Smoking Modifies the Association Between Radon Exposure and Incident Ischemic Stroke: The REGARDS Study.

BACKGROUND: Exposure to radon has been linked to lung cancer and other lung diseases. Although biologically plausible, research of residential radon exposure in relation to stroke risk is scarce. METHODS: Study participants were from the REGARDS (Reasons for Geographic and Racial Differences in Stroke) cohort (n=30 239), which consisted of male and female non-Hispanic Black and White adults aged 45 and older. After excluding participants with baseline stroke and transient ischemic attack, and missing information on exposure and outcome of interest, the final sample size was 26 950. The primary outcome was time to the first ischemic stroke through September 30, 2020. County-level radon measures from Lawrence Berkeley National Laboratory were linked to each participant based on their geocoded residential history. We used Cox proportional hazards regression models with a time-dependent exposure to estimate hazard ratios and 95% CIs for the association. RESULTS: After controlling for potential confounding factors including demographic, lifestyle, clinical variables, and PM2.5, radon exposure was significantly associated with incident ischemic stroke among never-smokers (hazard ratio, 1.39 [95% CI, 1.01-1.90]) but not ever-smokers. The results were generally consistent in the sensitivity analysis when using radon measures from state/Environmental Protection Agency residential radon survey. CONCLUSIONS: Findings from this study suggest that the association between residential radon exposure and incidence of ischemic stroke varies by smoking status and may be prominent in never-smokers. Further studies incorporating indoor-radon measures are needed to confirm these findings.

Telehealth Utilization Is Associated with Lower Risk of Discontinuation of Buprenorphine: a Retrospective Cohort Study of US Veterans.

OBJECTIVE: Treatment for opioid use disorder (OUD) may include a combination of pharmacotherapies (such as buprenorphine) with counseling services if clinically indicated. Medication management or engagement with in-person counseling services may be hindered by logistical and financial barriers. Telehealth may provide an alternative mechanism for continued engagement. This study aimed to evaluate the association between telehealth encounters and time to discontinuation of buprenorphine treatment when compared to traditional in-person visits and to evaluate potential effect modification by rural-urban designation and in-person and telehealth combination treatment. METHODS: A retrospective cohort study of Veterans diagnosed with OUD and treated with buprenorphine across all facilities within the Veterans Health Administration (VHA) between 2008 and 2017. Exposures were telehealth and in-person encounters for substance use disorder (SUD) and mental health, treated as time-varying covariates. The primary outcome was treatment discontinuation, evaluated as 14 days of absence of medication from initiation through 1 year. RESULTS: Compared to in-person encounters, treatment discontinuation was lower for telehealth for SUD (aHR: 0.69; 95%CI: 0.60, 0.78) and mental health (aHR: 0.69; 95%CI: 0.62, 0.76). There was no evidence of effect modification by rural-urban designation. Risk of treatment discontinuation appeared to be lower among those with telehealth only compared to in-person only for both SUD (aHR: 0.48, 95%CI: 0.37, 0.62) and for mental health (aHR: 0.46; 95%CI: 0.33, 0.65). CONCLUSIONS: As telehealth demonstrated improved treatment retention compared to in-person visits, it may be a suitable option for engagement for patients in OUD management. Efforts to expand services may improve treatment retention and health outcomes for VHA and other health care systems.

Does protracted radon exposure play a role in the development of dementia?

Radon is a ubiquitous radioactive gas that decays into a series of solid radioactive decay products. Radon, and its decay products, enter the human body primarily through inhalation and can be delivered to various tissues including the brain through systemic circulation. It can also reach the brain by neuronal pathways via the olfactory system. While ionizing radiation has been suggested as a risk factor of dementia for decades, studies exploring the possible role of radon exposure in the development of Alzheimer's Diseases (AD) and other dementias are sparse. We systematically reviewed the literature and found several lines of evidence suggesting that radon decay products (RDPs) disproportionally deposit in the brain of AD patients with selective accumulation within the protein fractions. Ecologic study findings also indicate a significant positive correlation between geographic-level radon distribution and AD mortality in the US. Additionally, pathologic studies of radon shed light on the potential pathways of radon decay product induced proinflammation and oxidative stress that may result in the development of dementia. In summary, there are plausible underlying biological mechanisms linking radon exposure to the risk of dementia. Since randomized clinical trials on radon exposure are not feasible, well-designed individual-level epidemiologic studies are urgently needed to elucidate the possible association between radon (i.e., RDPs) exposure and the onset of dementia.

Utility of death certificate data in predicting cancer incidence.

BACKGROUND: Studies often rely on death certificates to identify cancer occurrence. This research assessed the death certificate's ability to reflect cancer incidence and factors that influence agreement with cancer registry data. METHODS: This study compared death certificates to cancer incidence data for an occupational cohort of 1,795 deceased workers who were registered by the Iowa Cancer Registry (ICR) between 1973 and 2005. Logistic regression models examined the effects of factors such as survival time, age at diagnosis, and gender on the odds of agreement between death certificate and incidence data. RESULTS: Death certificates under-reported cancer incidence by 10-100%, depending on site. A 1-year increase in survival decreased the odds of agreement between death certificate and ICR data by 18%. Younger and female workers had increased odds of agreement. CONCLUSIONS: Death certificates can be useful predictors of cancer incidence, particularly for diseases with shorter survival and among subjects diagnosed earlier in life.

Prevalence of neonicotinoid insecticides in paired private-well tap water and human urine samples in a region of intense agriculture overlying vulnerable aquifers in eastern Iowa.

A pilot study among farming households in eastern Iowa was conducted to assess human exposure to neonicotinoids (NEOs). The study was in a region with intense crop and livestock production and where groundwater is vulnerable to surface-applied contaminants. In addition to paired outdoor (hydrant) water and indoor (tap) water samples from private wells, urine samples were collected from 47 adult male pesticide applicators along with the completions of dietary and occupational surveys. Estimated Daily Intake (EDI) were then calculated to examine exposures for different aged family members. NEOs were detected in 53% of outdoor and 55% of indoor samples, with two or more NEOs in 13% of samples. Clothianidin was the most frequently detected NEO in water samples. Human exposure was ubiquitous in urine samples. A median of 10 different NEOs and/or metabolites were detected in urine, with clothianidin, nitenpyram, thiamethoxam, 6-chloronicotinic acid, and thiacloprid amide detected in every urine samples analyzed. Dinotefuran, imidaclothiz, acetamiprid-N-desmethyl, and N-desmethyl thiamethoxam were found in ≥70% of urine samples. Observed water intake for study participants and EDIs were below the chronic reference doses (CRfD) and acceptable daily intake (ADI) standards for all NEOs indicating minimal risk from ingestion of tap water. The study results indicate that while the consumption of private well tap water provides a human exposure pathway, the companion urine results provide evidence that diet and/or other exposure pathways (e.g., occupational, house dust) may contribute to exposure more than water contamination. Further biomonitoring research is needed to better understand the scale of human exposure from different sources.

Juxtaposition of intensive agriculture, vulnerable aquifers, and mixed chemical/microbial exposures in private-well tapwater in northeast Iowa.

In the United States and globally, contaminant exposure in unregulated private-well point-of-use tapwater (TW) is a recognized public-health data gap and an obstacle to both risk-management and homeowner decision making. To help address the lack of data on broad contaminant exposures in private-well TW from hydrologically-vulnerable (alluvial, karst) aquifers in agriculturally-intensive landscapes, samples were collected in 2018-2019 from 47 northeast Iowa farms and analyzed for 35 inorganics, 437 unique organics, 5 in vitro bioassays, and 11 microbial assays. Twenty-six inorganics and 51 organics, dominated by pesticides and related transformation products (35 herbicide-, 5 insecticide-, and 2 fungicide-related), were observed in TW. Heterotrophic bacteria detections were near ubiquitous (94 % of the samples), with detection of total coliform bacteria in 28 % of the samples and growth on at least one putative-pathogen selective media across all TW samples. Health-based hazard index screening levels were exceeded frequently in private-well TW and attributed primarily to inorganics (nitrate, uranium). Results support incorporation of residential treatment systems to protect against contaminant exposure and the need for increased monitoring of rural private-well homes. Continued assessment of unmonitored and unregulated private-supply TW is needed to model contaminant exposures and human-health risks.

Occurrence of neonicotinoids and sulfoxaflor in major aquifer groups in Iowa.

A statewide assessment of neonicotinoids in groundwater was conducted among a sample of public water supply wells in Iowa from October 2017 to August 2018. Samples from all the state's major aquifer groups were initially collected from 118 wells in 69 counties. Subsets of 55 untreated samples and 45 paired pre- and post-treatment samples were then collected in summer 2018, post-planting season for primarily corn and soybeans, to assess seasonal differences and the efficacy of treatment. Samples prepared using solid phase extraction were analyzed using LC/MS/MS for six neonicotinoids: acetamiprid, clothianidin, dinotefuran, imidacloprid, thiacloprid, thiamethoxam, and a sulfoximine (i.e., sulfoxaflor). Clothianidin was the most frequently detected (34%, max: 13.4 ng/L), followed by thiamethoxam (14.4%, max: 20.6 ng/L), imidacloprid (13%, max: 2.3 ng/L), and dinotefuran (0.1%, max: 1.4 ng/L). Alluvial aquifers (unadjusted odds ratio (UOR) = 14.1; 95% CI (5.4-36.9), p=<0.0001), wells with confining layers <15 m (UOR = 13.5, 95% CI (4.8-38.4), p=<0.0001), and less than 19.4 m in depth (UOR = 20.0; 95% CI (6.5-58.0), p=<0.0001) had the greatest risk for contamination. In vulnerable aquifers, neonicotinoids were detected in 62% of winter and 46% of summer samples, with winter samples over 3 times (UOR = 3.2; 95% CI (1.2-8.8), p = 0.02) more likely to have at least two neonicotinoids detected. In 55 public water supply systems, the median concentrations of clothianidin (p = 0.6), imidacloprid (p = 0.7), and thiamethoxam (p = 0.7) were unchanged following treatment. These results suggest that neonicotinoid contamination may be present year-round in treated drinking water from vulnerable groundwater sources and represent a source of human exposure.

A critical review on the potential impacts of neonicotinoid insecticide use: current knowledge of environmental fate, toxicity, and implications for human health.

Neonicotinoid insecticides are widely used in both urban and agricultural settings around the world. Historically, neonicotinoid insecticides have been viewed as ideal replacements for more toxic compounds, like organophosphates, due in part to their perceived limited potential to affect the environment and human health. This critical review investigates the environmental fate and toxicity of neonicotinoids and their metabolites and the potential risks associated with exposure. Neonicotinoids are found to be ubiquitous in the environment, drinking water, and food, with low-level exposure commonly documented below acceptable daily intake standards. Available toxicological data from animal studies indicate possible genotoxicity, cytotoxicity, impaired immune function, and reduced growth and reproductive success at low concentrations, while limited data from ecological or cross-sectional epidemiological studies have identified acute and chronic health effects ranging from acute respiratory, cardiovascular, and neurological symptoms to oxidative genetic damage and birth defects. Due to the heavy use of neonicotinoids and potential for cumulative chronic exposure, these insecticides represent novel risks and necessitate further study to fully understand their risks to humans.

Recent advances in understanding the biomolecular basis of chronic beryllium disease: a review.

In this review we summarize the work conducted over the past decade that has advanced our knowledge of pulmonary diseases associated with exposure to beryllium that has provided a molecular-based understanding of the chemistry, immunopathology, and immunogenetics of beryllium toxicity. Beryllium is a strong and lightweight metal that generates and reflects neutrons, resists corrosion, is transparent to X-rays, and conducts electricity. Beryllium is one of the most toxic elements on the periodic table, eliciting in susceptible humans (a) an allergic immune response known as beryllium sensitization (BeS); (b) acute beryllium disease, an acutely toxic, pneumonitis-like lung condition resulting from exposure to high beryllium concentrations that are rarely seen in modern industry; and (c) chronic beryllium disease (CBD) following either high or very low levels of exposure. Because of its exceptional strength, stability, and heat-absorbing capability, beryllium is used in many important technologies in the modern world. In the early 1940s, beryllium was recognized as posing an occupational hazard in manufacturing and production settings. Although acute beryllium disease is now rare, beryllium is an insidious poison with a latent toxicity and the risk of developing CBD persists. Chronic beryllium disease-a systemic granulomatous lung disorder caused by a specific delayed immune response to beryllium within a few months to several decades after exposure-has been called the "unrecognized epidemic". Although not a disease in itself, BeS, the innate immune response to beryllium identified by an abnormal beryllium lymphocyte proliferation test result, is a population-based predictor of CBD. Genetic susceptibility to CBD is associated with alleles of the major histocompatibility gene, human leukocyte antigen DP (HLA-DP) containing glutamic acid at the 69th position of the beta chain (HLA-DPbeta-E69). Other genes are likely to be involved in the disease process, and research on this issue is in progress. The current Occupational Safety & Health Administration permissible exposure limit of 2 microg/m3 has failed to protect workers from BeS/CBD. As a safe exposure limit that will not lead to BeS or CBD has not yet been determined, the realization that the risk of CBD persists has led to a renaissance in research on the effects of the metal on human health. Current data support further reductions in exposure levels to help minimize the incidence of CBD. Steps that would directly impact both the power of epidemiologic studies and the cost of surveillance would be to develop and validate improved screening and diagnostic tests, and to identify more genetic factors that affect either sensitization or disease process. The major focus of this review is the recent research on the cellular and molecular basis of beryllium sensitization and disease, using a multidisciplinary approach of bioinorganic chemistry and immunology. First we present a historical background of beryllium exposure and disease, followed by occurrence of beryllium in the environment, toxicokinetics, biological effects, beryllium lung disease, and other human health effects.

Blind testing of commercially available short-term radon detectors.

A sample of commercially available, charcoal adsorption type, short-term radon detectors was blind tested under controlled laboratory conditions in order to obtain a "snapshot" of the accuracy and precision of the detectors. The results of the controlled exposures were then compared to a previous field study of the same type of commercially available radon detectors. Radon detectors, purchased from seven different commercial vendors, were exposed to a reference (222)Rn gas concentration at the U.S. Environmental Protection Agency's (EPA) Radon Chamber located at the Radiation and Indoor Environments National Laboratory in Las Vegas, Nevada. EPA Test 1 was performed under a controlled simulated field exposure paralleling, to the extent possible, the previous actual field exposure conditions. A second controlled exposure, EPA Test 2, was performed under a relatively steady state of (222)Rn gas concentration, at the same temperature, but a more moderate relative humidity. In the previous field setting evaluation of detectors, five out of six companies tested did not pass the accuracy guideline (all individual relative errors < or =25%) established during the EPA's former Radon Measurement Proficiency Program (EPA-RMPP). As compared to the field test, the detectors in this study generally exhibited better accuracy and precision. Not surprisingly, it appeared temporal fluctuations in radon concentrations and increased humidity had a negative influence on the accuracy and precision of detectors for some companies. The inability of three out of seven companies to meet former EPA-RMPP guidelines for accuracy, even under ideal exposure conditions (constant temperature, humidity, and radon concentration), highlights the importance of blind testing commercially available radon detectors. Furthermore, the consistent over-reporting or under-reporting trends in the overall results for all three tests suggest a potentially widespread systematic bias for the individual companies that merits further investigation. It is unknown if this one-time "snapshot" represents the overall reliability of commercially available charcoal-based radon detectors. Nonetheless, the findings suggest the need for improved vigilance to assure that the public can rely on commercially available radon detectors to make an informed decision whether or not to perform additional testing or to mitigate.

The unintended impact of smoking-risk information on concerns about radon: A randomized controlled trial.

OBJECTIVE: Health communications are often viewed by people with varying levels of risk. This project examined, in the context of radon risk messages, whether information relevant to high-risk individuals can have an unintended influence on lower-risk individuals. Two studies assessed whether information about lung cancer risk from smoking reduced concerns about lung cancer risk from radon among nonsmokers. METHOD: American nonsmokers viewed radon messages that varied in what they communicated about smoking's effect on lung cancer risk. Study 1 used a 4-arm factorial, randomized, controlled design in which smoking information was included or excluded from messages assembled from 2 existing radon pamphlets. Study 2 used a 3-arm parallel, randomized, controlled design in which a new radon message excluded smoking information, described smoking as a lung cancer risk, or also described smoking's synergistic effect with radon. RESULTS: In Study 1, the inclusion of smoking information reduced nonsmokers' (n = 462) concern-related reactions to possible radon exposure. In Study 2, nonsmokers' (n = 583) concern-related reactions were reduced in both smoking-information conditions; intentions to test their home for radon and perceived importance of testing were reduced in the synergistic condition. CONCLUSION: People reading health-risk information contextualize their risk relative to the risk of others. For people at midlevel risk, concern and related reactions prompted by a health message may be dampened when the message includes information about others who are more at risk. In the case of radon and smoking risks, the inclusion of smoking information can reduce the impact that radon messages have on nonsmokers. (PsycINFO Database Record (c) 2018 APA, all rights reserved).

Chronic lymphocytic leukaemia: an overview of aetiology in light of recent developments in classification and pathogenesis.

This overview of the epidemiology of chronic lymphocytic leukaemia (CLL) summarizes the evolution of classification and coding systems and describes the intersection of pathogenesis and aetiology. The role of the putative precursor to CLL, monoclonal B-cell lymphocytosis (MBL), is considered, and ideas for future investigations of the MBL-CLL relationship are outlined. We discuss the epidemiology of CLL, focusing on descriptive patterns and methodological considerations. Postulated risk factors are reviewed including the role of ionizing and non-ionizing radiation, occupational and environmental chemical exposures, medical conditions and treatments, and lifestyle and genetic factors. We conclude by raising key questions that need to be addressed to advance our understanding of CLL aetiology. Recommendations for future epidemiological studies are given, including the standardization of reporting of CLL across cancer registries, the clarification of the natural history of MBL, and the circumvention of the methodological shortcomings of prior epidemiological investigations in relation to radiation, chemical exposures and infectious agents.

Variation in yearly residential radon concentrations in the upper midwest.

It is well known that inhalation of 222Rn and 222Rn decay products increases the risk of lung cancer. While the occurrences of high radon areas in the United States are generally known, studies examining the temporal yearly radon variation in homes across different regions are lacking. This information is essential to assess the ability of a year-long radon measurement to predict the future radon concentration in a home or reconstruct the retrospective residential radon concentration. The purpose of this study is to help fill this gap by examining the temporal variation of residential radon concentrations in homes over several years as well as to explore factors that affect the yearly temporal variability of residential radon concentrations. The coefficient of variation was used as a measure of relative variation between multiple measurements performed across homes over several years. Generalized linear model analyses were applied to investigate factors affecting the coefficient of variation. The median coefficient of variation between the first and second test period was 12%, while a median coefficient of variation of 19% was found between the first and third test period. Factors impacting the coefficients of variation were found to vary for different types of homes and by floors of a home. This study provides important insights into the uncertainty of residential radon gas concentrations that can be incorporated into the sensitivity analyses for the risk estimates of both the North American and global pooling of residential radon studies to improve risk estimates.

Dosimetric challenges for residential radon epidemiology.

Radon concentration alone may not be an adequate surrogate to measure for lung cancer risk in all residential radon epidemiologic lung cancer studies. The dose delivered to the lungs per unit radon exposure can vary significantly with exposure conditions. These dose-effectiveness variations can be comparable to spatial and temporal factor variations in many situations. New technologies that use surface-deposited and implanted radon progeny activities make more accurate dose estimates available for future epidemiologic studies.

A combined analysis of North American case-control studies of residential radon and lung cancer.

Cohort studies have consistently shown underground miners exposed to high levels of radon to be at excess risk of lung cancer, and extrapolations based on those results indicate that residential radon may be responsible for nearly 10-15% of all lung cancer deaths per year in the United States. However, case-control studies of residential radon and lung cancer have provided ambiguous evidence of radon lung cancer risks. Regardless, alpha-particle emissions from the short-lived radioactive radon decay products can damage cellular DNA. The possibility that a demonstrated lung carcinogen may be present in large numbers of homes raises a serious public health concern. Thus, a systematic analysis of pooled data from all North American residential radon studies was undertaken to provide a more direct characterization of the public health risk posed by prolonged radon exposure. To evaluate the risk associated with prolonged residential radon exposure, a combined analysis of the primary data from seven large scale case-control studies of residential radon and lung cancer risk was conducted. The combined data set included a total of 4081 cases and 5281 controls, representing the largest aggregation of data on residential radon and lung cancer conducted to date. Residential radon concentrations were determined primarily by a-track detectors placed in the living areas of homes of the study subjects in order to obtain an integrated 1-yr average radon concentration in indoor air. Conditional likelihood regression was used to estimate the excess risk of lung cancer due to residential radon exposure, with adjustment for attained age, sex, study, smoking factors, residential mobility, and completeness of radon measurements. Although the main analyses were based on the combined data set as a whole, we also considered subsets of the data considered to have more accurate radon dosimetry. This included a subset of the data involving 3662 cases and 4966 controls with a-track radon measurements within the exposure time window (ETW) 5-30 yr prior to the index date considered previously by Krewski et al. (2005). Additional restrictions focused on subjects for which a greater proportion of the ETW was covered by measured rather than imputed radon concentrations, and on subjects who occupied at most two residences. The estimated odds ratio (OR) of lung cancer generally increased with radon concentration. The OR trend was consistent with linearity (p = .10), and the excess OR (EOR) was 0.10 per Bq/m3 with 95% confidence limits (-0.01, 0.26). For the subset of the data considered previously by Krewski et al. (2005), the EOR was 0.11 (0.00, 0.28). Further limiting subjects based on our criteria (residential stability and completeness of radon monitoring) expected to improve radon dosimetry led to increased estimates of the EOR. For example, for subjects who had resided in only one or two houses in the 5-30 ETW and who had a-track radon measurements for at least 20 yr of this 25-yr period, the EOR was 0.18 (0.02, 0.43) per 100 Bq/m3. Both estimates are compatible with the EOR of 0.12 (0.02, 0.25) per 100 Bq/m3 predicted by downward extrapolation of the miner data. Collectively, these results provide direct evidence of an association between residential radon and lung cancer risk, a finding predicted by extrapolation of results from occupational studies of radon-exposed underground miners.

An overview of the North American residential radon and lung cancer case-control studies.

Lung cancer has held the distinction as the most common cancer type worldwide since 1985 (Parkin et al., 1993). Recent estimates suggest that lung cancer accounted for 1.2 million deaths worldwide in 2002, which represents 17.6% of the global cancer deaths (Parkin et al., 2005). During 2002, the highest lung cancer rates for men worldwide reportedly occurred in North America and Eastern Europe, whereas the highest rates in females occurred in North America and Northern Europe (Parkin et al., 2005). While tobacco smoking is the leading risk factor for lung cancer, because of the magnitude of lung cancer mortality, even secondary causes of lung cancer present a major public health concern (Field, 2001). Extrapolations from epidemiologic studies of radon-exposed miners project that approximately 18,600 lung cancer deaths per year (range 3000 to 41,000) in the United States alone are attributable to residential radon progeny exposure (National Research Council, 1999). Because of differences between the mines and the home environment, as well as differences (such as breathing rates) between miners and the general public, there was a need to directly evaluate effects of radon in homes. Seven major residential case-control radon studies have been conducted in North America to directly examine the association between prolonged radon progeny (radon) exposure and lung cancer. Six of the studies were performed in the United States including studies in New Jersey, Missouri (two studies), Iowa, and the combined states study (Connecticut, Utah, and southern Idaho). The seventh study was performed in Winnipeg, Manitoba, Canada. The residential case-control studies performed in the United States were previously reviewed elsewhere (Field, 2001). The goal of this review is to provide additional details regarding the methodologies and findings for the individual studies. Radon concentration units presented in this review adhere to the types (pCi/L or Bq/m3) presented in the individual studies. One picocurie per liter is equivalent to 37 Bq/m3. Because the Iowa study calculated actual measures of exposure (concentration x time), its exposures estimates are presented in the form WLM(5-19) (Field et al., 2000a). WLM(5-19) represents the working level months for exposures that occurred 5-19 yr prior to diagnosis for cases or time of interview for control. Eleven WLM(5-19) is approximately equivalent to an average residential radon exposure of 4 pCi/L for 15 yr, assuming a 70% home occupancy.

Field comparison of commercially available short-term radon detectors.

We performed a comparison of commercially available short-term radon detectors in order to determine the accuracy and precision of the detectors under actual field conditions. We exposed fifteen radon detectors, under field conditions, from each of six companies to a reference radon concentration. Five of the six companies tested did not pass the U.S. Environmental Protection Agency's previously established accuracy guideline (all individual relative errors

Three Mile Island epidemiologic radiation dose assessment revisited: 25 years after the accident.

Over the past 25 years, public health concerns following the Three Mile Island (TMI) accident prompted several epidemiologic investigations in the vicinity of TMI. One of these studies is ongoing. This commentary suggests that the major source of radiation exposure to the population has been ignored as a potential confounding factor or effect modifying factor in previous and ongoing TMI epidemiologic studies that explore whether or not TMI accidental plant radiation releases caused an increase in lung cancer in the community around TMI. The commentary also documents the observation that the counties around TMI have the highest regional radon potential in the United States and concludes that radon progeny exposure should be included as part of the overall radiation dose assessment in future studies of radiation-induced lung cancer resulting from the TMI accident.