Recommended citation
ICRP, 2010. Lung Cancer Risk from Radon and Progeny and Statement on Radon. ICRP Publication 115, Ann. ICRP 40(1).
Authors on behalf of ICRP
M. Tirmarche, J.D. Harrison, D. Laurier, F. Paquet, E. Blanchardon, J.W. Marsh
Abstract - Recent epidemiological studies of the association between lung cancer and exposure to radon and its decay products are reviewed. Particular emphasis is given to pooled case-control studies of residential exposures and to cohorts of underground miners exposed to relatively low levels of radon. The residential and miner epidemiological studies provide consistent estimates of lung cancer risk with statistically significant associations observed at average annual concentrations of about 200 Bq m-3 and cumulative occupational levels of about 50 WLM, respectively. Based on recent results from combined analyses of epidemiological studies of miners, a lifetime excess absolute risk of 5 × 10-4 per WLM (14 × 10-5 per mJ h m-3) should now be used as the nominal probability coefficient for radon and radon progeny induced lung cancer, replacing the previous ICRP Publication 65 value of 2.8 × 10-4 per WLM (8 × 10-5 per mJ h m-3). Current knowledge of radon associated risks for organs other than the lungs does not justify the selection of a detriment coefficient different from the fatality coefficient for radon-induced lung cancer.
ICRP Publication 65 recommended that doses from radon and its progeny should be calculated using a dose conversion convention based on epidemiological data. It is now concluded that radon and its progeny should be treated in the same way as other radionuclides within the ICRP system of protection; that is, doses from radon and radon progeny should be calculated using ICRP biokinetic and dosimetric models. ICRP will provide dose coefficients per unit exposure to radon and radon progeny for different reference conditions of domestic and occupational exposure, with specified equilibrium factors and aerosol characteristics.
© 2011 ICRP Published by Elsevier Ltd.
Keywords: Radon; Lung cancer; Radiological protection; Risk.
AUTHORS ON UTHORS ON BEHALF OF ICRP M. TIRMARCHE, IRMARCHE, J.D. HARRISON ARRISON, D. LAURIER, F. PAQUET, E. BLANCHARDON LANCHARDON, J.W. MARSH
Reference
ICRP, 1993. Protection against radon-222 at home and at work. ICRP Publication 65. Ann. ICRP 23(2).
Key Points: Not included in this publication
Executive Summary
(a) Epidemiological studies of occupational exposures of miners and domestic exposures of the public have provided strong and complementary evidence of the risks of lung cancer following inhalation of radon and its progeny. In the large cohorts of underground miners, annual occupational exposures were considered for the whole working period of each individual. Consequently, these studies are able to analyse dose–response relationships taking account of time-dependent modifying factors, such as age at exposure and time since exposure. The risk of lung cancer associated with domestic exposures to radon has been evaluated in a large number of case–control studies, requiring estimates of radon exposure in houses over a period of 30 years preceding lung cancer diagnosis. A weakness of such studies is that measurements made during the study period are assumed to apply throughout the whole period of exposure. An important strength, however, is that the residential studies often include detailed interviews so adjustments can be made, in the statistical analysis, for tobacco smoking as well as exposure to other potential lung carcinogens in the home or at work.
(b) In 1999, the BEIR VI report presented a comprehensive analysis of available miner cohorts from China, Czech Republic, USA, Canada, Sweden, Australia, and France (NRC, 1999). Recent studies of lung cancer in miners include relatively low concentrations of radon and its progeny, long duration of follow-up, and good quality data for exposure of each individual (Tomášek et al., 2008; UNSCEAR, 2009). These results, consistent with previous analyses of combined miner studies, demonstrate significant associations between cumulative radon exposure and lung cancer mortality at levels of exposure as low as 50 working level months (WLM; i.e. 180 mJh/m3). Based on lifetime excess absolute risk (LEAR) calculations, reference background rates from Publication 103 (ICRP, 2007), and risk models derived from pooled analyses (NRC, 1999; Tomášek et al., 2008), a detriment-adjusted nominal risk coefficient of 5 x 104 per WLM [14 x 105 per (mJh/m3)] is now recommended for radiological protection purposes. This nominal risk coefficient replaces the Publication 65 value of 2.8 · 104 per WLM [8.0 · 105 per (mJh/m3)].
(c) Three comprehensive publications have provided joint analyses of data from domestic case–control studies for Europe (Darby et al., 2005), North America (Krewski et al., 2005, 2006), and China (Lubin et al., 2004). Each joint analysis demonstrated an increased risk of lung cancer with increasing domestic radon concentration, considering exposures over a period of 30 years preceding diagnosis. The estimates of an increase of lung cancer per unit of concentration in the three joint analyses are very close and statistically compatible: the values obtained were 1.08, 1.10, and 1.13 per 100 Bq/m3 from Europe, North America, and China, respectively. A combined estimate calculated for the studies in these three geographical areas was 1.09 per 100 Bq/m3 (UNSCEAR, 2009). All of these results were obtained after adjustment for smoking habits. The slope of the linear exposure–response relationship increased slightly to 1.11 per 100 Bq/m3 when analyses were restricted to cases 15 and controls with more complete estimation of cumulated individual exposure (UNSCEAR, 2009).
(d) The joint analyses also adjusted for uncertainties associated with variations in radon concentration. For example, in the European pooled analysis (Darby et al., 2005), adjustment for measurement uncertainties markedly increased the estimate of relative risk from 1.08 to 1.16 per 100 Bq/m3 . Limiting the European analysis to those cases and controls with a relatively low annual exposure, there was evidence of an increased risk below 200 Bq/m3. Analyses of the North American and Chinese studies were more variable and less statistically precise. It is concluded, however, that the residential studies provide consistent estimates of the risk of lung cancer and a basis for risk management related to low protracted radon exposures in homes, considering cumulative exposure over a period of at least 25 years.
(e) Although comparisons are complex, the cumulated excess absolute risk of lung cancer attributable to radon and its progeny estimated for residential exposures appears to be consistent with that obtained from miners at low levels of exposure.
(f) In the European pooled analysis of domestic exposures, a significant trend in the risk of lung cancer was observed among smokers, and also separately among non-smokers (Darby et al., 2006). Therefore, residential studies have demonstrated radon to be a lung carcinogen even in the absence of smoking, as shown previously in miner studies (Lubin et al., 1995). However, due to the dominant effect of tobacco use on lifetime risk of lung cancer, the excess absolute risk of lung cancer attributable to a given level of radon concentration is much higher among lifelong cigarette smokers than among non-smokers.
(g) The control of domestic exposures can be based directly on lung cancer risk estimates per unit exposure derived from epidemiological data; that is, in terms of radon concentrations in homes.
(h) However, for the purpose of control of occupational exposures using dose limits and constraints, estimates of dose per unit exposure are required. In Publications 65 and 66 (ICRP, 1993, 1994), the effective dose per unit exposure to radon and its progeny was obtained using the so-called ‘dose conversion convention’. This approach compared the detriment per unit exposure to radon and its progeny with the total detriment associated with unit effective dose, estimated largely on the basis of studies of Japanese atomic bomb survivors (ICRP, 1993). The values given were 5 mSv per WLM [1.4 mSv per (mJh/m3)] for workers and 4 mSv per WLM [1.1 mSv per (mJh/m3)] for members of the public.
(i) Doses from radon and its progeny can also be calculated using different dosimetric models. A review of published data on the effective dose per unit exposure to radon progeny obtained using dosimetric models is included as Annex B of this report. Values of effective dose range from about 6 to 20 mSv per WLM [1.7–5.7 mSv per (mJh/m3)], with results using the Human Respiratory Tract Model (HRTM; ICRP, 1994) in the range from approximately 10 to 20 mSv per WLM [3–6 mSv per (mJh/m3)] depending on the exposure scenario.
(j) ICRP has concluded that radon and its progeny should be treated in the same way as other radionuclides within the system of protection. That is, doses from radon and its progeny should be calculated using ICRP biokinetic and dosimetric 16 ICRP Publication 115 models, including the HRTM and ICRP systemic models. In the near future, ICRP will provide dose coefficients per unit exposure to radon and its progeny for different reference conditions of domestic and occupational exposure, with specified equilibrium factors and aerosol characteristics. It should be recognised, however, that these dose coefficients will be larger by about a factor of two or more.
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