Uranium mining and lung cancer: a legacy of the nuclear age

Abstract

The Nuclear Age spurred widespread mining of uranium for production of weapons and for nuclear power. The widespread mining of uranium, with historically limited control of radiation exposures, has resulted in high rates of lung cancer among the former miners. This paper reviews the long and ongoing story of lung cancer among miners of uranium.

Graphical Abstract

Graphical Abstract.

1. Introduction

The start of the “Nuclear Age” dates to the testing of the first atomic bomb at the Trinity Site in New Mexico in 1945, followed within weeks by the tragic bombings in Hiroshima and Nagasaki. Uranium, the fissile fuel for the Nuclear Age, was historically extracted primarily from underground mines [1]. Thousands of uranium miners have now died from lung cancer and other diseases caused by exposures in underground mines. They are also casualties of the Nuclear Age, dying one at a time in a toll that continues to increase. Here, we review the long and ongoing story of lung cancer among miners of uranium and other ores exposed to radon and its progeny, which come from the decay of uranium. The story dates back centuries [2]. More recently, when the problem of indoor radon was recognized, the epidemiological studies of the radon-exposed miners became the key resource for understanding the risks of radon in homes and other indoor settings.

While the Nuclear Age spurred widespread mining of uranium for production of weapons and for nuclear power, uranium-containing ores had long been mined for uranium and other metals, particularly silver, vanadium, and radium [1, 3]. These early mines were in Eastern Europe, the Four Corners region of the United States, Canada, and what was then referred to as the Belgian Congo (now Democratic Republic of Congo). The uranium used in the Manhattan Project came predominantly from the Belgian Congo, a fascinating history documented by Williams in a 2016 book [4]. After World War II and the onset of the Cold War, uranium extraction increased rapidly as multiple countries began to develop nuclear weapons and initiated nuclear power. While the geology of uranium is complicated, uranium deposits exist in many countries worldwide and it has been mined in most continents. Historically, uranium mining has been most prominent in the western United States, Canada, Eastern Europe, parts of Africa and Asia, and Australia. The uranium-containing ore is extracted through surface or underground mining and, more recently, also by in-situ recovery, which uses chemical solutions to leach out the uranium underground. The widespread mining of uranium, with historically insufficient control of radiation exposures, has resulted in high rates of lung cancer among the former miners.

The radiation exposures received by underground miners are sustained and continuous, not instantaneous like the initial exposures received from the nuclear detonations in Hiroshima and Nagasaki [5]. The cancer-causing radiation dose comes from radioactive progeny (sometime referred to as “daughters”) in the decay series of uranium-238 (Fig. 1). Radon (radon-222), an inert gas, is a naturally occurring decay product of radium-226, the fifth daughter of uranium-238. Radon decays with a half-life of 3.82 days into a series of solid, short-lived radioisotopes that are collectively referred to as radon progeny, or radon decay products (Fig. 1). Two of these decay products are particulate, polonium-218 and polonium-214. These polonium isotopes emit alpha particles: high-energy and high-mass particles, consisting of two protons and two neutrons that are highly effective in damaging cells as they pass through them. When these emissions take place within the lung from progeny deposited on the airways’ lining, the genetic material of the epithelial cells lining the airways may be damaged and lung cancer may ultimately result [6]. There are two additional decay series of radon—radon-220 and radon-219—referred to as thoron and acton, respectively [7]. As reported in the Biological Effects of Ionizing Radiation (BEIR) VI report, concentrations of radon-220 have been variable in those mines where measured and the radon-219 is not an important contributor to radiation dose delivered to the lungs because of its very short half-life.

Figure 1.

Uranium-234 decay series, including short-lived radon progeny from radon-222 through lead-210 [30]

Uranium miners are exposed to radon progeny from radon that diffuses from the uranium ore into the mine’s air. Depending on the richness of the ore, concentrations of radon and its progeny can become very high, unless there is ventilation with uncontaminated air. Historically, the concentration of radon and its progeny in mines is described by the Working Level (WL) with 1 WL being any combination of radon progeny in 1 L of air that ultimately releases 1.3 × 10⁵ MeV of alpha energy during decay. Exposure to a concentration of 1 WL for 170 h yields 1 Working Level Month (WLM) of exposure. These units of concentration and exposure are particular to the underground mining environment and are used in the epidemiological studies of uranium miners. In the United States for indoor environments, concentrations are expressed as picocuries per liter (pCi/L), a unit for the rate of decay. Globally, international units are generally used with concentration expressed as becquerel per meter³ (Bq m⁻³); 1 pCi/L translates to 37 Bq m⁻³.

Here, we focus on the lung cancer risk experienced by underground uranium miners. We point out that other workers are also exposed to ionizing radiation across the nuclear fuel cycle. Additionally, the impact of uranium mining and milling on communities has been substantial, arising from tailings and other wastes, abandoned mine sites, and contamination of water.

2. Historical background

Centuries ago, high rates of lung disease were documented among metal miners in the Schneeburg (now in Germany) and Joachimsthal (now in the Czech Republic) areas, on either side of the Erz mountains. In 1879, Harting and Hesse identified that the “miner’s disease” was a thoracic malignancy, later shown to be primary lung cancer [8]. In the first decades of the 20th century, radon was found in mines in both the Schneeburg and Joachimsthal districts and was considered as a possible cause of lung cancer in the miners. By the mid-20th century, as uranium mining proliferated, some considered that radon was a cause of lung cancer based on the experience in the European mines. In 1951, Bale and Harley worked out that radon itself did not cause the injury leading to lung cancer; rather it was the alpha particles released by radon’s decay products, polonium-218 and polonium-214, in the lung.

Underground uranium mining for the United States government began in the Four Corners states (Colorado, Utah, Arizona, and New Mexico) in the late 1940s, as it began to produce nuclear weapons and to build nuclear reactors [9]. The miners worked in small mines, sometimes referred to as “dog-holes” and also in larger mines owned by such companies as Union Carbide Corporation. Members of the Navajo tribe worked in small mines on the Navajo Nation. Suspecting that radon and its progeny were a likely cause of lung cancer, the US Public Health Service began the first epidemiological study of underground mines working in the Colorado Plateau in the early 1950s [10]. By the early 1960s, the study showed excess lung cancer. Large-scale underground uranium mining also began in Canada, France, and the former Soviet Union and epidemiological studies of cohorts of these miners were launched in the 1970s.

By the 1970s, results from the Colorado Plateau Study and other radon-exposed cohorts showed a clear excess of lung cancer and risk estimates were needed to develop standards to protect the miners [11]. Risk models were developed using various approaches, including biological considerations and dosimetry, expert judgement, and estimates based on epidemiological studies. For example, in 1982 Thomas and McNeill developed risk estimates for lung cancer using data from five cohorts (uranium miners in the United States Colorado Plateau Study, Ontario, and Czechoslovakia, fluorspar miners in Newfoundland, and metal miners in Sweden); in 1988, the BEIR IV Committee applied new time-dependent statistical models to four cohorts (uranium miners in the Colorado Plateau, Ontario, and Sasketchewan cohorts, and Swedish metal miners) as well [7, 12]. This general approach for estimating the risk of radon exposure is still used, albeit with more cohorts and more robust data (see below). In the early 1980s, there was widespread recognition in the United States and Europe that radon was ubiquitous in homes, even reaching concentrations as high as those measured in uranium mines. The miner-based risk models were extended to general population exposures to radon.

3. Cohort studies of uranium miners

Cohorts of uranium miners have been assembled in countries around the world, the first being the population assembled by the US Public Health Service in the Colorado Plateau from 1950 through 1960. Subsequently, studies were initiated in Canada, France, Australia, Czechoslovakia, and in the Grants area of New Mexico. The most recently launched cohort study, the WISMUT Cohort, includes workers in mines in the former East Germany employed between 1946 and 1989. Several of these cohorts were included in the pooled analyses of 11 cohorts reported by the US National Academies of Sciences BEIR VI committee [6]. That pooling effort included extant cohorts of uranium miners and also cohorts involving radon-exposed miners of other ores. The table below describes some of the major cohorts of uranium miners for which associations between exposure to radon progeny (in WLM) and lung cancer mortality have been reported and assembled in the pooled study of uranium miners carried out through the Pooled Uranium Miner Analysis (PUMA) project (Table 1).

Table 1.

Characteristics (period of follow-up, numbers of miners, lung cancer deaths, duration of employment, and mean cumulative and annual exposure to radon progeny) of some of the major cohorts of uranium miners for which associations between exposure to radon progeny and lung cancer mortality have been reported.

	Period of follow-up	Number of miners	Number of lung cancer deaths	Mean duration of employment (years)	Mean cumulative radon exposure in WLM	Mean annual exposure rate in WL
Eldoradoa (Canada)	1950–1999	13 574	517	2	122	8.3
Ontario (Canada)	1954–2007	28 546	1246	5	31	0.9
Czech (Czech Rep.)	1952–2014	9978	1176	8	73	0.8
France (France)	1946–2007	5086	213	17	37	0.8
Colorado (USA)	1960–2005	4137	612	4	579	11.7
New Mexico (USA)	1957–2012	3469	231	9	90	9.6
Wismut (Germany)	1946–2013	54 919	3759	14	304	1.9
PUMA total		119 709	7754	10	191	2.9

All cohorts in the Pooled Uranium Miners Analysis (PUMA) project [17].

^aIncludes Port Radium, Beaverlodge and Other facilities. “Other” was defined as workers who worked in more than one facility

There are similar design features among the studies. Participants were identified from rosters of companies and through contacts with health care facilities providing care for miners. Exposures were estimated using approaches that varied with the calendar time period. Generally, in the earlier time periods, measurements of radon progeny were limited or unavailable, requiring estimation by expert judgement and interpolation and extrapolation from available measurements to fill gaps. Over time, increasing numbers of measurements were made in the mines, facilitating more accurate exposure measurements. The occurrence of lung cancer was tracked through mortality searches, and relying on death certificate statement of cause of death, and in some cohorts, lung cancer incidence could be determined. The cohorts have now been followed for decades with follow-up ongoing in most.

Of course, there are important limitations to such occupational cohort studies. Exposure measurement error is among the most critical as the exposures of miners reflect the concentrations of radon in the mine areas where the miners were working during their worktime. Absent individual exposure measurements, made only in the French cohort in its later years, estimates of underground exposure are subject to misclassification at a level that likely depends on the time period when miners were working and that likely varies among the various cohort studies. In the early years of the industry for many of these cohorts, concentrations of radon progeny were extremely high and very poorly estimated. The density of measurements tended to be greater in later calendar periods and this time trend has been leveraged in some analyses to address concerns about bias due to exposure measurement error [13].

Moreover, for most of these cohorts, very little information has been collected on factors other than basic demographics and radon progeny exposures, including exposure to gamma radiation and long-lived radionuclides and diesel exhaust and other airborne carcinogens. One exception, however, is the substantial efforts made to collect information on smoking in the US cohorts. Information on cigarette use was obtained at study entry in the 1950s and 1960s for essentially all workers in the US cohorts (Colorado Plateau and New Mexico miners) and in subsequent follow-up surveys in the 1960s and 1980s. For the other cohorts, smoking data are available for some, but not all workers, based on questionnaires or surveys (in some cases on nested case-control samples) collected in the 1970s and 1980s. Information is needed on smoking to estimate the combined effect of radon progeny and smoking and also to address potential confounding by smoking.

4. Pooled analyses: BEIR VI/NCI

Estimates of the risk of lung cancer faced by underground uranium miners were needed for worker protection; with the identification of the problem of indoor radon that need was amplified. Before results of epidemiological studies of radon-exposed miners were available, the lung cancer risk associated with radon progeny exposure was estimated using a dosimetric approach; that is the dose delivered to the respiratory epithelium was calculated, adjusted for the relative biological effectiveness of alpha particles as compared to gamma rays, and combined with a lung cancer risk coefficient for gamma radiation derived from epidemiological studies of the Japanese atomic bomb survivors to calculate risk in relation to radon progeny exposure.

The BEIR IV Committee was convened in the mid-1980s to address internal emitters, including radon and radon progeny [7]. As it began its work, the problem of indoor radon was recognized in the United States and emphasis was given to the topic in its work and report, released in 1988. When the committee began its work, data from uranium miner cohorts were available and new analytical methods supported time-dependent analyses of the miner data, which included time-varying exposure to radon progeny. The committee modeled data from four cohorts and settled on a model in which the relative risk for lung cancer increased in a linear fashion with radon progeny exposure and declined with age attained and time elapsed since exposure. The modification of risk by attained age and by time since exposure was a novel finding.

The BEIR VI Committee began its work in 1992, releasing its final report in 1998 [6]. The committee’s approach to model development followed that of its predecessor, BEIR IV, but the committee had access to a pooled data set involving 11 cohorts that had been assembled with support from the US National Cancer Institute [14]. Its modeling approach expanded on the BEIR IV Committee’s with more in-depth exploration of the variation of the excess relative rate (ERR) with time since exposure, exposure rate, and attained age. The model took the form,

$$\mathrm{ERR}=\beta (w_{5-14}+{\theta }_{15-24}{w}_{15-24}+{\theta }_{25+}{w}_{25+}){\varphi }_{age}{\gamma }_z,$$

where β represents the slope of the radon progeny-lung cancer association at the reference levels of the exposure factors, w_5–14, w_15–24, and w₂₅₊, which represent radon progeny exposures at three windows of past time, and the modifying parameter ϕ_age allows the ERR to vary with attained age, and a second modifying factor, γ_z, allows the ERR to depend upon either the concentration or duration of radon progeny exposure. The exposure window variables, w_5–14, w_15–24, and w₂₅₊, allow the ERR to vary with time since exposure occurred. The first modifying parameter allows ERR to vary with attained age and the second modifying parameter allows the ERR to vary with the rate at which radon progeny exposure was received (or duration over which exposure was accrued).

The committee provided two final models, referred to as the exposure-age-concentration model and the exposure-age-duration model. These two models differ only with respect to the parameter γ_z, which represents either duration of exposure or the average concentration at which exposure was received. Table 2 provides the values for the coefficients in the exposure-age-concentration model. The ERR declines with attained age and also with lengthening time since exposure. It falls with increasing rate of exposure.

Table 2.

Comparison of reported estimates for the exposure–age–concentration model shown in the U.S. National Academy of Science’s BEIR VI committee report (without restriction by calendar period of hire) with those estimates obtained fitting a similar model to the Pooled Uranium Miners Analysis (PUMA) of uranium miners in Canada, Czech Republic, France, Germany, and the United States, male miners hired in 1960 or later.

	BEIR VI reporta	PUMA Full cohortb	PUMA 1960 + subcohortc
	Estimate (s.e.)	Estimate (95% CI)	Estimate (95% CI)
ERR/100 WLMd	7.68 (1.94)	4.68 (2.88, 6.96)	6.98 (1.97, 16.15)
Time since exposure (y)
5–14	1	1	1
15–24	0.78	0.77	0.64
25–34	0.51	0.54	0.89
≥35		0.39
Attained age (y)
<55	1.00	1.00	1.00
55–64	0.57	0.55	0.64
65–4	0.29	0.38	0.22
≥75	0.09	0.40	0.17
Mean exposure rate (WL)
<0.5	1	—	—
0.5–1.0	0.49	—	—
1.0–3.0	0.37	—	—
3.0–5.0	0.32	—	—
5.0–15.0	0.17	—	—
≥15.0	0.11	—	—
Annual exposure rate (WL)
<0.5	—	1	1
0.5−<1.0	—	0.60	1.00
1.0−<5.0	—	0.42	0.29
≥5.0		0.17
LEAR per WLM (×104)e	6.0	5.4	7.5

Cohorts of uranium miners in Canada, Czech Republic, France, and the United States are included in both the BEIR VI report and the PUMA analysis. —, not applicable; BEIR VI, Biological Effects of Ionizing Radiation VI; ERR/100 WLM, excess relative rate per 100 working level months; s.e., standard error; CI, confidence interval; WL, working level; LEAR, lifetime excess absolute risk.

^aAdjusted for attained age, calendar period and study cohort [6].

^bAdjusted for attained age, calendar period, study cohort, and duration of employment as a uranium miner [15].

^cAdjusted for attained age, calendar period, study cohort, and duration of employment as a uranium miner [16].

^dThe estimated ERR/100 WLM at the reference level of all effect measure modifiers, namely 5–14 years time since exposure, <55 years attained age, and <0.5 WL exposure rate.

^eLifetime excess absolute risk of lung cancer deaths per 10 000 persons following 1 WLM exposure [17].

Six of the cohorts included data on cigarette smoking. Examining the joint effects of smoking and radon progeny on lung cancer risk, the committee found synergism that was sub-multiplicative in magnitude, i.e. the combined effects of smoking and radon progeny were greater than additive, but less than multiplicative.

5. Pooled analyses: PUMA

In 2014, an international collaboration was launched to combine data from many of the most informative uranium miner cohorts that were ongoing in what was called the Pooled Uranium Miners Analysis (PUMA). The study assembled information on 124 507 underground uranium miners from seven cohorts with individual estimates of radon progeny exposures. Over 4.51 million person-years of follow-up, there have been 7253 lung cancer deaths. The study has reported on radon-lung cancer mortality associations among the sub-cohort of miners hired in 1960 or later with chronic low radon exposures and exposure rates mostly based on measurements, as well as in the full cohort, which includes those workers employed in the early years of mining who often encountered very high concentrations of radon progeny [15, 16].

The PUMA modeling approach built upon the BEIR VI Committee’s approach allowing variation of the ERR per WLM with time since exposure, attained age, and exposure rate, in a model very similar to the BEIR VI exposure-age-concentration model (as well as fitting a slightly different model that allowed variation of the ERR per WLM with age at exposure, exposure rate, and attained age) (Table 2). In general, analyses of the full PUMA cohort yield somewhat smaller estimates of ERR/WLM than analyses of the sub-cohort of miners hired in 1960 or later who had higher quality exposure information and lower average exposures to radon progeny; however, similar temporal patterns of effect measure modification are observed in the full cohort and sub-cohort of miners. In this subgroup of the PUMA data, risk increased in a linear fashion with cumulative exposure, starting from the lowest exposure level (Fig. 2).

Figure 2.

Estimated ERR of lung cancer mortality in male miners hired in 1960 or later (per 100 WLM) [16]

The model coefficients derived from the PUMA analyses have been used in combination with a BEIR VI model to estimate a person’s lifetime excess absolute risk (LEAR) of lung cancer, which provides the additional lung cancers occurring because of radon exposure at a particular level [17]. It is useful for extrapolating from the PUMA data to scenarios of indoor radon exposure and to occupational settings. Kreuzer and colleagues reported an estimate of ∼5.4–7.5 excess lung cancer deaths per 10 000 persons following 1 WLM exposure based on the PUMA data [17]. This figure is toward the upper end of reported values.

6. Application of risk models to indoor radon

Radium, the precursor of radon, is ubiquitous in soil. Consequently, radon is present in the soil under homes and enters homes through gaps in foundations and from basements. It is also present in some building materials and in water, particularly from deep wells. In 1956, Hultqvist report findings of a survey of homes in Sweden, documenting the presence of radon [18]. In the United States, the presence of radon in homes received wide recognition after a worker at a nuclear power plant repetitively set of the radiation alarm, on entering the plant [19]. His home was found to have radon concentrations comparable to higher levels in uranium mines. To guide policies on managing indoor radon, estimates were needed of the lung cancer risk associated with exposures in homes.

Models based on the studies of underground miners became the principal basis for estimating risk of domestic exposure. Estimates were used for various scenarios of exposure in homes with adjustment for factors related to the dosimetry of radon progeny that differed in homes and in mines. Case-control studies of lung cancer and radon exposure in the general population were also initiated with many including in-home radon measurements and collection of information on smoking and other factors. While there are population-based case-control studies that demonstrate an association between residential exposure to radon progeny and lung cancer, studies of residential radon exposures tend to be less conclusive, and less statistically precise, than occupational study findings.

Consequently, to-date, residential case-control studies have not served as the primary quantitative basis for deriving the radon-associated lung cancer risk estimates that guide policy recommendations. Surprisingly, however, evaluations based on pooling studies have concluded that the lung cancer risk per unit exposure in homes and in mines is comparable once we properly express radon progeny exposure in residential settings in units of WLM [20–22]. For example, using risk model derived from studies of underground miners, and an estimate of the average radon progeny concentration in a US home (expressed in WLM per year), the EPA has derived an estimate of the annual number of lung cancer deaths attributable to residential radon in the US (∼21 100 lung cancer deaths) [23].

7. Compensation for uranium workers—worldwide

After World War II, uranium was mined for national governments with two purposes: weapons manufacture and nuclear energy. Miners and other workers in the extraction phase of the uranium fuel cycle were exposed to cancer-causing radon progeny because of their government’s need for uranium. In the early years of uranium mining, workers experienced high levels of exposure to radon progeny that were only controlled in later years by ventilation when the hazard posed to miners was documented and indisputable. When the evidence on radon as a cause of lung cancer was certain remains a matter of historical dispute. By the early 1950s, the European experience with cancer in the mines of Schneeburg and Joachimsthal was well known and the key role of radon progeny in delivering alpha particles to the lung had been identified. Worldwide, thousands of uranium miners have likely developed lung cancer because of radon progeny exposure sustained when the risks were clear. Approaches to compensation have varied from none to formal compensation schemes [24, 25].

The epidemiological studies have provided an evidence base to inform compensation. In the United States, concern about lung cancer risk led to the initiation of the study of Colorado Plateau uranium miners by the Public Health Service in the early 1950s. Much later, the ethical rationale for starting a study without controlling levels of radon in mines was questioned by the Advisory Committee on Human Radiation Experiments [26]. By the 1960s, the study showed that lung cancer was occurring among the miners in excess of expectation based on the general population. Steps were taken by states and the industry to reduce radon progeny exposures in mines, but an ongoing excess risk of lung cancer was documented as the Colorado Plateau Study continued. The cohort study of New Mexico uranium miners reported increased risk for miners in that state in the early 1990s.

Through 1967, the only purchaser of uranium in the United States was the government agency, the Atomic Energy Commission, leaving the federal government responsible for the health and safety of the underground miners. That responsibility was largely abdicated, and a lung cancer epidemic followed, becoming evident by the late 1950s/early 1960s. Miners seeking compensation for their mining-related lung cancers through Workers’ Compensation and litigation were unsuccessful until the passage of the Radiation Exposure Compensation Act in 1990, later amended and extended through 2024. It was not renewed in spite of evidence for persistent excess risk in the Colorado Plateau Study. We could not identify formal government compensation programs specific to addressing harms to current and former uranium miners in the other countries where the PUMA cohorts are located. In Germany, miners were compensated through the German Workers’ Compensation Board [25].

8. The future

Epidemiological studies of underground miners exposed to radon progeny have supported the development of robust and informative risk models for policy purposes. The comparability of the models developed by the BEIR VI Committee and those based on PUMA is striking (Table 2). Radon-associated excess lung cancer risk varies quite similarly with attained age and time since exposure under the two models. Equally, important, estimates of lifetime excess lung cancer risk following 1 WLM exposure are very compatible under the two models (viz. 6 per 10 000 based on the BEIR VI model, and 5.4–7.5 per 10 000 under the PUMA models).

Analyses that focus on more recently hired uranium miners leverage higher quality exposure information available for miners who experienced far lower concentrations of radon progeny than the early underground miners. Those results support contemporary radon risk assessments and suggest similar, albeit slightly larger, risk estimates to those reported in the BEIR VI report. Longer follow-up of these contemporary miners should help to consolidate understanding of radon-associated lung cancer risks as more contemporary miners reach older attained ages.

These historical cohort studies of miners are used to inform radon risk assessments not only for contemporary workers, but also for members of the public. Importantly, the risk models based on the studies of miners have provided the foundation for programs directed at indoor radon. In contemporary settings, one critical source of uncertainty pertains to the combined effects of radon and cigarette smoking. Smoking surveys indicate that the uranium miners studied tended to smoke more than the general public today. However, these studies provide evidence that radon-associated excess lung cancer risks arise regardless of smoking, and add to the excess lung cancer risk conferred by smoking.

The future of uranium mining remains uncertain, although renewed interest in nuclear power generation and an expansion of nuclear weapons stockpiles globally over the past two decades suggest that demand for uranium remains and could grow. If underground uranium mining increases as a result, history indicates that radon progeny levels must be maintained at levels that are associated with acceptable risk. Another epidemic of lung cancer in underground uranium miners is avoidable. Of course, the findings from epidemiological studies of uranium miners inform the system of radioprotection more broadly than just as they pertain to people employed in the uranium mining industry. Studies of uranium miners have informed understanding of the potential health effects associated with other alpha-particle emitting radionuclides, and radon progeny are ubiquitous and present in homes as well as in many work environments other than uranium mines. Potential for relatively high occupational exposure occurs in metal and non-metal underground mines, particularly phosphate, fluorspar, talc and slate mines, where concentrations of airborne radon progeny can reach or exceed the radon levels typically encountered in uranium mines. Moreover, people may encounter high exposures in workplaces below ground, such as subways, tunnels, underground parking, and waste repositories; and, in work places above ground such as phosphate fertilizer plants, oil refineries, and natural gas and oil piping facilities. Remarkably, in spite of the firm knowledge of the lung cancer risk from radon progeny, there are still radon spas with exposed workers.

For contemporary workers, the epidemiological risk models derived in the BEIR VI and PUMA analyses suggest that occupational standards for exposure as WLM accrued annually are high: 4 WLM for underground miners per the US Mine Safety and Health Administration (MSHA) and 12 WLM under the US Occupational Safety and Health Administration for workers not covered by MSHA or the US Nuclear Regulatory Commission. These levels are associated with increased lung cancer risk based on biological understanding of the lung damage caused by alpha particles from radon progeny and the evidence from the studies of underground miners, particularly the recent findings from PUMA. Similarly, for members of the general public, lifetime risk estimates based on these models suggest that indoor exposure to radon progeny is associated with a large burden of lung cancer that can be reduced. EPA estimates for the US population based on BEIR VI models indicate that exposure to indoor radon progeny is the leading cause of lung among non-smokers. Recent reviews of radon epidemiology and dosimetry by the United Nations Scientific Committee on the Effects of Atomic Radiation and ongoing work of the International Commission for Radiological Protection aim to inform updated dose coefficients and recommendations for the system of radiation protection as it pertains to radon exposures for members of the public and workers [27–29]. Epidemiological findings from studies of underground miners will continue to help inform the models for determining acceptable levels of radon and the associated risks. Radon is a readily modifiable environmental risk factor through proper ventilation and other measures in indoor settings. However, in spite of decades of programs directed at reducing indoor radon, progress has been slow to implement interventions to reduce exposure and prevent the lung cancer cases caused by it.

Author contributions

J.M.S. and D.B.R. conceived and drafted the manuscript. Both authors participated in the revision of the manuscript and approved the submitted version.

Ethics statement

None to declare.

Funding

None declared.

Data availability

The data underlying this article are available in the article.