# Effective dose coefficients for radon progeny: A review of ICRP and UNSCEAR values.

James Marsh, Ladislav Tomášek, Dominique Laurier, John Harrison

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James Marsh, Ladislav Tomášek, Dominique Laurier, John Harrison. Effective dose coefficients for radon progeny: A review of ICRP and UNSCEAR values. Radiation Protection Dosimetry, 2021, 195 (1), pp.1-20. 10.1093/rpd/ncab106. hal-03515756

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**Effective dose coefficients for radon and progeny: A review of ICRP and UNSCEAR values**

James W. Marshª, Ladislav Tomášekᵇ, Dominique Laurierᶜ and John D. Harrisonª,ᵈ.

Running title: Radon dose coefficients

Corresponding author: J. W. Marsh (James.Marsh@phe.gov.uk)

<footnote>ªPublic Health England. Centre for Radiation, Chemical and Environmental Hazards, Chilton, Didcot, Oxon. OX11 0RQ, UK; PH (+44) 1235 831600; FAX (+44) 1235 833891</footnote>

<footnote>ᵇNational Radiation Protection Institute, Prague, Czech Republic</footnote>

<footnote>ᶜInstitut de Radioprotection et de Sûreté Nucléaire, Fontenay-aux-Roses, France</footnote>

<footnote>ᵈOxford Brookes University, Faculty of Health and Life Sciences, Oxford, UK.</footnote>
# Effective dose coefficients for radon and progeny: A review of ICRP and UNSCEAR values

James W. Marsh, Ladislav Tomášek, Dominique Laurier and John D. Harrison<sup>a,d</sup>.

## Abstract

The International Commission on Radiological Protection (ICRP) publishes guidance on protection against radon exposure in homes and workplaces. ICRP *Publication 137* recommends a dose coefficient of 3 mSv per mJ h m⁻³ (approximately 10 mSv WLM⁻¹) to be used in most circumstances of radon exposure, for workers in buildings and in underground mines. Recently, UNSCEAR reviewed radon epidemiology and dosimetry and concluded that its established dose coefficient of 1.6 mSv per mJ h m⁻³ (5.7 mSv WLM⁻¹) should be retained for use in its comparisons of radiation exposures from different sources in a population. This paper explains and compares the reviews of the scientific evidence from UNSCEAR and ICRP. It is shown that the UNSCEAR and ICRP reviews are consistent and support the use of the ICRP reference dose coefficients for radiation protection purposes. It is concluded that the ICRP dose coefficient should be used to calculate doses to workers.
INTRODUCTION

Radon has long been recognised as a cause of lung cancer. Since its 2007 Recommendations(1), the International Commission on Radiological Protection (ICRP) has published three reports on radon exposure: (i) Publication 115(2) on lung cancer risks from radon and radon progeny, (ii) Publication 126(3) on radiological protection against radon exposure and (iii) Publication 137 on Occupational Intakes of Radionuclides (OIR), Part 3(4). The latter document gives dose coefficients for the inhalation of radon, thoron and their airborne progeny as well as recommendations for their use for the protection of workers. As with all other radionuclides, the effective dose coefficients are calculated with ICRP reference biokinetic and dosimetric models. Sufficient information and dosimetric data are given so that site-specific dose coefficients can be calculated based on measured aerosol parameter values.

In Publication 115(2), ICRP reviewed epidemiological data of radon-induced lung cancers, focusing on low levels of exposure and low exposure rates in mines(5,6). Based on this review, a detriment adjusted nominal risk coefficient of 1.4 × 10⁻³ per mJ h m⁻³ [5 × 10⁻⁴ mSv per working level month (WLM)] was recommended for radiation protection purposes for a mixed adult population of smokers and non-smokers. This value is approximately twice the value given previously in ICRP Publication 65(7). Applying the epidemiological approach to calculating dose coefficients and using the revised nominal risk coefficient from ICRP Publication 115(2) and ICRP Publication 103(1) nominal detriment values, dose conversion convention values of effective dose of 3.4 mSv per mJ h m⁻³ (12 mSv WLM⁻¹) for adults and 2.6 mSv per mJ h m⁻³ (9 mSv WLM⁻¹) for all ages are derived(4,8,9,10,11). The latter value is obtained in the absence of any reliable information on risks of exposure to radon and progeny during childhood. In comparison, effective dose coefficients calculated with ICRP reference biokinetic and dosimetric models gave values of 3 to 4 mSv per mJ h m⁻³ (11 to 14 mSv WLM⁻¹) for workers in mines, sedentary indoor workers and exposures in homes(4). Thus, the consistency between the dose coefficients obtained by dosimetric calculations and by epidemiological comparisons is remarkable but the underlying uncertainties in both approaches should be recognised. Taking account of both approaches, ICRP Publication 137(4) recommends a single rounded value of 3 mSv per mJ h m⁻³ (approximately 10 mSv WLM⁻¹) to be used in most circumstances, for workers in buildings and in underground mines. ICRP also recommended a reference value of 6 mSv per mJ h m⁻³ (approximately 20 mSv WLM⁻¹) for specific situations of indoor work involving substantial physical activity, and for workers in tourist caves. However, ICRP now considers that these specific situations may be seen as special cases of requirements for more specific calculations when warranted(11,12).

Because the ICRP recommended nominal risk coefficient for radon(2) increased by about a factor of two in comparison to its previous publication in 1993(7), the upper reference level (URL) for radon in dwellings was reduced from 600 Bq m⁻³ to 300 Bq m⁻³. On the basis of a consistent and integrated protection strategy, ICRP recommends the same URL of 300 Bq m⁻³ for workplaces(3).

Although protection against radon is based on measurement and control of levels of radon concentration, dose estimates are required in certain situations for workers. If despite of optimisation, radon levels remain above the national reference level, then a dose assessment is
required(3,13). Dose estimates are also necessary for protection purposes when workers are exposed to more than one source of radiation as is the case for underground miners.

The United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR) uses an effective dose coefficient for radon to allow comparisons with other sources of radiation exposures(14). Their established value of 9 nSv per h Bq m⁻³ of equilibrium equivalent concentration (EEC) of ²²²Rn was based on a review of available dosimetric models by an expert group of the Nuclear Energy Agency(15). The UNSCEAR committee adopted this value for indoor radon exposures in its 1982 report(16) and it was retained for both indoor and outdoor exposures in UNSCEAR 1988, 2000 and 2006 Reports(14,17,18). This established value of 9 nSv per h Bq m⁻³ EEC of ²²²Rn corresponds to 1.6 mSv per mJ h m⁻³ or 5.7 mSv WLM⁻¹. It applies only to adults in the general population as stated in the UNSCEAR 1982 and 1988 reports(16,17).

Recently, in its 2019 report(19), UNSCEAR reviewed (i) the risk of lung cancer from radon progeny and (ii) the dosimetric calculations following inhalation of radon progeny. Because the uncertainties from both dosimetry and epidemiology gave rise to a broad range of risk estimates, UNSCEAR concluded that its established value of 9 nSv per h Bq m⁻³ EEC of ²²²Rn should be retained for use in its comparisons of radiation exposures from different sources among different countries.

This paper explains and compares the reviews of the scientific evidence from UNSCEAR and ICRP. It is shown that the ICRP reference dose coefficients used for radiation protection purposes are consistent with the UNSCEAR review. The UNSCEAR dose coefficient value is at the lower end of the range of calculated values whereas the ICRP reference dose coefficient is close to the central value. It is concluded that the UNSCEAR established value should not be used to calculate doses for radiation protection of workers but rather the ICRP dose coefficients should be used for this purpose.

## DOSIMETRIC APPROACH

Following the inhalation of radon and radon progeny the organ that receives the highest dose is the lung. The lung dose from inhaling the airborne radon progeny is about two orders of magnitude greater than the corresponding lung dose from inhaling radon gas(20). This is because most of the gas inhaled is subsequently exhaled whereas a large proportion of the inhaled radon progeny deposits in the lung. It is the bronchial and bronchiolar regions that receive the highest dose, consistent with observed regional lung cancer distributions(21). The equivalent dose to the lungs contributes more than 95% of the effective dose following inhalation of radon progeny.

Radon gas decays into a series of short-lived radionuclides creating an aerosol of solid particles suspended in air. These short-lived decay products are present in the air as unattached particles (with diameters around 0.5 to 5 nm in size) or can attach to existing particles in the atmosphere forming the so-called attached progeny. The attached progeny may consist of three modes, designated as the nucleation mode with activity median diameters (AMD) between 10 and 100 nm, the accumulation mode with AMD values of 100–450 nm, and a coarse mode with an AMD >
1 µm. Most of the potential alpha energy concentration (PAEC) is in the accumulation mode. The magnitude of the unattached fraction depends mainly on the ambient particle concentration, which depends on local conditions.

## Biokinetic and dosimetric models of the respiratory tract

Models of the respiratory tract describe the morphometry, the respiratory physiology, the deposition of the inhaled material, clearance from the respiratory tract, and the dosimetry including the location of target tissues and cells at risk. Basal and secretory cells are assumed to be the target cells for bronchial carcinomas located at different depths in the epithelium(22).

Airway generation models (i.e. anatomical models) have been used to calculate the absorbed dose to the sensitive target cells of each airway generation of the tracheobronchial tree. A weighting procedure for combining the target cell doses is applied to calculate an average lung dose. Two types of airways generation models have been used, namely deterministic airway generation models(23,24,25) and stochastic airway generation models(26,27). Deterministic airway generation models have a fixed number of bronchial generations (about 15) and all the airways in a given generation are identical in terms of length, diameter and branching angle. Thus, such deterministic models give single dose values for target cells in a given airway generation. In contrast, stochastic airway models describe the inherent asymmetry and variability of the human airway system. They have a variable number of airway generations (12 to 20) with airways in each generation having variable dimensions. Monte Carlo techniques are applied to obtain a distribution of absorbed doses to the sensitive target cells of each airway generation reflecting inter- and intra- subject variability in the morphology of the lung. Both the mucociliary clearance flow rates and the depth distribution of the targets cells are assumed to be a function of airway diameter(20,25,26,27). Hofmann et al.(26,20) approximated the average depths of the basal and secretory cell nuclei with polynomial functions of airway diameter based on the histological data of Mercer et al. (28). The basal and secretory cell nuclei were represented as spherical volumes of 9µm in diameter(29).

The ICRP Human Respiratory Tract Model (HRTM) (22,30) simplifies the anatomical representation of the respiratory tract by combining airway generations into compartments. For example, the lung is modelled as three regions: bronchial region (BB, airway generations 0-8), bronchiolar region (bb, airway generations 9-15), and the alveolar interstitial region (AI) where the gas exchange occurs. The radiosensitive target cells of the BB and bb regions are assumed to be restricted to tissue layers of given depths and thicknesses. These are the basal and secretory cells in the bronchial epithelium and the secretory cells in the bronchiolar epithelium. For the AI region it is assumed that the target cells are distributed homogeneously throughout the tissue mass and so the average dose to the target cells in the AI region is the same as that received by the whole tissue mass. Thus, the dose to the AI region from inhaling short-lived radon progeny is significantly lower than the doses to the BB and bb regions mainly because of the larger mass of the AI region (1100 g) compared with the masses of the target tissues in the BB (1 g) and bb (2 g) regions.

The equivalent dose to the lung calculated with the HRTM is given by:
$$H_{\text{lung}} = w_{\text{R}} \times [A_{\text{BB}}(D_{\text{bas}} + D_{\text{sec}})/2 + A_{\text{bb}} D_{\text{bb}} + A_{\text{AI}} D_{\text{AI}}], \text{ where}$$

* $D_{\text{bas}}$ and $D_{\text{sec}}$ are the absorbed doses to the basal and secretory target cell layers of the BB region, respectively.

* $D_{\text{bb}}$ and $D_{\text{AI}}$ are the absorbed doses to the bb and AI regions, respectively.

* $A_{\text{i}}$ are the apportionment factors representing the regional's estimate sensitivity relative to that of the lung and the assumed values are(30): $A_{\text{BB}}= 1/3$, $A_{\text{bb}}= 1/3$, $A_{\text{AI}}= 1/3$.

* $w_{\text{R}}$ is the radiation weighting factor for alpha particles (20) (1).

Because $H_{\text{lung}}$ contributes most of the effective dose following inhalation of radon and progeny, the effective dose can be approximated by multiplying $H_{\text{lung}}$ by the lung tissue weighting factor, $w_{\text{lung}}$ of 0.12. It should be noted that $H_{\text{lung}}$ and the effective dose are ICRP quantities used for radiation protection purposes. The effective dose is not an individual-specific dose quantity, but rather that for a Reference Person as defined by ICRP. The Reference Person can either be the Reference Worker or a Reference Member of the Public of a specified age(30). For the purposes of modelling intakes and deposition of radon progeny in the lung, the Reference Worker is assumed to be a healthy, non-smoking, normal nose-breathing, adult male at light work (with an average breathing rate of 1.2 m³ h⁻¹)(30). However, the tissue weighting factors, $w_{\text{T}}$ are based on the contributions of individual organs to the overall radiation detriment from stochastic effects, averaged over all ages and both sexes across the ICRP Reference populations, which include smokers and non-smokers. The $w_{\text{T}}$ values are rounded and only four different numerical values are assigned to the various organs to avoid the impression of unwarranted accuracy. The $w_{\text{T}}$ value for the lung is 0.12, compared with the value of relative detriment for lung of 0.16 for the whole population and 0.29 for adults(1).

## ICRP dose coefficients

### Workers

In ICRP Publication 137(4), equivalent doses to organs and effective doses to the Reference Worker, following inhalation of radon and progeny, have been calculated using the ICRP reference biokinetic and dosimetric models. Doses per unit potential alpha energy (PAE) exposure mainly depend on the breathing rate and the aerosols' properties, including the activity size distribution of the radon progeny aerosol and the unattached fraction. If the exposure is characterised by radon gas measurements, a value for the equilibrium factor, $F$, is required to estimate the radon progeny concentration in air, or more precisely the PAE. For radiological protection purposes, most of the parameters in the dosimetric models, such as breathing rate, correspond to values for the Reference Worker(22,30).

Reference aerosol parameter values were chosen for indoor workplaces, mines and tourist caves based on a literature review and expert judgement (Table 1). The justification of these parameter values is given by ICRP(4) and Marsh et al.(9).

Characterising aerosol parameter values for mines was difficult because of the highly variable conditions and because of the different types of mining conditions such as use of diesel or electric powered equipment, different ventilation rates, and the type of heating used during the winter
months. It is acknowledged that the reference values for mines were based on data published in the 1990s and that the exposure conditions in modern mines are significantly different. However, at the time of publication of ICRP Publication 137(4) there was insufficient information to provide an alternative set of parameter values.

In tourist caves, typically there is no additional ventilation as this may alter the humidity, affecting the geological formations that attract tourists. With high humidity and low ventilation, particle concentrations can be low resulting in high unattached fractions, $f_p$. Measurements of $f_p$ in tourist caves have resulted in a large range of values(31,32,33,34,35,36) with mean values ranging from 0.1 to 0.6 (Table 2). ICRP chose a reference $f_p$ value of 0.15 for tourist caves based on the measurements of Butterweck et al.(35) and Solomon et al.(31). If measurements of the activity radon gas concentration and F are made for accurate dose assessments, $f_p$ should also be measured, particularly if the doses are likely to be high. It should be noted that F and $f_p$ are negatively correlated(4,20).

Table 3 gives ICRP Publication 137(4) values of absorbed dose coefficients for the regions of the lung and the corresponding effective dose coefficients for workers inhaling radon progeny. The calculations have been carried out with the ICRP Human Respiratory Tract Model (HRTM)(30) and the ICRP systemic biokinetic models for polonium, lead and bismuth(4) using the aerosol parameter values of Table 2. The effective dose coefficients are 11 mSv WLM$^{-1}$ (3.1 mSv per mJ h m$^{-3}$) for mines, 20 mSv WLM$^{-1}$ (5.6 mSv per mJ h m$^{-3}$) for indoor workplaces and 23 mSv WLM$^{-1}$ (6.6 mSv per mJ h m$^{-3}$) for tourist caves. The ICRP reference breathing rate for a standard worker of 1.2 m$^3$ h$^{-1}$ was assumed, where one third of the time is spent sitting and two thirds of the time is spent undertaking light exercise(4,22). For sedentary occupations such as office workers, this reference breathing rate may be considered as an over-estimate(9). Assuming a lower breathing rate of 0.86 m$^3$ h$^{-1}$ (2/3 sitting, 1/3 light exercise) would reduce the dose coefficient from 20 mSv WLM$^{-1}$ to about 14 mSv WLM$^{-1}$ for an indoor workplace.

The equations for the effective dose per unit PAE exposure as a function of $f_p$ for the different exposure scenarios are given in Table 4. An $f_p$ of 0.60 that was measured at the lowest point of the Postojna cave, Slovenia, (Table 2) gives an effective dose of 56 mSv per WLM (16 mSv per mJ h m$^{-3}$). This is a factor of 2.4 greater than that obtained with the reference $f_p$ value of 0.15 for tourist caves (23 mSv WLM$^{-1}$; 6.6 mSv per mJ h m$^{-3}$).

## Public

For a male adult at home, the ICRP reference breathing rate is 0.78 m$^3$ h$^{-1}$ (55% sleep, 15% sitting and 30% light exercise)(22). The effective dose coefficient calculated by Marsh and Bailey, 2013(37) with the revised HRTM(30) is 13 mSv per WLM (3.6 mSv per mJ h m$^{-3}$). In its forthcoming publications on ‘Environmental Intakes of Radionuclides’, ICRP will publish dose coefficients for members of the public following exposure to radon and radon progeny. However, ICRP has already indicated in its summary of ICRP recommendations on radon (www.icrp.org) that the intention is that the dose coefficient of 3 mSv per mJ h m$^{-3}$ (approximately 10 mSv per WLM) for workers will also apply to members of the public exposed in homes(10).
## UNSCEAR's review of dosimetry

Recently, UNSCEAR carried out a review of published dosimetric calculations for radon progeny exposure in homes, indoor workplaces and mines(19). The review considered dose coefficients calculated with deterministic airway generation models(23,25,38,39), a stochastic airway generation model(25) and the ICRP HRTM(22,30). Important points raised by the review are summarised below and in Table 5.

Comparisons of dose calculations made with a deterministic airway generation model, a stochastic airway generation model and the HRTM with the same input parameter values for mine conditions gave similar results: 8.3, 8.9 and 12 mSv WLM⁻¹ respectively(25). Thus, the airway generation models gave results that were about 25 to 30% lower than that of the ICRP HRTM. The authors noted that one of the important issues affecting the comparison is the averaging procedure used in the airway generation models for combining the doses to target cell nuclei (i.e. cellular doses) over all airway generations. In this comparison, cellular doses were combined by calculating an arithmetic mean with equal weighting to basal and secretory cells.

The parameters most affecting the equivalent dose to the lung per WLM are the breathing rate, the parameters relating to the activity size distribution of the radon progeny, such as the unattached and nucleation fractions, the weighting given to the basal and secretory cell of the bronchial region, and the depth of the target cells(40). A parameter uncertainty analysis with the HRTM gave a lognormal distribution of effective dose with a geometric mean of 14 mSv WLM⁻¹ and a geometric standard deviation of 1.5 for exposures in homes(41). In this analysis, the weighting factors, $w_R$ and $w_T$ were fixed at their reference values. An uncertainty analysis with a stochastic airway generation model gave wider dose distributions, indicating that inter-subject variability in the morphology of the respiratory tract is an important source of uncertainty in the dose calculations(26). Dose coefficients calculated for Chinese males and females were 20 to 30% lower than that for Caucasian males, taking account of differences in lung morphology(38). However, it is acknowledged that effective dose is defined as a sex-averaged quantity and separate values for males and females do not conform to this definition(1).

### Target cell depths

Histological measurements of the basal and secretory cell depth in the human bronchial epithelium are the basis of the assumed target cell depth distributions in bronchial dose models. The target cell depth distribution of the HRTM(22,30), and the deterministic and stochastic airway generation models of Zock et al.(23), Winkler-Heil et al.(24,25) and Hofmann et al.(26,27) are all based on the histological measurements of Mercer, et al.(28). Mercer et al.(28) measured the distribution of nuclear cell depth for different cell types in the bronchi and bronchioles. The basal cell depths ranged mainly from 36 µm to 48 µm with most cells at 48 µm in large and small bronchi, and basal cells were absent in the bronchioles. In contrast, the data of Robbins et al.(42) showed smaller cell depths; the mean basal cell depth was 27 µm. Harley(43) estimated that the bronchial dose can change by ± 20% due to the different target cell assumptions selected in various models. With the HRTM, Marsh and Birchall(40) estimated that dose coefficients are increased by 40% if the target cell depth and thickness is decreased by a factor of 2.
The effects of calculating doses to targets cell layers as in the HRTM rather than to target cell nuclei using a microdosimetry approach was investigated by Nikezic et al. (44). In the microdosimetry approach, the nuclei of basal and secretory cells were approximated by cones and ellipsoids respectively. For indoor exposures, the effective doses calculated by the authors were 13 mSv per WLM with the cellular microdosimetry approach compared with 15 mSv per WLM obtained assuming target cell layers. Thus, simplifying the model by assuming target cell layers for the BB and bb regions rather than calculating cellular doses using microdosimetry increases the dose by 15%.

### Effects of smoking

Dosimetric calculations for inhaled radon progeny in smokers have been reported, taking account of changes in the morphological and physiological parameters of the lung due to smoking(45). For light, long-term smokers and heavy short-term smokers, the effective dose reduced by only about 10%, mainly due to a thickening of the mucous layer. For heavy long-term smokers the effective dose per unit exposure was estimated to increase by about a factor of two compared to never smokers, the determining factors considered being: thicker mucous layer, impaired mucociliary clearance, higher breathing frequencies and reduced lung volume due to obstructive lung diseases. The significant decrease in mucociliary clearance assumed by the authors is controversial(20,22) as some volunteer studies showed no difference in overall clearance between smokers and non-smokers(46) while other studies showed a decrease for smokers, especially in the large proximal airways(47,48,49,50,51). The significant reduction in mucociliary clearance assumed by Baias et al.(45) was based on histological data, which showed that heavy long-term smoking can damage and destroy cilia. For example, subjects that smoked about 40 cigarettes per day for more than 30 years had loss of cilia, with the epithelium becoming metaplastic (squamous cell metaplasia)(52). It was noted in ICRU Report 88(20) that physiological and morphological data of the influence of smoking vary widely among different sources, so the physiological effects of smoking categorized by Baias, et al.(45) represent only rough approximations.

### Recent dose assessment for modern mines

The most recent dose assessment for exposures in a mine, based on aerosol measurements carried out in a mine using modern mining practices, was made by Solomon et al(53). For work locations with high ventilation and low levels of PAEC (i.e. at underground workshop sites), the effective dose calculated with the HRTM was about 23 mSv per WLM (6.5 mSv per mJ h m⁻³). At these sites, the measured unattached fraction or the nucleation mode fraction was relatively high, giving rise to the high dose coefficient. This site-specific dose coefficient is about a factor of 2 greater than the recommended ICRP dose coefficient for mines (10 mSv per WLM or 3.0 mSv per mJ h m⁻³) (4). In comparison, for the operational sites with mining activities and higher levels of PAEC, the average effective dose was about 16 mSv per WLM (4.5 mSv per mJ h m⁻³).

### Apportionment factors

UNSCEAR reviewed data to estimate the relative sensitivity of the different lung regions (BB, bb, AI) to the development of cancer following uniform radiation exposure of the lung. In ICRP Publication 66(22) the regional distribution of lung cancer types in the general population was estimated. Overall values of 0.6 for the BB region, 0.3 for bb region and 0.1 for the AI region were obtained for a population of non-smokers and smokers. Saccomanno et al.(21) measured the distribution of tumours in the bronchial tree for a cohort of 467 miners and 311 non-miners. All
subjects were male, mostly with positive smoking histories. The data indicated that for smokers, the inhalation of radon progeny preferentially induces small cell carcinomas in the BB region, although an increase was also observed in the bb region (Figure 1). Adding up the number of tumours in each region (Figure 1) gave distributions of tumours in the BB:bb:AI regions as 0.68:0.15:0.16 for miners and 0.59:0.18:0.23 for non-miners. Winkler-Heil et al. (2015)⁽⁵⁴⁾ also estimated values of apportionment factors by comparing different radon and thoron exposures, which produce different regional dose distributions, with pathological observed regional cancer distributions⁽²¹⁾. The authors estimated apportionment factors of ~*A*<sub>BB</sub> = 0.65, *A*<sub>bb</sub> = 0.30, *A*<sub>AI</sub> = 0.05. The equivalent dose to the lung from inhaling radon progeny increases if more weight is given to the BB and bb regions compared with the AI region⁽²⁰,⁴⁰,⁵⁵⁾. Assuming apportionment factors, *A*<sub>BB</sub>:*A*<sub>bb</sub>:*A*<sub>AI</sub>, of 0.65:0.30:0.05⁽⁵⁴⁾ or 0.6:0.2:0.2⁽²¹⁾, rather than the 0.333:0.333:0.333⁽²²⁾ assumption of the ICRP HRTM, increases effective dose coefficients for exposures in homes to 21 or 17 mSv per WLM, respectively, compared with the ICRP value of 15 mSv per WLM.

ICRP⁽²²⁾ adopted apportionment factors of 1/3 for each of the three regions because, although the available evidence indicated that uniform irradiation is more likely to result in the development of tumours in the BB and bb airways, their precise origins within the lungs were uncertain and quantitative information remained unreliable. No change was made to this assumption when the model was updated⁽³⁰⁾. However, this apportionment gives a substantially greater sensitivity per unit mass of the central airways than the lung tissue represented by AI because of the much smaller mass of the target cell regions in the central airways than in AI⁽²²⁾.

*Summary statistics of UNSCEAR's dosimetric review*

Table 6 gives the results of UNSCEAR's recent review of dose coefficients for inhaled radon progeny in homes, indoor workplaces and mines⁽¹⁹⁾. The range of doses is large because of the use of different models and the uncertainties associated with model parameter values. For example, for exposures in homes, the range of the effective doses per unit of exposure is from 4 to 21 mSv per WLM with a mean of 11 mSv per WLM (Table 6). The mean values of the dose coefficients for exposures in homes, indoor workplaces and mines are about a factor of 2 or more greater than the UNSCEAR's established value of 5.7 mSv per WLM.

EPIDEMIOLOGICAL APPROACH

In total, about 15 epidemiological studies of miners have been conducted worldwide since the 1960s providing quantitative estimates of radon associated health risk used to inform the setting of protection standards⁽¹⁰,¹¹,⁵⁶⁾.

One of the major analyses was performed by the US National Academies of Sciences Biological Effects of Ionizing Radiation (BEIR) VI Committee in 1999. The BEIR VI report proposed two risk models, namely the exposure-age-concentration model and the exposure-age-duration model⁽⁵⁾, derived from the joint analysis of 11 miner cohorts. These cohorts were from: Beaverlodge, China, Colorado, Czechoslovakia, France, New Mexico, Newfoundland, Ontario, Port Radium, Radium Hill and Sweden. Since the publication of the BEIR VI report in 1999, several studies have been extended (Beaverlodge, Colorado⁽⁵⁷⁾, Czech Republic⁽⁵⁸⁾, France⁽⁵⁹⁾, Newfoundland⁽⁶⁰⁾, Ontario⁽⁶¹⁾, Port Radium, Sweden⁽⁶²⁾) and the new German WISMUT study⁽⁶³,⁶⁴,⁶⁵⁾ was established. The Beaverlodge and Port Radium miner cohorts were combined
with a cohort of workers from the Port Hope radium and uranium refinery and processing facility to form the Eldorado cohort study(66).

The epidemiological approach (also referred to as the dose conversion convention) has been used by ICRP to derive coefficients for the effective dose per unit exposure from radon and radon progeny(4,7). It compares the detriment associated with unit radon exposure and unit effective dose. Thus, the lifetime risk of lung cancer per unit exposure to radon progeny is divided by the detriment per unit effective dose. The former is determined from miner epidemiology and the latter determined mainly from epidemiological studies of Japanese atomic bomb survivors exposed largely to gamma rays(1). It was considered that the total detriment associated with unit radon exposure is approximately equal to the lifetime excess risk for lung cancer fatality because (i) lung cancer has a poor prognosis and (ii) most of the dose is delivered to the lungs.

ICRP Review of miner studies

In ICRP Publication 65(7), excess lifetime risk of lung cancer mortality, was calculated using the GSF model developed by Jacobi et al.(67) based on meta-analysis of existing studies of uranium miners (Colorado, New Mexico, Ontario, Beaverlodge, Czechoslovakia, France, and Sweden). The GSF model is a multiplicative projection model that takes account of age at exposure and time since exposure and these modifying factors were estimated from the Czechoslovakia study. It is noteworthy that the GSF model did not take account of the modifying effect of exposure rate. With this risk model, the excess lifetime risk was calculated as 2.8 x 10⁻⁴ per WLM using the ICRP Publication 60(68) reference population of five countries for baseline rates. ICRP Publication 65(7) adopted this value as the nominal risk coefficient for lung cancer after exposure to radon progeny during adulthood. Tomášek et al.(6) repeated the calculation with the GSF model but using the ICRP Publication 103(1) reference background rates of selected Asian and Euro-American reference populations and obtained a similar value for lifetime excess absolute risk (LEAR) of 2.7 x 10⁻⁴ per WLM (Table 7).

In Publication 115(2), ICRP reviewed epidemiological data of radon-induced lung cancers, focusing on low levels of exposure and low exposure rates in mines. Priority was given to models derived from pooled analyses rather than from single studies and to models able to consider exposure rate. These included:

* the BEIR VI risk models derived from the joint analysis of 11 miner cohorts(5), and

* the Czech-French risk model(69) derived from a joint analysis of the Czech and French miner cohorts focusing on the periods of work with the best quality of exposure assessment and low levels of exposure.

The BEIR VI risk models(5) have modifying factors of time since exposure (TSE), attained age and exposure rate. LEAR estimates calculated by Tomášek *et al.*(6) for the ICRP Asian and Euro-American reference population(1) based on the BEIR VI exposure-age-concentration model(5) and the Czech-French model(69) were 5.3 10⁻⁴ WLM⁻¹ and 4.4 10⁻⁴ WLM⁻¹, respectively (Table 7). The
increase in the LEAR estimates compared with the value of 2.7 $10^{-4}$ WLM$^{-1}$ obtained using the GSF model$^{(7,67)}$ is mainly due to the consideration of low levels of exposure and low exposure rates.

Publication 115 also considered other risk models obtained from single studies including the French CEA-AREVA cohort$^{(70)}$, Canadian Eldorado cohort$^{(71)}$ and German Wismut cohort$^{(63)}$. With these models the estimated LEAR varied from about 3 to $7 \times 10^{-4}$ per WLM.

Because the risk models discussed above are multiplicative projection (excess relative risk) models, the background lung cancer rates have a significant impact on the LEAR estimates. The higher the background lung cancer rates, the higher the LEAR estimates and vice-versa. For example, using the higher background lung cancer rates of the Euro-American males instead of the reference rates averaged over males and females and over Euro-American and Asian populations$^{(1)}$, the estimated LEAR is about $7 \times 10^{-4}$ per WLM$^{(2)}$. Conversely, using lower background lung cancer rates (such as females or non-smokers) gives lower estimates of LEAR per unit exposure.

Based on the Publication 115 review, ICRP adopted a detriment adjusted nominal risk coefficient of $5 \times 10^{-4}$ per WLM [$1.4 \times 10^{-3}$ per mJ h m$^{-3}$] for a mixed adult population of smokers and non-smokers to be used for radiation protection purposes. In choosing this value, priority was given to models derived from pooled analysis, focusing on low levels of exposure and exposure rates in mines, and good quality exposure assessment (i.e. the Czech-French model$^{(69)}$ and the BEIR VI model$^{(5)}$ with exposure rate modifying factors).

## UNSCEAR's review of miner studies

UNSCEAR$^{(19)}$ reviewed evidence of lung cancer risk from published extensions (after 2006) of existing miner studies including those of the Czech Republic$^{(58)}$, Eldorado$^{(66)}$, France$^{(59)}$, Newfoundland$^{(60)}$, Ontario$^{(61)}$, and Sweden$^{(62)}$, as well as the new German Wismut study$^{(65)}$. Linear estimates of the excess relative risk (ERR) per WLM were reported for each of these studies for both the entire cohort, and a sub-cohort of results for more recent work periods and lower exposures. Using a random effects meta-analysis model with inverse-variance weighting$^{(72)}$, a combined ERR estimate was calculated from the cohorts. The combined ERR estimate per 100 WLM from the entire cohorts was 0.60 (95% CI: 0.34, 0.87) whereas for the sub-cohorts, considering low exposures, the value was significantly higher at 1.53 (95% CI: 1.11, 1.94). This illustrates the point that it is important to consider the effect of exposure rate in risk models. Studies that considered exposure rate modifying factors showed that the ERR decreased with increasing exposure rates for cumulative exposures above 50 to 100 WLM$^{(19)}$.

In UNSCEAR's 2019 report$^{(19)}$, the BEIR VI exposure-age-concentration model$^{(5)}$ was fitted individually to the updated Czech Republic$^{(58)}$, Wismut$^{(65)}$ and Eldorado$^{(66)}$ miner studies as well as to the combined 11 miner studies$^{(5)}$ used in the BEIR VI report. With these risk models, LEAR was calculated up to 95 years of age for the ICRP composite Asian and Euro-American male population$^{(1)}$, assuming a constant exposure scenario of 2 WLM per year from 18 to 64 years of
age. A multiplicative projection model was assumed. Values ranged from 3.0 to 9.6 × 10⁻⁴ per WLM (Table 8).

To facilitate comparison with ICRP Publication 65, UNSCEAR also calculated lifetime risks for the combined male and female population (Table 8). The LEAR values for the sex-averaged population are lower than the corresponding values for the male population because the background lung cancer rates for females are lower than those for males. This may be because more males were smokers and started smoking at an earlier age compared with females, as seen in the European residential study(73). Darby, et al.(73) noted that studies indicate that women are as susceptible to lung cancer as men given similar cigarette smoking histories(74).

The BEIR VI risk model can lead to misleading results, as the exposure rate modifier considers the mean exposure rate over the period of employment rather than the actual exposure rate in each year(19,75). This can be important as the annual exposure rate can vary substantially, particularly for long-term employment, with generally higher rates in early periods. Consequently, Tomášek (2020)(75) developed a risk model which considers the exposure rate in each year, categorising the exposure from low and high annual exposure rates. The model also includes modifying factors of attained age and TSE as in the BEIR VI risk models(5). This model is also given in the electronic attachment of the UNSCEAR 2019 report(19) and is referred to here as the B2 model.

Tomášek(75) repeated lifetime risk calculations with the B2 model, by applying the model individually to the updated Czech Republic(58), Wismut(65) and Ontario miner studies(61) as well as to the combined 11 miner studies(5) used in the BEIR VI report. The LEAR estimates obtained with the B2 model for the ICRP Asian and Euro-American male population(1) ranged from 4.0 to 8.7 × 10⁻⁴ per WLM assuming a multiplicative risk projection model (Table 9, 1st row). These values are also given in the electronic attachment of the UNSCEAR 2019 report(19) as well as the results of lifetime risk calculations assuming an additive risk projection model (Table 9, 2nd row). The appropriateness of assuming an additive model is discussed below.

# DISCUSSION

## Dosimetry

In its 2019 report, UNSCEAR reviewed dosimetric calculations for radon progeny exposure in homes, indoor workplaces and mines published after 2006 (Table 6). The data given in the UNSCEAR report show that calculations with the HRTM for exposures in homes gives a range from 13 to 21 mSv per WLM with a mean of 16 mSv per WLM(37,40,76,77,78,79,80). Lower values were obtained with deterministic and stochastic airway generation models, ranging from 8-12 mSv per WLM with a mean of 9 mSv per WLM(24,38,39,81,82). Winkler-Heil(25) et al. also showed that their airway generation models gave effective dose coefficients (8-9 mSv per WLM) that were about 25% to 30% lower than that of the ICRP HRTM when comparisons were made with the same input parameter values for mine conditions (Table 5). In these dose assessments with airway generation models, the target cell doses were effectively averaged over the trachea-bronchial tree by taking the arithmetic mean with equal weighting to the secretory and basal cell nuclei.
Instead of assuming equal dosimetric weighting to basal and secretory cells, Hofmann et al. (26,27,55) calculated ‘weighted epithelial doses’ by weighting the doses to the basal and secretory cell nuclei by their relative volumetric densities. This reduces the dose coefficient by ~20% because both the depth and the frequency of the basal cells are greater than those of the secretory cells(27,55). However, with the stochastic airway generation model, a distribution of weighted epithelial doses for each airway generation was obtained reflecting the intra- and inter subject variability in the morphology of the lung(26,27). If the median of these distributions (instead of the arithmetic mean) are used to compute an average lung dose then even lower dose coefficients are obtained (4 or 5 mSv per WLM for exposures in mines and homes(26,27)). These values, although valid, are at the lower end of the range of the assessed doses reviewed by UNSCEAR in its 2019 report(19) (Table 6).

The UNSCEAR's established value of 5.7 mSv per WLM is a factor of two lower than the mean value (11 mSv per WLM) of UNSCEAR's recent review of effective dose coefficients for exposures in homes published in the literature after 2000. It is also at the lower end of the range of the assessed effective dose coefficients (4 to 21 mSv per WLM) for exposures in homes (Table 6).

For indoor workplaces, the assessed doses reviewed by UNSCEAR(19) ranged from 6 to 24 mSv per WLM with an arithmetic mean of 16 mSv per WLM (Table 6). The assessed mean dose coefficient (16 mSv per WLM) for indoor workers is higher compared with that for exposures in homes mainly because of the higher breathing rate assumed for workers compared with adults at home.

## Epidemiology

Both the BEIR VI risk model(5) and the B2 risk model developed by Tomášek (2020)(75) have been applied to calculate lifetime risks. The B2 risk model(75) is preferable to the BEIR VI risk model(5) because it takes account of the actual exposure rate in each year rather than the mean exposure rate over the period of employment. Furthermore, the B2 model gave more consistent fits (p-value ≈ 0.47) to the individual cohort studies than the BEIRVI model (p-value ≈ 0.088).

For comparison with ICRP Publication 65 and 115, Tomášek (2020)(75) calculated LEAR using the B2 model for the sex-averaged ICRP Asian and Euro-American population(1). Applying the B2 model individually to the updated Czech Republic(58), Wismut(65) and Ontario miner studies(61) as well as to the combined 11 miner studies(5) used in the BEIR VI report, the LEAR estimates ranged from 3.2 to 7.0 × 10⁻⁴ per WLM assuming a relative risk projection model (Table 10).

In this paper, a combined estimate of the LEAR values from all four studies is calculated using a random effects meta-analysis model with inverse-variance weighting(72) (Table 10). The combined estimate of the LEAR obtained with the B2 model is 5.0 × 10⁻⁴ per WLM (95% CI: 3.1 × 10⁻⁴, 6.8 × 10⁻⁴ per WLM). It is acknowledged that the combined estimate includes some ‘double counting’ as earlier data from the Czech Republic, and the Ontario miner cohorts are included in the combined 11 miner studies(5) used in the BEIR VI report: The Czech and Ontario cohorts contributed 42% of cohort members, 41% of person-years, and 35% of lung cancers of the 11 cohorts used in the BIER VI report. Calculating a combined estimate of LEAR using only the
three individual estimates from the Wismut, Czech and Ontario studies gives $4.3 \times 10^{-4}$ per WLM (95% CI: $2.5 \times 10^{-4}$, $6.0 \times 10^{-4}$ per WLM). These combined estimates are consistent with the detriment adjusted nominal risk coefficient of $5.0 \times 10^{-4}$ per WLM recommended by ICRP for a mixed adult population of smokers and non-smokers(2).

The dose conversion convention values calculated, here, using the LEAR estimates obtained with the B2 model are given in Table 10. These have been calculated by applying the detriment per Sv values from ICRP Publication 103(1), namely $4.2 \times 10^{-2}$ Sv$^{-1}$ for adults and $5.7 \times 10^{-2}$ Sv$^{-1}$ for all ages. For adults, the combined estimate of the dose conversion convention is 12 (95% CI: 7.3, 16) mSv per WLM from all four individual estimates and 10 (95% CI: 6.0, 14) mSv per WLM from the three individual estimates (Wismut, Czech and Ontario studies). Thus, the ICRP effective dose coefficient of 10 mSv per WLM, to be used in most circumstances for workers, is within the range and close to the central value whereas the UNSCEAR established value of 5.7 mSv per WLM is slightly lower than the lower limit of the assessed 95% CI.

The UNSCEAR value is within the range of possible values calculated using the B2 risk model applied to the Wismut study; 7.6 (95% CI: 4.8, 10) mSv per WLM (Table 10). The LEAR estimate for the Wismut study is lower than those from the other studies (Czech Republic, Eldorado, Ontario and the joint 11 studies from BEIR VI - see Tables 8-10). The reason for this is unclear. Notably, the Wismut cohort is one of the largest cohorts with many long-term workers, a long follow-up period (40 years) and many lung cancer deaths (3,940) and person-years at risk (2.3 million). This leads to high precision but not necessarily accuracy. Limitations of the WISMUT cohort include uncertainty in exposure assessment, particularly in the early years (< 1955) for which the assessment was based on expert judgement rather than ambient measurements. Like in other cohorts, large uncertainties associated to exposure estimates in the early years may lead to an underestimation of the excess relative risk(56). Of interest, risk assessments with the cohort restricted to low exposures and low exposure rates ($< 0.5$ WL, $< 50$ WLM, $< 100$ WLM) were similar to that from the 1960 + sub-cohort, which had better exposure assessment based on ambient measurements of radon progeny(65).

The dose conversion convention values for all ages given in Table 10 are lower than those for adults only because of the correspondingly higher detriment per Sv. The LEAR estimates and the ERR models for radon from miner studies are all based on adulthood exposure. It is only the Chinese tin miner study which provides data on exposure during adolescence(83, 84). In this study there was no clear indication of the effect of age at exposure, although there was a slight suggestion of a higher risk for those exposed at earlier ages(5,85). The effect of age at exposure in the 11 studies included in BEIR VI was investigated by Tomášek(86). The ERR/WLM adjusted for time since exposure were from 0.0097 to 0.0131 for age at exposure below 30 years and from 0.0044 to 0.0075 for age at exposure above 30 years. Currently, residential studies also mainly consider radon exposure during adulthood. Thus, the impact of radon exposure at young ages remains unclear(19, 85). On this basis, dose conversion convention values for adults are more reliable than those for all ages.
## Risk coefficients for males and females

In ICRP Publication 103, the detriment per Sv was calculated separately for males and females and then averaged<sup>(1)</sup>. For non-smokers, the lung cancer ERR per Gy for females was about a factor of 3 higher than that in males, estimated from the Life Span Study (LSS) of the Japanese atomic bomb survivors <sup>(87,88)</sup>. Lifetime risk estimates for radon exposure have been calculated with risk models derived from male miners and applied to the ICRP reference Asian and Euro-American population of male and females (Tables 8 and 10, and ICRP Publication 115<sup>(2)</sup>). Thus, implicitly it was assumed that the ERR model for males is the same as that for females. However, in the Czech Republic residential study<sup>(89)</sup> the ERR per 100 Bq m<sup>-3</sup> was a factor of two higher for women (0.36 for women and 0.16 in men)<sup>(90)</sup> and in the pooled residential North American study<sup>(91)</sup> the ERR per 100 Bq m<sup>-3</sup> was only slightly higher in women compared with men (0.18 for women and 0.16 for males for the restricted analysis). In contrast, in the European pooled residential study<sup>(73)</sup>, the ERR for women was not statistically significant and substantially lower than for males. As the ERR models are based on male miners and differences occur in the ERR between male and females, it is more appropriate to calculate the LEAR values for the Asian and Euro-American male population. For males, the LEAR estimates calculated by Tomášek<sup>(19,75)</sup> using the multiplicative B2 risk model ranged from 4.0 to 8.7 × 10<sup>-4</sup> per WLM (Table 9, 1st row). This corresponds to effective dose coefficients of 9 to 21 mSv per WLM for adults obtained using the epidemiological approach (i.e. dose conversion convention method).

The indication that the lung cancer ERR per unit exposure is greater for females compared with males based on the Czech residential study<sup>(90)</sup> may be due to lower prevalence of smoking among females. For example, among Mayak plutonium workers the ERR per absorbed dose to the lung was greater for females compared with males by a factor of 3<sup>(92)</sup>. However, when the ERR was calculated separately for smokers and non-smokers, similar estimates were obtained for males and females. Thus, more research is required to verify whether differences in the ERR occur between male and females.

## Additive or multiplicative projection models

A multiplicative projection model (based on an excess relative risk model) assumes that the interaction between radiation exposure and the underlying background rates is multiplicative whereas an additive projection model (based on an excess absolute risk model) assumes the interaction is additive. It should be noted that in LEAR calculations, excess relative risk models with cohort specific background rates are equivalent to excess absolute risk models. It is only when transferring the risk from one population to another (i.e. from the cohort population to the ICRP reference population) that estimates of LEAR differ between multiplicative and additive models.

To calculate radiation detriment, ICRP takes a weighted average of the risk estimates obtained with multiplicative and additive risk projection models derived from the LSS of the Japanese atomic bomb survivors<sup>(1)</sup>. For lung cancer, ICRP uses 0.7 weighting for the additive model and 0.3 for the multiplicative model<sup>(1)</sup>. The basis for this is that the LSS suggested that (i) radiation
induced lung cancer is more consistent with an additive model across the sexes and (ii) the interaction between smoking and radiation dose is additive(93). However, more recent analyses of the LSS showed that more complex generalized-interaction models(87,88) gave better fits to the data compared with simple additive or multiplicative interaction models. Furukawa et al.,(87) also noted that the joint effect appeared to be super-multiplicative for light/moderate-smokers but additive or sub-additive for heavy-smokers.

Two Czech nested case-control studies of miners and home occupiers showed that the combined effect from radon and smoking is close to an additive interaction(89). For the miner study, this was shown only when a modifying effect of time since exposure was used. In contrast, most uranium miner studies are consistent with a sub-multiplicative interaction between smoking and radon(5,65,94,95). For example, the findings from the WISMUT miner study(65) support a sub- to supra- multiplicative interaction between smoking and radon. Due to these conflicting results, more research is required to investigate the interaction between smoking and radiation induced lung cancer.

Because the baseline lung cancer rates for the miner cohorts are greater than that of the ICRP Reference Asia and Euro-American male population, higher estimates of LEAR are obtained with an additive as opposed to a multiplicative risk projection model (Table 9). However, if the baseline rates were the same for both populations then both projection models would give similar lifetime risk estimates. For males, the LEAR estimates calculated by Tomášek assuming 70% additive ranged from 5.0 to 17 × 10⁻⁴ per WLM (Table 9)(19). This corresponds to dose conversion convention values of effective dose of 12 to 40 mSv per WLM for adults.

## Use of dose and dose rate effectiveness factor (DDREF)

ICRP Publication 103(1) uses a dose and dose rate effectiveness factor (DDREF) to obtain nominal risk coefficients that apply at low doses and low dose rates of low-linear energy transfer (low-LET) radiation. The values of detriment per Sv of ICRP Publication 103(1) for solid cancers include a DDREF of 2. However, in the UNSCEAR 2017 Report, annex B(96), the Committee concluded that based on current scientific evidence it intends not to use a DDREF for radiation risks estimates at low doses and low dose rates. Nevertheless, for the purposes of calculating a dose conversion convention for radiation protection purposes, a DDREF of 2 is implicit in the use of the ICRP detriment values. Use of a different value of DDREF or no DDREF would result on a change in detriment per Sv. Thus, in the present paper, a DDREF of 2 is used for the purposes of calculations applying the ICRP dose conversion convention (i.e. epidemiological approach).

## CONCLUSIONS

In Publication 115(2), ICRP reviewed epidemiological data from studies of radon-induced lung cancers, focusing on low levels of exposure and exposure rates in mines. Priority was given to risk models derived from pooled analyses and with good quality exposure assessment data. Based
on this review, a detriment adjusted nominal risk coefficient of $5 \times 10^{-4}$ mSv per WLM [$1.4 \times 10^{-3}$ per mJ h m$^{-3}$] was recommended for a mixed adult population of smokers and non-smokers for radiation protection purposes. The increase of about a factor of 2 from ICRP's previous published value$^{(7)}$ was mainly due to consideration of low exposure and low exposure rates.

The effective dose coefficient per unit exposure to radon and progeny can be derived either by dosimetric calculations or by epidemiological comparisons. Taking account of both approaches, ICRP recommended a single rounded value of 3 mSv per mJ h m$^{-3}$ (approximately 10 mSv WLM$^{-1}$) to be used in most circumstances, for workers in buildings and in underground mines. ICRP also intends that this same dose coefficient applies to exposure in homes.

UNSCEAR has recently evaluated published dosimetric assessments and reviewed epidemiological data on radon-induced lung cancers. For occupational studies of miners published since 2006, linear estimates of the ERR per WLM derived from each of the full cohorts were reported and a combined estimate using a statistical weighting procedure was calculated. A statistically significant higher combined estimate (by a factor of 2.6) was obtained when restricting the analysis to more recent work periods and lower exposures. This difference, showing higher lung cancer risk per unit exposure at lower levels of exposure and exposure rate, is consistent with the conclusions of ICRP Publication 115.

Compared with the BEIR VI risk models, the B2 risk model of Tomášek$^{(75)}$ is preferable because it takes account of the exposure rate in each year rather than the mean exposure rate over the period of employment. LEAR estimates were calculated by applying the B2 risk model individually to the updated Czech Republic, Wismut and Ontario miner studies as well as to the combined 11 miner studies used in the BEIR VI report. LEAR values calculated for the ICRP sex-averaged reference population ranged from 3.2 to $7.0 \times 10^{-4}$ per WLM for the Wismut and the combined 11 miner studies respectively. The corresponding dose conversion convention values for adults range from 2.2 to 4.7 mSv per mJ h m$^{-3}$ (7.6 to 17 mSv per WLM). Lower values (1.6 to 3.5 mSv per mJ h m$^{-3}$ or 5.6 to 12 mSv per WLM) are obtained for the whole population assuming the same detriment per radon exposure for adults and children. However, these values are considered less reliable as the impact of radon exposure at young ages remains unclear.

UNSCEAR reviewed dosimetric calculations for radon progeny exposure in homes, indoor workplaces and mines published after 2006. For exposures in homes, the range of the effective doses per unit exposure is from 1.1 to 5.9 mSv per mJ h m$^{-3}$ (4 to 21 mSv per WLM) with an arithmetic mean of 3.1 mSv per mJ h m$^{-3}$ (11 mSv per WLM). The range for indoor workplaces was similar but the mean was higher (4.5 mSv per mJ h m$^{-3}$ or 16 mSv per WLM) because of the higher assumed breathing rate for workers compared with adults at home.

The UNSCEAR review of the epidemiological data and the published dosimetric assessments are consistent with the use of the ICRP reference effective dose coefficient of 3 mSv per mJ h m$^{-3}$ (about 10 mSv WLM$^{-1}$) for workers in buildings and in underground mines. It is close to the central value of the dosimetric assessments. Also, it is close to the epidemiological dose conversion convention values for adults that were calculated from the LEAR estimates obtained using the B2 risk model (Table 10). In contrast, the UNSCEAR's established value of 1.6 mSv per mJ h m$^{-3}$
(5.7 mSv per WLM or 9 nSv per h Bq m⁻³ EEC of <sup>222</sup>Rn) is at the lower end of the range of calculated values. The UNSCEAR's established value is not intended for radiological protection purposes; ICRP dose coefficients should be used for this purpose. This is in agreement with the conclusions of an IAEA Technical Meeting on radon dose coefficients at which the participants recommended the use of the ICRP Publication 137 reference effective dose coefficient of 3 mSv per mJ h m⁻³ (~10 mSv WLM⁻¹) as the default for workplaces unless a different dose coefficient is justified by specific aerosol characteristics<sup>(97)</sup>. UNSCEAR uses its established value when comparing radon exposure levels with other sources of radiation exposures among different countries.

Outstanding issues regarding the calculation of LEAR following exposure to radon that require further research include whether the ERR per WLM is independent of sex. The calculations of lifetime risks for a sex-average population assumes that the ERR is independent of sex status because the risk models are based on male miners. Thus, the question arises whether it is more appropriate to calculate LEAR estimates for a reference male population, which would yield higher values. Another issue is if a multiplicative or an additive projection risk model is more appropriate. The calculations carried out by Tomášek, which are reported here and in the electronic attachment of the UNSCEAR 2019 report<sup>(19)</sup>, give higher LEAR estimates for an additive projection model. Calculations of lifetime risks for populations with different levels of smoking prevalence would also be useful for radiation projection purposes. The impact of radon exposure at young ages remains unclear, as no epidemiological studies have been able to provide results on this point up to now.

Greater precision in dosimetric modelling can be obtained with more information on aerosol parameter values in a variety of residential and occupational conditions. For example, there is a lack of data on aerosol characteristics in modern mines, modern buildings, schools and tourist caves. Further research is required on the spatial dose distribution within the lung, the depth distribution of the target cells within the epithelium, and the regional sensitivity of the lung to radiation-induced cancer. More accurate dose calculations are required for specific groups such as smokers, persons with respiratory disease and children.

Most of these issues are being addressed in ongoing research projects such as the Pooled Uranium Miners Analysis (PUMA)<sup>(98,99)</sup> and the European research project RadoNORM on managing risks from radon and Naturally-Occurring Radioactive Materials (NORM)<sup>(100)</sup>.

## ACKNOWLEDGEMENTS

The authors would like to thank Dr Brian J Smith (from the University of Iowa, United States) for discussions and quality assurance checks on calculating the combined estimates using a random effects meta-analysis model with inverse-variance weighting. The authors also wish to thank to Dr Nora Fenske, Dr Paul Demers and Dr Lydia Zablotska for providing details on the uncertainties in risk models and for parameter estimates in the B2 model.

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<table><caption>**Table 1.** ICRP Publication 137<sup>(4)</sup> reference aerosol parameter values for different exposure scenarios for <sup>222</sup>Rn progeny<sup>(9)</sup>.</caption><thead><tr><th rowspan="2">Exposure scenario</th><th rowspan="2">Unattached fraction, f<sub>p</sub></th><th rowspan="2">Equilibrium factor, F</th><th colspan="5">Attached aerosol characteristics in the ambient air<sup>c,d</sup></th></tr><tr><th>Mode, i</th><th>f<sub>pi</sub></th><th>AMTD<sub>i</sub> (nm)</th><th>σ<sub>gi</sub></th><th>hgf<sub>i</sub><sup>e</sup></th></tr></thead><tbody><tr><td rowspan="2">Indoor workplace</td><td rowspan="2">0.08</td><td rowspan="2">0.4</td><td>n</td><td>0.2</td><td>30</td><td>2.0</td><td>2.0</td></tr><tr><td>a</td><td>0.8</td><td>250</td><td>2.0</td><td>2.0</td></tr><tr><td>Mine<sup>e</sup></td><td>0.01</td><td>0.2</td><td>a</td><td>1.0</td><td>250</td><td>2.0</td><td>1.0</td></tr><tr><td>Tourist cave</td><td>0.15</td><td>0.4</td><td>a</td><td>1.0</td><td>200</td><td>2.0</td><td>1.0</td></tr></tbody></table>

<sup>a</sup> f<sub>p</sub> = unattached fraction in terms of the potential alpha energy concentration (PAEC).

<sup>b</sup> The unattached progeny are assumed to have an activity median thermodynamic diameter (AMTD) of 1.0 nm with σ<sub>g</sub> = 1.3, and unit density and shape factor.

<sup>c</sup> Indices i = ‘n’ and ‘a’ represent the nucleation and accumulation modes, respectively. f<sub>pi</sub> = fraction of attached PAEC for mode i. σ<sub>gi</sub> = geometric standard deviation of mode i. hgf<sub>i</sub> = hygroscopic growth factor for mode i.

<sup>d</sup> The diesel powered mine aerosol is assumed to have an effective density, (i.e. ρ/χ) of 0.7 g cm<sup>-3</sup> whereas the tourist cave aerosol is assumed to have unit density and shape factor due to the high humidity in the caves<sup>(4,9)</sup>.

<sup>e</sup> It is assumed that the AMTD increases by hgf instantaneously as the particle enters the nose or the mouth. For simplicity, the hygroscopically enlarged particles are assumed to have unit density and shape factor.
<table><caption>**Table 2.** Published values of unattached fraction, *f*<sub>p</sub><sup>a</sup> and equilibrium factor, *F* for <sup>222</sup>Rn progeny obtained from measurements in tourist caves<sup>(4)</sup>.</caption><thead><tr><th>Tourist Caves</th><th>f<sub>p</sub><sup>a</sup></th><th>F</th><th>Reference</th></tr></thead><tbody><tr><td>Royal Cave, Victoria, Australia</td><td>0.14 (0.11-0.18)</td><td>0.19 - 0.52</td><td>Solomon, et al., 1992<sup>(31)</sup></td></tr><tr><td>Carlsbad Caverns, New Mexico</td><td>0.44 (0.25-0.59)</td><td>0.43 (0.36-0.48)</td><td>Cheng, Y. et al. 1997<sup>(32)</sup></td></tr><tr><td>Cantabria, Spain</td><td>0.26<sup>b</sup><br>0.86<sup>b</sup></td><td>-</td><td>Sainz et al. 2007<sup>(33)</sup></td></tr><tr><td>Bozkov Dolomite cave, Czech Republic</td><td>0.01-0.03</td><td>-</td><td>Rovenská et al. 2008<sup>(34)</sup></td></tr><tr><td>Postojna, Slovenia 1992:</td><td>0.1 (0.056-0.16)</td><td>0.36 (0.29-0.47)</td><td>Butterweck et al. 1992<sup>(35)</sup></td></tr><tr><td>Winter 1999<sup>c</sup>:</td><td>0.14 ± 0.08</td><td>0.58 ± 0.13</td><td>Vaupotič, 2008<sup>(36)</sup></td></tr><tr><td>Summer 2001<sup>c</sup>:</td><td>0.64 ± 0.12</td><td>0.32 ± 0.08</td><td></td></tr><tr><td>Summer 2001<sup>d</sup>:</td><td>0.17 ± 0.06</td><td>0.58 ± 0.13</td><td></td></tr></tbody></table>

a. *f*<sub>p</sub> = unattached fraction in terms of the potential alpha energy concentration (PAEC).

b. Estimated from particle concentration measurements made in the Monedas and Castillo caves respectively.

c. Measurements made at the lowest point of the cave.

d. Measurements made at the railway station in the cave.
<table><caption>**Table 3.** ICRP Publication 137<sup>(4)</sup> values of effective dose per unit exposure<sup>a</sup> to <sup>222</sup>Rn progeny for different exposure scenarios. Dose from inhaling <sup>222</sup>Rn gas is excluded. Calculations apply to a Reference Worker with an average breathing rate of 1.2 m<sup>3</sup> h<sup>-1</sup>.</caption><thead><tr><th rowspan="2">Place</th><th rowspan="2">f<sub>p</sub><sup>b</sup></th><th rowspan="2">F<sup>c</sup></th><th colspan="3">Absorbed dose to regions of the lung<sup>d</sup>, mGy per WLM</th><th colspan="2">Effective dose coefficient<sup>(e,f)</sup></th></tr><tr><th>BB</th><th>bb</th><th>AI</th><th>mSv per WLM</th><th>mSv per mJ h m<sup>-3</sup></th></tr></thead><tbody><tr><td>Indoor workplace</td><td>0.08</td><td>0.4</td><td>11</td><td>11</td><td>0.5</td><td>20</td><td>5.6</td></tr><tr><td>Mine</td><td>0.01</td><td>0.2</td><td>4.6</td><td>8.3</td><td>0.4</td><td>11</td><td>3.1</td></tr><tr><td>Tourist cave</td><td>0.15</td><td>0.4</td><td>14</td><td>14</td><td>0.4</td><td>23</td><td>6.6</td></tr></tbody></table>

a. 1 working level month (WLM) = 3.54 mJ h m<sup>-3</sup>; 1 WLM = (6.37 10<sup>5</sup>/F) Bq h m<sup>-3</sup> of <sup>222</sup>Rn gas.

b. $f_p$ = unattached fraction in terms of the potential alpha energy concentration (PAEC).

c. F = equilibrium factor.

d. The absorbed dose per WLM to regions of the lung averaged between male and females. BB=bronchial region, bb=bronchiolar region and AI = alveolar interstitial region.

e. Effective dose is computed from the equivalent doses assessed for all target organs and tissues of the Reference male and Reference Female defined by ICRP<sup>(1)</sup>. The dose to the lung contributes more than 93% of the effective dose depending on exposure scenario.

f. The extra effective dose from inhaling <sup>222</sup>Rn gas is 1.82E-7 mSv per Bq h m<sup>-3</sup> or (1.16E-1/F) mSv per WLM or (3.28E-2/F) mSv per mJ h m<sup>-3</sup>. Thus, for indoor workplaces and tourist caves with F=0.4, the extra effective dose is only 0.3 mSv per WLM.
<table><caption>**Table 4.** ICRP Publication 137(4) Effective doses per unit exposure to <sup>222</sup>Rn radon progeny as a function of the unattached fraction, $f_p^a$ for different exposure scenarios(4). Dose from inhaling <sup>222</sup>Rn gas is excluded. Calculations apply to a Reference Worker with an average breathing rate of 1.2 m<sup>3</sup> h<sup>-1</sup>.</caption><thead><tr><th rowspan="2">Place</th><th colspan="2">Effective dose per exposure<sup>b,c</sup></th></tr><tr><th>mSv per WLM</th><th>mSv per mJ h m<sup>-3</sup></th></tr></thead><tbody><tr><td>Indoor workplace</td><td>86 f<sub>p</sub> + 14 (1-f<sub>p</sub>)</td><td>24 f<sub>p</sub> + 3.9 (1-f<sub>p</sub>)</td></tr><tr><td>Mine</td><td>86 f<sub>p</sub> + 10 (1-f<sub>p</sub>)</td><td>24 f<sub>p</sub> + 2.9 (1-f<sub>p</sub>)</td></tr><tr><td>Tourist cave</td><td>86 f<sub>p</sub> + 12 (1-f<sub>p</sub>)</td><td>24 f<sub>p</sub> + 3.5 (1-f<sub>p</sub>)</td></tr></tbody></table>

<footnote>a $f_p$ = unattached fraction in terms of the potential alpha energy concentration (PAEC).</footnote>

<footnote>b 1 working level month (WLM) = 3.54 mJ h m<sup>-3</sup>.</footnote>

<footnote>c The extra effective dose from inhaling <sup>222</sup>Rn gas is 1.82E-7 mSv per Bq h m<sup>-3</sup> or (1.16E-1/F) mSv per WLM or (3.28E-2/F) mSv per mJ h m<sup>-3</sup>.</footnote>
<table><caption>**Table 5.** A selection of doses assessments reviewed by UNSCEAR<sup>(19)</sup>,<sup>a</sup></caption><thead><tr><th>Publication</th><th>Model Type<sup>b</sup></th><th>Comment</th><th>Effective dose coefficient<sup>c</sup><br>(mSv WLM<sup>-1</sup>)</th></tr></thead><tbody><tr><td colspan="4"><em>Home exposures</em></td></tr><tr><td>Marsh and Birchall, 2000<sup>(40)</sup></td><td>HRTM</td><td>Best estimate</td><td>15</td></tr><tr><td colspan="4"><em>Parameter sensitivity analysis:</em></td></tr><tr><td colspan="4">Breathing rate<sup>d</sup>: 0.45-1.5 m<sup>3</sup>h<sup>-1</sup></td></tr><tr><td colspan="4">Unattached fraction<sup>e</sup>, f<sub>p</sub> = 0.03 – 0.20</td></tr><tr><td colspan="4">Nucleation fraction<sup>f</sup>: 0 - 0.4</td></tr><tr><td colspan="4">Basal cell weighting factor<sup>g</sup>: 0-1</td></tr><tr><td colspan="4">Target cell layer depth:</td></tr><tr><td colspan="4">Reduced by factor of 2</td></tr><tr><td colspan="4">Apportionment factors, (A<sub>BB</sub>:A<sub>bb</sub>:A<sub>AI</sub>)<br>(1/3:1/3:1/3)<sup>(22)</sup> to (0.6:0.2:0.2)<sup>(21)</sup></td></tr><tr><td>Marsh, et al., 2002<sup>(41)</sup></td><td>HRTM</td><td>Parameter uncertainty analysis<sup>h</sup></td><td>GM=14<br>GSD=1.5</td></tr><tr><td rowspan="3">Yu, et al., 2001<sup>(38)</sup></td><td rowspan="3">Deterministic<br>airway generation<br>model</td><td>Caucasian male</td><td>9.2</td></tr><tr><td>Chinese male</td><td>7.4</td></tr><tr><td>Chinese female</td><td>6.5</td></tr><tr><td>Winkler-Heil and Hoffman, 2002<sup>(24)</sup></td><td>Deterministic<br>airway generation</td><td></td><td>8.8</td></tr><tr><td rowspan="2">Nikezic et al., 2006<sup>(44)</sup></td><td rowspan="2">HRTM</td><td>Target cell layer as in HRTM</td><td>15</td></tr><tr><td>Cellular dose approach</td><td>13</td></tr><tr><td colspan="4"><em>Mine exposures</em></td></tr><tr><td rowspan="3">Winkler-Heil, 2007<sup>(25)</sup></td><td rowspan="3">Deterministic<br>airway generation<br>Stochastic airway<br>generation<br>HRTM</td><td>Same input parameters for mine conditions</td><td>8.3</td></tr><tr><td></td><td>8.9</td></tr><tr><td></td><td>12</td></tr><tr><td rowspan="3">Baias, et al., 2010<sup>(45)</sup></td><td rowspan="3">Stochastic airway<br>generation</td><td>Never smoker</td><td>7.2</td></tr><tr><td>Light long-term smoker or heavy<br>short-term smoker<sup>i</sup></td><td>6.4</td></tr><tr><td>Heavy long-term smoker</td><td>13</td></tr><tr><td rowspan="2">Solomon, et al., 2018<sup>(53)</sup></td><td rowspan="2">Revised HRTM<sup>(30)</sup></td><td>Underground workshop</td><td>23</td></tr><tr><td>Operational sites</td><td>16</td></tr></tbody></table>

a. This is a sub-set of the dose assessments reviewed by UNSCEAR to illustrate the main points discussed in the text. The full set of reviewed dose assessments is tabulated in the UNSCEAR report<sup>(19)</sup>.

b. HRTM = ICRP Publication 66 Human Respiratory Tract Model<sup>(4)</sup>
c. The dose coefficient was calculated as $w_{lung} \times H_{lung}$, which approximates the effective dose, where $H_{lung}$ is the equivalent dose to the lung and $w_{lung}$ is the ICRP lung tissue weighting factor (0.12).

d. The ICRP reference ventilation rates for sleep and light exercise are 0.45 and $1.5 \text{ m}^3 \text{ h}^{-1}$ respectively(4).

e. $f_p$ = unattached fraction in terms of the potential alpha energy concentration (PAEC).

f. Expressed as a fraction of the attached PAEC.

g. The HRTM assumes that the basal and secretory cell populations in the bronchial epithelium are equally sensitive to dose(22,30). Thus $H_{BB} = 0.5H_{bas} + 0.5H_{sec}$. A basal cell weighting factor of 1.0 means that $H_{BB} = H_{bas}$ whereas a basal cell weighting factor of zero means that $H_{BB} = H_{sec}$.

h. The output was a lognormal distribution of doses characterised by the geometric mean (GM) and the geometric standard deviation (GSD).

i. For light, long-term smoker and the heavy short-term smoker it was assumed that the mucus thickness increases by 128%±5%. However, the authors noted that some publications argued that the increase in mucus thickness is much greater (500%±200%), and assuming these values would give an effective dose coefficient of $1.74 \text{ mSv WLM}^{-1}$ (Bais, et al.(45)).
<table><caption>**Table 6.** Summary statistics of UNSCEAR's dosimetric review of effective dose coefficients for inhalation of <sup>222</sup>Rn progeny<sup>(19),a</sup>. Arithmetic mean values are given with ranges in parentheses. The values are compared with UNSCEAR's established value, which applies to adults in the general population<sup>(16,17,19)</sup>.</caption><thead><tr><th rowspan="2">Place</th><th colspan="3">Effective dose coefficient<sup>a,b</sup> for <sup>222</sup>Rn progeny</th></tr><tr><th>mSv<br>per WLM</th><th>mSv per<br>mJ h m<sup>-3</sup></th><th>nSv per h Bq m<sup>-3</sup><br>EEC of <sup>222</sup>Rn</th></tr></thead><tbody><tr><td>Mines</td><td>12 (4-23)</td><td>3.4 (1.1-6.5)</td><td>18 (7-37)</td></tr><tr><td>Indoor workplace</td><td>16 (6-24)</td><td>4.5 (1.7-6.8)</td><td>25 (9-38)</td></tr><tr><td>Homes</td><td>11 (4-21)</td><td>3.1 (1.1-5.9)</td><td>18 (7-34)</td></tr><tr><td>UNSCEAR's established value</td><td>5.7</td><td>1.6</td><td>9</td></tr></tbody></table>

a. The dose coefficient was calculated as $w_{\text{lung}} \times H_{\text{lung}}$, which approximates the effective dose, where $H_{\text{lung}}$ is the equivalent dose to the lung and $w_{\text{lung}}$ is the ICRP lung tissue weighting factor (0.12).

b. 1 WLM = 3.54 mJ h m⁻³; EEC = equilibrium equivalent concentration of <sup>222</sup>Rn; 1 h Bq m⁻³ of EEC exposure of <sup>222</sup>Rn = $1.57 \times 10^{-6}$ WLM = $5.56 \times 10^{-6}$ mJ h m⁻³.
<table><caption>**Table 7** Estimates of lifetime excess absolute risks (LEAR)<sup>a</sup> per WLM presented in ICRP Publication 115<sup>(2)</sup>.</caption><thead><tr><th>Risk model</th><th>ICRP background reference rates</th><th>LEAR<sup>a</sup> [×10<sup>-4</sup> per WLM]</th><th>Reference</th></tr></thead><tbody><tr><td rowspan="2">GSF model, ICRP Publication 65<sup>(7)</sup></td><td>Reference population of 5 countries<sup>b</sup>; ICRP Publication 60<sup>(68)</sup></td><td>2.8</td><td>ICRP, 1993<sup>(7)</sup></td></tr><tr><td>Euro-American and Asian populations<sup>b</sup>; ICRP Publication 103<sup>(1)</sup></td><td>2.7</td><td>Tomášek et al. 2008<sup>(6)</sup></td></tr><tr><td>BEIR VI (exposure-age-concentration) model<sup>(5)</sup></td><td>Euro-American and Asian populations; ICRP Publication 103<sup>(1)</sup></td><td>5.3</td><td>Tomášek et al. 2008<sup>(6)</sup></td></tr><tr><td>Czech-French model<sup>(69)</sup></td><td>Euro-American and Asian populations; ICRP Publication 103<sup>(1)</sup></td><td>4.4</td><td>Tomášek et al. 2008<sup>(6)</sup></td></tr><tr><td>Models derived from single studies<sup>c</sup></td><td>Euro-American and Asian populations; ICRP Publication 103<sup>(1)</sup></td><td>3 to 7</td><td>ICRP, 2010<sup>(2)</sup></td></tr><tr><td>BEIR VI (exposure-age-concentration) model<sup>(5)</sup></td><td>Euro-American males of ICRP Publication 103<sup>(1)</sup></td><td>7</td><td>ICRP, 2010<sup>(2)</sup></td></tr><tr><td>Recommended value for radiation protection</td><td></td><td>5</td><td>ICRP, 2010<sup>(2)</sup></td></tr></tbody></table>

a. Lifetime excess absolute risks per WLM calculated for the reference population given in column 2 up to 95 years of age with an exposure scenario of 2 WLM per year from 18 to 64 years of age using a relative risk projection model. A lag time of 5 years was assumed.

b. The reference population consisted of both males and females.

c. Other risk models were considered obtained from single studies including the French CEA-AREVA cohort<sup>(70)</sup>, the Canadian Eldorado cohort<sup>(71)</sup> and the German Wismut cohort<sup>(63)</sup>.
<table><caption>**Table 8.** Lifetime excess absolute risks (LEAR)<sup>a</sup> per WLM calculated for the male and sex-averaged ICRP Asian and Euro-American population using the BEIR VI risk model<sup>(19,75)</sup>. The BEIR VI risk model<sup>b</sup> was applied individually to the Wismut, Czech and Eldorado cohort miner studies as well as to the joint analysis of the 11 cohort studies from BEIR VI report. Standard error given in parenthesis.</caption><thead><tr><th rowspan="2">Cohort</th><th colspan="2">LEAR<sup>a</sup> [× 10<sup>-4</sup> per WLM] (Standard error)</th></tr><tr><th>Male<sup>c</sup></th><th>Sex-averaged<sup>c</sup></th></tr></thead><tbody><tr><td>Wismut</td><td>3.0 (0.70)</td><td>2.4 (0.60)</td></tr><tr><td>Czech</td><td>5.0 (1.3)</td><td>3.9 (1.0)</td></tr><tr><td>Eldorado</td><td>9.6 (3.8)</td><td>7.5 (3.0)</td></tr><tr><td>11 studies from BEIR VI</td><td>7.0 (1.6)</td><td>5.6 (1.3)</td></tr></tbody></table>

a. Lifetime excess absolute risks per WLM calculated up to 95 years of age with an exposure scenario of 2 WLM per year from 18 to 64 years of age using a relative risk projection model. A lag time of 5 years was assumed.

b. The BEIR VI exposure-age-concentration with modifying factors of attained age, time since exposure (TSE), and mean exposure rate in terms of average concentration over period of exposure.

c. The ICRP reference baseline rates for general mortality and lung cancer mortality for males and sex-averaged of the Asia and Euro-American population<sup>(1)</sup> were used in the calculations.
<table><caption>**Table 9.** Lifetime excess absolute risks (LEAR)<sup>a</sup> per WLM calculated for the ICRP Asian and Euro-American male population [ICRP, 2007] using multiplicative and additive projection models<sup>(19,75)</sup>. The B2 risk model<sup>b</sup> was applied to the Wismut, Czech and Ontario cohort miner studies as well as to the joint analysis of the 11 cohort studies from BEIR VI report<sup>(19,75)</sup>. Standard error given in parenthesis.</caption><thead><tr><th rowspan="2">Projection Model</th><th colspan="4">LEAR<sup>a</sup> [ × 10<sup>-4</sup> per WLM] (Standard error)</th></tr><tr><th>Wismut</th><th>Czech</th><th>Ontario</th><th>11 studies from BEIR VI</th></tr></thead><tbody><tr><td>Multiplicative<sup>b</sup></td><td>4.0 (0.8)</td><td>5.6 (1.3)</td><td>8.3 (2.1)</td><td>8.7 (1.8)</td></tr><tr><td>Additive<sup>c</sup></td><td>5.4 (1.1)</td><td>13.4 (3.2)</td><td>11.8 (3.0)</td><td>21.0 (4.4)</td></tr><tr><td>Weighted mean<sup>d</sup></td><td>5.0 (1.0)</td><td>11 (3)</td><td>11 (3)</td><td>17 (4)</td></tr></tbody></table>

a. Lifetime excess absolute risks per WLM calculated for the ICRP Asian and Euro-American male population<sup>(1)</sup> up to 95 years of age with an exposure scenario of 2 WLM per year from 18 to 64 years of age. A lag time of 5 years was assumed.

b. Risk B2 model with modifying factors of attained age, TSE and annual exposure rate<sup>(19,75)</sup>. Multiplicative projection model: based on an Excess Relative Risk (ERR) coefficient.

c. Additive projection model: based on an Excess Absolute Risk (EAR) coefficient. EAR was calculated from the ERR as follows: EAR per person years per WLM = $r_B \times \text{ERR per WLM}$, where $r_B$ is the background lung cancer rate (per person years) estimated in the cohorts.

d. Weighted mean taken as 0.7 additive and 0.3 multiplicative as assumed in ICRP Publication 103 for the calculation of lung detriment<sup>(1)</sup>.
<table><caption>**Table 10** Dose conversion convention coefficients obtained by equating ICRP values for total radiation detriment with estimates of lifetime lung cancer risk from radon exposure obtained with the B2 risk model.</caption><thead><tr><th rowspan="3">Cohort</th><th rowspan="3">LEAR<sup>a</sup><br/>[× 10<sup>-4</sup> per WLM]<br/>(95% CI)</th><th colspan="4">Dose conversion convention<sup>b,c</sup> (95% CI)</th></tr><tr><th colspan="2">Workers (i.e. adults)</th><th colspan="2">Public (i.e. all ages)</th></tr><tr><th>mSv per<br/>WLM</th><th>mSv per<br/>mJ h m<sup>-3</sup></th><th>mSv per<br/>WLM</th><th>mSv per<br/>mJ h m<sup>-3</sup></th></tr></thead><tbody><tr><td>Wismut</td><td>3.2<br/>(2.0, 4.4)</td><td>7.6<br/>(4.8, 10)</td><td>2.2<br/>(1.4, 2.9)</td><td>5.6<br/>(3.6, 7.7)</td><td>1.6<br/>(1.0, 2.2)</td></tr><tr><td>Czech</td><td>4.5<br/>(2.3, 6.7)</td><td>11<br/>(5.6, 16)</td><td>3.0<br/>(1.6, 4.5)</td><td>7.9<br/>(4.1, 12)</td><td>2.2<br/>(1.2, 3.3)</td></tr><tr><td>Ontario</td><td>6.7<br/>(3.4, 10)</td><td>16<br/>(8.0, 24)</td><td>4.5<br/>(2.3, 6.7)</td><td>12<br/>(5.9, 18)</td><td>3.3<br/>(1.7, 5.0)</td></tr><tr><td>11 studies from<br/>BEIR VI</td><td>7.0<br/>(4.1, 9.9)</td><td>17<br/>(9.7, 24)</td><td>4.7<br/>(2.7, 6.7)</td><td>12<br/>(7.1, 17)</td><td>3.5<br/>(2.0, 4.9)</td></tr><tr><td colspan="6" style="text-align: center;">Combined estimates<sup>d</sup> (95% CI)</td></tr><tr><td>All 4 cohorts</td><td>5.0<br/>(3.1, 6.8)</td><td>12<br/>(7.3, 16)</td><td>3.3<br/>(2.1, 4.6)</td><td>8.7<br/>(5.4, 12)</td><td>2.5<br/>(1.5, 3.4)</td></tr><tr><td>Wismut,<br/>Czech, Ontario</td><td>4.3<br/>(2.5, 6.0)</td><td>10<br/>(6.0, 14)</td><td>2.9<br/>(1.7, 4.1)</td><td>7.5<br/>(4.4, 11)</td><td>2.1<br/>(1.3, 3.0)</td></tr></tbody></table>

a. Lifetime excess absolute risks (LEAR) per WLM calculated for the ICRP Asian and Euro-American population(1) up to 95 years of age with an exposure scenario of 2 WLM per year from 18 to 64 years of age using the multiplicative projection risk model B2(19,75). A lag time of 5 years was assumed. LEAR values calculated by Tomášek, 2020(75). CI = Confidence Intervals.

b. Dose conversion convention obtained by dividing the LEAR estimates (given in column 2) by the detriment per Sv values from ICRP Publication 103(1), namely 4.2 10⁻² Sv⁻¹ for adults and 5.7 10⁻² Sv⁻¹ for all ages.

c. 1 WLM = 3.54 mJ h m⁻³

d. A combined estimate was calculated using a random effects meta-analysis model with inverse-variance weighting(72).
<figure><img src="image_2.png" /><figcaption>**Figure 1.** Frequency distribution of the histologic subtypes of lung tumours in different regions of the lung in a group of uranium miners and a group of non-miners. Both groups were mainly cigarette smokers. Adapted from Saccomanno et al. (21).</figcaption></figure>