Radon and Non-Cancer Pulmonary Health Effects in Children: A State of The Art Review.

INTRODUCTION
Radon is a natural radioactive gas well-known for its carcinogenic effects, well-documented for its association with lung cancer, with radon exposure the leading cause of lung cancer in non-smokers and the second leading cause of lung cancer in smokers in adults.2,3 However, relatively little is known about the association between radon and non-cancer respiratory disease, particularly in children. Radon (222Rn), the heaviest noble gas, originates from the natural decay series of uranium-238 (Figure 1), a naturally occurring radioactive mineral present in the earth’s crust, rocks, and soils, with a half-life of 4.5 × 109 years. Radon may enter a house or building through fissures and cracks.4,5 Levels of uranium and subsequent decay into radon gas varies on earth depending on specific types of rocks and soils, such as uranium-enriched phosphatic rocks, granite, and shale.6 Compared to other naturally occurring isotopes of radon (such as 219Rn, also known as thoron, and 220Rn, also known as actinon, which have a short half-life of 3.96 s and 55.6 s, respectively), most of the radioactivity in the atmosphere is attributed to 222Rn (hereafter called radon).7,8
Radon-222 is the most harmful and most common form of radon, as 80% of all radon is Radon-222.9 Radon (222Rn), an inert, omnipresent, odorless, colorless, and radioactive gas with a half-life of 3.82 days, decays to produce more chemically reactive short-lived radionuclides and other radioactive decay products, including 218Polonium (Po), 214Lead (Pb), 214Bismuth (Bi), and 214Po (half-life equal to 3.1 min; 26.8 min; 19.9 min; and 1664 μs, respectively), which release harmful alpha (α) and beta (β) radiation, which can be inhaled or ingested.4,10,11 Radon exposure distribution is highly location-specific, which may be affected by variation in geologic factors (such as ground surface concentration of Uranium-238 and Thorium-232, which are parent elements that account for the generation of radon; distance to the closest geological fault, which influences the vertical movement of radon via fracture; the abundance of radon in soil gas; the age and granularity of surficial materials, which affects the generation and emanation of radon in the soil and soil parameters, such as available water capacity, saturated hydraulic conductivity, vertical permeability, bulk density, percent of organic matter, field capacity, depth, porosity, erodibility and the percent of soil components of different granularity, such as gravel, sand, and clay).12 Building characteristics, energy efficiency, the prevalence of radon mitigation, and the application of radon-resistant new construction may also affect radon levels, which may account for the heterogeneity of radon levels and affect generalizability of exposure.12

ROUTES OF EXPOSURE
The concentration of radon gas has been used as a reliable indicator of radon decay product concentration in indoor radon measurements.5 In the United States, 1 in 15 homes is estimated to have indoor radon levels at or above the U.S. Environmental Protection Agency’s (EPA) action level of 148 Bq/m3 [4 pCi per liter of air, pCi/L; based on the Citizen’s Guide to Radon (1990), which recommends the non-binding action level of 4 pCi/L and practical recommendations for testing and mitigation),14 with increasing indoor radon levels observed as a likely consequence of climate change and newer construction practices.15–18 Human exposure to radon occurs mainly through inhalation and ingestion, with the latter due to radon dissolved in groundwater. Rn decay products (Figure 1) form ultrafine clusters which may attach to airborne particulate matter (PM)19–25, causing ambient PM to become radioactive, known as particle radioactivity. Particle radioactivity is determined by collecting airborne PM and measuring gross α-, β-, and γ-activity (radiation). The PM with attached Rn decay products may be inhaled, depositing in human airways and alveolar regions, which may also lead to subsequent systemic transport due to particle translocation.26,27–30 The radioactive decay products result in cellular irradiation, oxidative stress, and cellular damage.31 Due to the high energy of α particles and its larger mass, α-emitting Rn decay products are considered to cause the most damage to nearby cells.32
While the concentration of outdoor radon is typically low, given radon escaping from the ground is diluted from the large volume of air and is rapidly degraded in the atmosphere, enclosed indoor spaces, such as homes, schools, and offices, often reach higher, and potentially harmful, concentrations. Radon gas and its radon decay products, the principal source of natural background ionizing radiation accounting for approximately half of all human exposure to radiation, is the largest source of background radiation exposure to the public, as it is present in all types of homes and buildings.9,33–37 While this naturally occurring radioactive emission exists in soil, rocks, and building materials, where it is generally trapped within these solids, Rn may accumulate in closed spaces and reach concerning indoor concentrations where it can be inhaled.38 Rn often settles in basements and other low-lying areas due to its high density, while outdoor radon tends to disperse rapidly.39 Higher indoor radon concentrations are typically found in colder climates, particularly in the winter, poorly ventilated spaces, areas supplied with groundwater, with its levels affected by building material properties. Low concentrations of radon may be found in building materials, such as tile, brick, concrete, and wallboard, which tend to have radon concentrations similar to the rock type they were manufactured and generally contribute a minimal amount to indoor radon concentrations, however, may contribute to a greater amount to indoor air levels if the building materials, such as wallboard, concrete, or blocks, were made from radioactive waste products or shale from uranium mining.40
On average, indoor radon levels are about 1000 times lower than radon in the soil beneath the home.40 Due to pressure differences driven by lower air pressure inside buildings, where the pressure difference leads to an upward flow of air from the ground with movement of air from a high to a low pressure area, radon and its decay products may diffuse through pores and cracks from the earth’s crust and released into the atmosphere, accumulating indoors. Radon in soil can traverse into a home via structural defects in the basement, which include gaps in concrete, floors, and around service pipes, crawl spaces, wall, construction joints, pores in walls, and cracks in floors and walls below construction level (Figure 2).10
Higher radon concentration in occupational settings is found in underground spaces with inadequate ventilation and in water treatment plans, with the highest concentration of radon associated with mine workers, where the first studies linking the health effects of radon exposure were conducted in miners of underground uranium mines.42 With regard to the general population, radon exposure is predominantly attributed to its presence in indoor dwellings, with levels of radon in buildings varying regionally and dependent on permeability of the ground material and building construction.43 Several additional factors that determine radon levels indoors include season (higher concentrations in colder months), building type (higher concentrations in buildings with poor ventilation), urban or rural setting, building floor level (higher concentrations in the basement and on lower floors of buildings), bedrock porosity and permeability, soil permeability, type of carrier fluids (such as surface water, groundwater, or carbon dioxide gas), weather, soil permeability, and building occupants’ lifestyle.44
Historically, radon’s health effects have been well-known to be associated with cancer, with the first studies of radon lung carcinogenicity originating from occupational studies in miners, particularly uranium miners, who were exposed to elevated levels of radon. Multiple cohort studies evaluating the association of lung cancer due to occupational exposure to radon decay products have been reported, with these cohort studies revealing a statistically significant association between exposure to radon in mines and lung cancer risk.40,45–48 Experimental evidence of mutagenesis studies in cell culture and laboratory animals also supports radon as an established human lung carcinogen.49 The International Agency for Research on Cancer (IARC) has also classified radon as a Group 1 carcinogen, based on sufficient evidence of its ability to cause cancer resulting from both human epidemiological studies and experimental laboratory experiments. Employing various modeling approaches, results of lung cancer risk in miners were also applied to project lung cancer risk for the general population exposed to residential radon, with results suggesting that 10–15% of total lung cancer mortality in the US may be caused by residential radon exposure, establishing radon as the second leading cause of lung cancer mortality following tobacco smoke in adults.40
While radon exposure is well-known to increase the risk of lung cancer in adults, radon’s association with childhood cancer, particularly leukemia,50 is still being investigated, with more research needed to fully understand the relationship between radon and childhood cancers given mixed findings of existing studies.51
While discussion of the well-known cancer effects of radon in adults, with suggestive effects in children, has been included above for historical context to provide an overview of the current state of knowledge of radon’s health effects, the purpose of this state of the art review is to synthesize how health outcome findings of this topic have developed over time to give rise to our current understanding of radon’s health effects, focusing primarily on non-cancer pulmonary findings in children to date.

Materials and Methods: Literature Search Strategy
A literature search on radon and non-cancer pulmonary health effects in children was performed in the English-language databases, including PubMed, EBSCO (psych info, CINAHL and Medline), Web of Science, and Cochrane, to obtain relevant articles published in the last 20 years from 12/12/2005 up to 2025. The literature search was performed using the following keywords: lung diseases, asthma, obstructive lung disease, COPD, lung function, bronchitis, cystic fibrosis, pulmonary disease, lung disease, radiation pneumonitis, respiratory, lung, non-cancer, radon, particle radioactivity, alpha particles, beta particles, radioactive pollutant, radioactive waste, or radioactive pollutants and pediatrics (Supplemental File 1, Supplemental File 2).

HEALTH RISKS OF RADON IN CHILDREN

Fetal, Perinatal, and Maternal Outcomes during Pregnancy
Several studies have examined the role of radon exposure during pregnancy, given ionizing radiation is a known risk factor for adverse fetal and maternal outcomes. In a review by Angley et al, exposure to radon and ambient particle radioactivity during pregnancy and adverse maternal, fetal, and perinatal outcomes were evaluated. In eight human studies, accumulated evidence suggests radon and particle radioactivity may be associated with adverse fetal, perinatal, and maternal outcomes, with data supporting prenatal particle radioactivity linked with smaller fetal growth measurements in anatomic scans (<24 weeks’ gestation), larger fetal growth measurements in growth scans (≥24 weeks’ gestation), reduced birth weight, associations with cleft lip with or without cleft palate and cystic hygroma/lymphangioma, and increased odds of gestational diabetes mellitus and hypertensive disorders of pregnancy.52–56

NON-CANCER PULMONARY HEALTH EFFECTS OF RADON

Obstructive Pulmonary Diseases

Chronic Obstructive Pulmonary Disease (COPD) in Adults:
More recent studies have linked radon with COPD morbidity and mortality.57,58 The study of radon exposure in patients with COPD and on pulmonary function in adults is relevant to understanding associations in children. Studies in COPD and effects on pulmonary function are highlighted in this review to synthesize how health outcome findings of this topic provide the foundation regarding the pathophysiology of how health effects have changed over time to give rise to our current understanding of radon and non-cancer pulmonary health effects in children.
In a study by Barbosa-Lorenzo et al, the relationship between residential radon exposure and COPD prevalence and hospital admissions at a municipal level was examined, where the authors reported residential radon increased the risk of hospital admissions in COPD patients.59 In a separate study, Wang et al investigated associations between indoor radon decay products, measured as particle radioactivity, with respiratory symptoms and health-related quality of life (HRQL) in patients with COPD and found that residential radon decay products are associated with cough, phlegm, and worse HRQL symptoms score in patients with COPD.60 Additional studies have shown radon decay product exposure associated with lung function changes, where Wang et al reported associations between measures of indoor particle radioactivity and reductions in FEV1 and FVC in a cohort study of 142 elderly, predominantly male patients, with COPD in Eastern Massachusetts who had 4 one-week long seasonal assessments of indoor home and ambient central site particle radioactivity and PM2.5 over one year.61 Radon and COPD mortality in an American Cancer Society Cohort (The Cancer Prevention Study-II, a large prospective cohort study of approximately 1.2 million Americans) was examined where a significant positive linear trend in COPD mortality with increasing concentrations of radon (p<0.05) was reported,62 suggesting residential radon may increase COPD mortality. The reported association between radon decay product particle radioactivity and COPD has also been described in a study assessing α-particle radioactivity (α-PR) with urinary biomarkers of oxidative tissue damage, where a higher ratio of indoor/ambient α-PR was positively associated with biomarkers of oxidative stress, such as total and free malondialdehyde (MDA), biomarkers of lipid oxidation, and 8-hydroxyl-2’-deoxyguanosine (8-OHdG), a biomarker of DNA oxidative damage.63 Associations with reduced pulmonary function have also been observed in association with ambient beta particle radioactivity in a community-based cohort of Veterans with little diagnosed COPD.64 One of the main features of COPD is chronic inflammation of airways and subsequent destruction of lung parenchyma and alveolar structure due to injury of the airway epithelium, causing release of endogenous intracellular molecules and danger-associated molecular patterns from stressed or dying cells.65 Antigen presenting cells capture these signals, which are transferred to lymphoid tissue, generating an adaptive immune response and contributing to ongoing chronic inflammation.65
The data on radon exposure and COPD causation and morbidity remains mixed, however, as other studies have not shown such associations,66–68 likely owing to the heterogeneity of available studies, some of which were smaller and generally only measured radon once, rather than measurement of long acting decay products, thus warranting an area of additional investigation and research to further understand the relationship between radon and COPD. Nevertheless, the most recent general population studies point to an association between radon exposure and the potential to contribute to worse pulmonary function and increased symptoms in patients with COPD, and additional studies would be of benefit to further strengthen the evidence, ideally with individual evaluations of exposure.29

Asthma
Based on recent findings in COPD in adults and mechanism of airway injury, which include oxidative stress, DNA damage, and chronic inflammation, particularly given radon’s reported role in obstructive lung disease outside its known carcinogenicity, the effect of radon on asthma morbidity in children has also been examined. Asthma, the most common non-communicable chronic disease in children worldwide, is an obstructive lung disease which affects approximately 14% of children globally.69,70 There is sufficient evidence that environmental factors, including indoor air pollutants, contribute to asthma development, morbidity, disability, and healthcare utilization in children.71–78 Oxidative stress is augmented in asthma, as well as by air pollution, causing oxidative damage of tissues, which promotes airway inflammation and hyperresponsiveness, including oxidative DNA damage, which results from exposure to irritants or inflammatory mediators which can lead to redox-dependent changes in cell signaling.79 Air pollutants may induce airway inflammation by driving Th2 immune responses through epithelial damage, promoting the release of Th2 cytokines, such as IL-4, IL-13 and IL-5.79
In a school-based cohort of children in the northeast US screened for asthma morbidity and respiratory symptoms which aimed to evaluate the effect of the indoor environment (School Inner-City Asthma Study), Mukharesh et al reported that modeled short- and long-term radon exposure at schools was associated with an increased odds of having an asthma diagnosis and school absenteeism.80 Monthly radon concentrations were calculated for each participant’s school ZIP Code Tabulation Area by a two-stage machine learning model.12 Asthma diagnosis, the primary outcome, was determined by answering “yes” to a physician diagnosis of asthma and/or current use of a medication for asthma on a study population screening eligibility form.80 Secondary outcomes included report of nighttime difficulty breathing, nocturnal cough, missed school days, and symptoms of wheezing.80
A study by Banzon et al assessed the effect of modeled radon, based on a spatiotemporal model predicting zip code-specific monthly exposure,12 on asthma symptom-days, fractional exhaled nitric oxide (FENO, a marker of eosinophilic inflammation), and lung function in inner-city asthmatic school children in the School Inner-City Asthma Study.81 In this study, a positive association was found between radon 1-month moving average (incidence rate ratio [IRR]= 1.014, 95% CI [1.002,1.027], p=0.0273) and 2-month moving average (IRR=1.015, 95% CI [1.002,1.028], p=0.0286) with maximum asthma symptom-days, which were assessed four times during the academic year (n=299, obs=1,167).81 Additionally, participants with high radon exposure (>50th percentile radon exposure) were found to have greater change in FENO from warm to cold periods compared to low radon exposure (interaction p = 0.0013; β = 0.29 [95% confidence interval [CI]: 0.04–0.54], p = 0.0240).81 The association found between radon and seasonal change in FENO, where participants with higher radon exposure had greater change in FENO from warm to cold periods compared to low radon exposure, was likely due to a combination of increased exposure levels and increased time spent indoors in cold weather. Indoor levels of radon are typically higher during winter months when natural ventilation is more limited as a result of doors and windows being shut during cold weather, use of heaters can cause warmer air to drive pressure differences in the home leading to radon gas traversing from the soil in the ground into the home, and cold weather can lead to the ground to be more compact, creating pressure for radon to escape from the ground into homes through porous entry points, holes, or cracks in the foundation.
To further explore the relationship found between radon and asthma morbidity and identify plausible mediators of this exposure-outcome relationship, in a separate exploratory study of children with asthma in the School Inner-City Asthma Study and modeled radon data, a positive association with radon exposure and interleukin 5 (IL-5) was reported, where higher radon was significantly associated with a greater increase in IL-5 compared to low radon exposure (observations 5 137; 1- month moving radon average [% change = 13.4%; 95% CI: 0.4%−28.0%; p = 0.044]).82 IL-5 is a TH2-cell cytokine known to recruit eosinophils to asthmatic airways, thus mediation analysis was performed revealing an indirect effect of IL-5 (β = 0.006; 95% CI:0.001–0.012; p = 0.024) on the association between radon exposure and absolute eosinophil count, suggesting the effect of radon on eosinophil count is mediated through IL-5. Collectively, these recent findings in the pediatric population identifies radon as a novel, modifiable environmental risk factor for asthma in children, where levels of radon exposure in the School Inner-City Asthma study were all lower in relation to the EPA recommended action level of 148 Bq/m3 advised for indoor radon mitigation,83,84 though all greater than the natural outdoor level of radon (14.8 Bq/m3), which are presently based on lung cancer risk.

NEW INSIGHTS
The literature reviewed in this article allows an expanded view of the adverse health effects of radon exposure, focusing on non-cancer pulmonary health effects in children reported to date. In recent pediatric studies in children with asthma, radon is associated as being a novel, modifiable risk factor to consider for asthma, linked with increased odds of having an asthma diagnosis, asthma morbidity, and school absenteeism (Table 1),80–82 warranting the need for confirmatory intervention studies, such as randomized clinical trials. Of note, recent studies in the pediatric population identifying radon as a risk factor for asthma in children were all found to have levels of modeled radon exposure lower than the EPA recommended actionable level of 148 Bq/m3, the World Health Organization (WHO) recommended indoor radon action level of 100 Bq/m3, and the International Commission on Radiological Protection (ICRP) recommended reference action level not to exceed 300 Bq/m3 advised for indoor radon mitigation,83–86 though all greater than the natural outdoor level of radon (14.8 Bq/m3), which is the level U.S. Congress has set as the target indoor radon level per the Indoor Radon Abatement Act of 1988, with current regulations based on lung cancer, rather than non-cancer effects.87 Recent findings associating radon exposure and asthma suggest radon may be an important contributor to asthma morbidity at levels below current existing EPA guidelines, which were developed specifically based on lung cancer risk associated with radon, and health effects of radon may be detrimental at lower levels which would not prompt an intervention in homes or buildings.
Additionally, due to smaller lungs, faster breathing rates, and lower proximity to the ground in children, radon may be drawn deeper into children’s lungs, where young children may experience even higher levels of radon exposure.88,89 Based on studies in adults, it is possible that exposure to radon and its decay products contributes to reduced pulmonary function in children, particularly given detrimental effects of exposure during a of immune system maturation, active lung development, and higher ventilation rates in children.88 Children may be more susceptible physiologically and particularly vulnerable to the adverse impacts of toxic environmental exposures, such as radon, as a result of modes of toxicant delivery and consumption, biological vulnerability during periods of rapid development, time spent indoors, and breathing and eating habits.88–92 Taylor et al reported chronic home radon exposure to be associated with higher inflammatory biomarker concentrations in children and adolescents, with the authors suggesting that chronic radon exposure starting early in life may contribute to later life pathology due to continuously elevated inflammation, including damage caused to respiratory epithelium, which may be linked to the incidence of respiratory diseases in childhood, such as asthma, well before any type of cancer is detected.90 Based on pediatric findings to date with modeled radon as a risk factor for asthma, these results may provide objective data to support reconsideration of current radon action level thresholds and reevaluation of future public policy regulations related to radon’s effect on asthma outcomes. Associations reported at levels below the EPA action level raise the possibility that non-cancer outcomes may occur at lower radon concentrations; however, these findings require replication with direct exposure measures and robust confounder control prior to clinical or regulatory thresholds are reconsidered. Given the study evaluating associations between radon exposure and biomarkers was an exploratory analysis, multiple testing corrections were not applied, and more directed studies are planned in future work.
While provocative, findings from cumulative pediatric studies of radon and asthma morbidity to date are based on residential radon models derived from validated zipcode-based geospatial models, rather than direct measurement of radioactivity inside buildings using scintillation, ionization chamber, or solid-state detection methods, which would offer more personalized and specific measures of exposure. Of note, the pediatric studies with modeled radon data included in this review were based a cross-sectional retrospective analysis, whose original objectives did not include the effects of radon. Therefore, direct home measurements were not available, and thus a radon prediction spatiotemporal model was employed. The assessment of exposure would be expected to be non-differential in regards to the outcomes assessed and bias the effect estimates towards the null and underestimate the true radon effects. Potential confounders in the modeled radon exposure analyses in pediatric asthma studies were addressed by the authors by conducting sensitivity analyses to assess potential confounding of ambient PM2.5, NO2 and O3, in which the association between each pollutant and health outcome were tested separately, adjusting for all covariates included in the original models. Pollutants significantly associated with each outcome were included with radon in a final adjusted model and the correlation between radon and pollutants was tested to assess potential for multicollinearity in adjusted models. In sensitivity analysis assessing confounding of the radon effect by PM2.5, NO2, and O3 on outcomes, the authors found results were consistent for all models with the exception of O3 and maximum symptom-days, in which O3 mitigated the effect of radon, however, the high collinearity of the exposures was noted. All statistical models which employed modeled radon data with pediatric asthma outcomes also adjusted for age, any sensitization, BMI, sex, ICS controller medication use, race, and household income <$25,000.
Potential risk of exposure misclassification may be minimized by future studies with concrete measurement methods and study design, such as continuous monitors, long-term alpha particle radioactivity tracking, classroom filter analysis for particle radioactivity, and seasonal sampling strategies. Future studies would benefit from design for causal inference, with individual exposure measurements, repeated measures, negative controls, instrumental variables, and randomized mitigation trials.
Ongoing research is currently underway which includes directly measured particle radioactivity from the classrooms in the School Inner-City Asthma Study (SICAS), where radon decay products (radon progeny) can be measured directly from air cleaner filters used from schools in the SICAS study and linked to health outcomes and biomarker data (NIH K23 ES035459). Short-lived radon progeny which is airborne can be inhaled, which is regarded as the most critical mode of internal exposure to the natural radiation dose delivered to the human lung.93 Dosimetry of alpha particles from radon progeny in the human airway distinguishes between unattached (free ions/clusters) and attached (bound to aerosols) fractions, with the amount of unattached progeny dependent on the concentration of aerosol in the air.94,95 The unattached fraction is higher in clean air, while in air which is dusty or smoky, the unattached fraction decreases as more progeny attach to particles.94,95 Dosimetry patterns depend on age and size of an individual, and compared to adults, children may receive a greater internal dose due to greater ventilation rate per body weight or lung surface area, in addition to metabolic differences which may lead to differing levels of tissue burden.96 This is supported by data from others who have shown radon to cause oxidative stress using in vivo murine models and in cell culture,97–99 with oxidative stress induction demonstrated by higher protein expression of Nrf-2 and its down-stream antioxidant proteins, which are suggestive of changes in oxidative stress indices and may play a significant role.99
Findings from directly measured particle radioactivity collected in the School Inner-City Asthma Study (SICAS) based on radon decay products may further aid in understanding the relationship between radon, particle radioactivity, and asthma, which may facilitate the design of public health intervention trials, directly inform activities regarding radon mitigation as an intervention to alleviate morbidity and disability from asthma, and identify biomarkers associated with particle radioactivity that may better phenotype patients and predict those who may have a more favorable response to personalized asthma treatment based on biomarkers. Future directions for research include the Radon Asthma Intervention Trial (ROME trial, ClinicalTrials.gov ID NCT06706336), which is a randomized, double-blind, sham controlled trial in children with asthma. This randomized controlled clinical trial aims to investigate the efficacy of radon mitigation in the homes of susceptible individuals and follow health outcomes in intervention vs. inactive (sham) control to provide evidence for health benefits by improving indoor air quality and determine if radon mitigation may improve asthma. Advantages of the ROME trial include minimizing bias through a randomized, double-blinded, sham controlled randomized controlled clinical trial to determine the effect of a home environmental radioactivity focused intervention with a home radon mitigation system on asthma symptoms, with use of IAQ monitors which will continuously measure radon and PM2.5, which serve as a surrogate for particle radioactivity using sensors for real-time direct assessment and remote transmission of data. Additionally, co-located integrated devices with filter collection of PM will collect particulate exposures and be used to calibrate the continuous monitors. Limitations of the ROME trial include the possibility that radon levels as a source contributing to particle radioactivity in the homes may be low due to naturally low levels (which may be accounted for by enriching the cohort with those with high exposure and recruiting participants from areas with historically elevated levels of radon and thus higher likelihood of elevated particle radioactivity). An additional limitation of the ROME randomized clinical trial includes the ability to evaluate the effect of unmeasured confounders, which is inherent with any epidemiologic exposure study.

CONCLUSIONS
Apart from radon’s known carcinogenicity, a growing body of literature supports an association between radon and non-cancer respiratory disease, although important knowledge gaps remain. In children, radon has been recently associated with asthma morbidity, and a greater understanding of the adverse health effects of exposure to radon and particle radioactivity in the pediatric population is critical to address important unanswered scientific questions, as studies to date have been based on modeled radon exposure, rather than directly measured particle radioactivity. Recent findings of radon’s non-cancer respiratory effects further highlight the role of avoidance of this environmental exposure and radon mitigation1 as an implementable strategy to improve lung health. Given health effects in studies to date linking radon with asthma in children falling below the EPA recommended actionable level of 148 Bq/m3 advised for indoor radon mitigation, further research is needed to expand our understanding of radon’s role in non-cancer respiratory health and how to optimize radon mitigation and intervention strategies which aim to reduce exposure to a potentially under-recognized threat to lung health, improve non-cancer pulmonary health morbidity and outcomes, and encourage policymakers to improve human respiratory health, which would be aided by the following actionable recommendations:
standardized exposure measurement in pediatric cohorts

investment in randomized mitigation trials for high-risk children

integration of radon monitoring into school health programs in high-risk areas

re-evaluation of guidelines in the setting of replicated evidence.

Supplementary Material
supplemental 1Supplemental 2