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Introduction Tobacco consumption and radon exposure are considered the first and second most common causes of lung cancer, respectively. The aim of this study was to analyze both whether selected genetic polymorphisms in loci that are in DNA repair pathways, are related to non-small-cell lung cancer (NSCLC) and whether they may modulate the association between residential radon exposure and lung cancer in both smokers and never smokers. Methods A multicentre, hospital-based, case–control study with 826 cases and 1201 controls was designed in a radon-prone area. Genotyping was determined in whole blood and residential radon exposure was measured in participants’ dwellings. Results Attending to tobacco exposure, the variant in the gene NBN (rs1805794) was associated with lung cancer in never smokers (OR 2.72; 95%1.44–5.2) and heavy smokers (OR 3.04; 95%CI 1.21–7.69). The polymorphism with the highest lung cancer association was OGG1 (rs125701), showing an OR of 8.04 (95%CI 1.64–58.29) for its homozygous variant genotype in heavy smokers. Attending to indoor radon exposure (>200 Bq/m3), rs1452584, for its homozygous variant genotype, showed the highest association (OR 3.04 (95%CI 1.15–8.48). Conclusion The genes analyzed seem to have no association with the fully adjusted model, but they might modulate lung cancer association when different categories of tobacco consumption are considered (i.e. heavy smokers). This association may similarly be elevated for those individuals having high indoor radon exposures, though at a minor extent.

Introduction and objectives: Exposure to environmental tobacco smoke (ETS) is associated with increased mortality and morbidity. The objective of this study was to estimate the impact of ETS exposure in Spain on mortality in 2020 in the population aged 35 years and over. Methods: A method of estimating attributable mortality (AM) based on the prevalence of ETS exposure was applied. Prevalence data were obtained from a representative study conducted in Spain and the relative risks were derived from a meta-analysis. AM point estimates are presented along with 95% confidence intervals (95% CI), calculated using a bootstrap naive procedure. AM, both overall and by smoking habit, was estimated for each combination of sex, age group, and cause of death (lung cancer and ischemic heart disease). A sensitivity analysis was performed. Results: A total of 747 (95% CI 676–825) deaths were attributable to ETS exposure, of which 279 (95% CI 256–306) were caused by lung cancer, and 468 (95% CI 417–523) by ischemic heart disease. Three quarters (75.1%) of AM occurred in men and 60.9% in non-smokers. When chronic obstructive pulmonary disease and cerebrovascular disease are included, the burden of AM is estimated at 2242 deaths. Conclusions: ETS exposure is associated with 1.5% of all deaths from lung cancer and ischemic heart disease in the population aged 35 and over. These data underline the need for health authorities to focus on reducing exposure to ETS in all settings and environments Instituto de Salud Carlos III (ISCIII), reference: PI22/00727, co-funded by the European Union SI

This study sought to ascertain whether there might be an association between radon concentrations and age, gender, histologic type, and tumor stage at diagnosis.Lung cancer cases from different multicenter case-control studies were analyzed, and clinical data were retrieved from electronic health records and personal interviews. A radon device was placed in all dwellings of participants, and we then tested the existence of an association between residential radon and lung cancer characteristics at diagnosis.Of the total of 829 lung cancer cases included, 56.7% were smokers or ex-smokers. There was no association between indoor radon concentrations and age, gender, histologic type or tumor stage at diagnosis. Median indoor radon concentrations increased with age at diagnosis for men, but not for women. When analyzing participants exposed to more than 1000 Bq/mThere seems to be no association between radon and age, gender, histologic type or tumor stage at diagnosis. Higher radon exposure is more frequent in the case of small-cell lung cancer.

In Spain, due to the lack of data at national level a lung cancer registry, the Thoracic Tumour Registry (TTR), was created. Such registry should demonstrate comparability with population-based data to ensure representativeness at population level. The aim is to compare the socio-demographic characteristics of the TTR with incidence data from the Red de Registros de Cáncer (REDECAN) and mortality data from the Instituto Nacional de Estadística (INE). Lung cancer data sources available to date, REDECAN and INE, were used. Lung cancer cases overall and disaggregated by sex and age groups were collected from each source of information and data were compared for the period 2017-2020. Sex and age group proportions of TTR were calculated for both databases (which collect incidence and mortality data), for the entire study period and broken down by year. A total of 17,109 incident lung cancer cases from the TTR, 58,668 estimated incident cases from REDECAN and 88,083 deaths registered from INE between 2017 and 2020 were included. In terms of sex, the proportions are very similar between the three sources and the differences do not exceed 4%. In terms of age, the differences are not large, being larger for mortality data in the older age group from the INE versus the TTR. The TTR seems to be representative of lung cancer cases diagnosed in Spain between 2019 and 2020, both by sex and age. This allows us to accurately characterise the status of this disease, which is the leading cause of cancer death in Spain, and that the analysis of results obtained from the RTT can be applied to cases of lung cancer diagnosed in our country.

Càncer de pulmó; Fumar; Diferències entre sexes Cancer de pulmón; Fumar; Diferencias entre sexos Lung neoplasms; Smoking; Sex Factors Background: Lung cancer causes approximately 25% of all cancer deaths. Despite its relevance, few studies have analyzed differences by sex at the time of diagnosis in terms of symptoms, stage, age or smoking status. We aim to assess if there are differences between men and women on these characteristics at diagnosis. Methods: We analyzed the Thoracic Tumour Registry (TTR), sponsored by the Spanish Lung Cancer Group using a case-series design. This is a nationwide registry of lung cancer cases which started recruitment in 2016. For each case included, clinicians fulfilled an electronic record registering demographic data, symptoms, exposure to lung cancer risk factors, and treatment received in detail. We compared men and women using descriptive statistics. Results: A total of 13,590 participants took part in this study, 25.6% women. Women were 4 years younger than men (64 vs. 69), and men had smoked more frequently. Adenocarcinoma was the most frequent histological type in both sexes. Stage IV at diagnosis was 50.8% in women compared to 43.6% in men. Weight loss/anorexia/asthenia was the most frequent symptom in both sexes and there were no differences in the number of symptoms at diagnosis. There were no relevant differences in the frequency or number of symptoms by sex when non-small cell lung cancer (NSCLC) and small-cell lung cancer (SCLC) were analyzed separately. Smoking status did not appear to cause different lung cancer presentation in men compared to women. Conclusions: There seems to be no differences in lung cancer characteristics by sex at the time at diagnosis on stage, specific symptoms or number of symptoms. This research received funding from the Spanish Lung Cancer Group

OBJECTIVE: In Spain, due to the lack of data at national level a lung cancer registry, the Thoracic Tumour Registry (TTR), was created. Such registry should demonstrate comparability with population-based data to ensure representativeness at population level. The aim is to compare the socio-demographic characteristics of the TTR with incidence data from the Red de Registros de Cáncer (REDECAN) and mortality data from the Instituto Nacional de Estadística (INE). METHOD: Lung cancer data sources available to date, REDECAN and INE, were used. Lung cancer cases overall and disaggregated by sex and age groups were collected from each source of information and data were compared for the period 2017-2020. Sex and age group proportions of TTR were calculated for both databases (which collect incidence and mortality data), for the entire study period and broken down by year. RESULTS: A total of 17,109 incident lung cancer cases from the TTR, 58,668 estimated incident cases from REDECAN and 88,083 deaths registered from INE between 2017 and 2020 were included. In terms of sex, the proportions are very similar between the three sources and the differences do not exceed 4%. In terms of age, the differences are not large, being larger for mortality data in the older age group from the INE versus the TTR. CONCLUSIONS: The TTR seems to be representative of lung cancer cases diagnosed in Spain between 2019 and 2020, both by sex and age. This allows us to accurately characterise the status of this disease, which is the leading cause of cancer death in Spain, and that the analysis of results obtained from the RTT can be applied to cases of lung cancer diagnosed in our country.

Background: Somatic EGFR mutations define a subset of non–small cell lung cancers (NSCLC) that have clinical impact on NSCLC risk and outcome. However, EGFR-mutation-status is often missing in epidemiologic datasets. We developed and tested pragmatic approaches to account for EGFR-mutation-status based on variables commonly included in epidemiologic datasets and evaluated the clinical utility of these approaches. Methods: Through analysis of the International Lung Cancer Consortium (ILCCO) epidemiologic datasets, we developed a regression model for EGFR-status; we then applied a clinical-restriction approach using the optimal cut-point, and a second epidemiologic, multiple imputation approach to ILCCO survival analyses that did and did not account for EGFR-status. Results: Of 35,356 ILCCO patients with NSCLC, EGFR-mutation-status was available in 4,231 patients. A model regressing known EGFR-mutation-status on clinical and demographic variables achieved a concordance index of 0.75 (95% CI, 0.74–0.77) in the training and 0.77 (95% CI, 0.74–0.79) in the testing dataset. At an optimal cut-point of probability-score = 0.335, sensitivity = 69% and specificity = 72.5% for determining EGFR-wildtype status. In both restriction-based and imputation-based regression analyses of the individual roles of BMI on overall survival of patients with NSCLC, similar results were observed between overall and EGFR-mutation-negative cohort analyses of patients of all ancestries. However, our approach identified some differences: EGFR-mutated Asian patients did not incur a survival benefit from being obese, as observed in EGFR-wildtype Asian patients. Conclusions: We introduce a pragmatic method to evaluate the potential impact of EGFR-status on epidemiological analyses of NSCLC. Impact: The proposed method is generalizable in the common occurrence in which EGFR-status data are missing.

Stage III non-small cell lung cancer (NSCLC) includes a highly heterogeneous group of patients with differences in the extent and localization of disease. Many aspects of stage III disease are controversial. The data supporting treatment approaches are often subject to a number of limitations, due to the heterogeneous patient populations involved in the trials. Furthermore, the definition of stage III disease has changed over time, and early studies were frequently inadequately powered to detect small differences in therapeutic outcome, were not randomized, or had a limited follow-up times. Major improvements in therapy, including the use of more active chemotherapy agents and refinements in radiation and surgical techniques, also limit the interpretation of earlier clinical trials. Lastly, improvements in pretreatment staging have led to reclassification of patients with relatively minimal metastatic disease as stage IV rather than stage III, leading to an apparent increase in the overall survival of both stage III and IV patients. Median overall stage III NSCLC survival ranges from 9 to 34 months. Higher survival rates are observed in younger Caucasian women with good performance status, adenocarcinoma, mutations, stage IIIA, and in patients with multidisciplinary-team-based diagnoses.

Radon is a colorless, odorless, and tasteless noble gas, causally related with the onset of lung cancer. We aimed to describe the distribution of radon exposure in the municipality of Manizales, Colombia, in order to estimate the population’s exposure and establish the percentage of dwellings that surpass reference levels. A cross-sectional study representing all geographical areas was carried out by measuring indoor radon concentrations. Participants answered a short questionnaire. Alpha-track type radon detectors were installed in all residences for six months. The detectors were subsequently processed at the Galician Radon Laboratory, an accredited laboratory at the University of Santiago de Compostela. A total of 202 homes were measured. Seventy-seven percent of the sampled houses were three stories high, their median age was 30 years, and half were inhabited by three people or fewer. For most dwellings, the building materials of walls and flooring were brick and covered cement, respectively. Results showed a geometric mean of radon concentration of 8.5 Bq/m3 and a maximum value of 50 Bq/m3. No statistically significant differences were found either between the geometric mean of the dwelling’s site, the height at which detectors were placed inside the home, or the wall and flooring materials, or between mean 222Rn concentrations in rural and urban areas. No dwelling surpassed the 222Rn reference level established by the WHO. This study shows that residential radon levels in Manizales, Colombia, seem to be low, though a more in-depth approach should be carried out. Despite these results, it is essential to create a national radon program and establish a radon concentration reference level for Colombia in line with international recommendations This study was funded by the Galician Radon Laboratory from the University of Santiago de Compostela (School of Medicine) and by the Institute of Health Research and Vicerrectorate of Research and post-graduate studies REF 0340220) of the University of Caldas (Manizales, Colombia) SI

Highlights • Alpha-1 antitrypsin deficiency (AATD) may increase the risk of lung cancer. • The lung cancer histological types most frequently associated with AATD are squamous carcinoma and adenocarcinoma. • No differences in lung cancer survival have been found acording to the carrier stuatus of alpha 1 antitrypsin deficient alleles., Introduction Alpha-1 antitrypsin deficiency (AATD) is an inherited genetic disorder associated with a risk of developing lung and liver disease. Several studies have examined its possible association with an increased risk of lung cancer. Materials and Methods Systematic review of the scientific literature on studies analyzing the risk of LC associated with AATD, as well as its impact on the histological type and survival. The information was located in the Medline (PubMed), Cochrane, and EMBASE databases. Results Six studies including a total of 4 038 patients with LC met the inclusion criteria. Most studies included seem to indicate that AATD increases the risk of developing LC, particularly of the squamous and adenocarcinoma types. This risk increases with exposure to tobacco smoke and the diagnosis of chronic obstructive pulmonary disease (COPD). Only one study analyzed the survival of LC patients without finding differences between AATD and non-AATD patients. Conclusions These results suggest that AATD may increase the risk of developing LC, particularly of the squamous and adenocarcinoma histological types, but no impact on patient survival has been demonstrated. However, the low quality of the included studies makes it necessary to carry out more studies with a larger sample size and preferably of a prospective nature to confirm these results.

Introduction Residential radon is considered the second cause of lung cancer and the first in never smokers. Nevertheless, there is little information regarding the association between elevated radon levels and small cell lung cancer (SCLC). We aimed to assess the effect of residential radon exposure on the risk of SCLC in general population through a multicentric case–control study. Methods A multicentric hospital-based case–control study was designed including 9 hospitals from Spain and Portugal, mostly including radon-prone areas. Indoor radon was measured using Solid State Nuclear Track Detectors at the Galician Radon Laboratory. Results A total of 375 cases and 902 controls were included, with 24.5% of cases being women. The median number of years living in the measured dwelling was higher than 25 years for both cases and controls. There was a statistically significant association for those exposed to concentrations higher than the EPA action level of 148 Bq/m3, with an Odds Ratio of 2.08 (95%CI: 1.03–4.39) compared to those exposed to concentrations lower than 50 Bq/m3. When using a dose-response model with 100 Bq/m3 as a reference, it can be observed a linear effect for small cell lung cancer risk. Smokers exposed to higher radon concentrations pose a much higher risk of SCLC compared to smokers exposed to lower indoor radon concentrations. Conclusions Radon exposure seems to increase the risk of small cell lung cancer with a linear dose-response pattern. Tobacco consumption may also produce an important effect modification for radon exposure.

Polymorphisms in DNA repair pathways may play a relevant role in lung cancer survival in never-smokers. Furthermore, they could be implicated in the response to chemotherapy and toxicity of platinum agents. The aim of this study was to evaluate the influence of various genetic polymorphisms in the BER and NER DNA repair pathways on survival and toxicity in never-smoker LC patients. The study included never-smokers LC cases diagnosed from 2011 through 2019, belonging to the Lung Cancer Research In Never Smokers study. A total of 356 never-smokers cases participated (79% women; 83% adenocarcinoma and 65% stage IV). Survival at 3 and 5 years from diagnosis was not associated with genetic polymorphisms, except in the subgroup of patients who received radiotherapy or chemo-radiotherapy, and presented with ERCC1 rs3212986 polymorphism. There was greater toxicity in those presenting OGG1 rs1052133 (CG) and ERCC1 rs11615 polymorphisms among patients treated with radiotherapy or chemo-radiotherapy, respectively. In general, polymorphisms in the BER and NER pathways do not seem to play a relevant role in survival and response to treatment among never-smoker LC patients.

Background Lung cancer is currently the leading cause of cancer death. Despite its high incidence and mortality, there are few studies describing its symptoms at diagnosis broken down by tumour stage and tobacco use. Accordingly, this study was proposed to describe the frequency of the most common symptoms of non-small cell lung cancer and small cell lung cancer (SCLC) at diagnosis, with a breakdown by stage and tobacco use. Patients and methods Cases were collected from the Spanish Thoracic Tumour Registry, a nationwide registry sponsored by the Spanish Lung Cancer Group. More than 50 hospitals recruited histologically confirmed lung cancer cases and information was gathered through personal interview plus data contained in the electronic clinical record. There were no data available on the lag between the appearance of the first symptoms and diagnosis of lung cancer. Results A total of 9876 patients (74% male, median age 64 years) were recruited from 2016 to 2019. Of these, 12.5% presented with SCLC. Stage IV was the most frequent stage at diagnosis (46.6%), and the most frequent symptom was cough (33.9%), followed by dyspnoea (26.7%). No symptom was present in 59% of patients diagnosed in stage I; 40% of stage I patients presented with at least one symptom, while 27.7% of patients in stage IV had no symptoms at diagnosis. Cough was the most frequent symptom in SCLC (40.6%), followed by dyspnoea (34.3%). The number of symptoms was similar across the respective smoking categories in SCLC, and differences between the symptoms analysed did not exceed 7% in any case. Conclusion The absence of the most frequent symptoms (ie, cough, pain, dyspnoea) should not lead to a decision to rule out the presence of lung cancer. A relevant percentage of stage IV patients displayed no symptoms at diagnosis.

BackgroundGlobally, radon is the leading risk factor for lung cancer in never-smokers (LCINS). In this study, we systematically reviewed and meta-analysed the evidence of the risk of LCINS associated with residential radon exposure.MethodsMedline and Embase databases were searched using predefined inclusion and exclusion criteria to identify relevant studies published from 1 January 1990 to 5 March 2020 focused on never-smokers. We identified four pooled collaborative studies (incorporating data from 24 case–control studies), one case–control study and one cohort study for systematic review. Meta-analysis was performed on the results of the four pooled studies due to different measures of effect and outcome reported in the cohort study and insufficient information reported for the case–control study. In a post hoc analysis, the corresponding risk for ever-smokers was also examined.ResultsRisk estimates of lung cancer from residential radon exposure were pooled in the meta-analysis for 2341 never-smoker cases, 8967 never-smoker controls, 9937 ever-smoker cases and 12 463 ever-smoker controls. Adjusted excess relative risks (aERRs) per 100 Bq·m−3 of radon level were 0.15 (95% CI 0.06–0.25) for never-smokers and 0.09 (95% CI 0.03–0.16) for ever-smokers, and the difference between them was statistically insignificant (p=0.32). The aERR per 100 Bq·m−3was higher for men (0.46; 95% CI 0.15–0.76) than for women (0.09; 95% CI −0.02–0.20) among never-smokers (p=0.027).ConclusionThis study provided quantified risk estimates for lung cancer from residential radon exposure among both never-smokers and ever-smokers. Among never-smokers in radon-prone areas, men were at higher risk of lung cancer than women.

Background Through a pooled case-control study design, we have assessed the relationship between residential radon exposure and lung cancer risk. Other objectives of the study were to evaluate the different risk estimates for the non-small cell lung cancer histological types and to assess the effect modification of the radon exposure on lung cancer risk by tobacco consumption. Methods We collected individual data from various case-control studies performed in northwest Spain that investigated residential radon and lung cancer. Cases had a confirmed anatomopathological diagnosis of primary lung cancer and controls were selected because they were undergoing ambulatory evaluation or surgical procedures that were unrelated to tobacco use. Residential radon was measured using alpha track detectors. Results were analyzed using logistic regression. Results 3704 participants were enrrolled, 1842 cases and 1862 controls. Data show that lung cancer risk increases with radon exposure, finding a significant association of radon exposure with lung cancer at radon exposures above 50 Bq/m3. The estimated adjusted OR for individuals exposed to concentrations >200 Bq/m3 was 2.06 (95% CI: 1.61–2.64) compared with those exposed to ≤50 Bq/m3. Within a smoking category, lung cancer risk increases markedly as radon concentration increases, reaching an OR of 29.3 (95% CI: 15.4–55.7) for heavy smokers exposed to more than 200 Bq/m.3 Conclusions This study confirms that residential radon exposure is a risk factor for lung cancer well below action levels established by international organizations. As expected, there is also an effect modification between radon exposure and tobacco consumption.

Introduction. Lung cancer is a major health problem. Mediastinal staging performed with the aid of imaging techniques is essential for appropriate disease treatment and prognosis. Accordingly, this study aimed to ascertain the usefulness of positron emission tomography (PET) in mediastinal staging, establish the best maximum standardized uptake value (SUVmax) cutoff point, compare its usefulness to that of computed tomography (CT), and determine the influence of histological tumour subtype. Methods. We conducted a retrospective study across a period of 3 years on 128 patients with suspicion of lung cancer and analyzed their demographic and radiological characteristics using CT and PET to perform the mediastinal examination. Histology was regarded as the gold standard. Results. PET displayed a high sensitivity (95%) and negative predictive value (NPV) (92%), outperforming CT (89% and 85%, respectively). Percentage agreement with histology was also higher (0.207 and 0.241 for CT and PET, respectively; p<0.001). Taking an SUVmax value of 0.5 as that which would ensure greatest diagnostic accuracy, S and NPV were 100%, though percentage agreement did not increase (0.189; p<0.001). PET discriminatory power was not affected by histological tumour subtype. Conclusions. The results of our study indicate that PET might be a useful test for examination of the mediastinum in lung cancer patients. Its high NPV suggests that the absence of mediastinal uptake could be used to proceed to surgical treatment without the need for further tests or examinations. Nevertheless, studies directly aimed to answer this specific question are needed.

Background Despite growing interest in increasing the efficiency and speed of the diagnosis, staging, and treatment of lung cancer (LC), the interval from signs and symptoms to diagnosis and treatment remains longer than recommended. The aim of this study was to analyze the factors that cause delays in the LC diagnosis/staging process and, consequently, delays in making therapeutic decisions. Methods We analyzed audit data from a prospective dataset of 1330 patients assessed at The Lung Cancer Rapid Diagnostic Unit from 26 June 2013 to 26 March 2016. The number and type of procedures and medical tests and the times of all procedures were recorded. Clinical and epidemiological variables and whether the diagnosis was performed on an inpatient or outpatient basis were also recorded. Results Malignancy was confirmed in 737 (55.4%) of the 1330 patients, with LC in 627 of these (85.2%). The mean interval to final diagnosis was 19.8 ± 13.9 days. Variables significantly related to a longer diagnostic time were the number of days until computed tomography (CT) was performed (odds ratio [OR], 95% confidence interval [CI] 1.347, 1.103-1.645; P = 0.003), until a histology sample was obtained (OR 1.243, 95% CI1.062-1.454; P = 0.007), and the total number of tests performed during the diagnostic and staging process (OR 1.823, 95% CI 1.046-3.177; P = 0.03). Conclusions A greater number of tests and more days to CT and histology led to longer delay times. Optimization of these factors should reduce delays in the LC diagnosis process.

Non-small cell lung cancer is the most common type of lung cancer. Both environmental and genetic risk factors contribute to lung carcinogenesis. We conducted a genome-wide interaction analysis between single nucleotide polymorphisms (SNPs) and smoking status (never- versus ever-smokers) in a European-descent population. We adopted a two-step analysis strategy in the discovery stage: we first conducted a case-only interaction analysis to assess the relationship between SNPs and smoking behavior using 13336 non-small cell lung cancer cases. Candidate SNPs with P-value

We aimed to evaluate lung cancer survival in never-smokers, both overall and specifically by sex, exposure to residential-radon, age, histological type, and diagnostic stage. We included lung cancer cases diagnosed in a multicentre, hospital-based, case-control-study of never-smoker patients, diagnosed from January-2011 to March-2015 (Lung Cancer Research In Never Smokers study). 369 never-smokers (79% women; median age 71 years; 80% adenocarcinoma; 66% stage IV) were included. Median overall survival, and at one, 3 and 5 years of diagnosis was 18.3 months, 61%, 32% and 22%, respectively. Higher median survival rates were obtained for: younger age, adenocarcinoma, actionable mutations, and earlier-stage at diagnosis. Higher indoor radon showed a higher risk of death in multivariate analysis. Median lung cancer survival in never-smokers seems higher than that in ever-smokers. Patients with actionable mutations have a significantly higher survival. Higher indoor-radon exposure has a negative effect on survival.

Introduction There are no studies analyzing the relationship between emphysema and lung cancer (LC). With this aim and in order to make some comparisons between different clinical variables, we carried out the present study. Methods This is a case–control study, patients with COPD and LC being the cases and subjects with stable COPD being the controls. Clinical and functional parameters, as well as the existence of radiological emphysema, were evaluated in a qualitative and quantitative way, using a radiological density of −950 Hounsfield units as a cutoff point in the images. The existence of several different types of emphysema (centrilobular, paraseptal, panacinar, or bullae) was analyzed, allowing patients to have more than one simultaneously. The extent to which lobes were involved was evaluated and the extension of emphysema was graduated for each type and location, following a quantitative scale. Differences between cases and controls were compared by using bivariate and multivariate analyzes with results expressed as OR and 95% CI. Results We included 169 cases and 74 controls, 84% men with a FEV1 (%) of 61.7±18.5, with 90.1% non-exacerbators. Most of them (50%) were active smokers and 47.2% were ex-smokers. Emphysema was found in 80.2% of the subjects, the most frequent type being centrilobular (34.4%). The only significantly different factor was the presence of paraseptal emphysema (alone or combined; OR =2.2 [95% CI =1.1–4.3, P = 0.03]), with adenocarcinoma being significantly more frequent in paraseptal emphysema with respect to other types (67.2% vs 32.8%, P =0.03). Conclusion Patients with COPD and paraseptal emphysema could be a risk group for the development of LC, especially adenocarcinoma subtype., Video abstract

Chronic obstructive pulmonary disease (COPD) is a known risk factor for developing lung cancer but the underlying mechanisms remain unknown. We hypothesise that the COPD stroma contains molecular mechanisms supporting tumourigenesis. We conducted an unbiased multi-omic analysis to identify gene expression patterns that distinguish COPD stroma in patients with or without lung cancer. We obtained lung tissue from patients with COPD and lung cancer (tumour and adjacent non-malignant tissue) and those with COPD without lung cancer for profiling of proteomic and mRNA (both cytoplasmic and polyribosomal). We used the Joint and Individual Variation Explained (JIVE) method to integrate and analyse across the three datasets. JIVE identified eight latent patterns that robustly distinguished and separated the three groups of tissue samples (tumour, adjacent and control). Predictive variables that associated with the tumour, compared to adjacent stroma, were mainly represented in the transcriptomic data, whereas predictive variables associated with adjacent tissue, compared to controls, were represented at the translatomic level. Pathway analysis revealed extracellular matrix and phosphatidylinositol-4,5-bisphosphate 3-kinase–protein kinase B signalling pathways as important signals in the tumour adjacent stroma. The multi-omic approach distinguishes tumour adjacent stroma in lung cancer and reveals two stromal expression patterns associated with cancer.

Introduction The objective of our study was to describe the characteristics of patients diagnosed with stage I and II lung cancer in the health area of A Coruna (Galicia) and to determine their overall survival according to certain variables. Methods Retrospective case series in patients diagnosed between January 2011 and December 2015 with stage I and II primary lung cancer with a minimum follow-up of 18 months. Results One hundred and fifty-eight patients were included, 99 at stage I, with a median age of 69 years [range 20–90], predominantly men (81%). Adenocarcinoma was the most common histology (52.9%), followed by epidermoid carcinoma (33.1%). Asymptomatic patients (35.9%) presented more frequently in stage I. Median survival was 57 months (95% CI: 48.1–65.9), with higher survival among women, patients under 70 years of age, and those who received surgical treatment. Conclusions Early-stage lung cancer in the health area of A Coruna occurs predominantly in men, in advanced age, and with adenocarcinoma histology. Survival was greater among patients with stage I disease, women, individuals aged under 70 years, and those treated surgically. Despite early diagnosis, median survival was less than 5 years.

Residential radon exposure is a serious public health concern, and as such appears in the recommendations of European Code Against Cancer. The objective of this study was to assess the association between residential radon levels and mortality due to different types of cancer, using misaligned data analysis techniques. Mortality data (observed cases) for each of the 313 Galician municipalities were drawn from the records of the National Statistics Institute for the study period (1999–2008). Expected cases were computed using Galician mortality rates for 14 types of malignant tumors as reference, with a total of 56,385 deaths due to the tumors analyzed. The effect estimates of indoor radon (3371 sampling points) were adjusted for sociodemographic variables, altitude, and arsenic topsoil levels (1069 sampling points), using spatial/geostatistical models fitted with stochastic partial differential equations and integrated nested Laplace approximations. These models are capable of processing misaligned data. The results showed a statistical association between indoor radon and lung, stomach and brain cancer in women in Galicia. Apart from lung cancer (relative risk (RR) = 1.09), in which a twofold increase in radon exposure led to a 9% rise in mortality, the association was particularly relevant in stomach (RR = 1.17) and brain cancer (RR = 1.28). Further analytical epidemiologic studies are needed to confirm these results, and an assessment should be made of the advisability of implementing interventions targeting such exposure in higher-risk areas., Unidad de Cáncer y Epidemiología Ambiental, Instituto de Salud Carlos III, España, Centro de Investigación Biomédica en Red de Epidemiología y Salud Pública, España, Departamento de Medicina Preventiva y Salud Pública, Universidad de Santiago de Compostela, España, Instituto Geológico y Minero de España, España, RADON Group, Universidad de Cantabria, España, Unidad de Medicina Preventiva, Hospital Clínico Universitario de Santiago de Compostela, España

Background: Lung cancer (LC) and chronic obstructive pulmonary disease (COPD) are associated with increased morbidity and mortality. The differential clinical and functional features among LC patients with or without COPD have not been defined. Objectives: The aims of this study were to examine the prevalence and underdiagnosis rate of COPD in LC patients and to compare the clinical and functional features of LC patients with and without COPD. Methods: We designed a multicenter hospital-based study including all LC cases diagnosed from January 2014 to August 2016. We assessed epidemiological, clinical, radiological, functional, and histological variables in all cases. Results: We recruited 602 patients with LC, most of them men (77.9%), with a median age of 67 ± 15 years. The COPD prevalence among LC patients was 51.5%, with a underdiagnosis rate of 71.6%. The LC+COPD patients were older and the proportion of men was higher compared with the LC-only patients. The LC+COPD patients had more pack-years, more squamous LC, a lower monoxide transfer coefficient (KCO), and higher Charlson index scores than patients with LC only. The median survival of LC-only patients was 37% longer than that of LC+COPD patients (22 vs. 16 months), but this difference was not statistically significant. Conclusions: Among LC patients, COPD is prevalent and underdiagnosed. Patients with LC+COPD more often have squamous LC, have greater comorbidities, and have a lower KCO. More effort should be made for an early diagnosis of COPD to select patients at higher risk of developing LC.

Lung cancer has the highest cancer mortality rate in developed countries. The principal risk factor for lung cancer is tobacco use, with residential radon being the leading risk factor among never smokers and the second among ever smokers. We sought to estimate mortality attributable to residential radon exposure in Spain and its Autonomous Regions, with correction for dwelling height and differentiation by tobacco use. We applied a prevalence-based method for estimating attributable mortality. For estimations, we considered exposure to radon in the different Autonomous Regions corrected for dwelling height, using the National Statistics Institute Housing Census and prevalence of tobacco use (never smokers, smokers and ex-smokers). The results showed that 3.8% (838 deaths) of lung cancer mortality was attributable to radon exposure of over 100 Bq/m3, a figure that rises to 6.9% (1,533 deaths) when correction for dwelling height is not performed. By Autonomous Region, the highest population attributable fractions, corrected for dwelling height, were obtained for Galicia, Extremadura, and the Canary Islands, where 7.0, 6.9, and 5.5% of lung cancer mortality was respectively attributable to radon exposure. The greatest part of the attributable mortality occurred in men and among smokers and ex-smokers. Residential radon exposure is a major contributor to lung cancer mortality, though this contribution is highly variable among the different territories, indicating the need for targeted prevention policies. Correction of estimates for dwelling height is fundamental for providing reliable estimates of radon-attributable mortality Carlos III Institute of Health (Instituto de Salud Carlos III) Project FIS PI19/00288 SI

Background Lung cancer is the deadliest cancer in developed countries but the etiology of lung cancer risk in never smokers (LCRINS) is largely unknown. We aim to assess the effects of alcohol consumption, in its different forms, on LCRINS. Methods We pooled six multi-center case-control studies developed in the northwest of Spain. Cases and controls groups were composed of never smokers. We selected incident cases with anatomopathologically confirmed lung cancer diagnoses. All participants were personally interviewed. We performed two groups of statistical models, applying unconditional logistic regression with generalized additive models. One considered the effect of alcohol type consumption and the other considered the quantity of each alcoholic beverage consumed. Results A total of 438 cases and 863 controls were included. Median age was 71 and 66, years, respectively. Adenocarcinoma was the predominant histological type, comprising 66% of all cases. We found that any type of wine consumption posed an OR of 2.20 OR 95%CI 1.12-4.35), and spirits consumption had an OR of 1.90 (95%CI 1.13-3.23). Beer consumption had an OR of 1.33 (95%CI 0.82-2.14). These results were similar when women were analyzed separately, but for men there was no apparent risk for any alcoholic beverage. The dose-response analysis for each alcoholic beverage revealed no clear pattern. Conclusions Wine and spirits consumption might increase the risk of LCRINSs, particularly in females. These results have to be taken with caution given the limitations of the present study.

Purpose The mechanisms of lung carcinogenesis are not fully understood. Not all smokers develop lung cancer, indicating that genetic variations and other environmental factors may play an important role in its development. The human glutathione S-transferases (GSTs) have been associated with an increased risk of lung cancer. Glutathione S-transferases are phase II biotransformation enzymes that play a role in detoxifying a wide range of exogenous agents including carcinogens but also anticarcinogenic drugs. Methods We assessed the effect of allelic deletions in the GSTM1 and GSTT1 genotypes on lung cancer overall survival through a systematic review of the scientific literature after applying predefined inclusion and exclusion criteria. Results Most of the included studies found no effect or a tendency to worse survival for individuals with deletion of GSTs. Conclusions Further studies are necessary to understand the magnitude of the effect of the deletion of both genes on lung cancer survival.

Background The aim of this study was to assess the relationship between do-it-yourself activities entailing the exposure to carcinogenic substances and the risk of lung cancer. Methods We pooled individual data from different case-control studies conducted in Northwestern Spain which investigated residential radon and lung cancer. Cases had an anatomopathologically confirmed primary lung cancer and controls were selected at the pre-surgery unit with uncomplicated surgeries. Both cases and controls were older than 30 years with no previous cancer history. All participants were interviewed face-to-face using a specific questionnaire. Painting, model building, furniture refinishing and woodworking or home carpentry were the do-it-yourself activities considered risky due to exposure to carcinogenic agents. Results We included 1528 cases and 1457 controls. Practicing do-it-yourself risk activities was more frequent among cases: 16.0% were exposed to carcinogenic exposures during leisure time, compared to 11.8% for controls. The overall adjusted OR for lung cancer risk among individuals who practiced do-it-yourself risk activities, was 1.77 (95% CI: 1.36–2.31); this was 2.17 (95% CI: 1.51–3.11) when the analysis was restricted to individuals who performed these activities for at least 10 years. These risks were greater when the analyses were carried out exclusively among never-smokers, with the respective ORs being 2.04 (95% CI: 1.38–3.01) and 3.10 (95% CI: 1.78–5.40). Conclusion These results support the hypothesis that do-it-yourself activities involving exposure to certain carcinogens are associated with an increased risk of lung cancer, both in ever and never-smokers.

Objectives To analyze the relationship of GSTT1, GSTM1, XRCC1 (rs25487), ERCC1 (rs11615, rs3212986), ERCC2 (rs13181), XRCC3 (rs861539), OGG1 (rs1052133), and Alpha-1-Antitrypsin mutations (AAT) with the risk of lung cancer in never-smokers, and ascertain if there is an effect modification between these polymorphisms and residential radon exposure. Material and methods We designed a multicenter hospital-based case-control study in a radon-prone area. 322 cases and 338 controls, all never-smokers, were included. They were selected using a frequency sampling based on sex and age distribution of the cases. Participants donated 3 ml. of whole blood used to determine genotype for polymorphisms. They placed a radon detector to measure residential radon exposure in their dwelling. Results The OR for deleted GSTM1 patients was 3.46 (95% CI = 1.52–7.89) at residential radon exposures above 200 Bq/m3. The ERCC1 rs3212986 polymorphism was the most associated with the risk of developing lung cancer, both for low and high radon exposures. The ERCC1 rs321986 GT and TT genotypes (at radon concentrations >200 Bq/m3) were more significantly associated with higher lung cancer risk (OR = 2.40, 95% CI = 1.29–4.45; OR = 4.45, 95% CI = 1.26–15.7, respectively). Conclusions These findings support the hypothesis that certain polymorphisms in genes involved in DNA-repair and carriers of GSTM1 deletion have an increased risk of lung cancer in never-smokers exposed to residential radon.

Background: Lung cancer is a public health problem worldwide. Small-cell lung cancer (SCLC) is the most aggressive histologic type, with a 5-year survival, This work was supported by the Instituto de Salud Carlos III (ISCIII)/PI15/01211/Cofinanciado FEDER, Spanish Society of Neumology and Thoracic Surgery (Project number 848. 2019 call)

Real-time endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA) is one of the major landmarks in the history of bronchoscopy. In the 10 years since it was introduced, a vast body of literature on the procedure and its results support the use of this technique in the study of various mediastinal and pulmonary lesions. This article is a comprehensive, systematic review of all the available scientific evidence on the more general indications for this technique. Results of specific studies on efficacy, safety and cost-effectiveness available to date are examined. The analysis shows that EBUS-TBNA is a safe, cost-effective technique with a high grade of evidence that is a valuable tool in the diagnosis and mediastinal staging of patients with suspected or confirmed lung cancer. However, more studies are needed to guide decision-making in the case of a negative result. Evidence on the role of EBUS-TBNA in the diagnosis of sarcoidosis and extrathoracic malignancies is also high, but much lower when used in the study of tuberculosis, lymphoma and for the re-staging of lung cancer after neoadjuvant chemotherapy. Nevertheless, due to its good safety record and lack of invasiveness compared to surgical techniques, the grade of evidence for recommending EBUS-TBNA as the initial diagnostic test in patients with these diseases is very high in most cases.

Real-time endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA) is one of the major landmarks in the history of bronchoscopy. In the 10 years since it was introduced, a vast body of literature on the procedure and its results support the use of this technique in the study of various mediastinal and pulmonary lesions. This article is a comprehensive, systematic review of all the available scientific evidence on the more general indications for this technique. Results of specific studies on efficacy, safety and cost-effectiveness available to date are examined. The analysis shows that EBUS-TBNA is a safe, cost-effective technique with a high grade of evidence that is a valuable tool in the diagnosis and mediastinal staging of patients with suspected or confirmed lung cancer. However, more studies are needed to guide decision-making in the case of a negative result. Evidence on the role of EBUS-TBNA in the diagnosis of sarcoidosis and extrathoracic malignancies is also high, but much lower when used in the study of tuberculosis, lymphoma and for the re-staging of lung cancer after neoadjuvant chemotherapy. Nevertheless, due to its good safety record and lack of invasiveness compared to surgical techniques, the grade of evidence for recommending EBUS-TBNA as the initial diagnostic test in patients with these diseases is very high in most cases.

Background: Lung cancer is the second most common cancer in both men and women. Mediastinal lymph node involvement in these patients, determined by imaging tests, indicates prognosis and modifies therapeutic attitude. Purpose: The aim of this study was to analyze the diagnostic capacity of magnetic resonance imaging (MRI) in the study of the mediastinum in comparison with conventional tests (computed tomography [CT] and positron-emission tomography [PET] or PET/CT scans), taking histology as the gold standard. Materials and Methods: An observational study was conducted on 16 patients with suspicion of primary lung cancer (June 2016 through December 2018). We studied their demographic characteristics and used CT, PET, or PET/CT scans and MRI (diffusion-weighted imaging-MRI sequence) to examine mediastinal disease and compare MRIs diagnostic yield and percentage agreement to that of conventional tests. Results: As compared to CT and PET scanning, MRI displayed a very low sensitivity and a specificity of 90 and 88%, respectively; positive predictive value was 0.67 (both) and negative predictive value (NPV) was 0.28 and 0.22, respectively. MRI showed a high degree of agreement in lymph node diagnosis when compared with histology (91.2%; P = 0.001): specificity in this case was high (E = 0.94), as was the NPV (NPV = 0.97). Conclusions: The results of this study would appear to indicate that MRI could play a relevant role in mediastinal staging of lung cancer. More prospective, multicenter studies are, however, needed to be able to draw up firm recommendations about the role of MRI and its place in lung cancer staging.

Emphysema and lung cancer (LC) are two diseases which share common risk factors, e.g., smoking. In recent years, many studies have sought to analyse this association. By way of illustration, we conducted a review of the scientific literature of the studies published to date, whose main designated aim was to demonstrate the relationship between emphysema and LC, and this association’s influence on the histology, prognosis and molecular mechanisms responsible. We included over 40 studies (ranging from case-control and cohort studies to systematic reviews and meta-analyses), which highlight the association between emphysema and LC, independently of smoking habit. These studies also report a possible influence on histology, with adenocarcinoma being the most frequent lineage, and an association with poor prognosis, which affects both survival and post-operative complications. Oxidative stress, which generates chronic inflammatory status as well as the presence of certain polymorphisms in various genes (CYP1A1, TERT, CLPTM1L, ERK), gives rise—in the case of patients with emphysema—to alteration of cellular repair mechanisms, which in turn favours the proliferation of neoplastic epithelial cells responsible for the origin of LC.

The authors regret not having included the following funding in the paper “Spanish Society of Neumology and Thoracic Surgery”. Project number 848. 2019 call. The authors would like to apologise for any inconvenience caused.

Background: Radon (and its decay products) is a known human carcinogen and the leading cause of lung cancer in never-smokers and the second in ever-smokers. The carcinogenic mechanism from radiation is a combination of genetic and epigenetic processes, but compared to the genetic mechanisms, epigenetic processes remain understudied in humans. This study aimed to explore associations between residential radon exposure and DNA methylation in the general population. Methods: Potential residential radon exposure for 75-metre area buffers was linked to genome-wide DNA methylation measured in peripheral blood from children and mothers of the Accessible Resource for Integrated Epigenomic Studies subsample of the ALSPAC birth cohort. Associations with DNA methylation were tested at over 450,000 CpG sites at ages 0, 7 and 17 years (children) and antenatally and during middle-age (mothers). Analyses were adjusted for potential residential and lifestyle confounding factors and were determined for participants with complete data (n = 786 to 980). Results: Average potential exposure to radon was associated in an exposure-dependent manner with methylation at cg25422346 in mothers during pregnancy, with no associations at middle age. For children, radon potential exposure was associated in an exposure-dependent manner with methylation of cg16451995 at birth, cg01864468 at age 7, and cg04912984, cg16105117, cg23988964, cg04945076, cg08601898, cg16260355 and cg26056703 in adolescence. Conclusions: Residential radon exposure was associated with DNA methylation in an exposure-dependent manner. Although chance and residual confounding cannot be excluded, the identified associations may show biological mechanisms involved in early biological effects from radon exposure.

Background: There is a relationship between Chronic Obstructive Pulmonary Disease (COPD) and the development of lung cancer (LC). The aim of this study is to analyse several blood markers and compare their concentrations in patients with only COPD and LC + COPD. Methods: Case-control study with cases presenting combined LC and COPD and two control groups (patients presenting only COPD and patients presenting only LC). We also included LC patients with descriptive purposes. In both groups, peripheral blood analyses of TNF-α, IL-6, IL-8, total leukocyte, lymphocyte and neutrophil counts, neutrophil-to-lymphocyte ratio, total platelet count, mean platelet volume, platelet-to-lymphocyte ratio, alpha 1-antitripsin (A1AT), IgE, C-reactive protein, fibrinogen, cholesterol and bilirubin were performed. We developed univariate and multivariate analyses of these markers, as well as a risk score variable, and we evaluated its performance through ROC curves. Results: We included 280 patients, 109 cases (LC + COPD), 83 controls (COPD) and 88 LC without COPD. No differences were observed in the distribution by sex, age, BMI, smoking, occupational exposure, lung function, GOLD stage or comorbidity. Patients with LC + COPD had significantly higher levels of neutrophils [OR 1.00 (95%CI 1.00–1.00), p = 0.03] and A1AT [OR 1.02 (95%CI 1.01–1.03), p = 0.003] and lower cholesterol levels [OR 0.98 (95%CI 0.97–0.99), p = 0.009] than COPD controls. We developed a risk score variable combining neutrophils, A1AT and cholesterol, achieving a sensitivity of 80%, a negative predictive value of 90.7% and an area under the curve of 0.78 (95%CI 0.71–0.86). Conclusions: COPD patients who also have LC have higher levels of neutrophils and A1AT and lower of cholesterol. These parameters could be potentially predicting biomarkers of LC in COPD patients. This work was supported by the project 110/2016 of the Spanish Society of Respiratory Pathology (SEPAR) SI

Introduction: Inherited susceptibility to lung cancer risk in never-smokers is poorly understood. The major reason for this gap in knowledge is that this disease is relatively uncommon (except in Asians), making it difficult to assemble an adequate study sample. In this study we conducted a genome-wide association study on the largest, to date, set of European-descent never-smokers with lung cancer. Methods: We conducted a two-phase (discovery and replication) genome-wide association study in never-smokers of European descent. We further augmented the sample by performing a meta-analysis with never-smokers from the recent OncoArray study, which resulted in a total of 3636 cases and 6295 controls. We also compare our findings with those in smokers with lung cancer. Results: We detected three genome-wide statistically significant single nucleotide polymorphisms rs31490 (odds ratio [OR]: 0.769, 95% confidence interval [CI]: 0.722-0.820; p value 5.31 x 10(-16)), rs380286 (OR: 0.770, 95% CI: 0.723-0.820; p value 4.32 x 10(-16)), and rs4975616 OR: 0.778, 95% CI: 0.730-0.829; p value 1.04 x 10(-14)). All three mapped to Chromosome 5 CLPTM1L-TERT region, previously shown to be associated with lung cancer risk in smokers and in never-smoker Asian women, and risk of other cancers including breast, ovarian, colorectal, and prostate. Conclusions: We found that genetic susceptibility to lung cancer in never-smokers is associated to genetic variants with pan-cancer risk effects. The comparison with smokers shows that top variants previously shown to be associated with lung cancer risk only confer risk in the presence of tobacco exposure, underscoring the importance of gene-environment interactions in the etiology of this disease. (C) 2019 International Association for the Study of Lung Cancer. Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

Objective : To explore whether there is a possible problem regarding indoor radon concentration surpassing the new European Directive 2013/59/Euratom threshold in Spanish workplaces. We also aim to find out whether radon concentration might be associated with certain characteristics of workplaces. Method : We performed a cross-sectional study to measure indoor radon concentrations in Spanish workplaces including five different sectors (education, public administration, the health sector, the tourist sector and the private sector). To be measured, the workplace should be occupied permanently by at least one worker. Alpha-track type radon detectors were placed for at least three months and read at the Galician Radon Laboratory at the University of Santiago de Compostela. A descriptive analysis was performed on radon distribution by sector, building characteristics and number of workers affected. Results : We faced enormous difficulties in finding volunteers for this study. Galicia and Madrid had the highest number of measurements. Of a total of 248 measurements, 27% had concentrations above 300 Bq/m3. Median radon concentration was 251 Bq/m3 in Galicia, followed by Madrid, with 61.5 Bq/m3. Forty-six percent of the workplaces measured in Galicia had radon concentrations higher than 300 Bq/m3 followed by 10.6% in Madrid. Nineteen percent of all workers were exposed to more than 300 Bq/m3 and 6.3% were exposed to radon concentrations higher than 500 Bq/m3. Conclusion : Indoor radon exposure might be a relevant problem in Spanish workplaces and the number of affected workers could be high. The prevalence of workers exposed to high radon concentrations probably depends on the geographical area. Objetivo: Explorar si podría existir un problema en cuanto a la concentración de radón en los puestos de trabajo en España por superación del umbral propuesto por la nueva Directiva Europea 2013/59/Euratom. También se pretende conocer si la concentración de radón puede estar asociada a las características de los puestos de trabajo. Método: Estudio transversal en seis regiones y diferentes sectores (educación, administración pública, sanitario, turístico y privado). El puesto de trabajo medido debía ser ocupado de manera permanente por al menos un trabajador. Los detectores de radón de tipo alfa-track estuvieron colocados al menos 3 meses y fueron revelados en el Laboratorio de Radón de Galicia, de la Universidad de Santiago de Compostela. Se realizó un análisis descriptivo de la concentración de radón por sector, por características de los edificios y por número de trabajadores afectados. Resultados: Hubo dificultades para encontrar voluntarios para este estudio. Galicia y Madrid tuvieron el mayor número de mediciones. Se midieron 248 lugares de trabajo, con el 27% por encima de los 300 Bq/m3. La concentración mediana fue de 251 Bq/m3 en Galicia, seguida de Madrid con 61,5 Bq/m3. El 46% de los puestos de trabajo en Galicia tenían concentraciones mayores de 300 Bq/m3, y el 10,6% en Madrid. El 19% de los trabajadores estuvieron expuestos a más de 300 Bq/m3 y el 6,3% a más de 500 Bq/m3. Conclusión: La exposición a radón podría ser un problema de salud relevante en los lugares de trabajo en España. El número de trabajadores expuestos parece elevado. La prevalencia de trabajadores afectados depende del área geográfica. This paper has been funded by a competitive research grant of the Fundación Prevent (2015) entitled Exposición laboral a radón interior en España – Estudio piloto. Instituto Sindical de Trabajo, Ambiente y Salud. SI