval in the fit to the solid cancer mortality data.
doses. An NAS Committee [15] has published an interim report that suggests—on the basis of the determination of fast neutron fluence through Ni-63 measurements in Hiroshima copper samples [17]—that the current dosimetry revision will lead to much smaller changes in the neutron doses than had been indicated by the thermal neutron activation measurements [18]. Some correction may be required at low doses, but at a total dose of 1 Gy—and this is the reference dose in the present analysis—the DS86 doses are not going to change much. The present results are therefore essentially independent of the current dosimetry revision.
5. Comparison to the ICRP nominal risk coefficient A central issue in the current discussion on neutron risk—with considerable impact on the practice of radiation protection—is, of course, the validity of the ICRP nominal risk coefficient if applied to neutrons. The ICRP risk coefficient [5] is expressed not in terms of
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the excess relative risk, ERR, but in terms of the lifetime attributable risk. One must therefore translate the ERR in the diagram for the risk coefficient into the lifetime attributable risk, LAR. In line with the conventions adopted by ICRP, one obtains for a working population [19]: LAR ¼ 0:11ERR:
ð5Þ
The values ERR/Gy = 8 and ERR/Gy = 16 that result (according to Fig. 4) to the neutron RBE of R1 = 20 and R1 = 50 correspond then to LAR/Gy = 0.9 and LAR/Gy = 1.8. ICRP gives the nominal solid cancer fatality risk coefficient 0.036/Sv for the occupational exposure [5]. Its radiation-weighting factor for neutrons has a maximal value around wR = 22 for fission energy neutrons [5]. Naively, one would use this factor to convert the risk estimate in terms of Sv to the risk estimate in terms of Gy, and this would provide the value: LAR=Gy ¼ 22 LAR=Sv ¼ 22 0:036 ¼ 0:8:
ð6Þ
The values 0.9 –1.8/Gy that result for the plausible range of neutron RBEs would then exceed the ICRP nominal risk coefficient. However, this numerical exercise would be erroneous. ICRP defines the neutron effective dose not as the product of the weighting factor, wR, and the neutron absorbed dose, i.e., the neutron tissue kerma. Instead, it applies the weighting factor to the mixture of the neutron and the g-ray dose that is caused by the neutrons incident on the human body [5]. This makes a substantial difference because at the most effective and most prevalent neutron energies, there is a considerable g-ray fraction [20] as shown in the diagram of Fig. 5. The ICRP radiation-weighting factor must, therefore, not be seen as representing a true neutron RBE. It represents an RBE of a mixed g-ray and neutron radiation. Once this difference is realized, it is fairly straightforward to derive the risk estimate for the unit neutron effective dose by summing the risk estimates for the g-ray and for the neutron component.
Fig. 5. The genuine neutron fraction, Fn, of the organ-weighted absorbed dose from a (anterior – posterior) neutron exposure (left ordinate – solid curve [20]) and the radiation-weighting factor, wR, (right ordinate – dashed curve [5]) in their dependence on neutron energy, En.
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Fig. 6. Lifetime solid cancer fatality risk (LAR/Sv) relative to the neutron effective dose for a working population. The values are given in their dependence on neutron energy, En. The solid curve results with R1 = 35. The grey band represents the possible values that result for R1 between 20 and 50. The assumed RBE values between 20 and 50 refer to the energy range 0.2 – 1 MeV where the neutrons are most effective. Outside this region, the values LAR/Sv need to be seen as conservative. For a population of all ages, roughly the same values are obtained in terms of the attained age model, while the age at exposure model provides values that are higher by a factor of 1.6. The current ICRP nominal risk coefficients are included for comparison as a dotted line (0.036/Sv, working population) and a dashed line (0.045/Sv, population of all ages).
Fig. 6 gives the result in terms of the shaded band. The values correspond to the assumed neutron RBE values between 20 and 50, which are realistic for the energy range 0.2– 1 MeV where the neutrons are most effective. Outside this energy range, the RBE values are lower, which makes the results conservative where the solid line is drawn lightly. It is seen that the present analysis provides a risk estimate for solid cancer mortality that slightly exceeds the ICRP nominal risk coefficient. The estimate agrees with the ICRP
Fig. 7. Lifetime attributable risk (LAR*/Sv) relative to the ambient dose equivalent of the neutrons (H*) in its dependence on neutron energy, En. The diagram is—apart from the difference between LAR/Sv and LAR*/Sv— analogous to Fig. 6.
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value for the fairly low energies that are of particular importance in moderated neutron spectra since they are typical for an occupational exposure or for a population exposure due to an accident as that in Tokaimura. The numerical risk estimates ought to be seen as guidelines and not as precise predictions. Any of the differences between the results that are obtained here and the current ICRP nominal risk coefficient are thus not very significant. An additional factor makes the difference even less essential. This is the fact that the neutron effective dose is, in practice, monitored in terms of the ambient dose equivalent, H* [21]. This operational quantity overestimates the effective dose at most neutron energies [22]. The ICRP risk coefficient is therefore (as shown in Fig. 7) strongly conservative against the risk coefficient of the neutrons relative to H*.
6. Conclusion The neutron risk coefficient that is derived from typical neutron RBE values and from the reliably known effect of larger doses on the A-bomb survivors is in remarkable agreement with the current ICRP nominal risk coefficient. Its numerical value is independent of the still somewhat controversial issue of the reduction factor DDREF for the photons, and it is also unlikely to be substantially affected by the outcome of the current revision of the A-bomb dosimetry. This conclusion is important since it may reduce some of the apprehension that has recently arisen with regard to neutron exposures from the handling and transport of nuclear fuel or from exposure in aviation. There are of course implications on risk modelling for g-rays. As has been suggested here, if the neutrons have had a higher contribution to the effects among the A-bomb survivors than previously assumed, the effect attribution to the g-rays is somewhat reduced. However, this is a separate issue and needs separate consideration.
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