Residential radon and risk of lung cancer in an Italian alpine area

To evaluate whether residential radon exposure explains the excess mortality for lung cancer in an Italian alpine valley with high natural radioactivity, the authors conducted a population-based case-control study on 138 deceased cases and 291 sex- and year-of-birth-matched controls. Year-long alpha-track measurements of radon were performed in the most recent residence, and information about occupational history and lifetime smoking habits was obtained. The authors adjusted for smoking, and radon was associated with lung cancer risk among men: compared with a radon level of < 40 becquerels (Bq) per cubic meter (m3), the odds ratios for 40-76 Bq/m3, 77-139 Bq/m3, 140-199 Bq/m3, and 200+ Bq/m3 were 2.1, 2.0, 2.7, and 1.4, respectively. The association between radon and lung cancer, as determined with a multiplicative model, was found only among male smokers.     

Radon-222 concentration in groundwater and cancer mortality in North Carolina

Summary In a geographic correlation study, we explored the possibility that residential exposure to radon in groundwater may be related to cancers other than lung cancer. Measurements of radon in groundwater and 1978–1982 cancer mortality data from North Carolina, USA were used to investigate this relationship. Counties were categorized in two levels of radon exposure according to measured radon concentration and geology. In the lower exposure group (unexposed) county mean radon concentrations ranged from 0–228 pCi/1 (0–8436 Bq/m³), and in the upper group (potentially exposed) the range of county average concentrations was 229–10892 pCi/1 (8473–403004 Bq/m³), (median 1375 pCi/1 (50875 Bq/m³)). Adjusted mortality ratios and 95% confidence intervals were calculated for selected cancers, including leukemias, gastro-intestinal tract cancers, and respiratory tract cancers excluding lung cancer. In contrast to other ecologic studies, we found no consistent association between radon level and cancer mortality.     

A cost-effectiveness analysis of lowering residential radon levels in Sweden—Results from a modelling study

PurposeResidential exposure to radon is considered as the second leading cause of lung cancer after smoking. The purpose of this study was to conduct a cost-effectiveness analysis of reducing the indoor radon levels in Sweden from the current reference level of 200 Bq/m³ to the WHO suggested reference level of maximum 100 Bq/m³.MethodsWe constructed a decision-analytic cost-effectiveness model using input data from published literature and administrative records. The model compared the increase in economic costs to the health benefits of lower indoor radon-levels in a Swedish policy context. We estimated the cost per life-year and quality adjusted life year (QALY) gained and assessed the robustness of the results using both deterministic and probabilistic sensitivity analysis.ResultsIncluding (excluding) costs of added life years the cost per QALY for existing homes was €130,000 (€99,000). For new homes the cost per QALY including (excluding) costs of added life years was €39,000 (€25,000).ConclusionsThe results indicate that it is not cost-effective to reduce indoor radon levels from 200 Bq/m³ to a maximum of 100 Bq/m³ in existing homes, whereas it is cost-effective for new homes.     

Residential radon and risk of lung cancer in Eastern Germany

BACKGROUND: There is suggestive evidence that residential radon increases lung cancer risk. To elucidate this association further, we conducted a case-control study in Thuringia and Saxony in Eastern Germany during 1990-1997. METHODS: Histologically confirmed lung cancer patients from hospitals and a random sample of population controls matched on age, sex and geographical area were personally interviewed with respect to residential history, smoking, and other risk factors. One-year radon measurements were performed in houses occupied during the 5-35 years prior to the interview. The final analysis included a total of 1,192 cases and 1,640 controls. Odds ratios (OR) and 95% confidence intervals (CI) were estimated by logistic regression. RESULTS: Measurements covered on average 72% of the exposure time window, with mean radon concentrations of 76 Bq/m3 among the cases and 74 Bq/m3 among the controls. The smoking- and asbestos-adjusted ORs for categories of radon (50-80, 80-140 and >140 Bq/m*3, compared with 0-50 Bq/m3) were 0.95 (CI = 0.77 to 1.18), 1.13 (CI = 0.86 to1.50) and 1.30 (CI = 0.88 to 1.93). The excess relative risk per 100 Bq/m? was 0.08 (CI = -0.03 to 0.20) for all subjects and 0.09 (CI = -0.06 to 0.27) for subjects with complete measurements for all 30 years. CONCLUSIONS: Our data indicate a small increase in lung cancer risk as a result of residential radon that is consistent with the findings of previous indoor radon and miner studies.     

Effects of work related confounders on the association between silica exposure and lung cancer: a nested case-control study among Chinese miners and pottery workers

Objective The role of silica in the causation of lung cancer is an ongoing debate. In order to explore whether observed association between silica exposure and lung cancer is confounded by exposure to other occupational carcinogens, we updated a previously nested case-control study among a cohort of male workers in 29 Chinese mines and factories on the basis of an extended follow-up. Methods Five hundred and eleven lung cancer cases and 1,879 matched controls were selected. Exposure to respirable silica as well as relevant occupational confounders were quantitatively assessed based on historical industrial hygiene data. The relationship between exposure to silica and lung cancer was analyzed by conditional logistic regression analysis adjusted for exposure to arsenic, polycyclic aromatic hydrocarbons (PAHs), radon, and smoking. Results In a crude analysis adjusted for smoking only, a significant trend of increasing risk of lung cancer with exposure to silica was found for tin, iron/copper miners, and pottery workers. But after adjustment for relevant occupational confounders, no relationship between silica and lung cancer can be observed. Instead, there is a significant association between lung cancer mortality and cumulative exposure to inorganic arsenic (OR = 1.86, 95% CI: 1.14, 3.04 for each mg/m³-year increase) and carcinogenic PAHs (OR = 1.35, 95% CI: 1.08, 1.69 for each 100 μg/m³-year increase). Conclusion This analysis does not provide any evidence to show that exposure to silica causes lung cancer in the absence of confounding factors.     

Case-control study on lung cancer and residential radon in western Germany

In a 1990-1996 case-control study in western Germany, the authors investigated lung cancer risk due to exposure to residential radon. Confirmed lung cancer cases from hospitals and a random sample of community controls were interviewed by trained interviewers regarding different risk factors. For 1 year, alpha track detectors were placed in dwellings to measure radon gas concentrations. The evaluation included 1,449 cases and 2,297 controls recruited from the entire study area and a subsample of 365 cases and 595 controls from radon-prone areas of the basic study region. Rate ratios were estimated by using conditional logistic regression adjusted for smoking and for asbestos exposure. In the entire study area, no rate ratios different from 1.0 were found; in the radon-prone areas, the adjusted rate ratios for exposure in the present dwelling were 1.59 (95% confidence interval (CI): 1.08, 2.27), 1.93 (95% CI: 1.19, 3.13), and 1.93 (95% CI: 0.99, 3.77) for 50-80, 80-140, and >140 Bq/m3, respectively, compared with 0-50 Bq/m3. The excess rate ratio for an increase of 100 Bq/m3 was 0.13 (-0.12 to 0.46). An analysis based on cumulative exposure produced similar results. The results provide additional evidence that residential radon is a risk factor for lung cancer, although a risk was detected in radon-prone areas only, not in the entire study area.     

A study on natural radioactivity in khewra salt mines, pakistan

The Khewra Salt Mines, the second largest salt mines in the world, are located 160 km south of Islamabad, the capital of Pakistan. Around 1000 workers are involved in the removal of salt from these mines. More than 40,000 visitors come annually to see the mines. The visitors and workers are directly exposed to the internal and external radiological hazards of radon and gamma rays in these mines. The general public is affected by the intake of the salt containing the naturally occurring radionuclides. Therefore the concentration of radon (²²²Rn) in the Khewra Salt Mines and activity concentrations of the naturally occurring radionuclides in the salt samples from these mines were measured. Both active and passive techniques were employed for the measurement of radon with Radon Alpha Detector (RAD-7) and SSNTD respectively. The concentration of ²²²Rn was 26 ± 4 Bq m^-3 measured by the active method while 43 ± 8 Bq m^-3 was measured by the passive method. The activity concentration of the radionuclides was measured using gamma ray spectrometry with HPGe detector. The mean activity of ⁴⁰K in salt samples was found to be 36 ± 20 Bq kg^-1 and the concentration of ²²⁶Ra and ²³²Th in the salt samples was below the detection limits. Gamma radiation hazard was assessed in terms of the external gamma dose from salt slabs and the rooms made of salt and the annual effective dose due to gamma radiation. The exposure to radon daughters, annual effective dose and excessive lifetime cancer risk due to radon in the mines were estimated. The mean annual effective dose due to an intake of ⁴⁰K from the salt was calculated as 20.0 ± 11.1 μSv, which is lower than the average annual effective dose rate of 0.29 mSv, received by the ingestion of natural radionuclides. Due to the low concentration values of primordial radionuclides in the salt and radon (²²²Rn) in the mines, a 'low level activity measurement laboratory' is suggested to be established in these mines.     

The impact of declining smoking on radon-related lung cancer in the United States

Objectives. We examined the effect of current patterns of smoking rates on future radon-related lung cancer.Methods. We combined the model developed by the National Academy of Science''s Committee on Health Risks of Exposure to Radon (the BEIR VI committee) for radon risk assessment with a forecasting model of US adult smoking prevalence to estimate proportional decline in radon-related deaths during the present century with and without mitigation of high-radon houses.Results. By 2025, the reduction in radon mortality from smoking reduction (15 percentage points) will surpass the maximum expected reduction from remediation (12 percentage points).Conclusions. Although still a genuine source of public health concern, radon-induced lung cancer is likely to decline substantially, driven by reductions in smoking rates. Smoking decline will reduce radon deaths more that remediation of high-radon houses, a fact that policymakers should consider as they contemplate the future of cancer control.The Environmental Protection Agency (EPA) estimates that radon in the home is responsible for over 21 000 lung cancer deaths annually among Americans, making radon the major cause of lung cancer after tobacco use. The agency considers radon a major public health problem and, since 1986, has mounted an aggressive campaign urging the public to test their homes for radon and take remedial actions when airborne concentrations of radon exceed 4 picocuries per liter of air (4 pCi/L).¹For its most current risk assessment, the EPA employed the BEIR VI model, developed by the Committee on Health Risks of Exposure to Radon (the BEIR VI committee) of the National Academy of Sciences (NAS).² The BEIR VI model''s calculation of radon-related risk (as was the case for its predecessor, BEIR IV) was estimated from data on miners, who are subject to much higher levels of radon than is the average population and have shown a significant correlation between lung cancer risk and radon exposure. Although the extrapolation of the results from miners to the much less exposed general public initially caused controversy, the BEIR VI implications of risk have been validated by recent case–control studies at the population level.^3–5 The BEIR VI model is thus broadly accepted as a valid predictor of the radon-related risk for typical individuals.The available data suggest a strong interaction effect between radon exposure and smoking status in the determination of lung cancer risk, which means that smokers are at a much higher risk of dying from radon-induced lung cancer than are nonsmokers. This interaction is recognized in the BEIR VI model, which postulates a superadditive (but less than multiplicative) interaction between smoking and radon. To appreciate the magnitude of this interaction, consider the fact that the background lung cancer risk ratio between ever and never smokers is 13 to 1.⁶ A multiplicative interaction between radon and smoking would imply that, at the same level of radon exposure, the ratio of radon-induced excess risk between ever and never smokers would be the same as the ratio of background lung cancer risks between those 2 groups (i.e., 13 to 1). On the other hand, an additive relationship between radon and smoking would imply that radon would add the same extra risk to ever and never smokers exposed to the same dosage, making the excess risks ratio between the 2 groups equal 1 to 1. Using the BEIR VI model, the EPA calculates that, at a radon level of 4 pCi/L, the lifetime risk of radon-induced lung cancer death is 62 per 1000 for ever smokers and 7 per 1000 for never smokers, yielding an excess risk ratio of 8.86 to 1 between the 2 groups.¹ As 8.86 falls between 1 and 13, the BEIR VI model implies that radon adds more risk to ever smokers than to never smokers, but that excess risk is less than proportional to the lung cancer background risk of those 2 groups, suggesting a submultiplicative (but superadditive) relationship between smoking and radon. The BEIR VI model does not distinguish between current and former smokers.Given this implied superadditive interaction, the number of future radon deaths will heavily depend on population smoking rates. As smoking rates in the United States have been falling for several decades and are expected to continue declining, the overall magnitude of the radon death toll is likely to decline as well. The question we try to address is what is the magnitude of this expected decline?We extend the EPA''s analysis by examining the sensitivity of radon-related lung cancer in the United States to future smoking rates. We estimate the proportional decline in the number of lung cancer deaths caused by radon for the period 2006 through 2100, assuming a likely scenario for smoking rates. We do not forecast specific numbers of radon-induced lung cancer deaths because these numbers will depend on many factors likely to change over such a long period of time. Instead, we concentrate on the relative impact of the smoking decline on the overall radon death toll and also examine the benefits of remediating houses with high radon levels given the results of our analysis. Following the EPA''s approach, in our computations, we employ the BEIR VI model, thereby assuming a submultiplicative relationship between smoking and radon. In the remaining sections of the report, we discuss the assumptions, models, and data employed in our analysis, our findings, and the implications of the results for both the magnitude of radon-related risk to the population and the effectiveness of housing remediation in reducing such risk.     

Residential radon and lung cancer risk in a high-exposure area of Gansu Province, China

In the general population, evaluation of lung cancer risk from radon in houses is hampered by low levels of exposure and by dosimetric uncertainties due to residential mobility. To address these limitations, the authors conducted a case-control study in a predominantly rural area of China with low mobility and high radon levels. Included were all lung cancer cases diagnosed between January 1994 and April 1998, aged 30-75 years, and residing in two prefectures. Randomly selected, population-based controls were matched on age, sex, and prefecture. Radon detectors were placed in all houses occupied for 2 or more years during the 5-30 years prior to enrollment. Measurements covered 77% of the possible exposure time. Mean radon concentrations were 230.4 Bq/m(3) for cases (n = 768) and 222.2 Bq/m(3) for controls (n = 1,659). Lung cancer risk increased with increasing radon level (p < 0.001). When a linear model was used, the excess odds ratios at 100 Bq/m(3) were 0.19 (95% confidence interval: 0.05, 0.47) for all subjects and 0.31 (95% confidence interval: 0.10, 0.81) for subjects for whom coverage of the exposure interval was 100%. Adjusting for exposure uncertainties increased estimates by 50%. Results support increased lung cancer risks with indoor radon exposures that may equal or exceed extrapolations based on miner data.     

Increased lung cancer risk due to residential radon in a pooled and extended analysis of studies in Germany

Residential radon has been shown to be a risk factor for lung cancer in several studies-but with limited power in each single study. The data of two case-control studies performed during 1990-1997 in Germany and used for previous publications have been extended and pooled. Both studies have identical study designs. In total, data of 2,963 incident lung cancer cases and 4,232 population controls are analyzed here. One-year radon measurements were performed in houses occupied during the 5-35 y prior to the interview. Conditional logistic and linear relative risk regression was used for the analysis. Measurements covered on average 70% of the exposure time window, with an average radon exposure of 61 Bq m(-3). The smoking and asbestos-adjusted ORs were 0.97 [95% confidence interval (CI) 0.85 to 1.11] for 50-80 Bq m(-3), 1.06 (95% CI 0.87 to 1.30) for 80-140 Bq m(-3) and 1.40 (95% CI 1.03 to 1.89) for radon concentrations above 140 Bq m(-3), compared to the reference category <50 Bq m(-3). The linear increase in the odds ratio per 100 Bq m(-3) was 0.10 (95% CI -0.02 to 0.30) for all subjects and 0.14 (95% CI -0.03 to 0.55) for less mobile subjects who lived in only one home in the last 5-35 y. The risk coefficients generally were higher when measurement error in the radon concentrations was reduced by restricting the population. With respect to histopathology, the risk for small cell carcinoma was higher than for other subtypes. This analysis strengthens the evidence that residential radon is a relevant risk factor for lung cancer.     

Indoor radon and lung cancer in France

BACKGROUND: Several case-control studies have indicated an increased risk of lung cancer linked to indoor radon exposure; others have not supported this hypothesis, partly because of a lack of statistical power. As part of a large European project, a hospital-based case-control study was carried out in 4 areas in France with relatively high radon levels. METHODS: Radon concentrations were measured in dwellings that had been occupied by the study subjects during the 5- to 30-year period before the interview. Measurements of radon concentrations were performed during a 6-month period using 2 Kodalpha LR 115 detectors (Dosirad, France), 1 in the living room and 1 in the bedroom. We examined lung cancer risk in relation to indoor radon exposure after adjustment for age, sex, region, cigarette smoking, and occupational exposure. RESULTS: We included in the analysis 486 cases and 984 controls with radon measures in at least 1 dwelling. When lung cancer risk was examined in relation to the time-weighted average radon concentration during the 5- to 30-year period, the estimated relative risks (with 95% confidence intervals) were: 0.85 (0.59-1.22), 1.19 (0.81-1.77), 1.04 (0.64-1.67), and 1.11 (0.59-2.09) for categories 50-100, 100-200, 200-400, and 400+ becquerels per cubic meter (Bq/m), respectively (reference <50 Bq/m). The estimated relative risk per 100 Bq/m was 1.04 (0.99-1.11) for all subjects and 1.07 (1.00-1.14) for subjects with complete measurements. CONCLUSIONS: Our results support the presence of a small excess lung cancer risk associated with indoor radon exposure after precise adjustment on smoking. They are in agreement with results from some other indoor radon case-control studies and with extrapolations from studies of underground miners.     

Residential radon and lung cancer among never-smokers in Sweden.

In this study, we attempted to reduce existing uncertainty about the relative risk of lung cancer from residential radon exposure among never-smokers. Comprehensive measurements of domestic radon were performed for 258 never-smoking lung cancer cases and 487 never-smoking controls from five Swedish case-control studies. With additional never-smokers from a previous case-control study of lung cancer and residential radon exposure in Sweden, a total of 436 never-smoking lung cancer cases diagnosed in Sweden between 1980 and 1995 and 1,649 never-smoking controls were included. The relative risks (with 95% confidence intervals in parentheses) of lung cancer in relation to categories of time-weighted average domestic radon concentration during three decades, delimited by cutpoints at 50, 80, and 140 Bq m(-3), were 1.08 (0.8--1.5), 1.18 (0.9--1.6), and 1.44 (1.0--2.1), respectively, with average radon concentrations below 50 Bq m(-3) used as reference category and with adjustment for other risk factors. The data suggested that among never-smokers residential radon exposure may be more harmful for those exposed to environmental tobacco smoke. Overall, an excess relative risk of 10% per 100 Bq m(-3) average radon concentration was estimated, which is similar to the summary effect estimate for all subjects in the main residential radon studies to date.     

Exposure to residential radon and lung cancer in Spain: a population-based case-control study

Although high radon concentrations have been linked to increased risk of lung cancer by both experimental studies and investigations of underground miners, epidemiologic studies of residential radon exposure display inconsistencies. The authors therefore decided to conduct a population-based case-control study in northwest Spain to determine the risk of lung cancer associated with exposure to residential radon. The study covered a total of 163 subjects with incident lung cancer and a population sample of 241 cancer-free subjects since 1992-1994. Odds ratios for radon were estimated using logistic regression adjusted for sex, age, lifetime tobacco use, family history, and habitat. The adjusted odds ratios for the second, third, and fourth quartiles of radon (breakpoints: 37.0, 55.2, and 148.0 Bq/m(3)) were 2.73 (95% confidence interval (CI): 1.12, 5.48), 2.48 (95% CI: 1.29, 6.79), and 2.96 (95% CI: 1.29, 6.79), respectively. An additive synergic effect between radon and tobacco was found. The results from this study suggest that, even at concentrations far below official guideline levels, radon may lead to a 2.5-fold rise in the risk of lung cancer. Furthermore, the synergy found between smoking and radon may prove useful when it comes to drafting public health recommendations.     

Canadian individual risks of radon-induced lung cancer for different exposure profiles

BACKGROUND: Indoor radon has been determined to be the second leading cause of lung cancer after tobacco smoking. There is an increasing need among radiation practitioners to have numerical values of lung cancer risks for men and women, ever-smokers and never-smokers exposed to radon in homes. This study evaluates individual risks for the Canadian population exposed to radon in homes at different radon concentrations and for different periods of their lives. METHODS: Based on the risk model developed recently by U.S. Environmental Protection Agency (EPA), individual risks of radon-induced lung cancers are calculated with Canadian age-specific rates for overall and lung cancer mortalities (1996-2000) as well as the Canadian smoking prevalence data in 2002. RESULTS: Convenient tables of lifetime relative risks are constructed for lifetime exposures and short exposures between any two age intervals from 0 to 110, and for various radon concentrations found in homes from 50 to 1000 Bq/m3. CONCLUSIONS: The risk of developing lung cancer from residential radon exposure increases with radon concentration and exposure duration. For short exposure periods, such as 10 or 20 years, risks are higher in middle age groups (30-50) compared especially to the later years. Individuals could lower their risks significantly by reducing radon levels earlier in life. The tables could help radiation protection practitioners to better communicate indoor radon risk to members of the public.     

Residential randon exposure and lung cancer risk in Misasa, Japan: a case-control study

In order to investigate an association between residential radon exposure and risk of lung cancer, a case-control study was conducted in Misasa Town, Tottori Prefecture, Japan. The case series consisted of 28 people who had died of lung cancer in the years 1976-96 and 36 controls chosen randomly from the residents in 1976, matched by sex and year of birth. Individual residential radon concentrations were measured for 1 year with alpha track detectors. The average radon concentration was 46 Bq/m3 for cases and 51 Bq/m3 for controls. Compared to the level of 24 or less Bq/m3, the adjusted odds ratios of lung cancer associated with radon levels of 25-49, 50-99 and 100 or more Bq/m3, were 1.13 (95% confidence interval; 0.29-4.40), 1.23 (0.16-9.39) and 0.25 (0.03-2.33), respectively. None of the estimates showed statistical significance, due to small sample size. When the subjects were limited to only include residents of more than 30 years, the estimates did not change substantially. This study did not find that the risk pattern of lung cancer, possibly associated with residential radon exposure, in Misasa Town differed from patterns observed in other countries.     

Residential radon exposure and lung cancer in Swedish women.

A case-control study was undertaken to investigate the role of residential radon exposure for lung cancer. The study included 210 women with lung cancer diagnosed from 1983-1986 in the county of Stockholm and 191 hospital and 209 population controls. Interviews provided information on lifetime residences and smoking. Radon concentrations measured in 1,573 residences of the study subjects showed a lognormal distribution with arithmetic and geometric means of 127.7 and 96.0 Bq m-3, respectively. Lung cancer risks tended to increase with estimated radon exposure, reaching a relative risk of 1.7 (95% confidence interval: 1.0-2.9) in women having an average radon level exceeding 150 Bq m-3 (4 pCi L-1). Stronger associations were suggested in younger persons and risk estimates appeared to be within the same range as those projected for miners. However, further studies are needed to clarify the level of risk associated with exposure to residential radon.     

Meta-analysis of residential exposure to radon gas and lung cancer

OBJECTIVES: To investigate the relation between residential exposure to radon and lung cancer. METHODS: A literature search was performed using Medline and other sources. The quality of studies was assessed. Adjusted odds ratios with 95% confidence intervals (CI) for the risk of lung cancer among categories of levels of exposure to radon were extracted. For each study, a weighted log-linear regression analysis of the adjusted odds ratios was performed according to radon concentration. The random effect model was used to combine values from single studies. Separate meta-analyses were performed on results from studies grouped with similar characteristics or with quality scores above or equal to the median. FINDINGS: Seventeen case-control studies were included in the meta-analysis. Quality scoring for individual studies ranged from 0.45 to 0.77 (median, 0.64). Meta-analysis based on exposure at 150 Bq/m3 gave a pooled odds ratio estimate of 1.24 (95% CI, 1.11-1.38), which indicated a potential effect of residential exposure to radon on the risk of lung cancer. Pooled estimates of fitted odds ratios at several levels of randon exposure were all significantly different from unity--ranging from 1.07 at 50 Bq/m3 to 1.43 at 250 Bq/m3. No remarkable differences from the baseline analysis were found for odds ratios from sensitivity analyses of studies in which > 75% of eligible cases were recruited (1.12, 1.00-1.25) and studies that included only women (1.29, 1.04-1.60). CONCLUSION: Although no definitive conclusions may be drawn, our results suggest a dose-response relation between residential exposure to radon and the risk of lung cancer. They support the need to develop strategies to reduce human exposure to radon.     

Predictors of Indoor Radon Concentrations in Pennsylvania, 1989–2013

Background

Radon is the second-leading cause of lung cancer worldwide. Most indoor exposure occurs by diffusion of soil gas. Radon is also found in well water, natural gas, and ambient air. Pennsylvania has high indoor radon concentrations; buildings are often tested during real estate transactions, with results reported to the Department of Environmental Protection (PADEP).

Objectives

We evaluated predictors of indoor radon concentrations.

Methods

Using first-floor and basement indoor radon results reported to the PADEP between 1987 and 2013, we evaluated associations of radon concentrations (natural log transformed) with geology, water source, building characteristics, season, weather, community socioeconomic status, community type, and unconventional natural gas development measures based on drilled and producing wells.

Results

Primary analysis included 866,735 first measurements by building, with the large majority from homes. The geologic rock layer on which the building sat was strongly associated with radon concentration (e.g., Axemann Formation, median = 365 Bq/m³, IQR = 167–679 vs. Stockton Formation, median = 93 Bq/m³, IQR = 52–178). In adjusted analysis, buildings using well water had 21% higher concentrations (β = 0.191, 95% CI: 0.184, 0.198). Buildings in cities (vs. townships) had lower concentrations (β = –0.323, 95% CI: –0.333, –0.314). When we included multiple tests per building, concentrations declined with repeated measurements over time. Between 2005 and 2013, 7,469 unconventional wells were drilled in Pennsylvania. Basement radon concentrations fluctuated between 1987 and 2003, but began an upward trend from 2004 to 2012 in all county categories (p < 0.001), with higher levels in counties having ≥ 100 drilled wells versus counties with none, and with highest levels in the Reading Prong.

Conclusions

Geologic unit, well water, community, weather, and unconventional natural gas development were associated with indoor radon concentrations. Future studies should include direct environmental measurement of radon, as well as building features unavailable for this analysis.

Citation

Casey JA, Ogburn EL, Rasmussen SG, Irving JK, Pollak J, Locke PA, Schwartz BS. 2015. Predictors of indoor radon concentrations in Pennsylvania, 1989–2013. Environ Health Perspect 123:1130–1137; http://dx.doi.org/10.1289/ehp.1409014     

Glass-based radon-exposure assessment and lung cancer risk

Lung cancer risk estimation in relation to residential radon exposure remains uncertain, partly as a result of imprecision in air-based retrospective radon-exposure assessment in epidemiological studies. A recently developed methodology provides estimates for past radon concentrations and involves measurement of the surface activity of a glass object that has been in a subject's dwellings through the period for exposure assessment. Such glass measurements were performed for 110 lung cancer subjects, diagnosed 1985 to 1995, and for 231 control subjects, recruited in a case-control study of residential radon and lung cancer among never-smokers in Sweden. The relative risks (with 95% confidence intervals) of lung cancer in relation to categories of surface-based average domestic radon concentration during three decades, delimited by cutpoints at 50, 80, and 140 Bq m(-3), were 1.60 (0.8 to 3.4), 1.96 (0.9 to 4.2), and 2.20 (0.9 to 5.6), respectively, with average radon concentrations below 50 Bq m(-3) used as reference category, and with adjustment for other risk factors. These relative risks, and the excess relative risk (ERR) of 75% (-4% to 430%) per 100 Bq m(-3) obtained when using a continuous variable for surface-based average radon concentration estimates, were about twice the size of the corresponding relative risks obtained among these subjects when using air-based average radon concentration estimates. This suggests that surface-based estimates may provide a more relevant exposure proxy than air-based estimates for relating past radon exposure to lung cancer risk.