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WHO Handbook on Indoor Radon: A Public Health Perspective. Geneva: World Health Organization; 2009.

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WHO Handbook on Indoor Radon: A Public Health Perspective.

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1Health effects of radon

KEY MESSAGES

  • Epidemiological studies confirm that radon in homes increases the risk of lung cancer in the general population. Other health effects of radon have not consistently been demonstrated.
  • The proportion of all lung cancers linked to radon is estimated to lie between 3% and 14%, depending on the average radon concentration in the country and on the method of calculation.
  • Radon is the second most important cause of lung cancer after smoking in many countries. Radon is much more likely to cause lung cancer in people who smoke, or who have smoked in the past, than in lifelong non-smokers. However, it is the primary cause of lung cancer among people who have never smoked.
  • There is no known threshold concentration below which radon exposure presents no risk. Even low concentrations of radon can result in a small increase in the risk of lung cancer.
  • The majority of radon-induced lung cancers are caused by low and moderate radon concentrations rather than by high radon concentrations, because in general less people are exposed to high indoor radon concentrations.

This chapter discusses current knowledge on health risks from radon, including both lung cancer and other potential health effects. It also gives estimates of radon concentrations in various countries and summarizes recent estimates of the burden of radon-induced lung cancer. Radon is the largest natural source of human exposure to ionizing radiation in most countries. In the general population most exposure occurs indoors, especially in small buildings such as houses (UNSCEAR 2000), although there are some groups for whom occupational exposure presents a greater risk.

Evidence of increased mortality from respiratory disease among certain groups of underground miners in central Europe dates back to the sixteenth century, but it was not until the nineteenth century that it was appreciated that the disease was in fact lung cancer. Radon was first suspected as the primary cause of these cancers in radon-exposed miners in the twentieth century, and its causal role in lung cancer became firmly established in the 1950s. Further historical details are presented elsewhere (BEIR IV 1988). Studies of underground miners exposed occupationally to radon, usually at high concentrations, have consistently demonstrated an increased risk of lung cancer for both smokers and non-smokers. Based primarily on this evidence, radon was classified as a human carcinogen by the International Agency for Research on Cancer in 1988 (IARC 1988).

Since the 1980s, a large number of studies have directly examined the relationship between indoor radon and lung cancer in the general population. Individually, these studies are generally too small either to rule out a material risk, or to provide clear evidence that one existed. The investigators of the major studies in Europe, North America, and China have therefore brought their data together, and re-analyzed it centrally (Lubin et al. 2004, Krewski et al. 2005, 2006, Darby et al. 2005, 2006). These three pooled-analyses present very similar pictures of the risks of lung cancer from residential exposure to radon. Together, they provide overwhelming evidence that radon is causing a substantial number of lung cancers in the general population and they provide a direct estimate of the magnitude of the risk. They also suggest that an increased risk of lung cancer cannot be excluded even below 200 Bq/m3, which is the radon concentration at which action is currently advocated in many countries.

1.1. Lung cancer risks in radon-exposed miners

Lung cancer rates in radon-exposed miners have generally been studied using a cohort design in which all men employed in a mine during a particular time period are identified. The men are then followed up over time, regardless of whether they remain employed in the mine, and the vital status of each man is established at the end of the follow-up period. For those who have died, the date and cause of death is ascertained, and the death rate from lung cancer calculated, both overall and after subdivision by factors such as age, calendar period and cumulative exposure to radon. In these studies, exposure to radon was usually estimated retrospectively and in many of the studies the quality of the exposure assessment was low, particularly in the early years of mining, when the exposures were highest and no radon measurements were performed. In studies of radon-exposed miners radon progeny concentrations are generally expressed in terms of “working levels” (WL). The working level is defined as any combination of the short-lived progeny in one litre of air that results in the ultimate release of 1.3 × 105 MeV of potential alpha particle energy. The cumulative exposure of an individual to this concentration over a “working month” of 170 hours (or twice this concentration over half as long, etc.) is defined as a “working level month” (WLM).

A review of the major studies of underground miners exposed to radon that were available in the 1990s was carried out by the Committee on the Biological Effects of Ionizing Radiation (BEIR VI 1999). Eleven cohort studies were considered, including a total of 60 000 miners in Europe, North America, Asia and Australia, among whom 2 600 deaths from lung cancer had occurred. Eight of these studies were of uranium miners, and the remainder were of miners of tin, fluorspar or iron. Lung cancer rates generally increased with increasing cumulative radon exposure, but in one study (Colorado cohort) the rate increased at moderate cumulative exposures and then decreased again at high cumulative exposures. After exclusion of cumulative exposures above 3 200 WLM in this study, the lung cancer rate increased approximately linear with increasing cumulative radon exposure in all 11 studies, although the size of the increase per unit increase in exposure varied by more than a factor of ten between the studies, and this variation was much greater than could be explained by chance. Despite the substantial variation in the magnitude of the risk that was suggested by the different studies, the BEIR VI committee carried out a number of analyses considering pooled data from all 11 studies, giving different weights to the different studies. One such analysis estimated that the average increase in the lung cancer death rate per WLM in the 11 studies combined was 0.44% (95% confidence interval 0.20-1.00%). The percentage increase in the lung cancer death rate per WLM varied with time since exposure, with the highest percentage increase in risk in the period 5-14 years after exposure. It also varied with the age that the person concerned had reached, with higher percentage increases in risk at younger ages. Another finding of the BEIR VI study was that miners exposed at relatively low radon concentrations had a larger percentage increase in lung cancer death rate per WLM than miners exposed at higher radon concentrations. In order to summarize the risks seen in the studies of radon-exposed miners and to make projections about the likely risks in other radon-exposed populations, the BEIR VI committee developed a number of models. For illustration, the exposure-age-concentration model is summarized in Table 1.

Table 1. Patterns of radon-related lung cancer in miners in the studies considered by the BEIR VI Committee and the study of German uranium miners.

Table 1

Patterns of radon-related lung cancer in miners in the studies considered by the BEIR VI Committee and the study of German uranium miners.

Since the publication of the BEIR VI report, further follow-up has been conducted for the Czech study of radon-exposed miners (Tomasek et al. 2002, 2004) and for the French study (Rogel et al. 2002, Laurier et al. 2004). Several papers have been published giving further analyses of some other groups (Langholz et al. 1999, Stram et al. 1999, Hauptmann et al. 2001, Hornung et al. 2001, Duport et al. 2002, Archer et al. 2004, Hazelton et al. 2001, Heidenreich et al. 2004). In addition, cohorts of radon-exposed coal miners in Poland (Skowronek et al. 2003) and Brazil (Veiga et al. 2004) have been established, as well as a large cohort of uranium miners in the former German Democratic Republic (Kreuzer et al. 2002).

The German cohort includes a total of 59 001 men who had been employed by the Wismut Company in Eastern Germany (Grosche et al, 2006). By the time of the first mortality follow-up, a total of 2 388 lung cancer deaths had occurred. The German cohort is of particular interest, as it is nearly as large as all the 11 cohorts available to the BEIR VI Committee combined. In addition, the miners were all from the same geographical area and had the same social background, and the entire cohort was subject to the same follow-up procedure and the same system of exposure assessment. In this study, the average increase in lung cancer death rate per WLM was 0.21% (95% confidence interval 0.18-0.24%), just over half that seen in the BEIR VI analysis. When an exposure-age-concentration model similar to that used by the BEIR VI Committee was fitted to the German cohort, the highest percentage increase in the death rate per WLM was during the period 15 to 24 years after exposure, compared to 5 to 15 years in the BEIR VI model (cf. Table 1). The percentage increases were lower at older ages, as in the BEIR VI model, although the age-gradient was less steep. In both studies, the percentage increase in death rate per unit exposure decreased with increasing radon concentration, with exposures at 15.0+ WL carrying about one tenth the risk of those at <0.5 WL.

For some of the miner studies available to the BEIR VI Committee, information on smoking was available and in these studies the lung cancer death rate increased by 0.53% per WLM on average (95% confidence interval 0.20-1.38%), similar to the average percentage increase for all eleven studies considered by the BEIR VI Committee. When the analysis was carried out separately for never smokers (i.e. lifelong non-smokers) and for ever smokers (i.e. current and ex-smokers combined) the lung cancer death rate increased by 1.02% per WLM (95% confidence interval 0.15-7.18%) for the never smokers and 0.48% per WLM (95% confidence interval 0.18-1.27%) for the ever smokers. Thus, the percentage increase in lung cancer risk per WLM was larger in the never-smokers than in the ever-smokers, but the difference was not statistically significant (BEIR VI 1999).

Information on smoking habits is not generally available in the German cohort study. However, a case-control study of lung cancer among former employees of the German uranium mining company diagnosed at certain clinics during the 1990s has been carried out (Brueske-Hohlfeld et al. 2006). This study also found that the percentage increase in the lung cancer death rate per WLM was larger in never-smokers than in ex-smokers, and larger in ex-smokers than in current smokers (current smokers: 0.05% (95% confidence interval 0.001-0.14%); ex-smokers: 0.10% (95% confidence interval 0.03-0.23%); never-smokers: 0.20% (95% confidence interval 0.07-0.48%)).

Whether or not the true percentage increase in the lung cancer death rate per WLM differs between never-smokers and ever-smokers, it should be noted that the absolute increase in death rate per WLM will be much higher for current smokers than for never-smokers. This is due to the fact that for a given radon concentration, smokers have much higher lung cancer rates than never-smokers. For ex-smokers, the absolute increase per WLM will lie between those for current and for never-smokers, depending on factors such as the duration of smoking and the number of cigarettes per day smoked before quitting, and also the time since smoking cessation.

1.2. Lung cancer risks in the general population from indoor radon

Background

The magnitude of lung cancer risk seen in underground miners exposed to radon strongly suggests that radon may be a cause of lung cancer in the general population due to the exposure that occurs inside houses and other buildings. The conditions of exposure in mines and indoors differ appreciably (NRC 1991), and the smoking-related risks in the miners that have been studied differ from the smoking-related risks in the general populations of today. Other determinants of lung cancer risk differ between exposure in mines and indoors. For example, many of the miners were exposed to other lung carcinogens, such as arsenic, in addition to radon. All these differences mean that there is substantial uncertainty in extrapolating from the miner studies to obtain a quantitative assessment of the risk of lung cancer from radon in the home.

Much of the uncertainty associated with quantitative extrapolation from the studies of miners can be avoided by directly studying the association between indoor radon and risk of lung cancer. In such studies, radon exposures are usually expressed as the average concentration of radon gas per cubic metre of air to which an individual has been exposed at home over the previous few decades, and the unit is Becquerel per cubic metre (Bq/m3), where 1 Bq corresponds to one disintegration per second. Indoor radon concentrations in an individual house are usually subject to systematic diurnal and seasonal variation and the annual average radon concentration is also usually subject to substantial random year-to-year variation related to numerous factors (e.g. weather patterns and occupant behaviour such as window opening).

Initial attempts to study the risk of lung cancer from indoor radon included a number of geographical correlation studies (sometimes known as “ecological studies”), which examined the correlation between average radon concentrations and average lung cancer rates in different geographical areas. However, the usefulness of such studies is severely limited since they cannot control adequately for other determinants of lung cancer risk, such as cigarette smoking, which causes a much larger number of lung cancers than radon in most populations. Therefore, ecological studies often provide biased and misleading estimates of the radon-related risk. Further details and some illustrations of the biases that can occur are presented elsewhere (Puskin 2003).

A more appropriate way to examine the association between lung cancer and residential radon exposure is a case-control study, in which a predetermined number of individuals who have developed lung cancer are identified, together with a predetermined number of control individuals who have not developed the disease, but who are otherwise representative of the population from which the cases of lung cancer were drawn. In these studies, the controls are usually matched to the cases by age and sex. Detailed residential histories then need to be obtained for each individual in the study, as well as detailed information on smoking histories and other factors that determine each person's risk of developing lung cancer. In order to estimate the average radon concentration to which each individual in the study has been exposed over the previous few decades, measurements of the radon concentration need to be made both in his or her present home and, if the individual has moved in the last few decades, in other homes where the individual has lived. Once this is done, the radon concentrations can be compared between individuals who have developed lung cancer and the control individuals. Special statistical methods have been developed to account for variations in the other factors that influence the risk of developing lung cancer so that, in effect, comparisons are made only between individuals who have similar smoking histories and also similar values for other factors that determine the risk of lung cancer. Using such methods, the relationship between the risk of lung cancer and the average indoor radon concentration over the previous few decades can be estimated.

At least 40 case-control studies of indoor radon and lung cancer have now been conducted. Individually, most of these studies have not been large enough either to rule out an increased risk or to provide clear evidence that an increased risk existed. Therefore, in order to combine the information from more than one study, a number of authors have considered the published results from several studies to obtain a pooled estimate (Lubin and Boice 1997, Lubin 1999, Pavia et al. 2003). These systematic reviews of published papers have all concluded that the radon-related risk of lung cancer, as published in the individual studies, varies appreciably from one study to another. However, the methodology used to analyze the various studies differs considerably from study to study, notably in the extent to which the differing smoking-related risks of lung cancer for different individuals have been taken into account and in the quantification of the radon exposure histories of each individual. Such divergences may well lead to differences between the risk estimates in the individual studies and cannot be eliminated without access to basic data for each individual involved in the studies (Field et al. 2002).

In order to compare the findings of the different case-control studies of radon and lung cancer appropriately, and to ensure that the different smoking-related risks for different individuals are fully taken into account, it is necessary to assemble the component data on radon concentration, smoking history and other relevant factors for each individual in each of the original studies and to collate the data in a uniform way. When this has been done, parallel analyses of the different studies can be carried out, and the findings from the individual studies can be compared. Then, if the data from the different studies are consistent, they can be combined and an estimate of the risk of radon-related lung cancer can be derived based on all the studies included. Three analyses collating and comparing the individual information from a number of component studies have now been carried out, including 13 European studies (Darby et al. 2005, 2006), 7 North American studies (Krewski et al. 2005, 2006), and 2 Chinese studies (Lubin et al. 2004), respectively. All three analyses concluded that it was appropriate to derive a pooled estimate of the risk of lung cancer from radon in the home from the component studies. A summary of the findings of these pooled analyses appears in Table 2 and further details are presented below.

Table 2. Summary of risks of lung cancer from indoor radon based on international pooling studies that have combined individual data from a number of case-control studies and on studies of radon exposed miners.

Table 2

Summary of risks of lung cancer from indoor radon based on international pooling studies that have combined individual data from a number of case-control studies and on studies of radon exposed miners.

The European pooling study

The European pooling study (Darby et al. 2005, 2006) included data from all thirteen European studies of residential radon and lung cancer that satisfied selected inclusion criteria. These criteria required that studies had to be of a certain size (minimum 150 people with lung cancer and 150 control individuals without lung cancer, drawn from the same population) and that detailed smoking histories for each individual were available. In terms of exposure, radon measurements in homes where the individual had lived during the past 15 years or more were required. In total, over 7 000 lung cancer cases and more than 14 000 controls were entered into the pooled analysis. The study considered the effect on lung cancer risk of exposures to radon during the 30 year period ending 5 years prior to the diagnosis of lung cancer, or prior to a comparable reference date for control individuals. The available radon measurements covered a mean of 23 years and, where necessary, were adjusted for seasonal variation so that each measurement was representative of the radon concentration in a home over an entire year. For homes where no radon measurements could be obtained (e.g. the house had been demolished) the concentration was estimated indirectly as the mean of all the radon measurements in the residences of control group members in the relevant study area. To obtain the “measured radon concentration” for each individual, a time-weighted average of the radon concentrations in all the homes occupied over the past 5 to 34 years was calculated, with weights proportional to the length of time that the individual had lived in each of them.

After detailed allowance for the different lung cancer risks due to the varying smoking histories for individuals, the variation between the proportionate increase in risk per unit increase in radon concentration in the European studies was no larger than expected from random variation. It was therefore appropriate to pool the data. When this was done, a clear positive association between radon and lung cancer emerged. The risk of lung cancer increased by 8% per 100 Bq/m3 increase in measured radon concentration (95% confidence interval 3-16%). The estimated percentage increase in lung cancer rate for each unit increase in residential radon concentration did not vary according to the age or sex of the individual more than would be expected by chance, nor did it vary (on this proportionate scale) more than would be expected by chance according to his or her smoking history (cf. Table 3).

Table 3. Risk increase of radon-related lung cancer per 100 Bq/m3 of measured indoor radon concentration based on the results of the European and North American pooling studies.

Table 3

Risk increase of radon-related lung cancer per 100 Bq/m3 of measured indoor radon concentration based on the results of the European and North American pooling studies.

In the European pooling study, the exposure-response relationship appeared to be approximately linear with no evidence for a threshold below which there was no risk. In particular, the results were incompatible with a threshold above 150 Bq/m3 (i.e. 150 Bq/m3 was the 95% upper confidence limit for any threshold). Furthermore, the investigators found a statistically significant association between radon concentration and lung cancer, even when the analysis was restricted to people in homes with measured radon concentrations below 200 Bq/m3. The risk of lung cancer was 20% higher (95% confidence interval 3-30%) for those individuals with measured radon concentrations 100-199 Bq/m3 (mean: 136 Bq/m3) when compared to those with measured radon concentrations under 100 Bq/m3 (mean: 52 Bq/m3).

As mentioned above, there is substantial year-to-year random variation in the average annual radon concentration in a home, depending, for example, on variation in the weather (Zhang et al. 2007). Therefore, if the risk of lung cancer due to radon from the case-control studies is estimated based only on the measured radon concentrations and without taking this variation into account, then the risk is likely to be underestimated. Therefore, in the European pooling study, the analysis was repeated using “long-term average radon concentration” (i.e. taking into account the random year-to-year variability in measured radon concentration). The final estimated risk coefficient, based on the long-term average radon concentration, was 16% per 100 Bq/m3 (95% confidence interval 5-31%). Once again, on this proportionate scale, the risk did not vary more than would be expected by chance with age or sex or according to the smoking status of the individual, and the dose-response relationship was approximately linear, as demonstrated in Figure 1.

Figure 1. Relative risk of lung cancer versus long-term average residential radon concentration in the European pooling study.

Figure 1

Relative risk of lung cancer versus long-term average residential radon concentration in the European pooling study. Source: Darby et al. 2005 Relative risks and 95% confidence intervals are shown for categorical analyses and also best fitting straight (more...)

The North American pooling study

The North American Pooling study (Krewski et al. 2005, 2006) involved 3 662 cases and 4 966 controls from seven studies in the USA and Canada. The methodology was similar to that used for the European study. As with the European study, the radon-related risk in the component studies was found to be consistent, once the data for individual subjects had been collated. When data from all seven studies were combined, the risk of lung cancer increased by 11% per 100 Bq/m3 increase in measured radon concentration (95% confidence interval 0-28%). When the analyses were restricted to the subsets of data with greater exposure accuracy, the lung cancer risk estimates increased. For example, for individuals who lived in only one or two houses in the period 5 to 30 years prior to recruitment, with at least 20 years covered by dosimetry, the investigators reported a percentage increase of 18% (95% confidence interval 2-43%) per 100 Bq/m3. The estimated percentage increase in lung cancer rate for each unit increase in measured residential radon concentration did not vary according to the age or sex of the individual more than would be expected by chance, nor did it vary more than would be expected by chance according to his or her smoking history (cf. Table 3).

As with the European pooling study, the results of the North American pooling were consistent with a linear dose-response relationship with no threshold. However, unlike the European Pooling study, no formal adjustments for variations in yearly residential radon concentrations have been performed so far. When further analyses become available, a direct comparison between the findings of the North American and European pooled studies after accounting for year-to-year variations in indoor radon concentration will be feasible.

The Chinese pooling study

Lubin and colleagues (2004) analysed 1050 cases and 1996 controls from two studies in two areas: Gansu and Shenyang. For the pooled data, the risk per 100 Bq/m3 measured radon concentration increased by 13% (95% confidence interval 1-36%). This effect was chiefly due to the data from the much larger Gansu study, although the results of the two component studies were compatible with each other. As with the European and North American pooling studies, the results were consistent with a linear dose-response relationship with no threshold.

Overall evidence on the risk of lung cancer from residential radon

The three pooling studies present a very similar picture of the risk of lung cancer from residential exposure to radon (cf. Table 2). There is overwhelming evidence that radon is acting as a cause of lung cancer in the general population at concentrations found in ordinary homes. In particular, in all three pooling studies there was no evidence that the proportionate increase in risk per unit increase in radon concentration varied with the age, sex or smoking habits of the study subjects more than would be expected by chance. In addition, the dose-response relationship appeared to be linear, with no evidence of a threshold, and there was substantial evidence of a risk increase even below 200 Bq/m3, the concentration at which action is currently advocated in many countries.

The three major pooling studies reported increased risks of lung cancer based on a measured radon concentration of 8% (95% confidence interval 3-16%), 11% (0-28%) and 13% (1-36%) per 100 Bq/m3 increase in measured radon concentration (Table 2). As these three estimates are statistically compatible with each other, a weighted average, with weights proportional to their variances, can be calculated. This gives a joint estimate from the three pooling studies, based on measured radon concentrations, of 10% per 100 Bq/m3.

As described above, estimates based on measured radon concentration are likely to under estimate the true risks associated with residential radon, due to the year-to-year random variation in radon concentrations in a home. The only pooling study to date that has carried out a detailed analysis of the risks of residential radon based on a long-term average, as opposed to measured radon concentrations, is the European pooling. In this study, the risk estimate based on long-term average concentrations was twice the risk estimate based on measured radon concentrations. Data from repeated radon measurements made in separate years in the same home in China show a similar year-to-year variation as in the European studies (Lubin et al. 2005), while data from the United States also suggest considerable year-to-year random variation (Zhang et al. 2007). If it is assumed that the effect of adjusting for year-to-year random variation in the three pooling studies combined is the same as in the European study, then a joint risk estimate from the three pooling studies, based on long-term radon concentrations, would be around 20% per 100 Bq/m3 (cf. Table 2).

Other potential sources of radon exposure misclassification include detector measurement error, spatial radon variations within a home, missing data from previously occupied homes that are currently inaccessible, failure to link radon concentrations with subject mobility, and measuring radon gas concentration as a surrogate for radon progeny exposure (Field et al. 2002). It is generally difficult to assess the impact of these potential exposure measurement errors. However, if the misclassification does not differ systematically between cases and controls, the observed results tend to be biased towards zero (i.e. the true effect is underestimated). In fact, empiric models with improved retrospective radon exposure estimates were more likely to detect an association between residential radon exposure and lung cancer (Field et al. 2002).

A number of other factors have not been included in the formal analyses for the majority of indoor radon studies. In particular, there are frequently errors in the assignment of individuals to smoking categories and, in some countries, there may have been systematic changes in the radon concentrations over the last few decades, due to increased energy efficiency and the introduction of air conditioning. The overall effect of these factors, as described above, may indicate that the true effect of radon may be somewhat higher than the estimated risk in the residential radon studies, even after correction for year-to-year random variation in measured radon concentrations.

Direct comparison of the risks of lung cancer in studies of indoor radon with risks based on studies of radon-exposed miners is complicated. The generally higher exposures and also the inverse exposure-rate effect in the miners' data (cf. Table 1) contribute to this. Summary risk estimates from miners' studies are somewhat lower than from residential radon studies. For example, when all the miners included in the BEIR VI analysis are considered, the estimated risk is approximately 5% per 100 Bq/m3, with somewhat lower estimates for the large German study. For the BEIR VI study, an additional analysis including only miners with cumulative exposures below 50 WLM (i.e. the exposure that would be received from living in a house with a radon concentration of around 400 Bq/m3 for 30 years) has been carried out (Lubin et al. 1997) and suggests an increase of 14% per 100 Bq/m3, while a further analysis considering only miners with cumulative exposures below 50 WLM and exposed only at <0.5 WL (i.e. <∼2 000 Bq/m3) suggests an increase in risk of 30% per 100 Bq/m3. Similarly, results from an analysis of French and Czech cohorts that are restricted to workers with low exposure rates, an exposure window of 5 to 34 years and a comparatively high precision of exposure assessment indicate a risk increase in the order of 32% per 100 Bq/m3 as shown in Table 2 (Tomasek et al. 2008).

In summary, there is good agreement between the estimates of radon-related risk based on the studies of indoor radon and the studies of underground miners with relatively low cumulative exposures accumulated at low concentrations.

1.3. Radon and diseases other than lung cancer

When an individual spends time in an atmosphere that contains radon and its decay products, the part of the body that receives the highest dose of ionizing radiation is the bronchial epithelium, although the extra thoracic airways and the skin may also receive appreciable doses. In addition, other organs, including the kidney and the bone marrow, may receive low doses (Kendall et al 2002). If an individual drinks water in which radon is dissolved, the stomach will also be exposed.

The evidence for radon-related increases in mortality from cancers other than lung cancer has been examined in the same studies of radon-exposed miners that were included in the BEIR VI analyses (Darby et al. 1995), and no strong evidence was found that radon was causing cancers other than lung cancer. However, further investigations are focusing on this issue. For example, a recent case-cohort study evaluating the incidence of leukaemia, lymphoma, and multiple myeloma in Czech uranium miners (Rericha et al. 2007) found a positive association between radon exposure and leukemia, including chronic lymphocytic leukemia. The relationship between radon exposure and cardiovascular disease has been examined in a number of cohorts of radon-exposed miners, but none has found evidence that radon is causing heart disease (Villeneuve et al. 1997, 2007, Xuan et al. 1993, Tomasek et al. 1994, Kreuzer et al. 2006). A case-control study of stomach cancer in an area where there were high concentrations of natural uranium and other radionuclides in drinking water gave no indication of an increased risk (Auvinen et al. 2005).

About 20 ecological studies of exposure to radon in the general population and leukaemia either in children or in adults have been carried out. Several of these, including a recent methodologically advanced study by Smith et al. (2007), have found associations between indoor radon concentration and the risk of leukaemia (including chronic lymphocytic leukaemia in the Smith et al. study) at the geographic level (for a review see: Laurier et al. 2001). An ecological study performed in Norway showed an association between multiple sclerosis and indoor radon concentration (Bolviken 2003). Generally, these associations has been confirmed in a high-quality case-control or cohort study, either in radon-exposed miners or in the general population, although several such studies have been carried out (Laurier et al. 2001, Möhner et al. 2006). As with the studies of radon exposure and lung cancer, these ecological studies are prone to a number of biases. They are therefore likely to give misleading answers and should not be taken as evidence that radon is acting as a cause of these diseases.

1.4. Burden of lung cancer caused by indoor radon

From the evidence presented above, it is clear that exposure to radon is a well established cause of lung cancer in the general population. In any particular country, the proportion of lung cancers occurring each year which are radon-induced will be determined chiefly by the indoor radon concentrations in that country. Surveys have been carried out to determine the distribution of residential radon concentrations in most of the 30 member countries of the Organization for Economic Co-operation and Development (OECD). The worldwide average indoor radon concentration has been estimated at 39 Bq/m3 (Table 4).

Table 4. Indoor radon concentrations in OECD countries.

Table 4

Indoor radon concentrations in OECD countries.

Detailed calculations of the numbers of radon-induced lung cancers attributable to radon exposure have previously been published for a number of countries. The calculations are based on the estimated concentrations of indoor radon from the surveys together with the indirect estimates of risk provided either by the studies of miners in the BEIR VI analysis or by the direct evidence provided by the European pooling studies (Table 5).

Table 5. Estimates of the proportion of lung cancer attributable to radon in selected countries.

Table 5

Estimates of the proportion of lung cancer attributable to radon in selected countries.

In most populations, lung cancer rates are much higher in current cigarette smokers than in lifelong non-smokers. The proportionate increase in the risk of lung cancer per unit increase in indoor radon concentration is similar in lifelong non-smokers and cigarette smokers in studies of residential radon (Table 3). Furthermore, in the miner studies for which smoking information is available, the proportionate increase in the risk of lung cancer per unit increase in indoor radon concentration is also similar. It follows that the majority of radon-induced lung cancers are caused jointly by radon and by smoking, in the sense that lung cancer would not have occurred if either the individual had not smoked cigarettes or had not been exposed to radon.

At an individual level, the risk of radon-induced lung cancer following exposure to a given radon concentration is much higher among current cigarette smokers than among lifelong non-smokers. This has been illustrated by the pooled analysis of European residential radon studies (Darby et al. 2005). For lifelong non-smokers, it was estimated that living in a home with an indoor radon concentration of 0, 100 or 800 Bq/m3 was associated with a risk of lung cancer death (at the age of 75) of 4, 5 or 10 in a 1000, respectively. However, for a cigarette smoker, each of these risks would be substantially greater, namely 100, 120 and 220 in 1000. For those having stopped smoking, the radon-related risks are substantially lower than for those who continue to smoke, but they remain considerably higher than the risks for lifelong non-smokers.

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