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Abstract

Background:

Inflammatory bowel disease (IBD) develops from a dysregulated immune response influenced by environmental exposures. Radon, a radioactive gas, has known biological effects, but its role in IBD remains unexplored.

Objectives:

To examine the association between residential radon exposure and the risk and clinical course of IBD.

Design:

A case–control study with 1-year prospective follow-up of cases.

Methods:

We included 178 newly diagnosed IBD patients and 178 age- and sex-matched controls in Santiago de Compostela, Spain, from June 2020 to September 2023. Residential radon levels were measured using passive detectors for 3 months. Outcomes included IBD diagnosis, disease extent, hospitalizations, and flares. Logistic regression was used to estimate odds ratios adjusted for age and sex.

Results:

Median residential radon was 144.5 Bq/m³ in IBD cases and 189.5 Bq/m³ in controls. Higher radon levels were associated with reduced odds of IBD (OR 0.5 for 100–299 and >299 Bq/m³ vs 0–99 Bq/m³). No significant association was found between radon levels and hospitalizations or flares. Among ulcerative colitis patients, higher radon was linked to more extensive disease.

Conclusion:

Higher residential radon exposure might be inversely associated with IBD risk. However, it does not appear to influence disease progression. Further studies are needed to confirm these findings, since this is the first study on this topic, and chance or selection bias might be present.

Plain language summary

Does radon in homes affect the risk and severity of inflammatory bowel disease?

This study looked at whether home radon levels affect inflammatory bowel disease (IBD). People with IBD had lower radon exposure than those without. Higher radon levels were linked to less IBD, but didn’t affect how the disease progressed. Radon might play a protective role, especially in ulcerative colitis cases.

Keywords

Crohn’s disease environmental factors inflammatory bowel diseases radon ulcerative colitis

Introduction

The development of inflammatory bowel disease (IBD) depends on the occurrence of an uncontrolled immune-mediated inflammatory response in an individual genetically predisposed, in combination with environmental factors, only partially known, which interact with the gut microbiome.^1–4 Some factors have been shown to be protective, such as breastfeeding or rural living, and others are risk factors, such as consumption of ultra-processed food or urban living.^5–7 The place of residence could also be related to the phenotype and clinical course of the disease, with living on the coast being associated with ileocolonic Crohn’s disease, extensive ulcerative colitis, and a greater need for immunosuppressive therapy.⁶

A recent systematic review by Estevinho et al.⁸ of 32 studies on environmental pollutants and their link to IBD risk and outcomes reveals that exposure to heavy and transition metals, air pollutants, industrial contaminants, and insecticides is associated with an increased IBD risk, while zinc may offer protective effects. This reveals how acting on the environment could influence the course or the development of the disease. In the same line of investigation, the study of Rodríguez-Lago et al.⁹ investigates the potential link between environmental exposures to heavy metals and minerals and the preclinical phase of IBD. Examining scalp hair samples from patients with subclinical IBD and comparing their mineral and metal concentrations to healthy controls, they found significant differences in certain elements, including higher levels of sodium, potassium, and boron, and lower levels of zinc, uranium, copper, and germanium in the IBD group. These findings suggest that environmental exposures, possibly affecting gut permeability and gut microbiome, may play a role in the early stages of IBD development. However, further studies are needed to understand the biological effects and potential clinical implications of these differences.

Radon is a noble gas naturally produced by the radioactive decay of uranium and radium in soil and rocks. During this process—particularly through its progeny polonium-218 and polonium-214—it emits ionizing alpha particles which, when inhaled, can damage bronchial epithelial cells. Although radon disperses easily outdoors, it tends to accumulate indoors, especially in poorly ventilated spaces or buildings with structural defects such as cracks in the foundation. Classified by the IARC as a Group 1 carcinogen, residential radon is the second leading cause of lung cancer worldwide, after tobacco use. Studies conducted in areas with high natural radon exposure, such as Galicia (Spain), have shown a significantly increased risk even among never-smokers. One case–control study reported an odds ratio (OR) of 2.42 (95% confidence interval (CI): 1.45–4.06) for individuals exposed to concentrations ⩾200 Bq/m³ compared to those exposed to <100 Bq/m³,¹⁰ findings that were later confirmed by pooled analyses. Notably, this risk also extends to adenocarcinoma, the most common subtype in never-smokers.¹¹ These epidemiological data emphasize the oncogenic potency of radon, particularly its synergistic effect with environmental tobacco smoke, and affirm the need for preventive measures, such as long-term α-track monitoring and home mitigation, in radon-prone areas.

Concurrently, there is growing interest in understanding the molecular mechanisms behind lung cancer in never-smokers, including driver gene alterations such as EGFR mutations and ALK rearrangements. In this context, a study by Ruano-Ravina et al.,¹² involving 323 never-smoking lung cancer patients from Galicia, examined the potential link between residential radon exposure and these genetic alterations. While no overall association was found between radon levels and the presence of EGFR mutations, patients with exon 19 deletions had nearly double the radon exposure compared to those with the exon 21 (L858R) point mutation. Similarly, ALK-positive patients showed substantially higher radon concentrations than ALK-negative patients. Although these results were not statistically significant—mainly due to small sample sizes—they suggest that alpha radiation may contribute to specific genetic alterations in never-smokers.

In addition, evidence concerning the genetic basis of small-cell lung cancer (SCLC) remains limited. Existing genome-wide association studies are scarce and heterogeneous, primarily due to small sample sizes and methodological differences. However, certain loci—most notably the CHRNA5/A3/B4 gene cluster on chromosome 15—have shown consistent associations with increased SCLC risk. Other implicated variants include those in CDK6, SH3RF1, TERT, CLPTM1L, MAP4, and CDC25A, many of which are involved in signaling pathways such as PI3K-Akt and MAPK, often activated by tobacco-derived carcinogens like NNK and NNN. The transcription factor ASCL1, characteristic of a major SCLC subtype, may also regulate nicotinic receptor gene expression, adding further biological relevance.¹³ Taken together, these findings underscore the need for more targeted and large-scale studies to better understand the interplay between radon exposure, genetic susceptibility, and lung carcinogenesis—especially in never-smokers.

Nevertheless, radon has been used in the treatment of multiple inflammatory diseases such as pemphigus,¹⁴ rheumatoid arthritis,¹⁵ or bronchial asthma due to the proposed anti-inflammatory and immune-inhibiting effects. The induction of changes on the immune status, for example the decrement of TNF-α levels, and the release of some factors such as TGF-β1 and β-endorphin were posed.¹⁶ Inhalation of radon, the main source of human exposition, produces reactive oxygen species (ROS), increases antioxidants levels, and activates antioxidant enzymes.¹⁷ With regard to autoimmune diseases, there is an imbalance of Th1/Th2, and it was observed that low doses of radiation might regulate T cells. This induction favors the recovery of the Th1/Th2 balance.¹⁴

The World Health Organization (WHO) recommends residential radon exposure levels below 100 Bq/m³. If this cannot be achieved, it should be as low as possible and always below 300 Bq/m³.¹⁸ Galicia, a region located in north-western Spain and in which the health area of Santiago de Compostela (where the study was conducted) is located, is a radon-prone area due to the geological composition of the subsoil.¹⁹ The median radon levels in the region are 132 Bq/m³, with 18% of the dwellings with levels above 300 Bq/m³.²⁰ This region has also a high incidence of IBD compared to the rest of the country.²¹ This makes this area a perfect place to investigate if radon levels could have any role on the development and evolution of IBD.

Although the association between radon exposure and lung cancer is well-documented and supported by extensive evidence, this is not the case for other diseases. This topic is receiving increasing attention at the international level, so additional case–control studies are warranted to investigate the potential relationship between radon and a broader range of health outcomes, for several critical reasons²²:

First, most existing studies examining associations between radon and non-pulmonary diseases have employed ecological designs, relying on average radon concentrations assigned to broad geographic units rather than utilizing individual-level exposure data. This methodology fails to account for substantial intra-regional variability in radon levels, leading to exposure misclassification. Given that residential radon concentrations can differ significantly even between adjacent dwellings, individual-level measurements are essential for accurately assessing exposure–disease relationships.

Second, the current body of evidence linking radon exposure to diseases other than lung cancer is inconclusive and highly dependent on study design, geographic location, and population characteristics. To strengthen causal inference and improve the validity of observed associations, more rigorous and well-designed studies (particularly those using case-control methodologies) are urgently needed.

Moreover, such studies should be conducted specifically in radon-prone areas. These regions are characterized by high heterogeneity in residential radon levels, enabling the assessment of potential dose–response relationships, a key criterion in establishing causality. Prior research has shown that associations with certain health outcomes are more readily observable in these high-exposure settings, reinforcing the importance of focusing future investigations in these areas.

This study aims to analyze the role of individual residential radon exposure on the probability of IBD and its possible impact on hospitalizations or flares during the follow-up in a radon-prone area. To the best of our knowledge, this is the first study of this nature conducted in the context of IBD.

Materials and methods

Design, subjects, and settings

A case–control study was conducted in the health area of Santiago de Compostela (Galicia, Spain) between June 2020 and September 2023. All incident cases of IBD who met the inclusion criteria were included, and matched with controls, recruited in parallel, by age and sex. Cases were recruited at the IBD consultations at the Clinic Hospital of Santiago de Compostela, a referral center for this condition, while controls were recruited from general gastroenterology consultations or the endoscopy unit after checking that they did not have IBD.

Inclusion criteria were living in the same dwelling at least 5 years before the diagnosis (or before the inclusion for controls), being 18 years old or more, comprehension of the study procedures, and signing the informed consent. For cases, they have to be diagnosed in the last 3 months prior to inclusion. Exclusion criteria were a recent change of address, being underage, inability to measure radon levels in the subject’s home or to comprehend the study procedures, and, in the case of patients with IBD, having been diagnosed more than 3 months before the planned time of inclusion.

To diagnose a patient with IBD, the diagnostic consensus guideline by the Crohn’s and Colitis Organisation and the European Society of Gastrointestinal and Abdominal Radiology was used.²³

In patients with UC, mild activity is defined as a partial Mayo score between 2 and 4 points, moderate activity between 5 and 7 points, and severe activity >7 points. In the total Mayo classification, mild activity is between 3 and 5 points, moderate activity between 6 and 10 points, and severe activity >10 points. In patients with CD, mild activity is defined as a Crohn’s Disease Activity Index (CDAI) score between 151 and 219 points or a Simple Endoscopic Score for Crohn’s Disease (SES-CD score) between 3 and 6 points, moderate activity with CDAI between 220 and 450 points or SES-CD between 7 and 15 points, and severe activity with CDAI >450 points or SES-CD >15 points.

The study protocol and consent forms were approved by the Santiago de Compostela-Lugo Ethics Committee (REF 2020/013).

The reporting of this study conforms to the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) statement.²⁴

Information retrieval

At the time of inclusion, all participants were given a questionnaire to complete, which included not only their sociodemographic data (age, sex, date of birth) but also epidemiological data (vaccination status, type of drinking water, occupational activity, tobacco use, alcohol consumption), and information regarding their residence: type of dwelling (apartment or house), location (coastal/interior, urban/rural area), age of the dwelling, presence or absence of a wood stove, and the number of years living there, among others.

In addition, patients with IBD completed a questionnaire with information on the type of disease, its extent, as well as analytical parameters and endoscopic indices at the time of diagnosis. The type of IBD was registered using the Montreal classification²⁵ and the endoscopic and clinical index (total and partial Mayo index for UC and CDAI and SES-CD for CD).²⁶

The questionnaire is not validated, but was developed specifically for this study (Supplemental Table 1).

Radon measurements

Radon levels were measured during 3 months in the participants’ homes. To measure them, a passive alpha-track radon detector (RSKS, from Radosys INC, Hungary) was given to all participants the day they were included in the study. The radon detector was provided by the Galician Radon Laboratory (www.radon.gal), which is accredited by the National Accreditation Entity in Spain (ENAC) for radon measurement in air.

After 3 months, participants returned the radon detector via regular mail to the Galician Radon Laboratory, where radon concentration was analyzed. All participants received feedback on their residential radon concentration. Figure 1 shows the process.

Figure 1.

Process of radon level measurement.

Follow-up of IBD cases

All IBD patients underwent a prospective follow-up for 1 year. Clinical and analytic parameters such as fecal calprotectin, hemoglobin, ferritin, iron, and C-reactive protein were collected at the time of diagnosis and 1 year after to determine whether radon levels affected the evolution of the disease in terms of flares and hospitalizations related to the disease.

Hospitalization was defined as any admission related to a worsening of IBD. A flare was defined as the recurrence or exacerbation of symptoms such as diarrhea, abdominal pain, rectal bleeding, and fatigue that require treatment. To classify the severity, the modified Truelove-Witts scale for UC (mild 11–15, moderate 16–21, and severe >21 points) and the Harvey Bradshaw Index for CD (mild 5–7, moderate 8–16, and severe >16 points) were used.

Statistical analysis

For the descriptive statistics, we used percentages for categorical variables and medians and interquartile range (IQR) for continuous variables. Radon levels were classified into three categories: 0–99, 100–299, and >299 Bq/m³ according to the WHO.¹⁸

The characteristics of cases and controls were compared using a bivariate analysis. This was followed by a logistic regression where the dependent variable was the case or control status and the main independent variable was radon concentration classified in the aforementioned categories. The regression was adjusted by age and sex. Results were expressed as ORs with 95% CIs.

Spearman’s test was used to determine whether there was any correlation between the extent of the disease and radon concentration.

Stata^® 15 (StataCorp LP, College Station, TX, USA) was used for statistical analysis.

Results

Between June 2020 and September 2023, 178 patients with IBD were included (102 ulcerative colitis, 70 Crohn’s disease, and 6 unclassified colitis), and compared with 178 controls recruited in parallel. In total, 172 cases and 172 controls handed over the radon detector at the end of the 3 months, and 175 patients with IBD completed 1 year of follow-up, while 3 patients were lost because they did not return to the hospital and they did not answer the phone. Figure 2 shows radon concentration comparing cases and controls. Median radon concentration for cases was 144.5 Bq/m³ compared to 189.5 Bq/m³ in controls (p value = 0.00). In Figure 3, radon levels are broken down not only by cases and controls but also by the type of IBD. Median radon level of controls is 189.5 Bq/m³, while the median radon levels of UC patients are 134 Bq/m³, being 177 Bq/m³ in CD patients.

Figure 2.

Comparison of radon concentrations between cases and controls.

Figure 3.

Radon levels broken down by IBD type.

Table 1 shows the sample characteristics broken down by case and control status.

Table 1.

Sample size description.

	Cases	Controls
N	178	178
Age (median, IQR)	51 (39–59)	51 (42–60)
Sex (% females)	53.4	50.0
Housing area (N, %)
Urban	44 (24.7)	62 (34.8)
Rural	134 (75.3)	116 (65.2)
Years living in the dwelling (median, IQR)	21 (14–30)	22 (13–35)
Age of the dwelling (median, IQR)	30.5 (20–50)	37 (23–56)
Work activity (N, %)
Inside	133 (74.7)	144 (80.9)
Outside	42 (23.6)	31 (17.4)
No answer/don’t know	3 (1.7)	3 (1.7)
Blue collar	79 (44.4)	80 (44.9)
White collar	78 (43.8)	75 (42.1)
No answer/don’t know	21 (11.8)	23 (12.9)
Smoking habit (N, %)
Never smoker	67 (37.6)	92 (51.7)
Active smoker	31 (17.4)	24 (13.5)
Ex-smoker	80 (44.9)	62 (34.8)
Comorbidities (N, %)
Yes	37 (20.8)	58 (32.6)
No	141 (79.2)	120 (67.4)
Radon levels (Bq/m³)	144.5 (83–260)	189.5 (112–292.5)
IBD classification	Crohn’s disease (N, %): 70 (39.3) L1 46 (65.7) L2 9 (12.9) L3 12 (17.1) L4 3 (4.3) B1 41 (58.6) B2 22 (31.4) B3 7 (10.0) Ulcerative colitis (N, %): 102 (57.3) E1 36 (35.3) E2 41 (40.2) E3 25 (24.5) Unclassified (N, %): 6 (3.4)

IBD, inflammatory bowel disease; IQR, interquartile range.

Comparing the median radon level of the controls with the expected level in the region where the study was conducted, it is observed that the included population exhibits higher levels.

After adjusting by age and sex, and using levels of 0–99 Bq/m³ as a reference, it was found that higher radon levels showed a negative association with the development of IBD (Table 2). Stratifying by sex, higher radon levels showed a trend to a negative association too, but without achieving a statistically significant difference, probably because of the reduction in the sample size.

Table 2.

Comparison of radon levels between cases and controls, adjusted by age and sex.

Radon levels	Controls (N, %)	Cases (N, %)	OR (95% CI)
0–99	34 (19.8)	59 (34.3)	1
100–299	96 (55.8)	77 (44.8)	0.5 (0.3–0.8)
>299	42 (24.4)	36 (20.9)	0.5 (0.3–0.9)

CI, confidence interval; OR, odds ratio.

Radon levels between the different types of IBD are similar (p = 0.176), being median radon levels of UC, CD, and unclassified colitis 134 Bq/m³ (IQR 78–221), 177 Bq/m³ (IQR 86–306), and 239 Bq/m³ (IQR 111–410), respectively.

Endoscopic involvement of patients with ulcerative colitis, measured by the Montreal classification, was correlated with radon levels. Patients with extensive affectation at the diagnosis had higher radon levels (Spearman’s rho = 0.2123, Prob > |t| = 0.0331). Montreal classification for Crohn’s disease did not show correlation with radon levels (p > 0.05 for all the items).

IBD patients were followed for 1 year, and radon levels were compared between patients with flares and patients without flares. There were no statistically significant differences between patients who had flares in comparison with patients without any flare, taking 0–99 Bq/m³ as reference (OR = 0.7 (95% CI 0.3–1.5) for 100–299 Bq/m³, OR = 1.3 (95% CI 0.5–3.2) for >299 Bq/m³). Median radon levels of patients with at least one flare are 134 Bq/m³ (IQR 79–303), while median radon levels of patients with any flare are 150 Bq/m³ (IQR 83–251). Dividing patients into hospitalized and non-hospitalized ones, radon levels (taking 0–99 Bq/m³ as a reference) were no statistically significant different (OR = 0.7 (95% CI 0.1–5.3) for 100–299 Bq/m³, OR = 3.9 (95% CI 0.7–23.4) for >299 Bq/m³; Table 3). Median radon levels of patients who had at least one hospitalization are 269 Bq/m³ (79–414), while median radon levels of patients without any hospitalizations are 144 Bq/m³ (IQR 83–248).

Table 3.

Relationship between hospitalizations, flares, and radon concentration.

Radon concentration (Bq/m³)	HospitalizationOR (95% CI)	FlareOR (95% CI)
0–99	1	1
100–299	0.8 (0.3–2.1)	0.6 (0.3–1.7)
>299	1.7 (0.6–5.0)	1.5 (0.5–4.5)

CI, confidence interval; OR, odds ratio.

When analytic parameters such as C-reactive protein (CPR), calprotectin, hemoglobin, ferritin, and iron were correlated with radon levels (both at the time of inclusion of the cases and 1 year after), none of them showed any significant correlation (p > 0.05 for all comparisons, being for CPR, 0.32 at the time of inclusion and 0.40 1 year after. For calprotectin, 0.92 at the time of inclusion and 0.73 1 year after, for hemoglobin, 0.17 at the time of inclusion and 0.15 1 year after, for ferritin 0.26, at the time of inclusion and 0.14 1 year after, and for iron, 0.45 at the time of inclusion and 0.49 1 year after).

Discussion

In this study, the exposure to higher levels of radon showed a negative association with IBD, without influencing its evolution in terms of augmenting or diminishing the hospitalizations or flares during 1 year of follow-up. To our knowledge, this is the first study that analyzed this association in IBD. Despite the observed negative association, the findings should be interpreted with caution, as they are likely to be highly speculative due to the limitations discussed below.

In addition, in patients with ulcerative colitis, it has been observed that the greater the extent of the disease, the higher the radon concentration. This is of great interest, as extensive colitis is associated with a higher risk of colorectal cancer and a greater need for long-term treatment. Elevated radon levels could suggest the need for closer monitoring.

Regarding environmental factors, a systematic review of 32 human studies⁸ on environmental pollutants and their relationship to the risk and outcomes of IBD shows that exposure to heavy metals, transition metals, air pollution, industrial contaminants, and insecticides is linked to a higher risk of developing IBD, whereas zinc may have protective effects. Studies suggest that pollutants like PM2.5, PFAS, and pesticides affect IBD outcomes, including hospitalizations and surgery. The mechanisms behind these effects involve gut microbiome alterations, intestinal barrier dysfunction, and systemic inflammation. Despite these findings, there are knowledge gaps, particularly concerning the long-term and combined effects of pollutants, and the need for more detailed exposure assessments.

People are exposed to environmental radon and its decay products Po-214 and Po-218, which are inhaled. Compartmental biokinetic models have been developed to understand the movement and behavior of inert gases like radon within the body. These models rely on physical laws that govern gas transfer between tissues and fluids, focusing on factors such as blood-to-air partition coefficients, blood perfusion rates, and tissue volumes. After inhalation or absorption, radon equilibrates between the lung air and pulmonary blood and then distributes to systemic tissues based on blood flow. The gas is eventually exhaled as the body eliminates the accumulated radon.²⁷ It has been described in different studies that radon increases antioxidant enzymes like superoxide dismutase and catalase, diminishing ROS and therefore decreasing inflammation (augments TGF-β and decreases TNFα, incrementing regulatory T-lymphocytes). And this radon gas is proposed to have different effects on the individual, such as pain relief and an increase in quality of life.¹⁶ However, it should not be forgotten that it also increases the risk of lung cancer,¹¹ being the second cause of this type of cancer after tobacco exposure. In this article by Ruano-Ravina et al., the authors highlight the particular vulnerability of never-smokers exposed to high indoor radon concentrations, with studies reporting an OR of lung cancer as high as 2.42 for concentrations exceeding 200 Bq/m³. Importantly, adenocarcinoma, the most frequent histological subtype among never-smokers, has shown a consistent association with radon exposure, suggesting a specific pathogenic pathway independent of tobacco-related mechanisms. Regarding other types of cancer, its association is unclear.^28–30 But there are no data about the risk in this respect from exposure at therapeutic doses in humans. Mitchel³¹ suggests, after analyzing different doses and lengths of exposure in mice, that there is a window of exposure (between 1 and 100 mGy) that can provide adaptive response protection. Doses below those values could reduce the tumor latency rather than incidence, and doses above increase the risk gradually. This affirmation contrasts with what was shown in the pooling study on radon and lung cancer, which observed that the association with this disease is linear, with no threshold effect.³²

For years, low doses of radon radiation have been used to treat some inflammatory conditions and relieve the pain caused by some chronic degenerative diseases such as rheumatoid arthritis,¹⁵ lupus, scleroderma, psoriasis, ankylosing spondylitis, bronchitis, and asthma.³³ In the article by Kojima et al.,³⁴ a patient with ulcerative colitis was treated with radon exposure in a prepared room, radon-containing water, and with exposure to a radon sheet at bedtime. This allowed the patient to stop corticoid therapy, and the patient improved clinically and endoscopically.

Radon levels have been studied in relation to other diseases, such as lung cancer or COPD, being a well-known risk factor for lung cancer. Although the link between radon exposure and lung cancer is well established, its association with other diseases remains unclear and understudied. Growing international interest highlights the need for additional case–control studies to explore these potential relationships. Most existing research has relied on ecological designs that use regional average radon levels, which overlook significant variability between individual homes and result in exposure misclassification. Furthermore, the current evidence on non-pulmonary diseases is inconsistent and heavily influenced by study design and population differences. To enhance causal inference, future studies should focus on individual-level exposure data and be conducted in radon-prone areas, where the wide range of radon levels allows for better assessment of dose–response relationships.²²

The study of radon concentrations in relation to IBD had not been conducted until now. The area chosen for the study has three principal advantages, the incidence of IBD is higher in comparison with the neighboring regions,²¹ the study was conducted at a referral center for IBD allowing the inclusion of all diagnosed cases from the catchment area (this area comprises a population of approximately 320,400 inhabitants based on 2020 estimates), making the study population representative of the regional IBD burden, and it is a radon-prone area. Therefore, this study delves further into the potential epidemiological factors that could be linked to the development and progression of these diseases for the purpose of their control. Having used a radon-prone area should facilitate the finding of a potential dose–response effect, should it exist. A very important advantage is to have individual radon measurements at each participant’s dwelling, since it is known that radon concentrations are highly heterogeneous even in houses a few meters away. Finally, all included cases had a thorough clinical exploration, and their diagnosis was confirmed using standard and accepted procedures.

This possible association between radon levels and IBD might explain the lower incidence of IBD in rural areas,⁶ as these are regions where radon levels are higher due to the presence of single-family homes.

This study has some limitations. First, only residential radon is taken into account, ignoring occupational radon levels. But most of the hours are spent at home, including bedtime, being those levels the most representative of the doses to which one is exposed throughout the day. And adjusting by working hours, results do not vary. Although radon was measured using devices placed for at least 3 months (which is recommended by WHO), ideally radon exposure should be measured for 1 year, but this is logistically more difficult and the return rate could be lowered when using such a long period. Second, although there is a significant number of patients included, as one of the strengths of this study is that it was conducted in a referral center for IBD, there is a low proportion of them who were hospitalized or had a flare during the follow-up. Third, the results could be influenced by the selection of controls, as their median concentration is 189.5 Bq/m³, considerably higher than the median concentration of 119 Bq/m³ observed in the subjects from the radon map of Galicia. This difference in concentration between the controls and the study subjects maybe because the radon distribution for cases compared to controls (i.e., controls living in lower storeys than cases, older houses or houses with a cellar, compared to cases) may impact the findings and potentially change their interpretation. Moreover, the selected controls were not drawn from the general population but were instead chosen by convenience from among all patients attending the Gastroenterology outpatient clinics or the Endoscopy unit who did not have an IBD. Fourth, the questionnaire used is not validated, but it was developed specifically for this study.

Conclusion

Higher concentrations of residential radon might have a negative association with IBD. Residential radon does not have an influence on the evolution of the disease in terms of hospitalizations or flares. Furthermore, high radon levels could have some association with a more extensive UC. These findings should be interpreted cautiously in light of methodological limitations. They could have been obtained by chance, something possible in any epidemiological study that we cannot disregard since this is the first study on the topic, due to a selection bias of controls, which have higher indoor residential radon concentrations compared to that observed for Galician population, or lack of association because radon might not be related with this disease. Additional research is warranted to confirm these results.

Supplemental Material

sj-docx-1-tag-10.1177_17562848251374190 – Supplemental material for Indoor radon concentration and risk and severity of inflammatory bowel diseases: a case–control study

Supplemental material, sj-docx-1-tag-10.1177_17562848251374190 for Indoor radon concentration and risk and severity of inflammatory bowel diseases: a case–control study by Violeta Mauriz-Barreiro, Alberto Ruano-Raviña, Rocío Ferreiro-Iglesias, Iria Bastón-Rey, Cristina Calviño-Suárez, Laura Nieto-García, Sol Porto-Silva, Xurxo Martínez-Seara, Lucía Martín-Gisbert, J. Enrique Domínguez-Muñoz and Manuel Barreiro-de Acosta in Therapeutic Advances in Gastroenterology

Footnotes

Acknowledgements

This has been possible thanks to the grant Janssen-Antonio Obrador to support scientific publication, allowing further advancement in the knowledge of IBD.

Declarations

ORCID iDs

Violeta Mauriz-Barreiro

J. Enrique Domínguez-Muñoz

Supplemental material

Supplemental material for this article is available online.

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