Health Effects and Preventive Strategies for Radon Exposure: A Systematic Review of the Literature

Abstract

Introduction: Radon is a radioactive noble gas formed from uranium decay in the Earth’s crust. The most significant isotope, 222Rn, emits alpha particles capable of damaging lung tissue and inducing cancer. Radon exposure is affected by geophysical and building characteristics and is recognized as a Group 1 carcinogen by the IARC. Despite regulatory thresholds (e.g., EURATOM standards), health risks remain. Various mitigation methods aim to reduce indoor radon exposure and its impact. Materials and Methods: This systematic review followed PRISMA guidelines. PubMed, Scopus, and Web of Science were searched up to 28 February 2025, using a defined string. Studies with original data on radon exposure and lung cancer risk or mitigation efficacy were included. Independent screening and quality assessment (Newcastle–Ottawa Scale) were conducted by multiple reviewers. Results: Of the 457 studies identified, 14 met the inclusion criteria. Eleven of these investigated the link between indoor radon and lung cancer risk, and three evaluated mitigation strategies. Radon levels were commonly measured using passive alpha track detectors. Levels varied depending on geographical location, season, building design and ventilation, these were higher in rural homes and during the colder months. Case–control studies consistently found an increased lung cancer risk with elevated radon exposure, especially among smokers. Effective mitigation methods included sub-slab depressurisation and balanced ventilation systems, which significantly reduced indoor radon concentrations. Adenocarcinoma was the most common lung cancer subtype in non-smokers, whereas squamous and small cell carcinomas were more prevalent in smokers exposed to radon. Discussion and Conclusions: This review confirms the robust association between indoor radon exposure and lung cancer. Risks persist even below regulatory limits and are amplified by smoking. While mitigation techniques are effective, their application remains uneven across regions. Stronger public education, building codes, and targeted interventions are needed, particularly in high-risk areas. To inform future prevention and policy, further research should seek to clarify radon’s molecular role in lung carcinogenesis, especially among non-smokers.

1. Introduction

Radon is a noble gas produced through the radioactive decay of uranium found in the rocks that make up the Earth’s crust. It is colourless, odourless, and tasteless, and during its decay, it emits ionising alpha radiation. There are several isotopes of radon, but the most relevant, from a public health perspective, is 222Rn, which originates primarily from 238U in its radioactive decay chain. 222Rn has an average lifetime of about 3.8 days and quickly transforms into short-lived daughter isotopes, such as 218Po and 214Po, which also emit alpha radiation [1].

Radon concentration varies significantly from one location to another. It is entirely dependent on the geological and geographical features of the area. 222Rn is continuously released into groundwater from the rocks of the Earth’s crust, and due to its solubility in water, it can travel long distances through the soil [2].

Radon levels in indoor environments can be measured using a variety of instruments and technologies. One of the most reliable and commonly used methods for assessing residential radon concentration involves devices that detect alpha particle impacts on a surface. These are known as alpha track detectors or solid-state nuclear track detectors [3]. To ensure accurate results, these detectors should be left in place for at least three months.

Radon is a Group 1 human carcinogen, according to the World Health Organization (WHO) and the International Agency for Research on Cancer (IARC) [4].

The harmful health effects of radon have been acknowledged by international legislation, such as the Basic Safety Standards (BSS) of EURATOM (European Council, 2013) [5]. For example, Article 103/3 of the EURATOM-BSS obliges Member States to identify areas—referred to as “radon priority areas” (RPAs)—where the annual average concentration of radon is expected to exceed the relevant national reference level in a significant number of buildings [5].

Epidemiological studies carried out on miners and the general population have consistently provided evidence of radon’s carcinogenic effect on the lungs [6,7,8].

The role of radon in the development of lung cancer has been linked to the emission of alpha particles, which have a high potential to damage the respiratory epithelium. Alpha particles can directly affect epithelial cells, causing various cytotoxic and genotoxic effects that promote carcinogenesis. These genotoxic effects lead to significant molecular alterations, including DNA double-strand breaks, translocations, deletions, substitutions, and chromosomal rearrangements. Ultimately, this results in cytokine dysregulation and increased production of proteins associated with cancer development [9,10].

Additionally, alpha radiation impacts the immune system within the tumour microenvironment. Chronic radon exposure leads to the overproduction of reactive oxygen species (ROS) in the lungs, triggering oxidative stress and pulmonary inflammation. Moreover, radon can enhance tumour immunogenicity by increasing genomic instability and inducing clustered mutations in cancer cells [9,10].

For decades, studies worldwide have assessed the effectiveness of various radon mitigation strategies, including active techniques, which rely on electric fans, passive methods that utilize only natural ventilation, and combined approaches which integrate both systems [11].

A systematic review identified effective radon mitigation systems for both new and existing homes. In existing houses, active techniques proved to be more efficient than passive ones. Among all methods, the active sub-slab depressurization system (SSDS) was found to be the most effective, followed by active ventilation systems. Passive ventilation and stand-alone passive barriers, such as membranes used in new constructions, showed limited effectiveness. In areas with high radon levels or in large buildings, a combination of long-term, customised mitigation techniques is preferable, particularly in countries with very cold climates [12]. This study aims to demonstrate that radon exposure remains a significant cause of lung cancer and that effective mitigation can prevent disease onset. Public awareness campaigns are essential to promote measurement and reduction in exposure to this invisible gas.

2. Materials and Methods

2.1. Selection Protocol and Search Strategy

This systematic review was registered in PROSPERO under the following ID: CRD420251066104 and was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) Methodology [13]. PubMed, Scopus and Web of Science were the three databases used for the research in the literature.

All of the literature accessible through the databases, up to 28 February 2025, using the following search string was included: “radon AND lung AND (effects OR impact OR toxicity OR carcinogenesis OR pathology) AND (therapy OR treatment OR prevention OR protective AND measures)”.

2.2. Inclusion Criteria for the Study

The titles and abstracts of every article were examined first, followed by the complete text. Independent screening was carried out by each of the authors (L.C., M.S., F.P., A.M., S.S, C.C., L.P.) The whole texts were separately read by the same writers (L.C., M.S., F.P., A.M., S.S., C.C., and L.P.). Following a discussion of any uncertainties and conflicts, the writers reached a consensus to resolve any issues. Only articles that presented direct measurements of environmental, residential or occupational radon aimed at assessing cause and effect in lung cancer or aimed at evaluating mitigation interventions were considered. Case studies, symposia, editorials, reviews, meta-analyses, and other types of research were not allowed. Admissible papers were only those that presented original data. In order to determine which articles were included in the references, every reference of the included papers was reviewed. Only English or Italian-language publications were included.

2.3. Data Extraction and Quality Assessment

Data from every study was gathered, including author, year, country, patients, case, sampling period, sampling location, environmental concentration measurement, environmental measurement methodology, and preventative techniques. Additionally, the information was arranged to specify the radon concentrations that were crucial for evaluating the environmental influence on human health. The Newcastle–Ottawa Quality Assessment Scale (NOS) was used to do a quality assessment. The Newcastle–Ottawa Scale (NOS) was selected due of its widespread use in assessing observational research, particularly its ability to evaluate comparability, exposure result clarity, and selection bias in non-randomized studies [14]. Each article was evaluated by two independent reviewers, and disagreements were resolved through discussion in order to minimise selection and publishing bias. Furthermore, only original research with precise outcome definitions and direct radon measurements was considered.

3. Results

The databases PubMed, Web of Science, and Scopus were used to obtain a total of 457 studies. Of these, 408 were screened based on title and abstract, and 49 duplicates were eliminated. Because they did not fit the inclusion criteria selected by all of the authors (L.C., M.S., F.P., A.M., S.S., C.C., L.P.), 319 publications were eliminated at this stage.

The whole text was then used to screen the remaining 89 articles. Following an examination of the remaining 89 full texts, 2 papers were eliminated as it involved animals, and 73 articles were eliminated for lacking a direct measurement. Only the 14 publications that satisfied the inclusion criteria were ultimately included (Figure 1, Supplementary Figure S1).

The NOS was then used to measure the quality of each included study. Following a series of questions, the NOS for observational studies assesses the study’s quality. Each study can receive up to nine points based on three criteria. The selection of the study groups, sample size, respondent information, and whether the risk factor was clearly determined are all taken into account in the first area, “SELECTION” (4 points). The comparability of the various outcome groups and whether or not confounding variables are controlled make up the second category, “COMPARABILITY,” which is worth two points. The final domain, “OUTCOME” (3 points), examines whether the exposure and outcome are clearly determined or whether the statistical test, if it is employed, is suitable. After the points were added up, the quality was classified as “Good” if the sum was greater than 7, “Fair” if the points were between 5 and 7, or “Poor” if it was less than 5 [15].

Table 1. Included studies and their characteristics.

Author, Year, Country	Field R. W. et al. 2001 USA [16]	Cucu M. et al. 2022 Romania [17]	Steck D. J. 2012 Minnesota [18]
n° Patients (sex F%, M%; mean age years, range + SD)	case 413 (100% F; 40–84 years); control 614 (100% F; 40–64 years)	-	-
Case	Primary invasive lung carcinoma; residence for 20 consecutive years or more in the current home	-	-
Sampling location	Large areas of western Iowa	Urban areas	Minnesota
Sampling period	May 1993 and 30 October 1996	February 2021–June 2021	Between 1 February and 15 March 2008
Anatomopathological changes	Histologic typing of lung tumours and included the major categories of small cell carcinoma, squamous cell carcinoma, adenocarcinoma, and large cell carcinoma	-	-
Environmental concentration measurement	Approximately 60% of the basement radon concentrations and 30% of the first floor radon concentrations of study participants’ homes exceeded the US Environmental Protection Agency Action level of 150 Bq m−3(4 pCi l−1) Large areas of western Iowa had outdoor radon concentrations comparable to the national average indoor value of 55 Bq m−3(1.5 pCi l−1) Excess odds of 0.24 (95 CI = −0.05–0.92) and 0.49 (95% CI = −0.03–1.84) per 11 WLM (Working Level Month) 5–19 were calculated using the continuous radon exposure estimates for all cases and live cases, respectively. Slightly higher excess odds of 0.50 (95% CI = −0.004–1.80) and 0.83 (CI = 0.11–3.34) per 11 WLM5-19 were noted for the categorical radon exposure estimates for all cases and the live cases.	The highest indoor radon concentration was 219 Bq m−3, in the cold season. The lowest measured value for indoor radon concentration (17 Bq m−3) was found in the hot season. The air exchange rate varied from 0.2 to 4.2 h−1. In the cold season (wintertime), the outdoor–indoor exchange of air is made possible by two mechanisms: diffusion and convection.	The pre-mitigation concentration was lognormally distributed with an average of 380 Bq m−3 (10.3 pCi L−1), geometric mean of 295 Bq m−3, and a factor of 1.8 variations (geometric standard deviation). These post-mitigation concentrations averaged 45 Bq m−3 (1.2 pCi L−1).
Methodology of environmental measurement	The radon dosimetry assessment consisted of five components: on-site residential assessment survey; on-site radon measurements; regional outdoor radon measurements; assessment of subjects’ exposure when in another building; and linkage of historic subject mobility with residential, outdoor and other building radon concentrations.	5 residential apartments were subjected to testings of radon concentration and air exchange rates between February 2021 and June 2021. Sample collection for each detector ranged from 4 to 24 h. Two devices were used to carry out indoor radon measurements: a RAD7 active radon detector and an Airthings Wave Plus detector. Temperatures and atmospheric state were also recorded. Other parameters of interest impacting the air exchange rate are: tightness of the building, habitual opening of windows by occupants and outside atmospheric conditions.	A 4 d long and also a winter radon measurement with the activated charcoal detector (AC). Two alpha track detectors (ATD) were sent for long-term measurements in then home during an extensive period of normal house operation. One ATD was to be placed at the primary site. The second ATD was to be placed in a frequently occupied room on another level if possible, preferably a bedroom. The ATDs were returned after 90 or more days of exposure between mid-June and the end of September 2008.
Methods of prevention	-	Indoor radon levels are influenced by air exchange rates (ACH), building design, ventilation, materials, and outdoor Indoor radon levels are influenced by air exchange rates (ACH), building design, ventilation, materials, and outdoor conditions. With ACH between 0.2 and 4.2 h−1, radon typically reaches steady state within 24–48 h. Heating and cooling systems mainly recirculate air and do not reduce radon effectively. To lower levels, increased ventilation—such as opening windows—is needed. The critical ACH (ACH_critical) required to reduce radon can range from −1 to 135 h−1, depending on indoor-outdoor differences. Airtight, well-insulated buildings often have higher radon, especially in winter (average 133 Bq/m3) compared to summer (23 Bq/m3).	All the mitigation systems used active soil ventilation.
Conclusion	Lung cancer risk is substantially correlated with cumulative radon exposure.	Findings indicate that levels of indoor radon concentration depend on ventilation rates of the unit, but also on building materials, wind speed around building, time of day (higher around noon) and season of the year (higher in the cold season when ventilation rate is lower).	If that reduction was maintained over the lifetime, radon-related lung cancers can be prevented.
Author, Year, Country	Finne I. E. et al. 2019 Norway [19]	Barros-Dios J. M. et al. 2012 Spain [20]	Park E. Y. et al. 2020 Korea [21]
n° Patients (sex F%, M%; mean age years, range + SD)	-	Case 349 (13.5% F, 86.5% M; 6.6% < 50 y, 50.7% 51–70 y, 42.7% > 70 y) Control 513 (12.3%F, 87.7% M; 10.1% < 50 y, 61.4% 51–70 y, 28.5% >70 y)	Case 519 (51.25% F, 48.75% M; 64, 57–72 y) Control 519 (51.25% F, 48.75% M; 64, 59–72 y)
Case	-	Lung cancer	Non-small cell lung cancer
Sampling location	Norway	Galicia, Ourense	Seoul, Suwon, Wonju, Changwon, Yangsan
Sampling period	2008 and 2016	Between 2004 and 2008	Between October 2015 and March 2018
Anatomopathological changes	-	46.4% squamous cell carcinoma; 26.4% adenocarcinoma; 15.5% SCC; 5.7% large cell carcinoma; 6.0% other types	-
Environmental concentration measurement	For detached houses where the average radon concentration was almost halved from 76 (under construction in 2008) to 40 (under construction in 2016) Bq/m3. For Terraced house/semi-detached houses (vertically divided) were a reduction from 44 (under construction in 2008) to 29 (under construction in 2016) Bq/m3. For Block of flats/terraced apartments, ground and 1st floors were a reduction from 35 (under construction in 2008) to 34 (under construction in 2016) Bq/m3.	About 18.6% and 20.1% of cases were exposed to 101–147 and >147 Bq/m3 compared with 14% and 15% of controls.	Mean residential radon levels were 65.46 Bq/m3 and 73.75 Bq/m3 (p = 0.013) in the case and control groups, respectively. Among the cases and controls, the proportions of individuals exposed to high levels of residential radon (≥100 Bq/m3) were 13.7% and 17.7% (p = 0.007); smokers comprised 42.8% and 34.9% (p = 0.009); and second-hand smokers accounted for 46.1% and 21.2% (p < 0.001), respectively.
Methodology of environmental measurement	Integrated radon measurements were performed with alpha track detectors for two months or longer, in two occupied rooms, preferably in the living room and a bedroom.	Radon measurements were conducted with alpha-track detectors. Detectors were placed away from doors, windows, and electric devices, between 60 and 180 cm from the floor. Radon was measured for a period of 3 to 6 months.	Residential radon levels were measured in the living room and the bedroom with Alpha-track detectors, as a passive radon measuring device. The measuring devices were positioned away from household electrical appliances, windows, or sealed drawers. The measurements were made over 3 months, and the average of measurements at both locations in the house was taken. Given that indoor radon levels are highest in the winter and lowest in the summer, seasonal corrections were made with average temperature and wind speed.
Methods of prevention	Balanced ventilation (mechanical supply and exhaust ventilation) with heat recovery in new buildings.	-	-
Conclusion	It appears that radon concentrations are lower in terraced and semi-detached homes, which were previously thought to be about the same as detached homes in terms of radon hazards.	Compared to people exposed to lesser quantities, those exposed to concentrations greater than 50 Bq/m3 are about twice as likely to get lung cancer. Additionally, radon exposure modifies the effects of tobacco use. The increased radon exposure raises the risk of lung cancer for people who smoke regularly.	Residential radon exposure and cigarette smoking were synergistically associated with a greater risk of lung cancer. Although addictive interaction (p = 0.344) and multiplicative interaction (p = 0.367) did not reach statistical significance, the difference in ORs for lung cancer according to radon exposure was much greater in current smokers than in non-smokers.
Author, Year, Country	Rodríguez-Martínez A. et al. 2021 Spain [22]	Torres-Duràn M. et al. 2015 Spain [23]	Xiang-Zhen X. et al. 1993 China [24]
n° Patients (sex F%, M%; mean age years, range + SD)	Case 375 (24.5% F, 75.5% M; 6.4% < 50 y, 62.4% 51–70 y, 29.9% > 70 y) Control 902 (33.0%F, 77.0% M; 20.2% < 50 y, 61.5% 51–70 y, 18.1% > 70 y)	Case 199 (79.9% F, 13.5% M; 70, 61–77 y) Control 275 (78.8%F, 21.2% M; 70, 63–79 y)	17,000 male and 2800 female employees
Case	Small cell lung cancer	Never-smoking cases with primary lung cancer	Lung cancer
Sampling location	Santiago de Compostela, Ourense, A Coruna, Asturias, Ávila, Puerta de Hierro, Porto	Galicia and Asturias	Workers of the Yunnan Tin Corporation (YTC) in Yunnan Province, Southern China
Sampling period	-	Between January 2011 and October 2013	The mean durations of radon exposure and of arsenic exposure are about 13 years
Anatomopathological changes	-	Squamous cell carcinoma; Adenocarcinoma; Small cell carcinoma; Large cell carcinoma; other histological types	-
Environmental concentration measurement	Median radon concentration (25–75th percentiles) 152,5 Bq/m3 (91–260) in case’s houses; 142 Bq/m3 (89–267) in control’s houses	Median radon concentration (25–75th percentiles): 223 Bq/m3 (123–587) in squamous cell carcinoma; 189 Bq/m3 (106–375) in adenocarcinoma; 173 Bq/m3 (57–218) in small cell carcinoma; 109 Bq/m3 (77–130) in large cell carcinoma; 309 Bq/m3 (238–516) in other histological types.	The mean lifetime cumulative radon exposure was 275.4 WLM with a maximum exposure of 1653 WLM.
Methodology of environmental measurement	Alpha-track device which was placed for a period of at least three months in each dwelling.	Alpha-track types were placed for a minimum of 3 months in the participant’ s bedroom, away from doors, windows, heating and electrical devices and at a height between 60 and 180 cm off the floor.	-
Methods of prevention	-	-	-
Conclusion	It can be observed that for people exposed to more than 147 Bq/m3 the risk of lung cancer increased with tobacco consumption. For heavy smokers, the risk of lung cancer also increases with radon exposure. Those exposed to more than 147 Bq/m3 and heavy smokers showed an OR of 72.6 (95%CI 18.0–499.4) compared to never-smokers exposed to less than 50 Bq/m3. The synergy index, calculated for 2 categories of radon exposure (<100 and >147 Bq/m3) and tobacco consumption (never smokers and heavy smokers) was not significant: 2.18 (95%CI: 0.88–5.43).	We can observe that the risks are very similar for the different histologies, though there is statistical significance only for adenocarcinoma (OR 2.19; 95% CI 1.44–3.33). The remaining histological types did not reach statistical significance, though for all histological types, the lowest confidence interval was 0.85.	The risk of lung cancer declines significantly with attained age, radon exposure rate, and years since last radon exposure, and does not vary in a consistent way with age at first radon exposure.
Author, Year, Country	Grzywa-Celińska A. et al. 2023 Poland [25]	Kelly-Reif K. et al. 2022 USA [26]	Tomasek L. et al. 2012 Czech Republic [27]
n° Patients (sex F%, M%; mean age years, range + SD)	102 patients 39 women (38.2%) and 63 men (61.8%).	16,434 underground uranium miners	11842 people (5858 men and 5984 women)
Case	lung cancer	-	Lung cancer
Sampling location	Lublin	Uranium miners in the Czech Republic.	80 villages of Mid-Bohemia Pluton
Sampling period	-	The cohort included male workers who were listed in the employment registry between 1 January 1949 and 31 December 1975, worked underground for at least 1 year	The study was established in 1990 as a retro-prospective follow-up covering period since 1961
Anatomopathological changes	38.2% of the study group. Patients with the diagnosis of non-small cell carcinoma accounted for 78.4% (n = 80), 41.2% (n = 42) had adenocarcinoma subtype, squamous subtype occurred in 26.5% (n = 27), and not otherwise specified (NOS) due to an uncertain histological subtype was found in 6.9% (n = 7). Four patients were diagnosed with rare types of lung cancer. In this subgroup of patients, there were neuroendocrine, mixed histology of adenosquamous and two patients with large cell tumours. Small cell carcinoma was treated in 21.6% (n = 22) of patients.	-	-
Environmental concentration measurement	The average concentration of radon during the exposure of the detector in the residential premises of the respondents was at the level of 69.0 Bq/m3 [37.0–117.0]. Significantly higher values of the average radon concentration during the exposure of the detector in residential premises were observed if the measurement was performed in the countryside compared to a large city (82.0 vs. 3 9.5 B q/m3; p = 0.0232; It was found that there were significantly lower values); in the cases where the basement floors were wooden compared to other possible materials (wood vs. ceramic tiles or concrete or soil, respectively: 30.5 vs. 119.0 or 69.0 or 76.5 Bq/m3; p = 0.0024); Significantly higher values of the average radon concentration during detector exposure were observed in patients with air conditioning (95.0 vs. 67.0 Bq/m3; p = 0.0456). Moreover, in patients whose window frames were made of plastic instead of wood, the mean values of radon concentration during detector exposure were significantly higher (75.0 vs. 40.0 Bq/m3; p = 0.0350)	Radon (WLM) 115 (0–1022)	The measurement as were conducted in 2154 houses (mean 499 Bq/m3).
Methodology of environmental measurement	The measurements of indoor radon concentration were made with the use of a passive method with solid-state nuclear track detectors (SSNTD) of CR-39 type. The detectors of RSKS type (Radosys Ltd., Hungary) have been used. One month of radon exposure measurement was performed with alpha-track detectors.	-	Passive track detectors and radon gas by electrets and closed CR-39 detectors
Methods of prevention	There are some practical solutions to reduce indoor radon, using wooden window frames rather than plastic frames and limiting the use of air conditioning.	-	-
Conclusion	That higher concentrations of radon occurs in buildings located in the countryside. The level of radon was higher in the presence of air conditioning, which intensifies the transport of radon from the soil to the interior of the building. The higher radon concentrations were also associated with the presence of plastic window frames compared to wooden frames.	There is a positive exposure-response relationship between cumulative exposure to radon and lung cancer.	The study confirmed that the risk from radon exposure in houses is indubitable.
Author, Year, Country	Torres-Duran M. et al. 2014 Spain [28]	Turner M. et al. 2011 Canada [29]
n° Patients (sex F%, M%; mean age years, range + SD)	521 (192 cases and 329 controls); Female 153 (79.7) 259 (78.7) Male 39 (20.3) 70 (21.3)	811,961 (55.3%F, 44.7%M; 4.6% < 40 y, 21.4% 40–49 y; 36.6% 50–59 y; 26.3% 60–69 y; 9.4% 70–79 y; 1.7% > 80)
Case	Lung cancer	-
Sampling location	Hospitals of Northwest of Spain (Galicia and Asturias)	Florida, New Jersey, South Carolina, New Hampshire, New York, Iowa, Idaho, Ohio, Utah
Sampling period	Between January 2011 and June 2013	1982–1986
Anatomopathological changes	Adenocarcinoma, Squamous cell carcinoma, Small cell carcinoma, Large cell carcinoma, Other histological types	-
Environmental concentration measurement	48% of cases had residential radon exposure >200 Bq·m−3; ≤100 to ≥200	Mean Bq/m3 (SD): Northeast 58.3 (42.3); South 35.6 (21.7); Midwest 73.7 (36.6); West 46.9 (40.3)
Methodology of environmental measurement	Alpha-track type	Mean county level residential radon concentrations were linked to study participants according to ZIP code information
Methods of prevention	-	-
Conclusion	The results of the present study show that residential radon increases the risk of lung cancer in never-smokers when they are exposed to indoor levels >200 Bq·m−3.	A significant positive linear trend was observed between categories of radon concentrations and lung cancer mortality (p ¼ 0.02). A 15% (95% CI, 1–31) increase in the risk of lung cancer mortality was observed per 100 Bq/m3 increase in radon. Participants with mean radon concentrations above the EPA guideline value (148 Bq/m3) experienced a 34% (95% CI, 7–68) increase in risk for lung cancer mortality relative to those below the guideline value.

summarizes the results from each of the included investigations.

The articles included were published between the years 1993 [24] and 2023 [25]. Studies were conducted in the United States of America [16,18,26], Spain [20,22,23,28], Canada [29], Czech Republic [27], Poland [25], Korea [21], Norway [19], Romania [17] and China [24] (Figure 2).

Most of the articles describe how to trace back cases of lung cancer diagnosed in local nosocomial sites through indoor radon measurements [16,20,21,22,23,24,25,26,27,28,29], while only three articles describe mitigation methods, evaluating their effectiveness through direct pre- and post-intervention measurements [17,18,19]. No article addressed either the preventive issue or the correlation between radon and lung cancer or the method of diagnosis/treatment of the disease. All authors assessed the effect of confounding factors such as cigarette smoking.

All authors used a passive detection method, through the use of alpha track detection placed for several months in the homes of subjects with cancer and in healthy subjects identified as controls or in homes chosen for the evaluation of mitigation methods [16,17,18,19,20,21,22,23,24,25,26,27,28,29].

Radon levels varied significantly among the trials based on the kind of dwelling, season, geographic location, and ventilation techniques (Figure 3). In remote regions, during colder seasons, especially in buildings with inadequate ventilation or airtight construction, radon concentrations were often higher [17,18,19].

For instance, Grzywa-Celińska et al. found mean concentrations considerably higher in dwellings in rural areas and in buildings with air conditioning or plastic window frames [25], while Cucu et al. showed seasonal radon fluctuation ranging from 17 Bq/m³ to 219 Bq/m³ [14].

A number of case–control studies showed a consistent positive correlation between increasing indoor radon exposure and a higher risk of lung cancer, including those conducted by Field et al., Barros-Dios et al., Park et al., and Rodríguez-Martínez et al. [16,20,21,22]. Those individuals exposed to radon levels exceeding 100–150 Bq/m³, especially smokers, had odds ratios that were generally higher [20,21,22,23,24,25,26,27,28]. When comparing heavy smokers exposed to radon levels above 147 Bq/m³ to never-smokers exposed to levels below 50 Bq/m³, Rodríguez-Martínez et al. found an odds ratio of 72.6 (95% CI 18.0–499.4) [22].

Significant reductions in indoor radon concentrations were reported by Steck et al. and Finne et al., who demonstrated the effectiveness of active mitigation techniques such as balanced mechanical ventilation and sub-slab depressurization, a mitigation technique used to prevent harmful vapours, like radon and volatile organic compounds (VOCs), from entering a building from the soil beneath the foundation [18,19]. Steck et al. specifically reported a reduction from an average of 380 Bq/m³ to 45 Bq/m³ following mitigation [18].

The histological subtypes of lung cancer in people exposed to radon were thoroughly described in a number of the studies that were part of this study. In line with the larger epidemiological profile of lung cancer in the general population, the most commonly reported histologies were small cell carcinoma, squamous cell carcinoma, and adenocarcinoma [16,20,22,25,28].

Histologic type in the large case–control study by Field et al. (2001) included small cell carcinoma, squamous cell carcinoma, adenocarcinoma, and large cell carcinoma. The cumulative radon exposure increased the excess probabilities of lung cancer [16].

Among the 349 cases, 46.4% had squamous cell carcinoma and 26.4% had adenocarcinoma, according to Barros-Dios et al. This suggests that there is a higher correlation between radon exposure and squamous cell cancer in their research population [20].

According to Grzywa-Celińska et al., 78.4% of cases were non-small cell lung cancer (NSCLC), with adenocarcinoma accounting for the most common subtype (41.2%) and squamous cell carcinoma (26.5%) coming in second and third, respectively. There were other rare histological kinds like giant cell tumours, adenosquamous carcinoma, and neuroendocrine tumours [25].

Interestingly, adenocarcinoma was the most statistically significant histological type linked to radon exposure (OR 2.19; 95% CI 1.44–3.33) in the study by Torres-Durán et al., which only included never-smokers. However, elevated radon levels were observed across all histological types, including squamous, small cell, and large cell carcinomas [23].

Park et al. and Rodríguez-Martínez et al. also emphasized the relationship between radon exposure and histological subtype, particularly in smokers, where small cell and squamous cell types were more common in high-exposure groups [21,22].

Torres-Durán et al.’s observation that adenocarcinoma consistently predominates in never-smokers gained statistical significance, supporting the idea that radon may cause cancer in this population via a different molecular pathway. This raises the possibility of a preferred carcinogenic route in this population. However, despite the fact that other histological categories (such as small cell carcinoma and squamous cell carcinoma) were similarly more prevalent among smokers exposed to radon, their correlations did not achieve statistical significance, with confidence intervals exceeding unity [20,21,22,23].

The geographic analysis reinforces the need for region-specific radon surveillance, building code regulations, and targeted public health interventions based on local geological and architectural characteristics.

Indoor radon concentrations in Spain, especially in the Galicia region, were routinely among the highest, with readings reaching 587 Bq/m³ [20,22,23,24]. According to reports, pre-mitigation indoor radon concentrations in Midwestern areas like Iowa and Minnesota were as high as 380 Bq/m³ [13,15,26]. In Poland, especially in the Lublin region, indoor radon levels were found to be moderate, with rural areas having greater levels than urban ones [25]. Comparing South Korea to other high-exposure nations, the average residential radon concentrations were lower (~74 Bq/m³) [21]. Average residential radon concentrations in the Czech Republic were found to be quite high (up to 499 Bq/m³), especially in granite-rich areas like Mid-Bohemia [27]. The cumulative occupational exposure levels of tin miners in Yunnan Province, China, were exceptionally high [up to 1653 WLM (Working Level Month) [24]. The preventive potential of architectural interventions was portrayed by Norwegian studies that showed how contemporary building design and ventilation systems may dramatically lower radon levels in new constructions—from 76 Bq/m³ in 2008 to 40 Bq/m³ in 2016 [19]. Lastly, Canada provided a comprehensive national analysis that demonstrated that for every 100 Bq/m³ rise in home radon concentration, there was a 15% increase in lung cancer mortality [20]. This supported data from other high-exposure nations and demonstrated the worldwide significance of radon-related health hazards.

Regarding the Quality Assessment, only 1 study was considered “Fair” [29], while the others were considered “Good” [16,17,18,19,20,21,22,23,24,25,26,27,28].

4. Discussion

This systematic analysis supports the robust and reliable link between indoor radon exposure and the risk of lung cancer, especially for those who are exposed to high quantities for extended periods of time. The results are consistent with international classifications, such as the International Agency for Research on Cancer’s (IARC, 1988) classification of radon as a Group 1 human carcinogen [6,27]. Furthermore, Member States are required by the European Directive 2013/59/EURATOM, which establishes fundamental safety standards for safeguarding against the risks associated with ionizing radiation exposure, to designate Radon Priority Areas (RPAs) and to set national reference levels for indoor air that do not surpass 300 Bq/m³ (Article 74). [30,31]

Numerous studies in this review highlight the significance of taking preventative measures even in groups with moderate exposure since they show that health hazards can arise even at concentrations below this threshold. The necessity for coordinated public health treatments is further supported by the synergistic effect of tobacco smoking and radon exposure that has been shown in several studies [32,33,34].

Nevertheless, the efficiency of mitigation techniques has been the subject of very little research. Based on the research that is currently available, active methods that considerably reduce indoor radon concentrations include balanced mechanical ventilation with heat recovery and sub-slab depressurization (SSD) [13,35]. These results are in line with the WHO Handbook on Indoor Radon (2009), which encourages the use of radon-resistant measures in new construction and suggests radon treatment in buildings when concentrations surpass national guideline limits [5,7].

The information also shows that public knowledge and the application of radon-related health regulations vary from one nation to another. The degree of enforcement and public involvement varies greatly, despite the fact that national agencies are required by the EURATOM Directive to create radon action plans [5,31].

According to these findings, squamous cell carcinoma and small cell carcinoma may be more strongly correlated with high radon exposure, especially in smoking populations, but adenocarcinoma is still the most prevalent histological subtype of lung cancer, especially in non-smokers. This trend might be the result of varying cellular sensitivity to alpha radiation or the combined mutagenesis effects of tobacco and radon carcinogens [36,37].

To better understand the pathogenic pathways and investigate the function of radon in tumour histogenesis—particularly in lung malignancies that develop in non-smokers—more molecular profiling research is required [38].

Lung carcinogenesis is facilitated by alpha radiation from radon by intricate and subtype-specific mechanisms. Alpha particles’ high linear energy transfer (LET) produces dense ionization tracks that lead to large-scale chromosomal abnormalities such translocations, deletions, and inversions as well as clustering DNA damage, especially double-strand breaks (DSBs) [9,10]. The bronchioalveolar stem cells, which are believed to be the cells of origin for adenocarcinoma, (the most common histological subtype among never-smokers exposed to indoor radon), are particularly susceptible to these lesions [23].

Simultaneously, long-term exposure to radon encourages the overproduction of reactive oxygen species (ROS) in lung tissues, maintaining a micro-environment that is pro-inflammatory and pro-oncogenic [9,10]. In addition to amplifying DNA damage, ROS also cause epigenetic changes, such as histone acetylation and promoter hypermethylation, which can silence tumour suppressor genes and cause abnormal oncogenic pathway activation [38].

According to recent molecular research, radon exposure may be linked to mutations in genes such as EGFR, ALK, and KRAS [38] that frequently occur in lung cancer. These data suggest that radon may selectively influence particular carcinogenic pathways in non-smokers, although a direct causal relationship is still being studied. Additionally, in the tumour microenvironment, radiation-induced activation of signalling cascades such ATM-p53, NF-κB, and HIF-1α may be a factor in both immune evasion and DNA repair failure [9,10,38].

When combined, these processes offer a tenable biological explanation as to why adenocarcinoma is prevalent in non-smokers exposed to radon and emphasize the need for more studies that integrate exposure information with the genomic profiling of cancers in affected individuals.

The high-risk areas in this research, including Yunnan (China), Bohemia (Czech Republic), Iowa and Minnesota (USA), and Galicia (Spain), have similar geological and environmental features that lead to high indoor radon levels. These include frigid climates where homes are tightly sealed for energy efficiency, eliminating natural ventilation; uranium-rich granitic bedrock; and permeable soils that allow radon mitigation. Radon can also be trapped within architectural elements like air conditioners, basements, and windows with plastic frames. Exposure is made worse in some places by past mining operations or the recycling of uranium-contaminated items. These results highlight the necessity of radon mitigation plans and urban development regulations that are specific to a given region [39,40,41,42,43,44].

Before building new homes, or workplaces, or meeting places, it would be advisable to include radon exposure in the health impact assessment in order to avoid future lung damage [45].

There are certain restrictions on this review. Because the examined studies were so heterogeneous, a meta-analysis could not be conducted. The legislative differences among the several nations that carried out the studies represent another drawback. There are not any studies that simultaneously describe and assess the effects of radon on the lungs, treatment options, and mitigation techniques.

5. Conclusions

In conclusion, radon continues to be a neglected yet avoidable cause of lung cancer. To encourage household testing, guarantee adherence to construction codes, and fund remediation projects in high-risk locations, stronger national rules are required. Campaigns for public awareness should highlight the health advantages of mitigation, the invisible character of radon, and its synergistic relationship with tobacco. Future studies should support the implementation of the goals of the European Radon Action Plan, standardize exposure assessment procedures, and analyse the cost-effectiveness of various remediation strategies.