Recommended citation
ICRP, 2021. Cancer risk from exposure to plutonium and uranium. ICRP Publication 150. Ann. ICRP 50(4).
Authors on behalf of ICRP
M. Tirmarche, I. Apostoaei, E. Blanchardon, E.D. Ellis, E. Gilbert, J.D. Harrison, D. Laurier, J.W. Marsh, M. Sokolnikov, R. Wakeford, S. Zhivin
Abstract - The objective of this publication is to provide a detailed review of results from recent epidemiological studies on the risk of cancer from exposure to plutonium and uranium, and how these results relate to the assumptions currently used for protection against alpha radiation. For plutonium, the two main studies are of the cohorts of workers employed at the nuclear installations at Mayak in the Russian Federation and at Sellafield in the UK. The analysis of the Mayak worker cohort provides an estimate of the slope of the dose–response curve for the risk of lung cancer, while at lower levels of plutonium exposure, the Sellafield worker cohort provides results that, within relatively large confidence intervals, are consistent with those for the Mayak worker cohort. Results from the Mayak worker cohort also show an association between plutonium exposure and the risk of liver and bone cancers, but not the risk of leukaemia. Lifetime excess risk of lung cancer mortality has been calculated for scenarios of acute and chronic inhalation of plutonium nitrate and plutonium oxide, similar to work performed previously for radon and its decay products in ICRP Publication 115. Estimated lifetime excess risk of lung cancer mortality per unit absorbed dose is close to that derived from miner studies for exposure to radon and its progeny, and is compatible with the assumption of a radiation weighting factor of 20 for alpha particles. Epidemiological studies of the risk of cancer associated with uranium exposure have been conducted among cohorts of European and North American workers involved in the nuclear fuel cycle. Current results do not allow the reliable derivation of dose–risk models for uranium for any cancer type. Continuation of efforts to improve dose assessment associated with plutonium and uranium exposure is recommended for future research.
© 2021 ICRP. Published by SAGE.
Keywords: Plutonium; Uranium; Alpha emitter; Epidemiology; Cancer; Health risk.
Key Points
This publication complements the review of risk from exposure to radon and its decay products given in Publication 115 (ICRP, 2010).
For plutonium, the cohorts of workers from Mayak in the Russian Federation and from Sellafield in the UK provide quantitative information on the risk of lung cancer, with the Mayak worker cohort also indicating associations with the risk of liver and bone cancers, but not with the risk of leukaemia. Most of the data for lung cancer relate to male smokers, with limited information for other groups.
The lifetime excess risk of lung cancer mortality per unit absorbed dose to the lung attributable to acute and chronic exposures to plutonium nitrate and oxide varies between 1.4 and 1.7 per 10,000 individuals per mGy. These values are similar to those derived from miner studies for exposure to radon and its progeny.
Comparing the lifetime excess risk of lung cancer mortality calculated for plutonium and radon progeny exposures with that for external gamma irradiation suggests a biological effectiveness of alpha particles relative to high-energy photons that is compatible with the radiation weighting factor of 20 assumed for alpha particles.
However, applying no dose and dose-rate effectiveness factor to the lifetime risk derived from the Japanese Life Span Study would suggest relative biological effectiveness of approximately 7–8. . Epidemiological studies of uranium exposure remain insufficient to provide reliable estimates of risk due to limits in dose reconstruction.
Executive Summary
1. Objectives
(a) In the current radiological protection system, estimation of radiation risk and detriment is primarily based on the risks observed in the Life Span Study cohort of the Japanese atomic bomb survivors, who were exposed at a high dose rate, mainly to an external source of gamma rays. It is assumed that these observed risk estimates can also be applied to different situations of exposure, such as internal contamination by radionuclides emitting alpha radiation, leading to protracted and heterogeneous irradiation, once account is taken of the relative biological effectiveness of alpha particles compared with low-level exposure to gamma rays, and of the organs/ tissues irradiated.
(b) The results of several epidemiological studies reported over the last two decades allow the direct estimation of the risk of cancer related to exposure to alpha particle-emitting radionuclides. A critical analysis of these results can be used to evaluate the validity of the assumptions applied to protection against alpha emitters.
(c) This publication provides a detailed review of results from recent epidemiological studies of the risk of cancer and occupational exposure to isotopes of plutonium (mainly 238Pu, 239Pu, and 240Pu) and uranium (mainly 234U, 235U, and 238U). It updates previous reviews published by national and international organisations, specifically the Fourth Committee on Biological Effects of Ionizing Radiation (BEIR IV) Report of the US National Research Council (NRC, 1988), the International Agency for Research on Cancer monograph on internal emitters (IARC, 2012), and the United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR) 2016 Report on the biological effects of uranium (UNSCEAR, 2017). The present publication constitutes the first comprehensive review of health risks associated with plutonium exposure to be published in over 30 years.
(d) This publication presents calculations of the lifetime excess risk of lung cancer mortality associated with example scenarios of plutonium inhalation, similar to those performed previously for radon and its decay products in Publication 115 (ICRP, 2010). It discusses the uncertainties associated with these results, and their potential impact for radiological protection.
2. Methodology used
(e) This publication focuses essentially on epidemiological studies published since 2000 in which organ-/tissue-specific dose estimates are based on individual monitoring of internal exposure to plutonium or uranium. Individual annual exposure data, long duration of health surveillance in the cohort, and validation of the dosimetric models used for individual organ-/tissue-specific dose assessment were the major criteria considered for inclusion of a study in the analysis of lifetime risk. Consequently, results contributing to this analysis derive from a limited number of cohorts.
(f) For plutonium, several studies have been performed in North America, Europe, and Russia. One joint case–control study has been performed in Europe, but was limited by its size. The two main studies are the cohorts of workers employed at the nuclear installations at Mayak in the Russian Federation and at Sellafield in the UK. Assessments of intakes and organ-/tissue-specific doses for Mayak workers arising from the inhalation of plutonium have been based primarily on the interpretation of measurements of urinary excretion, taking account of workers’ occupational histories and the physicochemical forms of the inhaled plutonium aerosols. Results from autopsy data have also been used to determine model parameter values. There has been a progression of biokinetic and dosimetric models used for this purpose over the last 20 years, most recently applying the methodology of the Commission. This publication details the recent Mayak Worker Dosimetry Systems (MWDS-2008 and MWDS-2013) and the system developed for the joint analysis of Mayak and Sellafield plutonium workers as part of a European Union SOLO (epidemiological studies of exposed Southern Urals populations) project.
(g) The assessment of uranium-specific doses for workers employed in the nuclear fuel cycle (processing, concentration, enrichment, and reprocessing operations) is difficult due to the relatively fast clearance of uranium from blood circulation, variability of exposure to uranium compounds, and differences in the methods used to monitor internal exposure. The solubility of the uranium compounds to which workers are exposed is a particularly important parameter in determining lung doses from bioassay data. Cohorts of uranium miners were not considered in this publication, as they were discussed extensively in Publication 115 (ICRP, 2010), and the major risk of lung cancer identified in these cohorts is due to radon and its decay products.
3. Review of epidemiological results
(h) The epidemiological evidence on risks associated with plutonium is less extensive than that for radon and its progeny. Indeed, the first epidemiological results from underground hard-rock miner studies were published at the end of the 1960s, whereas most of the results related to plutonium were published after the 1990s. Furthermore, the number of studies providing results on risks associated with plutonium exposure is more limited than for radon progeny. In addition, the assessment of doses due to plutonium exposure is more complicated due to the chemical nature of plutonium compounds, and the retrospective reconstruction of plutonium doses from bioassay measurements.
(i) Risk of lung cancer resulting from plutonium exposure has been quantified through extensive study of the Russian Mayak workers, which includes a wide range of exposure levels. Risks at lower levels of plutonium exposure can be complemented by analysing other cohorts in Europe and North America. One of the major risks related to plutonium exposure is lung cancer. Several successive analyses of the Mayak worker cohort, based on different dosimetry systems and periods of follow-up, have provided estimates of the dose–response relationship. Estimates of the risk of lung cancer for Mayak workers are compatible with estimates obtained in two European studies published in 2017, but which have relatively wide confidence intervals. Much of the evidence derives from male smokers. The impact of statistical power, uncertainty in dose estimates, and co-factors (e.g. tobacco smoking) that may influence cancer development are considered, together with alternative dosimetric approaches.
(j) Results from the Mayak worker cohort also suggest an association between plutonium exposure and risks of liver and bone cancers, although data are limited. There is no consistent evidence of a positive dose–response relationship between the risk of leukaemia and plutonium exposure.
(k) Epidemiological studies of the risk of cancer associated with uranium exposure are primarily of cohorts of workers exposed to different chemical forms of uranium. Published studies are collated and evaluated, but most do not provide information that fulfils all the criteria mentioned above for the estimation of risks specific to uranium exposure. In recent years, several studies have been published using improved organ-/tissue-specific dose calculations, but they remain inconclusive because statistical power was limited and some of the information needed to reconstruct doses was not recorded in the past. Therefore, at present, it is not possible to quantify the risk of cancer per organ-/tissue-specific dose of uranium on the basis of the published studies.
(l) A few recently published studies have also considered possible health effects other than cancer, mainly circulatory diseases (Annex A). Some results are suggestive of an association between plutonium or uranium exposure and increased risk of circulatory diseases, especially results from the Mayak worker cohort. However, at present, these studies do not permit definitive conclusions on the existence of noncancer diseases associated with internal exposure to plutonium or uranium.
4. Quantification of the lifetime risk of lung cancer associated with plutonium exposure
(m) It is now possible to estimate the lifetime excess risk of lung cancer following inhalation of plutonium directly from epidemiological studies of plutonium workers. Calculations have been performed for illustrative scenarios with a total plutonium intake of 1 Bq, assuming either an acute inhalation event at 20 years of age or chronic inhalation at 20–29 years of age of either insoluble plutonium oxide or soluble plutonium nitrate. Lung doses were calculated using models from Publication 141 (ICRP, 2019). Lifetime risk was calculated using ICRP baseline rates for a composite Euro-American male population, as provided in Publication 103 (2007), and the risk model derived from the SOLO project analysis of Gillies et al. (2017). These unitary intake scenarios should be considered as examples, ignoring the impact of variations in important factors such as smoking, to provide an estimated order of magnitude of risk and to illustrate variations in dose and risk for the inhalation of plutonium.
(n) For the same intake, the cumulative doses to lung tissues from plutonium oxide are higher than those from plutonium nitrate, but the lifetime excess risk of lung cancer mortality per mGy varies little, with estimates between 1.4 and 1.7 per 10,000 persons, depending on the solubility (plutonium oxide or plutonium nitrate) and exposure rate (acute or chronic intake). In comparison, the lifetime baseline risk of lung cancer mortality is 631 per 10,000 persons for a Euro-American male population.
(o) For comparison, exposure to 222Rn progeny under the scenario considered in Publication 115 (ICRP, 2010) of 7.1 mJ h m-3 (2 working-level months) per year from 18 to 64 years of age, when converted to lung dose, leads to a lifetime excess risk of lung cancer mortality per mGy of 1.6 per 10,000 persons. 5. Implications for radiological protection and future research
(p) A comparison of the lifetime excess risk of lung cancer mortality from exposure to an external source of gamma radiation (based on the Life Span Study of the Japanese atomic bomb survivors) and from internal exposure to plutonium (based on the Mayak workers study) indicates that, for the same absorbed dose to the lung and dose distribution, the risks from plutonium exposure are larger than those from external gamma exposure by a factor of approximately 16. The risk for radon progeny exposure appears to be consistent with that from plutonium exposure, and larger than that from external gamma exposure by a factor of approximately 14, despite the very different distribution of alpha-particle dose within the lung.
(q) These comparisons suggest a biological effectiveness of alpha particles relative to high-energy photons of approximately 14–16 for lung cancer. These values are compatible with the current radiation weighting factor, wR, of 20 used by ICRP for alpha particles in the calculation of equivalent and effective doses (ICRP, 2007).
(r) It should be noted that this comparison is based on lung absorbed dose and lifetime excess risk of lung cancer mortality, with application of a dose and dose-rate effectiveness factor (DDREF) of 2 to the risk derived from the Japanese Life Span Study. Not applying a DDREF would lead to relative biological effectiveness of approximately 7–8 for lung cancer. Also, care has to be taken in making comparisons with wR as the latter is intended to embrace the risk of all stochastic effects, whereas lung cancer mortality alone is considered in the present calculations. Further, it was considered premature to quantify lifetime excess risks for bone and liver cancers, for which associations have also been demonstrated for plutonium, and different relative biological effectiveness values for alpha radiation may apply for these cancer types.
(s) Further research is needed to improve the assessment of health risks associated with plutonium or uranium exposure in epidemiology, dosimetry, and risk modelling. Uncertainties associated with plutonium and uranium exposure and dose reconstruction are substantial, and inhalation of different chemical forms leads to very different cumulative organ-/tissue-specific absorbed doses. For lung cancer, a better determination of the distribution in the different parts of the lung is important. Important efforts have been made in recent years to improve dose assessment and to consider the potential impact of uncertainties on risk estimates, and should be maintained in the future. Also, extension of existing cohorts and combined analyses of data are needed to increase power, and allow improved estimation of the risks associated with plutonium and uranium exposures. In addition, better consideration of the effect of smoking in future analyses is highly desirable. For uranium, more information on the intake of different chemical forms is required. Future research may better characterise the risks associated with alpha particles emitted by plutonium for cancer induction in organs/tissues other than the lung.
ICRP, 2021. Cancer risk from exposure to plutonium and uranium. ICRP Publication 150. Ann. ICRP 50(4).
Authors on behalf of ICRP
M. Tirmarche, I. Apostoaei, E. Blanchardon, E.D. Ellis, E. Gilbert, J.D. Harrison, D. Laurier, J.W. Marsh, M. Sokolnikov, R. Wakeford, S. Zhivin
Abstract - The objective of this publication is to provide a detailed review of results from recent epidemiological studies on the risk of cancer from exposure to plutonium and uranium, and how these results relate to the assumptions currently used for protection against alpha radiation. For plutonium, the two main studies are of the cohorts of workers employed at the nuclear installations at Mayak in the Russian Federation and at Sellafield in the UK. The analysis of the Mayak worker cohort provides an estimate of the slope of the dose–response curve for the risk of lung cancer, while at lower levels of plutonium exposure, the Sellafield worker cohort provides results that, within relatively large confidence intervals, are consistent with those for the Mayak worker cohort. Results from the Mayak worker cohort also show an association between plutonium exposure and the risk of liver and bone cancers, but not the risk of leukaemia. Lifetime excess risk of lung cancer mortality has been calculated for scenarios of acute and chronic inhalation of plutonium nitrate and plutonium oxide, similar to work performed previously for radon and its decay products in ICRP Publication 115. Estimated lifetime excess risk of lung cancer mortality per unit absorbed dose is close to that derived from miner studies for exposure to radon and its progeny, and is compatible with the assumption of a radiation weighting factor of 20 for alpha particles. Epidemiological studies of the risk of cancer associated with uranium exposure have been conducted among cohorts of European and North American workers involved in the nuclear fuel cycle. Current results do not allow the reliable derivation of dose–risk models for uranium for any cancer type. Continuation of efforts to improve dose assessment associated with plutonium and uranium exposure is recommended for future research.
© 2021 ICRP. Published by SAGE.
Keywords: Plutonium; Uranium; Alpha emitter; Epidemiology; Cancer; Health risk.
Key Points
This publication complements the review of risk from exposure to radon and its decay products given in Publication 115 (ICRP, 2010).
For plutonium, the cohorts of workers from Mayak in the Russian Federation and from Sellafield in the UK provide quantitative information on the risk of lung cancer, with the Mayak worker cohort also indicating associations with the risk of liver and bone cancers, but not with the risk of leukaemia. Most of the data for lung cancer relate to male smokers, with limited information for other groups.
The lifetime excess risk of lung cancer mortality per unit absorbed dose to the lung attributable to acute and chronic exposures to plutonium nitrate and oxide varies between 1.4 and 1.7 per 10,000 individuals per mGy. These values are similar to those derived from miner studies for exposure to radon and its progeny.
Comparing the lifetime excess risk of lung cancer mortality calculated for plutonium and radon progeny exposures with that for external gamma irradiation suggests a biological effectiveness of alpha particles relative to high-energy photons that is compatible with the radiation weighting factor of 20 assumed for alpha particles.
However, applying no dose and dose-rate effectiveness factor to the lifetime risk derived from the Japanese Life Span Study would suggest relative biological effectiveness of approximately 7–8. . Epidemiological studies of uranium exposure remain insufficient to provide reliable estimates of risk due to limits in dose reconstruction.
Executive Summary
1. Objectives
(a) In the current radiological protection system, estimation of radiation risk and detriment is primarily based on the risks observed in the Life Span Study cohort of the Japanese atomic bomb survivors, who were exposed at a high dose rate, mainly to an external source of gamma rays. It is assumed that these observed risk estimates can also be applied to different situations of exposure, such as internal contamination by radionuclides emitting alpha radiation, leading to protracted and heterogeneous irradiation, once account is taken of the relative biological effectiveness of alpha particles compared with low-level exposure to gamma rays, and of the organs/ tissues irradiated.
(b) The results of several epidemiological studies reported over the last two decades allow the direct estimation of the risk of cancer related to exposure to alpha particle-emitting radionuclides. A critical analysis of these results can be used to evaluate the validity of the assumptions applied to protection against alpha emitters.
(c) This publication provides a detailed review of results from recent epidemiological studies of the risk of cancer and occupational exposure to isotopes of plutonium (mainly 238Pu, 239Pu, and 240Pu) and uranium (mainly 234U, 235U, and 238U). It updates previous reviews published by national and international organisations, specifically the Fourth Committee on Biological Effects of Ionizing Radiation (BEIR IV) Report of the US National Research Council (NRC, 1988), the International Agency for Research on Cancer monograph on internal emitters (IARC, 2012), and the United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR) 2016 Report on the biological effects of uranium (UNSCEAR, 2017). The present publication constitutes the first comprehensive review of health risks associated with plutonium exposure to be published in over 30 years.
(d) This publication presents calculations of the lifetime excess risk of lung cancer mortality associated with example scenarios of plutonium inhalation, similar to those performed previously for radon and its decay products in Publication 115 (ICRP, 2010). It discusses the uncertainties associated with these results, and their potential impact for radiological protection.
2. Methodology used
(e) This publication focuses essentially on epidemiological studies published since 2000 in which organ-/tissue-specific dose estimates are based on individual monitoring of internal exposure to plutonium or uranium. Individual annual exposure data, long duration of health surveillance in the cohort, and validation of the dosimetric models used for individual organ-/tissue-specific dose assessment were the major criteria considered for inclusion of a study in the analysis of lifetime risk. Consequently, results contributing to this analysis derive from a limited number of cohorts.
(f) For plutonium, several studies have been performed in North America, Europe, and Russia. One joint case–control study has been performed in Europe, but was limited by its size. The two main studies are the cohorts of workers employed at the nuclear installations at Mayak in the Russian Federation and at Sellafield in the UK. Assessments of intakes and organ-/tissue-specific doses for Mayak workers arising from the inhalation of plutonium have been based primarily on the interpretation of measurements of urinary excretion, taking account of workers’ occupational histories and the physicochemical forms of the inhaled plutonium aerosols. Results from autopsy data have also been used to determine model parameter values. There has been a progression of biokinetic and dosimetric models used for this purpose over the last 20 years, most recently applying the methodology of the Commission. This publication details the recent Mayak Worker Dosimetry Systems (MWDS-2008 and MWDS-2013) and the system developed for the joint analysis of Mayak and Sellafield plutonium workers as part of a European Union SOLO (epidemiological studies of exposed Southern Urals populations) project.
(g) The assessment of uranium-specific doses for workers employed in the nuclear fuel cycle (processing, concentration, enrichment, and reprocessing operations) is difficult due to the relatively fast clearance of uranium from blood circulation, variability of exposure to uranium compounds, and differences in the methods used to monitor internal exposure. The solubility of the uranium compounds to which workers are exposed is a particularly important parameter in determining lung doses from bioassay data. Cohorts of uranium miners were not considered in this publication, as they were discussed extensively in Publication 115 (ICRP, 2010), and the major risk of lung cancer identified in these cohorts is due to radon and its decay products.
3. Review of epidemiological results
(h) The epidemiological evidence on risks associated with plutonium is less extensive than that for radon and its progeny. Indeed, the first epidemiological results from underground hard-rock miner studies were published at the end of the 1960s, whereas most of the results related to plutonium were published after the 1990s. Furthermore, the number of studies providing results on risks associated with plutonium exposure is more limited than for radon progeny. In addition, the assessment of doses due to plutonium exposure is more complicated due to the chemical nature of plutonium compounds, and the retrospective reconstruction of plutonium doses from bioassay measurements.
(i) Risk of lung cancer resulting from plutonium exposure has been quantified through extensive study of the Russian Mayak workers, which includes a wide range of exposure levels. Risks at lower levels of plutonium exposure can be complemented by analysing other cohorts in Europe and North America. One of the major risks related to plutonium exposure is lung cancer. Several successive analyses of the Mayak worker cohort, based on different dosimetry systems and periods of follow-up, have provided estimates of the dose–response relationship. Estimates of the risk of lung cancer for Mayak workers are compatible with estimates obtained in two European studies published in 2017, but which have relatively wide confidence intervals. Much of the evidence derives from male smokers. The impact of statistical power, uncertainty in dose estimates, and co-factors (e.g. tobacco smoking) that may influence cancer development are considered, together with alternative dosimetric approaches.
(j) Results from the Mayak worker cohort also suggest an association between plutonium exposure and risks of liver and bone cancers, although data are limited. There is no consistent evidence of a positive dose–response relationship between the risk of leukaemia and plutonium exposure.
(k) Epidemiological studies of the risk of cancer associated with uranium exposure are primarily of cohorts of workers exposed to different chemical forms of uranium. Published studies are collated and evaluated, but most do not provide information that fulfils all the criteria mentioned above for the estimation of risks specific to uranium exposure. In recent years, several studies have been published using improved organ-/tissue-specific dose calculations, but they remain inconclusive because statistical power was limited and some of the information needed to reconstruct doses was not recorded in the past. Therefore, at present, it is not possible to quantify the risk of cancer per organ-/tissue-specific dose of uranium on the basis of the published studies.
(l) A few recently published studies have also considered possible health effects other than cancer, mainly circulatory diseases (Annex A). Some results are suggestive of an association between plutonium or uranium exposure and increased risk of circulatory diseases, especially results from the Mayak worker cohort. However, at present, these studies do not permit definitive conclusions on the existence of noncancer diseases associated with internal exposure to plutonium or uranium.
4. Quantification of the lifetime risk of lung cancer associated with plutonium exposure
(m) It is now possible to estimate the lifetime excess risk of lung cancer following inhalation of plutonium directly from epidemiological studies of plutonium workers. Calculations have been performed for illustrative scenarios with a total plutonium intake of 1 Bq, assuming either an acute inhalation event at 20 years of age or chronic inhalation at 20–29 years of age of either insoluble plutonium oxide or soluble plutonium nitrate. Lung doses were calculated using models from Publication 141 (ICRP, 2019). Lifetime risk was calculated using ICRP baseline rates for a composite Euro-American male population, as provided in Publication 103 (2007), and the risk model derived from the SOLO project analysis of Gillies et al. (2017). These unitary intake scenarios should be considered as examples, ignoring the impact of variations in important factors such as smoking, to provide an estimated order of magnitude of risk and to illustrate variations in dose and risk for the inhalation of plutonium.
(n) For the same intake, the cumulative doses to lung tissues from plutonium oxide are higher than those from plutonium nitrate, but the lifetime excess risk of lung cancer mortality per mGy varies little, with estimates between 1.4 and 1.7 per 10,000 persons, depending on the solubility (plutonium oxide or plutonium nitrate) and exposure rate (acute or chronic intake). In comparison, the lifetime baseline risk of lung cancer mortality is 631 per 10,000 persons for a Euro-American male population.
(o) For comparison, exposure to 222Rn progeny under the scenario considered in Publication 115 (ICRP, 2010) of 7.1 mJ h m-3 (2 working-level months) per year from 18 to 64 years of age, when converted to lung dose, leads to a lifetime excess risk of lung cancer mortality per mGy of 1.6 per 10,000 persons. 5. Implications for radiological protection and future research
(p) A comparison of the lifetime excess risk of lung cancer mortality from exposure to an external source of gamma radiation (based on the Life Span Study of the Japanese atomic bomb survivors) and from internal exposure to plutonium (based on the Mayak workers study) indicates that, for the same absorbed dose to the lung and dose distribution, the risks from plutonium exposure are larger than those from external gamma exposure by a factor of approximately 16. The risk for radon progeny exposure appears to be consistent with that from plutonium exposure, and larger than that from external gamma exposure by a factor of approximately 14, despite the very different distribution of alpha-particle dose within the lung.
(q) These comparisons suggest a biological effectiveness of alpha particles relative to high-energy photons of approximately 14–16 for lung cancer. These values are compatible with the current radiation weighting factor, wR, of 20 used by ICRP for alpha particles in the calculation of equivalent and effective doses (ICRP, 2007).
(r) It should be noted that this comparison is based on lung absorbed dose and lifetime excess risk of lung cancer mortality, with application of a dose and dose-rate effectiveness factor (DDREF) of 2 to the risk derived from the Japanese Life Span Study. Not applying a DDREF would lead to relative biological effectiveness of approximately 7–8 for lung cancer. Also, care has to be taken in making comparisons with wR as the latter is intended to embrace the risk of all stochastic effects, whereas lung cancer mortality alone is considered in the present calculations. Further, it was considered premature to quantify lifetime excess risks for bone and liver cancers, for which associations have also been demonstrated for plutonium, and different relative biological effectiveness values for alpha radiation may apply for these cancer types.
(s) Further research is needed to improve the assessment of health risks associated with plutonium or uranium exposure in epidemiology, dosimetry, and risk modelling. Uncertainties associated with plutonium and uranium exposure and dose reconstruction are substantial, and inhalation of different chemical forms leads to very different cumulative organ-/tissue-specific absorbed doses. For lung cancer, a better determination of the distribution in the different parts of the lung is important. Important efforts have been made in recent years to improve dose assessment and to consider the potential impact of uncertainties on risk estimates, and should be maintained in the future. Also, extension of existing cohorts and combined analyses of data are needed to increase power, and allow improved estimation of the risks associated with plutonium and uranium exposures. In addition, better consideration of the effect of smoking in future analyses is highly desirable. For uranium, more information on the intake of different chemical forms is required. Future research may better characterise the risks associated with alpha particles emitted by plutonium for cancer induction in organs/tissues other than the lung.
