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Estimating Rn-induced Lung Cancer in the United States
Abstract
The proportion of lung cancer deaths attributable to Rn among residents of single-family homes in the U.S. (approximately 70% of the housing stock) is estimated using the log-normal distribution of Rn concentrations proposed by Nero et al. (1986) and the risk model developed by the National Academy of Sciences' BEIR IV Committee. The risk model, together with the exposure distribution, predicts that approximately 14% of lung cancer deaths among such residents (about 13,300 deaths per year, or 10% of all U.S. lung cancer deaths) may be due to indoor Rn exposure. The 95% confidence interval is 7%-25%, or approximately 6600 to 24,000 lung cancer deaths. These estimated attributable risks due to Rn are similar for males and females and for smokers and nonsmokers, but higher baseline risks of lung cancer result in much larger absolute numbers of Rn-attributable cancers among males (approximately 9000) and among smokers (approximately 11,000). Because of the apparent skewness of the exposure distribution, most of the contribution to the attributable risks arises from exposure rates below 148 Bq m-3 (4 pCi L-1), i.e., below the EPA "action level." As a result, if all exposure rates that exceed 148 Bq m-3 (approximately 8% of homes) were eliminated, the models predict that the total annual lung cancer burden in the U.S. would drop by 4-5%, or by about 3800 lung cancer deaths, in contrast to a maximum reduction of 14% if all indoor Rn exposure above the 1st percentile were eliminated.
... Accordingly, there exists a close relationship between human health and living environment. It has been estimated that 6600-24000 lung cancer deaths per year may be related to indoor radon in the United States in the late 1980s [5]. Indoor radon accounts for nearly half of all radiation exposure among the general population [6]. ...
... The annual effective radiation dose of indoor 222 Rn and 220 Rn exposure was calculated with the equation below retrieved from the UNSCEAR [5]. ...
To evaluate the health risk of radon and its progeny, a large amount of accurate monitoring data is needed according to the theory and practice of health risk assessment. However, the indoor radon levels in different regions in China and worldwide reveal temporal and spatial variations. In addition, the residents living in different areas follow distinct living modes. Therefore, it is recommended and accepted by many researchers to detect the radon level in local areas and subsequently conduct health risk assessments based on local detection data. In this study, 21 bedrooms of households in Weifang city were selected, and the indoor ²²² Rn and ²²⁰ Rn levels were detected with RAD7 radon detector in winter, while the annual effective radiation dose was calculated for ordinary residents in Weifang city. Our investigation showed that the 24- and 12-hour average levels of ²²² Rn were 35.7±15.2 Bq/m ³ and 36.2±15.8 Bq/m ³ , respectively. The 24- and 12-hour average levels of ²²⁰ Rn were 30.4±12.3 Bq/m ³ and 22.4±11.6 Bq/m ³ , respectively. There were significant differences in the average levels of ²²² Rn and ²²⁰ Rn between floors. The estimated annual effective radiation dose received by ordinary residents in Weifang city was 1.7193 mSv, of which 0.9479 mSv originated from ²²² Rn and its progeny and 0.7714 mSv originated from ²²⁰ Rn and its progeny, accounting for 55.1% and 44.9%, respectively, of the total dose. Our findings suggest that ²²⁰ Rn should not be ignored by local residents in Weifang city, and more attention should be paid to ²²⁰ Rn in future research.
... In 1998, Health Canada first established a radon guideline with an action level of 800 Bq/m 3 . This guideline was based on data from studies of uranium miners, which was the best information at that time (Chen et al., 2012;Lubin and Boice, 1989). In June 2007, this guideline reduced the action level from 800 Bq/m 3 to 200 Bq/m 3 . ...
... The proportion of lung cancer cases related to indoor radon is assessed by population attributable risk (PAR), which is theoretically the proportion of lung cancer cases prevented by reducing indoor radon concentration Lubin and Boice (1989). Several occupational and residential models derived from epidemiological studies to estimate PAR (Prüss-Üstün et al., 2003). ...
Methods:
Using Canadian observed first floor radon data collected by Health Canada during the period October 2010 to March 2011, seven common PAR radon models used for North American miners and dwelling scenarios were applied. The death rates used for this study were from the period 2006-2009. Smoking data (Ever Smoking ES and Never Smoking NS) collected in 2009 was also used in this study. The original discrete radon data for Canada overall and for each of its provinces are estimated using log-normal and Gaussian kernel density estimator distributions. PAR was then calculated for Canada and its provinces using the empirical, log-normal, and Gaussian kernel estimates distributions. Finally, cancer death cases attributable to radon are reported for the constant relative risk model for the three distributions and the reduction in the cases when the action level 200Bq/m(3) is applied.
Results:
PAR for the Canadian data is sensitive to the model choice, and it varies with a range of 10% for ES and 32% for NS, respectively. There is little difference in results between miners' models and dwelling models. PAR values for ES females are greater than those for ES males, except in Saskatchewan, Northwest Territories, Nunavut, and Yukon. The male-female range overlaps. Gaussian kernel estimator produces PAR estimates similar to the commonly used log-normal distribution.
Conclusion:
Many lung cancer cases could be prevented in Canada by reducing indoor radon. PAR is sensitive to the choice of RR model. Miners' models can be used for residential radon. Empirical, log-normal, and Gaussian kernel density estimation with support [0,∞) can all be applied to radon data.
... AR is a measure of how much of the disease risk is attributable to a certain exposure, and thus, indicates the potential for prevention if the exposure could be eliminated [12]. Explicitly, the AR of lung cancer deaths due to indoor radon exposure refers to the proportion of lung cancer deaths that could be prevented if indoor radon concentrations were remediated to outdoor levels [13]. In fact, since most homes are deemed to have low levels of radon, the majority of lung cancer deaths attributable to radon would occur among persons exposed to indoor radon concentrations below commonly used reference levels [4]. ...
... The effects of radon mitigation on lung cancer were assessed in studies conducted in the US [2], Germany [14], and Canada [1,17]. In the US, under the EAC model, mitigating radon levels in homes at or above 148 Bq/m 3 , the EPA action level [13], would result in an estimated reduction in lung cancer mortality of 4.2 % if indoor radon were completely eliminated, 3.7 % if homes were mitigated to 0-148 Bq/m 3 , or 1.7 % if homes were remediated to exactly 148 Bq/m 3 [2]. In Germany, reducing radon levels below 100 Bq/m 3 (WHO guideline [4]) in homes would prevent 302 lung cancer deaths (15.9 % of all lung cancer deaths attributable to radon) every year [14]. ...
Exposure to radon gas is the second most common cause of lung cancer after smoking. A large number of studies have reported that exposure to indoor radon, even at low concentrations, is associated with lung cancer in the general population. This paper reviewed studies from several countries to assess the attributable risk (AR) of lung cancer death due to indoor radon exposure and the effect of radon mitigation thereon. Worldwide, 3-20 % of all lung cancer deaths are likely caused by indoor radon exposure. These values tend to be higher in countries reporting high radon concentrations, which can depend on the estimation method. The estimated number of lung cancer deaths due to radon exposure in several countries varied from 150 to 40,477 annually. In general, the percent ARs were higher among never-smokers than among ever-smokers, whereas much more lung cancer deaths attributable to radon occurred among ever-smokers because of the higher rate of lung cancers among smokers. Regardless of smoking status, the proportion of lung cancer deaths induced by radon was slightly higher among females than males. However, after stratifying populations according to smoking status, the percent ARs were similar between genders. If all homes with radon above 100 Bq/m(3) were effectively remediated, studies in Germany and Canada found that 302 and 1704 lung cancer deaths could be prevented each year, respectively. These estimates, however, are subject to varying degrees of uncertainty related to the weakness of the models used and a number of factors influencing indoor radon concentrations.
... According to the data, the population impact of exposure to the US Environmental Protection Agency's action levelmeasured as attributable risk (9.0 percent)-does not differ much from that reported by other authors, who place it at somewhere between 5 percent and 10 percent (61-63). However, because these results indicate that a clear effect is already in evidence at low exposures, this gives a population attributable risk that is from 5 to 6 times higher in this study versus others (61,62). ...
... The high concentrations of residential radon observed here are probably due to the granite nature of the subsoil in the study area, an area that has a geologic profile closely akin to that of north Portugal and southwest England. Nevertheless, this characteristic alone cannot explain the appearance of risk at concentrations much lower than those defined as the "action level" in the United States for many years (61). It is arguable that these results might, in part, be due to inter- (73) or intraannual (74) variations in radon concentrations. ...
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 (Cl): 1.12, 5.48), 2.48 (95% Cl: 1.29, 6.79), and 2.96 (95% Cl: 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.
... Detailed investigations of this area revealed these high levels of radon could be correlated with a particular bedrock type found within the Reading Prong geological province. The concerns, or stigma, associated with excess radon in the household are well warranted due to a direct correlation between elevated radon exposure and lung cancer (Lubin et al., 1989). The fact that elevated levels of radon could be traced to particular geological provinces has lead to much research into the origins and transport mechanisms of radon gas. ...
... The Surgeon General has declared radon the second leading cause of lung cancer within the United States, behind smoking (USEPA, 1992). A direct correlation among indoor radon and lung cancer has been found using the BEIR IV model of risk assessment (Lubin et al., 1989). Detailed epidemiology studies of uranium miners and single-family homes have shown that increased radon exposure increases the lifetime chance of lung cancer (Nazaroff et al., 1988;USEPA, 1992). ...
... The presence of radon and thoron at high levels in dwellings increases the risk of lung cancer significantly [8,9]. Inhaling radon or thoron gas and accumulation of alphaemitting decay product in the lungs can damage the cells lining the airways and lead to lung cancer in the long run. ...
The present study is based on the measurement of the radon and thoron concentrations in the indoor environment of the tectonically active zone of the Garhwal Himalaya region using the portable SMART RnDuo monitor. The concentration of the indoor radon and thoron varies from 60 ± 17 to 213 ± 49 Bq m−3 (with an arithmetic mean of 100 ± 27 Bq m−3) and 33 ± 18 to 217 ± 94 Bq m−3 (with an arithmetic mean of 76 ± 33 Bq m−3), respectively. The significant contribution of thoron concentration was observed in the present study. The average values of indoor radon and thoron concentrations measured from the sampling sites are well below the recommended level of the World Health Organization.
... There is little question that high radon concentrations in uranium mines and related absorbed radiation doses to the respiratory tract combined with the worker environment and worker lifestyle resulted in an increase in lung cancer [1,[7][8][9]. The radiation dose estimates and lung cancer data for uranium miners were combined with the dose derived from within-home radon exposure to estimate lung cancer risk from radon inhalation for a range of exposure levels [1,10,11]. Epidemiology research has been combined with multivariate risk models to demonstrate the influence of radon in homes on lung cancer frequency. Use of multivariate models allows for addressing multiple risk factors and making adjustments for some covatiate influences. ...
The National Academy of Sciences (USA) conducted an extensive review on the health effects of radon (BEIR VI). This was a well written and researched report which had impact on regulations, laws and remediation of radon in homes. There were a number of problems with the interpretation of the report and three are focused on here. First, most of the radiation dose used to estimate risk was from homes with radon levels below the US Environmental Protection Agency's action level so that remediation had minor impact on total calculated attributable risk. Remediation of the high level homes (i.e., above the action level) would therefore have a minor impact on the calculated “population attributable risk”. In individual homes with very high levels of radon, remediation may minimally reduce individual risk. Second, the conclusion communicated to the public, regulators and law makers was “Next to cigarette smoking radon is the second leading cause of lung cancer.” This is not an accurate evaluation of the report. The correct conclusion would be: Next to cigarette smoking, high levels of radon combined with cigarette smoking is the second leading cause of lung cancer. In the never-smokers, few cancers could be attributable to radon. Thirdly, there is little question that high levels of radon exposure in mines combined with cigarette smoke and other significant insults in the mine environment produces excess lung cancer. However, the biological responses to low doses of radiation are different from those produced by high levels and low doses may result in unique protective responses (e.g. against smoking-related lung cancer). These three points will be discussed in detail. This paper shows that in contrary to the BEIR VI report, risk of lung cancer from residential radon is not increased and radon in homes appears to be helping to prevent smoking-related lung cancer. Thus, laws requiring remediation of homes for radon are providing little if any public health benefits.
... 23 In the U.S., mitigation level of indoor radon concentration is the same as that in Korea at 148 Bq/m 3 . 24 A study in the U.S. estimated that remediating indoor radon concentrations in all homes below 148 Bq/m 3 could reduce lung cancer mortality by 3.7%. 1 The study further reported that if mitigation level was lowered to 74 Bq/m 3 , 6.5% of all lung cancer deaths could be prevented every year. These estimates are similar to ours with a 3.2-4.7% ...
Purpose
Exposure to indoor radon is associated with lung cancer. This study aimed to estimate the number of lung cancer deaths attributable to indoor radon exposure, its burden of disease, and the effects of radon mitigation in Korea in 2010.
Materials and Methods
Lung cancer deaths due to indoor radon exposure were estimated using exposure-response relations reported in previous studies. Years of life lost (YLLs) were calculated to quantify disease burden in relation to premature deaths. Mitigation effects were examined under scenarios in which all homes with indoor radon concentrations above a specified level were remediated below the level.
Results
The estimated number of lung cancer deaths attributable to indoor radon exposure ranged from 1946 to 3863, accounting for 12.5–24.7% of 15623 total lung cancer deaths in 2010. YLLs due to premature deaths were estimated at 43140–101855 years (90–212 years per 100000 population). If all homes with radon levels above 148 Bq/m³ are effectively remediated, 502–732 lung cancer deaths and 10972–18479 YLLs could be prevented.
Conclusion
These findings suggest that indoor radon exposure contributes considerably to lung cancer, and that reducing indoor radon concentration would be helpful for decreasing the disease burden from lung cancer deaths.
... Variations in population risk estimation among various models are presented and discussed. (8) , the attributable risk (AR) of lung cancer due to ionizing radiation is defined as the proportion of lung-cancer deaths attributable to radon progeny exposure. This risk indicates the proportion of lung cancer deaths that theoretically could be prevented by reducing indoor radon concentrations to outdoor levels. ...
To address public concerns regarding radon risk and variations in risk estimates based on various risk models available in the literature, lifetime lung cancer risks were calculated with five well-known risk models using more recent Canadian vital statistics (5-year averages from 2008 to 2012). Variations in population risk estimation among various models were assessed. The results showed that the Canadian population risk of radon induced lung cancer can vary from 5.0 to 17% for men and 5.1 to 18% for women based on different radon risk models. Averaged over the estimates from various risk models with better radon dosimetry, 13% of lung cancer deaths among Canadian males and 14% of lung cancer deaths among Canadian females were attributable to long-term indoor radon exposure.
... One of the main contributors to indoor radon concentrations are the materials from which buildings are constructed (13,14) . Radon, a noble gas, can easily diffuse from the surface of the Earth and building materials and can be a source of health hazard related to bronchus and lungs (15,16) . Studies on natural radioactivity were carried out in many other South Indian rivers in the past (17 -19) . ...
The activity concentration of the natural radionuclides (226)Ra, (232)Th and (40)K was measured for sediment samples collected from thirty-three different locations along the Bharathapuzha river basin by using high-resolution gamma-ray spectrometry. The concentrations of the natural radionuclides were found to vary from location to location, and their mean values are 19.6, 82.87 and 19.44 % higher than the worldwide mean values of (226)Ra, (232)Th and (40)K, respectively. The value of (232)Th was found to be higher than that of (226)Ra in 82 % of the samples collected for this study. The calculated values of indoor gamma dose rate (DIN) ranged between 89.55 and 194.24 nGy h(-1), and the overall mean value is 63.2 % higher than the recommended safe and criterion limit by UNSCEAR. The internal and external hazard indices (Hin and Hex), the representative gamma index and alpha index (Igamma and Ialpha), the annual gonad dose equivalent (AGDE) and the excess lifetime cancer risk (ELCR) were also calculated and compared with the international recommended values. Multivariate statistical analyses were also carried out to determine the relation between the natural radionuclides and various radiological parameters.
... The population risk of radon-induced lung cancer is assessed by an attributable risk (AR). The AR of lung cancer due to ionising radiation is defined as the proportion of lung-cancer deaths attributable to indoor radon exposure (5) . This risk indicates the proportion of lung cancer deaths that could be theoretically prevented by reducing indoor radon # The Author 2012. ...
Exposure to indoor radon has been determined to be the second leading cause of lung cancer after tobacco smoking. Canadian population risk of radon induced lung cancer was assessed in 2005 with the radon distribution characteristics determined from a radon survey carried out in the late 1970s in 19 cities. In that survey, a grab sampling method was used to measure radon levels. The observed radon concentration in 14 000 Canadian homes surveyed followed a log-normal distribution with a geometric mean (GM) of 11.2 Bq m(-3) and a geometric standard deviation (GSD) of 3.9. Based on the information from that survey, it was estimated that ∼10 % of lung cancers in Canada resulted from indoor radon exposure. To gain a better understanding of radon concentrations in homes across the country, a national residential radon survey was launched in April 2009. In the recent survey, long-term (3 month or longer) indoor radon measurements were made in roughly 14 000 homes in 121 health regions across Canada. The observed radon concentrations follow, as expected, a log-normal distribution with a GM of 41.9 Bq m(-3) and a GSD of 2.8. Based on the more accurate radon distribution characteristics obtained from the recent cross-Canada radon survey, a re-assessment of Canadian population risk for radon induced lung cancer was undertaken. The theoretical estimates show that 16 % of lung cancer deaths among Canadians are attributable to indoor radon exposure. These results strongly suggest the ongoing need for the Canadian National Radon Program. In particular, there is a need for a focus on education and awareness by all levels of government, and in partnership with key stakeholders, to encourage Canadians to take action to reduce the risk from indoor radon exposure.
... It has been estimated that -10% (or -13,000 per year) of all lung cancer deaths in the U.S. are directly attributable to exposure to Rn and its decay products (Lubin and Boice 1989). Both ^"Rn and ^Rn are significant contributors to the indoor radiation environment; it has been estimated that 10-20% of the effective dose equivalent from all indoor Rn progeny is due to ""Rn progeny (UNSCEAR 1982). ...
Soil gas 220Rn and 222Rn concentrations were measured at sites in Chester and Aberdeen, New Jersey (NJ). Two years of 222Rn and 220Rn data were obtained from a depth of 0.85 m, followed by two years from depths of 0.28, 0.56, 0.85, and 1.28 m. Variations of 220Rn and 222Rn, before the first winter that sample tubes were installed, were larger than later, indicating that the soil structure, disturbed during installation of the tubes, may have significantly redistributed after the first winter, thus ensuring that the sample was drawn from near the bottom of the tube. At the Chester site, autumn 222Rn concentrations were found to be up to 10 times higher than winter values, variations larger than predicted assuming diffusion-only transport. Spatial variations up to an order of magnitude were observed over distances of a few meters. The 220Rn concentrations were typically ∼2 to 3 times higher during summer than during winter. At the Aberdeen site, 220Rn and 222Rn concentrations were about an order of magnitude less than the lowest Chester site values with no statistically significant temporal or spatial variations. Permeability, thought to be an indicator of parameters controlling soil gas Rn variations, showed poor correlations with 220Rn or 222Rn at both sites.
... The risk, as extrapolated from miners to the general population, was remarkable: owing to the widespread presence of radon in the indoor air of workplaces and dwellings, many thousands of lung cancers were attributed to residential radon exposure (e.g. Lubin and Boice, 1989). As a consequence, many countries and international organizations introduced recommendations and regulations to limit radon exposure in workplaces and/or in dwellings (ICRP, 1987(ICRP, , 1993Åkerblom, 1999;WHO-ROE, 2001). ...
An important achievement of nuclear track detectors is that they render it possible to measure a large number of radon concentrations. These are necessary for epidemiological studies aimed to estimate the lung cancer risk due to exposure to radon and its decay products in dwellings. Many case–control studies were conducted in the last 15 years in Europe, North America and China, in order to avoid the uncertainties associated with the risk extrapolation from epidemiological studies on miners exposed in underground mines. In this review paper, the main methodological issues of these studies are introduced: confounding factors, the impact of radon exposure uncertainties on the estimated risk, the retrospective assessment of radon exposure through the measurement of surface concentration on glass objects, the interaction between radon and smoking, statistical methods to analyze data and combine studies, etc. As regards the estimated risk of lung cancer, the main characteristics and results of each study are reported and discussed, together with the results of meta-analyses and, most importantly, of the three recently published analyses that pool 2 Chinese, 7 North American, and 13 European studies. Finally, some conclusions are given and a brief reference is made to ongoing studies.
Description
Radon was recognized as a potential public health threat in the United States more than 30 years ago. To understand and effectively deal with radon, one needs to understand the physics of radon, its health effects, measurement techniques and protocols, the extent of its occurrence in the United States, mitigation principles and practices, and legislative and regulatory actions.
Manual 15 addresses these areas and provides a well-rounded look at the radon issue. Ten peer-reviewed chapters include:
• Radon -- A Multifaceted Environmental Problem: An Overview
• Radon and the Natural Environment
• Health Effects of Radon
• Measurement Methods and Instrumentation
• Radon Measurement Protocols
• Geology and Occurrence
• Concentration Patterns
• Radon Control Strategies
• EPA's Strategy to Reduce Risk of Radon
• Current and Future Perspectives.
After smoking, residential radon is the second risk factor of lung cancer in general population and the first in never-smokers. Previous studies have analyzed radon attributable lung cancer mortality for some countries. We aim to identify, summarize, and critically analyze the available data regarding the mortality burden of lung cancer due to radon, performing a quality assessment of the papers included, and comparing the results from different countries. We performed a systematic scoping review using the main biomedical databases. We included original studies with attributable mortality data related to radon exposure. We selected studies according to specific inclusion and exclusion criteria. PRISMA 2020 methodology and PRISMA Extension for Scoping Reviews requirements were followed. Data were abstracted using a standardized data sheet and a tailored scale was used to assess quality. We selected 24 studies describing radon attributable mortality derived from 14 different countries. Overall, 13 studies used risk models based on cohorts of miners, 8 used risks from residential radon case-control studies and 3 used both risk model options. Radon geometric mean concentration ranged from 11 to 83 Becquerels per cubic meter (Bq/m3) and the population attributable fraction (PAF) ranged from 0.2 to 26%. Studies performed in radon prone areas obtained the highest attributable mortality. High-quality publications reported PAF ranging from 3 to 12% for residential risk sources and from 7 to 25% for miner risk sources. Radon PAF for lung cancer mortality varies widely between studies. A large part of the variation is due to differences in the risk source used and the conceptual description of radon exposure assumed. A common methodology should be described and used from now on to improve the communication of these results.
We compare lung cancer (LC) rates, smoking percentages and radon levels in Manitoba (MN) and Prince Edward Island (PE). Smoking does not explain high LC in MN, but indoor radon does. We show that population attributable risk in PE is only 37% of that in MN. Radon above 200 Bq m −3 increases LC in PE by only 4 cases, but in MN by 195 cases.
This paper reviews adjusted methods of estimation of attributable risk (AR), that is methods that allow one to obtain estimates of AR while controlling for other factors. Estimability and basic principles of AR estimation are first considered and the rationale for adjusted AR estimators is discussed. Then, adjusted AR estimators are reviewed focusing on cross-sectional, cohort and case-control studies. Two inconsistent adjusted estimators are briefly commented upon. Next, adjusted estimators based on stratification, namely the weighted-sum and Mantel-Haenszel (MH) approaches, are reviewed and contrasted. It appears that the weighted-sum approach, which allows for full interaction between exposure and adjustment factors, can be affected by small-sample bias. By contrast, the MH approach, which rests on the assumption of no interaction between exposure and adjustment factors may be misleading if interaction between exposure and adjustment factors is present. Model-based adjusted estimators represent a more general and flexible approach that includes both stratification approaches as special cases and offers intermediate options. Bruzzi et al.’s and Greenland and Drescher’s estimators are reviewed and contrasted. Finally, special problems of adjusted estimation are considered, namely estimation from case-cohort data, estimation for risk factors with multiple levels, for multiple risk factors, for recurrent events, estimation of the prevented and preventable fractions, and estimation of the generalized impact fraction. Comments on future directions are presented.
Lifetime risks of radon induced lung cancer were assessed based on epidemiological approaches for Canadian, Swiss and Chinese populations, using the most recent vital statistic data and radon distribution characteristics available for each country. In the risk calculation, the North America residential radon risk model was used for the Canadian population, the European residential radon risk model for the Swiss population, the Chinese residential radon risk model for the Chinese population, and the EPA/BEIR-VI radon risk model for all three populations. The results were compared with the risk calculated from the International Commission on Radiological Protection (ICRP)'s exposure-to-risk conversion coefficients. In view of the fact that the ICRP coefficients were recommended for radiation protection of all populations, it was concluded that, generally speaking, lifetime absolute risks calculated with ICRP-recommended coefficients agree reasonably well with the range of radon induced lung cancer risk predicted by risk models derived from epidemiological pooling analyses.
With the rapidly growing interest in improving environmental performance in new buildings, it is sometimes easy to forget the inherent environmental hazards posed by many development sites. The reality is that, following large-scale industrial restructuring over the past 20 years, many industrial and commercial developments now take place on or adjacent to land that was formerly put to contaminative use. In some parts of the UK, and especially in SE England, the available landbank is so small that sites are almost invariably redeveloped rather than developed for the first time. In other areas, naturally occurring pollutants such as radon can pose special problems for the developer. On some sites, health hazards from the electromagnetic fields generated by overhead power lines may need to be considered. These are the major issues addressed in this chapter.
Lung cancer is the most common cause of cancer and cancer death throughout the world. In the United States alone, lung cancer is expected to account for an estimated 169,400 of the 1.28 million new cases of cancer and 154,900 of 555,500 cancer deaths for 2002 (Jemal et al. 2002). Because the widespread incidence of lung cancer around the world mirrors the high rates of the United States, it is vital that the disease be studied in an effort to reduce the incidence of this disease. It is clear that cigarette smoking is the primary cause of lung cancer, thus making it a largely preventable disease. Epidemiology is the field of study that investigates the frequency, etiologies, incidence, and mortality of various disease states. This chapter will endeavor to highlight lung cancer incidence and mortality worldwide, identify changing trends in the lung cancer epidemic, and discuss the numerous etiologies of this deadly cancer.
Epidemiological evidence is accumulating on cancer risks related to non-occupational exposures with primary sources indoors, such as environmental tobacco smoke, radon, cooking fumes and mineral fibres. Most of the data is focused on lung cancer risks and on women because they are believed to receive the heaviest residential exposures. For clarity the different exposure factors will be treated separately, although it is realised that they often occur together, and that interactions may be of importance.
The presented work tried to compare of lifestyles of lung carcinoma patients with control subjects without the disease. The most common cause of malignant tumour death is lung carcinoma responsible for 1 320 000 deaths worldwide in 1996. Lung carcinoma is a disease with multifactor etiology smoking being the main risk factor for developing the disease. Smoking is the cause of the disease in 83-94% of males and 57-80% of females. However, other factors must not be ignored. These are risk factors in the working environment, ionizing radiation, polluted air, passive smoking, nutrition, family history etc. The so called clustering of risk factors is common. The study was performed as a hospital-based analytical observation study of cases and controls in the Teaching Hospital in Olomouc. The group consisted of 91 subjects (70 males and 21 females) with lung carcinoma and the same number of subjects was in the control group. The subjects provided information directly during interviews and these were recorded in questionnaires. The questions were related to lifestyle and other risk factors - education, domicile including cooking and heating habits, polluted environment, height and weight, non-tumour lung diseases in the case-history, number of X-ray examinations, smoking, passive smoking, alcohol consumption, dietary habits and family history.
Radon and Lung Cancer Outdoor Radon Indoor Radon The Other Radon, 220Rn, Thoron Radon Epidemiology in Underground Mines Residential Epidemiology Lung Dosimetry Lung Cancer Models for Humans Childhood Exposure Animal Studies Smoking and Radon Summary References
A study was conducted to measure indoor radon concentrations in dwellings of the Abbottabad city. In this regard, CR-39 based radon detectors were installed in drawing rooms and bedrooms of 40 selected houses and were exposed to indoor radon for 3 months. After exposure, the CR-39 detectors were etched for 8 hrs in 6M NaOH solution at 70 C and tracks were counted under an optical microscope. The observed tracks densities were related to radon
concentrations using a calibration factor of 2.7 tracks.cm .h /kBq.m . The mean annual estimated effective dose received by the residents of the studied area was found to be 1.48 ± 0.47 mSv y . Comparing the current indoor radon results with the published data of international agencies, it was found that the houses surveyed in the present study were within the safe limits
This paper examines the problem of estimating indoor radon concentrations for radon-induced lung cancer risk assessment. Previous authors have identified various problems and possible corrections for the use of generally available radon screening measurements. Bias evident in data collected from volunteers is described; regional databases developed from voluntary data generally exhibit higher mean values than those obtained from random samples. Tools are developed to better characterize the differences in voluntary and random concentration distributions. Application is demonstrated using voluntary and random radon survey data for the state of North Dakota.
The association between tobacco smoking and lung cancer has been noted for more than 50 years and continues to dominate the etiologic milieu of this malignant disease. Other agents, many discovered in the occupational setting, have also been substantiated as lung carcinogens. Inherent predisposition to the disease has long been suspected, and recent investigations suggest several potential mechanisms and a possible mode of inheritance. Considerable progress has been made in deciphiring the molecular defects present in lung cancer cells. These recent findings have been incorporated into two well-known models of lung carcinogenesis. As the details of the carcinogenic process are unraveled, one goal is to identify intermediate (preneoplastic) markers of exposure and inherent predisposition that will help assess the risk of lung cancer for individuals as well as for groups.
This paper includes the results of measurements of natural radioactivity in building materials and raw building materials. The dose rate indoors was calculated on the basis of the contents of K-40, Ra-226 and Th-232 in building materials and the results were compared with literature data of measurements (in situ). The standard procedure for qualifying building materials for building houses designed for habitation was used.
Radon generated within the upper few meters of the Earth's crust by the radioactive decay of radium can migrate during its brief lifetime from soil into the atmosphere. This phenomenon leads to a human health concern as inhalation of the short-lived decay products of radon causes irradiation of cells lining the respiratory tract. This paper reviews the factors that control the rate at which two radon isotopes, 222Rn and 220Rn, enter outdoor and indoor air from soil. The radium content of surface soils in the United States is usually in the range 10–100 Bq kg−1. The emanation coefficient, which refers to the fraction of radon generated in a material that enters the pore fluids, varies over a wide range with a typical value being 0.2. Radon in soil pores may be partitioned among three states: in the pore air, dissolved in the pore water, and sorbed to the soil grains. Except in the immediate vicinity of buildings, radon migrates through soil pores principally by molecular diffusion. Average reported flux densities from undisturbed soil into the atmosphere are 0.015–0.048 Bq m−2 s−1 for 222Rn and 1.6–1.7 Bq m−2 s−1 for 220Rn. Soil is the dominant source of radon in most buildings. Advective flow of soil gas across substructure penetrations is a key element in the transport process. The advective flow is driven by the weather (wind and indoor-outdoor temperature differences) and by the operation of building systems, such as heating and air conditioning equipment. A typical radon entry rate into a single-family dwelling of 10–15 kBq h−1 can be accounted for by weather-induced pressure-driven flow through moderately to highly permeable soils. The extent to which diffusion through soil pores contributes to radon entry into buildings is not known, but in buildings with elevated concentrations, diffusion is believed to be less important than advection.
The BEIR IV report gives graphs and tables that are used to estimate the risks due to radon (Rn-222) and its decay products. The BEIR IV hypothesis predicts that the lifetime risks will depend upon the ''normal'' incidence of fatal lung cancers for nonsmokers and smokers and the life expectancies of both groups. This paper examines the influence of recent information on these health risks. The factors considered are a) the life tables for both sexes and for those who never smoked, formerly smoked, are currently light smokers, or are currently heavy smokers, and b) the age-dependent fatal lung cancer rates for the same groups of people. In general, the calculations indicate that people who have never smoked would have the same risks as those listed in the BEIR IV report as nonsmokers. For males, those who smoke or formerly smoked would have calculated risks that are greater than people who never smoked; however, for males, the smokers and former smokers considered in this paper have lower calculated risks than the BEIR IV smokers. For females, the heavy smokers examined here would have greater calculated risks than the BEIR IV smokers. The reasons for these differences are presented.
Studies of the natural γ-emitting radionuclides in different types of cements manufactured by different companies in Egypt (e.g. Iron (HI), Karnak (HK), and Super fine (HSu) products from Helwan Ltd.) have been done to determine their natural levels of radioactivity using a high-purity germanium detector (HPGe). Knowledge of radioactivity present in cement materials enables one to assess any possible radiological risks to human health. The results show that the highest mean values of Ra and Th activity are 234.01±20.12 and 46.56±4.65 Bq kg, respectively, measured in cement sample ‘Iron’ from Helwan company (HI). The corresponding value of K is 333.53±26.68 Bq kg measured in cement sample ‘Karnak’ from Helwan company (HK). For Cs, this value is 3.27±0.31 Bq kg measured in cement sample (HI). The average concentrations of measured radionuclides in the different cement samples are 72.21±6.39, 24.98±2.24, 134.49±10.45, and 0.58±0.08 Bq kg for Ra, Th, K, and Cs, respectively. The measured activity concentrations for these radionuclides were compared with the reported data of other countries. Radium equivalent (Raeq) activities and different hazard indices were calculated to assess the radiation hazard. Iron HI cement sample shows a higher Raeq activity of 311.91±31.10 Bq kg. Calculations of absorbed doses in nGy h show that the Iron (HI), Karnak (HK), and Super fine (HSu) products from Helwan company have higher activities than the permissible level (80 nGy h). On the basis of the external hazard index (Hex), Raeq activities, and annual effective dose rates for organs (Horgan), the natural radioactivity of cement samples is not greater than the recommended values in the established standards and hence safe for use in building constructions and therefore for inhabitants.
The use of an activated charcoal sampler for radon monitoring has become popular in recent years because of its passiveness and low price. Dynamics of adsorption on a passive sampler have been described with theoretical models. However, extrapolation of the measured results of radon on charcoal to the diurnal fluctuations of the ambient radon concentration is often difficult and even misleading because of the oversimplification of these models. A more generalized approach is undertaken by treating the diurnal variations in radon concentrations as poly-exponential functions and by solving for explicit particular solutions of Fick's equation. The application of these solutions to various practical situations is explored. This includes their use for charcoal sampler calibration. Estimated values of the adsorption coefficients, k, and diffusion constant, D, appear to be agreeable with corresponding reported values. A triple-sampler protocol is also proposed for radon survey in areas of high diurnal fluctuations.
Short-term measurements of 222Rn concentrations using diffusion barrier charcoal canisters were made in living areas at the request of volunteer households in Tennessee, Kentucky, Georgia, and Florida from 1986 through 1989. We analyzed the observed radon concentrations in regional sub-areas within these states. After adjusting for oversampling that had occurred in some areas, we estimated state-wide geometric means of radon concentrations in living rooms as 59.7 Bq m−3 in Kentucky, 51.9 Bq m−3 in Tennessee, and 60.0 Bq m−3 in Georgia. Measurements in Florida were scattered over the state and the coverage was inadequate to allow a state-wide estimate. Estimates of the percentage of homes having indoor radon levels equal to or above the action level of 148 Bq m−3 are 21.6% in Kentucky, 17.0% in Tennessee, and 6.8% in Georgia, respectively.
bjectives: To date, the pattern of spermatogenic failure in patients
undergoing chemotherapeutic treatment has yet to be clarified. The
mechanisms responsible for the testicular cytotoxicity of the
neoplastic drugs cisplatin, adriamycin, and 5-fluorouracil remain to be less
explored.
Methods: Twenty-four mature male albino rats of the Wistar strain were
divided into four groups: control (saline-treated), adriamycin (i.p. 0.2 mg/kg
BW), cisplatin (i.p. 0.2 mg/kg BW), and 5-fluorouracil (i.p. 20 mg/kg BW).
Drug-treatment were carried every other day for 30 days followed by
assessments of testis weight, light and transmission electron microscopy
examinations, DNA fragmentation experiments, and measurements of
biochemical markers of testicular damage.
Results: The drugs altered the absolute and relative testicular weights of the
rats compared to the effects of control treatment. There were marked
reductions in the number of germ cells, decreases in germ cell height, and
thinning of the tubular basal lamina in the treatment groups. 5-Fluorouracil
treatment led to the sclerosis of seminiferous tubules, and enhanced
conjugation between spermatogenic cells led to the formation of
multinucleated giant cells with different structural patterns. Apparent DNA
damage, reduced testicular vascular endothelial growth factor (VEGF),
increased heat shock protein 70(HSP-70) and 8-hydroxy-2-guanosine (8-
OHdG), and reduced both intercellular and vascular cell adhesive molecules
(ICAM-1, VCAM-1) were observed after chemotherapeutic drug -treatment.Conclusions: We concluded that chemotherapeutic drugs cause testicular
cell death, as confirmed by altered 8-OHdG, VEGF, and HSP-70 expression
and genomic damage.
Lung‐cancer mortality (LCM) is elevated in underground miners who chronically inhaled the mutagenic, cytotoxic α‐decay products of radon gas. Epidemiologie studies of LCM rates vs. residential‐radon concentration levels are generally considered inconclusive. However, Cohen (Health Physics 68, 157–174, 1995) has hypothesized that data on LCM vs. residential radon concentrations at the U.S. county level are clearly inconsistent with a linear no‐threshold (LN) dose‐response model, and rather are consistent with threshold or hormesis model. Cohen's hypothesis has been criticized as “ecological fallacy,”; particularly because LN (but not threshold or hormesis) models are generally considered biologically plausible for agents like α radiation that damage DNA in linear proportion to dose. To assess the biological plausibility of Cohen's hypothesis, a preliminary study was made of whether a biologically realistic, cytodynamic 2‐stage (CD2) cancer model can provide a good, joint fit to Cohen's set of U.S. county data as well as to underground‐miner data. The CD2 model used adapts a widely applied, mechanistic, 2‐stage stochastic model of carcinogenesis to realistically account for interrelated cell killing and mutation (both assumed to have a LN dose‐response), cell turnover, and incomplete exposure of stem cells. A CD2 fit was obtained to combined summary data on LCM vs. radon‐exposure in white males in 1, 601 U.S. counties (from Cohen) and in white male Colorado Plateau (CP) uranium miners (from the National Research Council's “BEIRIV”; report). The CD2 fit is shown to: (i) be consistent with the combined data; (ii) have parameter values all consistent with biological data; and (iii) predict inverse dose‐rate‐effects data for CP and other radon‐exposed miners, despite the fact that optimization had not involved any of these dose‐rate data. The latter data were not predicted by a simplified CD2 model in which all stem cells were presumed to be exposed. It is concluded that this study provides preliminary evidence that Cohen's hypothesis is biologically plausible.
Solid state alpha track detectors using CR-39 plastic detectors were used to measure the radon concentration and the radon exhalation rates from building materials used in Egypt. The radon flux emitted from the surface of the building material was measured by placing CR-39 detector within the hollow holder. Tracks due to alpha particles from radon that migrate from the building materials into the air space in the chamber were registered on the CR-39 detector. The detectors were etched in 6M NaOH solution at 70 °C for 18 hours. An image analyzer system was used to record the tracks on the CR-39 detector. This technique can be used to give a database for average radon exhalation rates from all available building materials and walls or floors.
A major aim of epidemiologic research is to measure disease occurrence in relation to various characteristics such as exposure
to environmental, occupational, or lifestyle risk factors, genetic traits or other features. In this chapter, various measures
will be considered that quantify disease occurrence, associations between disease occurrence and these characteristics as
well as their consequences in terms both of disease risk and impact at the population level. As is common practice, the generic
term exposure will be used throughout the chapter to denote such characteristics. Emphasis will be placed on measures based
on occurrence of new disease cases, referred to as disease incidence. Measures based on disease prevalence, i. e., considering
newly occurring and previously existing disease cases as a whole will be considered more briefly.
Although studies of radon exposure have established that Rn decay products are a cause of lung cancer among miners, the lung cancer risk to the general population from indoor radon remains unclear and controversial. Our epidemiological investigation of indoor radon influence on lung cancer incidence was carried out for 201 patients from the Osijek town. Ecological method was applied by using the town map with square fields of 1 km2 and the town was divided into 24 fields. Multiple regression study for the lung cancer rate on field, average indoor radon exposure and smoking showed a positive linear double regression for the mentioned variables. Case-control study showed that patients, diseased of lung cancer, dwelt in homes with significantly higher radon concentrations, by comparison to the average indoor radon level of control sample.
Lung cancer risk in relation to indoor radon was examined in three case-control studies in Stockholm (Sweden), New Jersey (United States), and Shenyang (People's Republic of China). Year-long measurements of radon gas were made in current and past homes of 966 women who developed lung cancer and of 1,158 control women, included in the combined analysis. Nearly 14 percent of the participants were estimated to have a time-weighted, mean, radon concentration in their homes of more than 4 pCi/l (150 Bq/m3) during the period from five to 35 years prior to the date of lung cancer diagnosis (or comparable date for controls). There was a tendency for risk to increase with increasing levels of randon in NJ and Stockholm, but the trends for individual studies and overall were not statistically significant. The estimates of the excess relative risk for indoor exposure per pCi/l were 0.18 (95 percent [CI]=–0.04–0.70) in NJ, 0.06 (CI=–0.05–0.34) in Stockholm, and –0.02 (CI=––0.03) for Shenyang; these estimates did not differ significantly from each other. The overall excess RR per pCi/l was 0.00 (CI=–0.05–0.07); the confidence limits were sufficiently broad, however, that the overall estimate was still compatible with extrapolations of risks from miners. Cigarette smoking was the predominant cause of lung cancer with the RR significantly elevated in all studies. Within smoking categories, the trend in risk with increasing mean radon concentration was inconsistent. Analyses of data from several studies are complicated by the possibility that there may exist important differences in study bases which might affect results, and which may be controlled only partially through adjustment procedures. Future efforts to combine various residential studies will need to be attentive to the intrinsic limitations of studies to detect low levels of risk as well as the unique uncertainties associated with estimating, accurately, cumulative exposure to indoor radon.
The considerable radiosensitivity of the human lung together with the highly localized α-doses in the bronchial and pulmonary regions from naturally occurring and man-enhanced radon decay products make the respiratory tract the most critical organ for cancer from exposure to ionizing radiation in our environment. From indoor radon, the tracheobronchial region of the lung generally receives radiation doses which are at least an order of magnitude above the total dose to any other organ. Excess lung cancer deaths found in epidemiological studies on heavily exposed populations of miners can be fitted reasonably well to a relative risk model, when declines in relative risk with both age at risk evaluation, and time since exposure, are incorporated. Smoking seems to act synergistically. A comparison of the major radon risk projections shows considerable discrepancies in the best estimates of risk, indicating that the uncertainties remain large.
This paper presents the results of radon concentration measurements in the drinking water from the municipal water supply system and private wells of Xian, Xianyang and Baoji city of Shaanxi province of China. The measurements were carried out on 38 samples. Radon levels in drinking water in Xian, Xianyang and Baoji were found to be 5.78, 13.04 and 15.01kBqm–3, respectively. The AM radon concentration of private well water from Xianyang and Baoji is 28.84kBqm–3 and 38.85kBqm–3, respectively, which is 2.56 times and 3.14 times as high as that of tap water radon, respectively. The radiation risk of radon in water would be due to degassing and not due to drinking water. The domestic use of showers, humidifiers, and cooking, washing up, laundering, etc. may lead to an additional increase of the radon concentration in the indoor air. The observed radon concentration in drinking water from three main cities of Shaanxi Province can contribute to a 4.86 to 32.63% increase in indoor radon concentration and can cause 0.0680.016mSvy–1 to 0.1770.045mSvy–1 extra annual effective dose to males, 0.0600.014mSvy–1 to 0.1550.039mSvy–1 to females. The mean annual effective dose equivalents to males and females of Xianyang and Baoji from well water account for 25.94 to 39.75% of environmental radon and radon daughters annual effective dose equivalents. The radon concentrations in the well water from Xianyang and Baoji will bring a definite additional risk to the population.
Measurements of indoor radon concentrations in the village Umhausen (2600 inhabitants, Ötztal valley, Tyrol, Austria) revealed unusually high indoor radon concentrations up to 274,000 Bq m−3. The medians measured on the basements were 3750 Bq m−3 in winter and 361 Bq m−3 in summer, those on the ground floors were 1180 Bq m−3 and 210 Bq m−3, respectively. Seventy-one per cent of the houses showed basement radon concentrations above the Austrian action level of 400 Bq m−3 in winter, 33% in summer. There are indications that the high radon concentrations are due to a giant rock slide about 8700 years ago. The unusually high radon concentrations in Umhausen coincide with a statistically significant increase in lung cancer mortality. For the period 1970–1991 the age and sex standardized mortality rate is 3.85 (95% confidence interval: 2.9 to 5.1). The control population is the total population of Tyrol (630,000 inhabitants).
Most members of the general public tend to regard their homes and the buildings in which they work as relatively safe havens from the physical and chemical stresses of the ambient environment. However, during recent decades a hazardous phenomenon concerning the built environment has become apparent: it can have a detrimental effect on occupants' health and has implications for energy usage. Radon gas is the culprit! It has no taste, smell or colour and its presence is therefore neither immediately apparent or readily detectable.
Active sub-slab depressurization (SSD) systems are an effective means of reducing indoor radon concentrations in residential buildings. However, energy is required to operate the system fan and to heat or cool the resulting increased building ventilation. We present regional and national estimates of the energy requirements, operating expenses and CO2 emissions associated with using SSD systems at saturation (i.e. in all US homes with radon concentrations above the EPA remediation guideline and either basement or slab-on-grade construction). The primary source of uncertainty in these estimates is the impact of the SSD system on house ventilation rate. Overall, individual SSD system operating expenses are highest in the Northeast and Midwest at about $99 y−1, and lowest in the South and West at about $66 y−1. The fan consumes, on average, about 40% of the end-use energy used to operate the SSD system and accounts for about 60% of the annual expense. At saturation, regional impacts are largest in the Midwest because this area has a large number of mitigable houses and a relatively high heating load. We estimate that operating SSD systems in US houses, where it is both appropriate and possible (about 2,6 million houses), will annually consume 1.7 × 104 (6.4 × 103 to 3.9 × 104) TJ of end-use energy, cost $230 (130 to 400) million (at current energy prices), and generate 2.0 × 109 (1.2 × 109 to 3.5 × 109) kg of CO2. Passive or energy efficient radon mitigation systems currently being developed offer opportunities to substantially reduce these impacts.
A population-based, case-control study of incident lung cancer among women in Missouri (United States) who were lifetime nonsmokers and long-term exsmokers was conducted between 1986 and 1992. The study included 538 lung cancer cases and 1183 population-based, age matched controls. Information on lung cancer risk factors was obtained by interviewing cases, next-of-kin of cases, and controls. Year-long radon measurements were also sought in every dwelling occupied for the previous 5–30 y. The Missouri study was among the first studies specifically-designed to evaluate the effects of residential radon on lung cancer risk. The mean radon level found in homes was 1.6 pCi/L. This level of radon exposure is somewhat higher than that observed in the United States as a whole (mean 1.25 pCi/L). A small nonsignificant risk was found for study subjects exposed to a median domestic radon concentration of 4 pCi/L (25 y time-weight average). Since only a small fraction of the population is exposed at this level, it is estimated that the population attributable risk (PAR) for domestic radon is between 1 and 4% in Missouri. The growing body of residential studies has not clearly shown an elevation in lung cancer risk due to low-level, long-term radon exposure. It may be difficult to demonstrate a statistically significant increase in risk due in part to the inherent methodologic difficulties associated with assessing the potential carcinogenic effect of low-level radon exposure, errors in reconstructing past radon exposures, and population mobility which tends to homogenize exposures. A complementary method of radon exposure measurement, now being used in a second epidemiologic evaluation of lung cancer in Missouri, which uses heirloom glass to assess actual historic cumulative dose, is discussed, and may help strengthen future studies.
The risk estimates for the general population extrapolated from the risk obtained from the miner studies leaded many national and international health organizations to estimate that residential exposure to radon and its decay products can be considered one of the main lung cancer risks after the tobacco smoking, which is responsible of a very large fraction of the total number of lung (and other) cancers. Due to this health relevance and to uncertainties in the extrapolation from studies on miners, many residential case-controls studies have been conducted in Europe, North America and China, are shortly reviewed in this paper. Most of these studies estimated an increased risk, proportional to the radon expo- sure, although a statistical significance of the estimated risk was reached only in few studies or restricted analyses, due to the low statistical power related to the relatively small study size and the presence of not negligible uncertainties in the evaluated radon exposure. The effects of these uncertainties were analyzed in some studies, and it was estimated to reduce the risk by 50% to 100%. Moreover, some restricted analyses showed that selecting subjects with a presumably better evaluation of radon exposure, for example with radon measurement covering all the exposure period of interest, the estimated risk increases by a factor of about two. The use of retrospective dosimetry compared with contemporary radon concentration measurements produce higher risks, too. In most of the studies a multiplicative interaction between tobacco smoking and radon is suggested, which implies that the lung cancer risk due to radon exposure is much higher for a smoker, compared with the risk for a never-smoker. More precise and definitive results are expected from pooled analysis. The just published pooled analyses of two Chinese studies and seven North American estimate a (slightly) significant excess odds ratio of 14% and 11% respectively. A more precise and comprehensive assessment is expected from the forthcoming results of the European pooling of 13 studies and the following pooling of all the studies. Other studies will be probably needed to answer some question on the risk for never-smokers and the interaction with passive smoking.
A case-referent study on the possible association between radon emanating from the ground and bronchial cancer was carried out on 292 female lung cancer cases and 584 matched population referents. Both groups had lived for at least 30 years in the city of Stockholm, Sweden. The cases were diagnosed during 1972 to 1980 with oat-cell and other types of anaplastic pulmonary carcinomas. A sample of about 10% of the dwellings where cases and referents had lived was selected for measurements of radon and radon daughters. There was a relative risk of 2.2 (P = 0.01) for lung cancer associated with living in dwellings close to the ground in areas with an increased risk of radon emanation. Smoking habits did not appear to be a major confounding factor for this association, although a detailed evaluation was not possible. The measurements indicated increased radon daughter concentrations in ground level dwellings within radon risk areas where lung cancer cases had lived, suggesting that this exposure was of etiologic importance.
Values of the radon and radon daughter concentration in different types of Norwegian dwellings are reported. The mean radon concentrations found were 1.3 pCi/l., 2.0 pCi/l. and 1.0 pCi/l. for buildings with outer walls of wood, concrete and brick, respectively. An equilibrium factor of 0.5 was found to be representative for the dwellings. The variations of the radon concentration due to ventilation and atmospheric pressure were investigated by continuous measurements with an ionization chamber inside a room with very poor ventilation and a room with strong artificial ventilation. A daily decrease of 1 mmHg was found to give an increase in the radon concentration of about 6% of the mean value. The population average dose to the bronchial epithelium from inhalation of radon's short-lived daughters was found to be about 220 mrad/yr in Norway.
Measurements of the indoor radon and radon daughter concentrations were performed in several thousand Swedish houses during the years 1979-1984 with the solid state nuclear track detector technique (SSNTD technique). The investigation focused on structures containing building materials of light-weight concrete with enhanced amounts of U. The detectors used nuclear track films exposed for 1 mo. The film basically measures total airborne alpha activity but may be calibrated in units of EER in an environment with known 222Rn and daughter concentrations. (EER is here the equilibrium equivalent concentration of Rn with the equilibrium factor F = 0.5.) The investigation was performed in various municipalities in collaboration with the local public health and environmental authorities. The investigation included 6700 individual measurements in detached (single-family) houses as well as in apartment houses. A small percentage of the dwellings exhibited Rn daughter concentrations (EER) exceeding 400 Bq m-3. It was found in detached houses that the concentrations were higher in the basement floor than in the entrance floor of a house. The Rn daughter values in the bedrooms were similar to values in any other room (mainly on the same floor) of the structure. The Rn daughter levels in apartment houses were lower than in single-family houses. The seasonal variations of the Rn daughter levels are presented and show that the levels in summertime are approximately equal to the levels in the winter.
Data on five mining populations exposed to Rn progeny have been used to estimate the lifetime risk of lung cancer resulting from occupational and environmental exposure under current standards. Slopes of dose-response relations for lung cancer show a tendency to decrease with increasing dose. Our best estimate of curvilinearity is given by raising dose to the power 0.92 +/- 0.07, but the improvement in fit beyond simple linearity is not significant. On the other hand, the addition of a cell-killing term significantly improves the fit of the linear model. In any event, linear extrapolation is unlikely to underestimate the excess risk at low doses by more than a factor of 1.5. However, these inferences about curvilinearity are highly subject to error from the choice of reference populations, dosimetry, and latency. Under the linear-cell-killing model, our best estimate of excess relative risk is 2.28 +/- 0.35 per 100 working level month (WLM) (a doubling dose of 44 WLM). Attributable risks in these five studies range from 3.4-17.8 per 10(6) person-yr WLM-1. Risks from Rn progeny appear to interact with age and smoking in a form intermediate between additive and multiplicative. The "relative risk" model is therefore preferable for projecting lifetime risks, but life-table projections are described for a wide variety of assumptions. Our best estimate of the effect of a 50-yr occupational exposure to 4 WLM yr-1 is 130 excess lung cancer deaths per 1000 persons (0.65 per 1000 person-WLM), with a range from 60-250 per 1000. Similar calculations for lifetime exposure to an additional 0.02 working level (WL) beyond normal background produces an estimate of 20 excess lung cancers per 1000 persons.
The National Institute for Occupational Safety and Health (NIOSH) has recently updated the vital status of the U.S. cohort of U miners through the end of 1982. This represents 69 additional lung cancer deaths since the last published follow-up through 1977. This more recent data was used to generate quantitative risk estimates of lung cancer after exposure to Rn daughters. Relative risks were estimated through use of the Cox proportional hazards model with an internal referent group. Results indicated that the exposure-response relationship was a slightly convex curve, predicting excess relative risks between 0.9 and 1.4 per 100 working level months (WLM) in the lower cumulative exposure range. Other findings of interest include a significant exposure-rate effect with low exposure rates more harmful per unit of cumulative exposure (WLM). Two temporal effects which modify relative risk estimates were also found. Relative risk increased with age at initial exposure to underground U mining. However, relative risk of lung cancer fell dramatically in the years following cessation of exposure.
A goal of analyses of occupational cohort data is the specification of how covariate information relates to age-specific disease risks. In describing this relationship, certain assumptions or models must be defined. For example, the usual standardized mortality ratio assumes a constant multiplicative increase in the age and calendar period disease rates of an exposed cohort over rates in a unexposed referent group. For analyzing several exposures, some of which may be continuous, such as cumulative dose, dose rate, duration of employment, and smoking patterns, or for analyzing complex associations between disease rate and covariates, flexible regression procedures are required. Using a crossclassification of the data and a Poisson probability model, relative risk regression methods are outlined. Breslow and Storer [1985], Guerrero and Johnson [1982], and Thomas [1981] propose general models for the relative risk as alternatives to, but which include, the usual exponential form. We review these models, discuss some limitations (in particular when there is more than one covariate) and present alternatives. Methods and models are illustrated by examining the joint effects of radon exposure and tobacco use on lung cancer mortality among a group of uranium miners.
The potential contribution to U.S. lung cancer deaths from 1930 to 1987 from indoor 222Rn exposures is investigated from the standpoint of a constant relative risk model. Based on this model, which assumes a Rn risk proportional to the baseline lung cancer risk from other causes, the rate of Rn-induced lung cancer mortality has been increasing sharply since 1930. However, the estimated proportion of lung cancer deaths attributable to Rn has remained fairly constant. Applying the range of coefficients the U.S. Environmental Protection Agency employs in assessing the risk from indoor Rn, it is estimated that 8-25% of all current lung cancer deaths are "attributable to" past Rn exposures. The major sources of uncertainty in the estimates are discussed.
Public concern was expressed regarding the possibility of adverse health effects with the disposal of radioactive waste in
Port Hope, Ontario. A case-control study was carried out to estimate the relative importance of domestic radon gas exposure
in the causation of lung cancer in the town over a ten-year period. Twenty-seven cases met the entry criteria. Statistical
analyses of results did not provide conclusive results that linked an increased risk of lung cancer and elevated domestic
alpha radiation levels, when all factors were considered. However, a very strong association was demonstrated between cigarette
smoking and lung cancer.
Sixteen counties in New York, Pennsylvania, and New Jersey that are associated with the Reading Prong granite deposits have significantly higher age-adjusted lung cancer rates among whites of both sexes (1950-1979) than do 17 nearby control counties. Elevated radon daughter concentrations have been found in homes near the Reading Prong granites. Fraction of populations living in cities with over 5,000 persons, industrial centers, cities with populations above 20,000, and median incomes did not differ significantly for three county groups (those which include the granite, fringe area, and control areas). Weaknesses were inadequate home measurements of radon and lack of smoking information. Findings are consistent with several other studies relating radon in homes to lung cancer.
The results of a pilot study on radon in Norwegian dwellings are presented together with a discussion on the feasibility of an epidemiological study on the correlation between lung cancer and radon progeny exposure in dwellings. There are large variations in the mean radon concentration in Norwegian municipalities, and the population average indoor radon concentration is high (80-100 Bq m-3). The large variations and high absolute values, together with excellent lung cancer and smoking habit data, make it feasible to conduct epidemiological studies based on representative exposure data in the Norwegian population.
A survey of 222Rn levels in 453 houses of physics professors from 101 universities in 42 states (plus the District of Columbia) was carried out with 1-y exposures of nuclear track detectors, accompanied by an extensive questionnaire. The geometric mean concentration was 38 Bq/m3 (1.03 pCi/l), the standard deviation was times divided by 2.36, and the arithmetic average was 54 Bq/m3 (1.47 pCi/l). Correlations were studied with age of the house, environs, location of the detector in the house, number of floors in the house, what is beneath the house, integrity of the barrier between the house and the ground, wind conditions, draftiness, construction materials, ventilation, use of gas, and source of water. In general, these correlations were found to be much weaker than expected, indicating that geographical variations are the dominating effect.
A survey of inhabitant exposures arising from the inhalation of 222Rn and 220Rn progeny, and lung cancer mortality has been carried out in two adjacent areas in Guangdong Province, People's Republic of China, designated as the "high background" and the "control" area. Annual exposure rates are 0.38 working level months (WLM) per year in the high background, and 0.16 WLM/yr in the control area. In 14 yr of continuous study, from 1970 to 1983, age-adjusted mortality rates were found to be 2.7 per 10(5) living persons of all ages in the high background area, and 2.9 per 10(5) living persons in the control area. From this data, we conclude that we are unable to determine excess lung cancers over the normal fluctuations below a cumulative exposure of 15 WLM. This conclusion is supported by lung cancer mortality data from Austrian and Finnish high-background areas. A theoretical analysis of epidemiological data on human lung cancer incidence from inhaled 222Rn and 220Rn progeny, which takes into account cell killing as competitive with malignant transformation, leads to the evaluation of a risk factor which is either a linear-exponential or a quadratic-exponential function of the alpha-particle dose. Animal lung cancer data and theoretical considerations can be supplied to support either hypothesis. Thus we conclude that at our current stage of knowledge both the linear-exponential and the quadratic-exponential extrapolation to low doses seem to be equally acceptable for Rn-induced lung cancer risk, possibly suggesting a linear-quadratic transformation function with an exponential cell-killing term, or the influence of risk-modifying factors such as repair or proliferation stimuli.
Apparently large exposures of the general public to the radioactive decay products of radon-222 present in indoor air have led to systematical appraisal of monitoring data from U.S. single-family homes; several ways of aggregating data were used that take into account differences in sample selection and season of measurements. The resulting distribution of annual-average radon-222 concentrations can be characterized by an arithmetic mean of 1.5 picocurie per liter (55 becquerels per cubic meter) and a long tail with 1 to 3% of homes exceeding 8 picocuries per liter, or by a geometric mean of 0.9 picocurie per liter and a geometric standard deviation of about 2.8. The standard deviation in the means is 15%, estimated from the number and variability of the available data sets, but the total uncertainty is larger because these data may not be representative. Available dose-response data suggest that an average of 1.5 picocuries per liter contributes about 0.3% lifetime risk of lung cancer and that, in the million homes with the highest concentrations, where annual exposures approximate or exceed those received by underground uranium miners, long-term occupants suffer an added lifetime risk of at least 2%, reaching extraordinary values at the highest concentrations observed.
This paper presents an evaluation of the inhalation and ingestion doses from exposure to Rn and Rn progeny; an overview of the human and animal health-effects data; estimations of the cancer risks from Rn and Rn-progeny exposures; and suggested limits for Rn concentrations in drinking water and indoor air. We suggest that a rounded Rn-in-water concentration limit of 10,000 pCi/l can be supported by health-effects considerations alone, based on the conservative "tolerance dose" concept and other conservative assumptions regarding lung dose. A practical concentration limit (or action level) of 20,000 pCi/l has been derived by estimations of exposure distributions in the United States and in relation to current U.S. Environmental Protection Agency (EPA) standards for U-tailings-contaminated buildings. Research needed for resolution of the uncertainties in these estimates is suggested. We conclude that before a maximum contaminant level (MCL) for Rn in water can be firmly established, the broader issue of setting the MCL for Rn in indoor air must be addressed.
The possible association between the geological nature of the soil, as related to radioactivity, and lung cancer occurrence has been explored in an Italian province. Lung cancer mortality rates for the period '69-'78, in population 35-74 years old, have been calculated for two areas with different lithological features and radioactivity levels. Direct standardization has been used to take into account possible confounding factors such as age, degree of urbanization and cigarette sales. The area with high background radioactivity levels has higher lung cancer mortality rates in both sexes but the results are not statistically significant.
Solid state nuclear track detectors were used in a regional survey of radon in indoor air. The study area comprises seven rural municipalities and two towns in an area of 80 X 50 km2 with a population of about 65,000. Measurements were made in 754 houses in 31 subareas. The highest and lowest subarea means were 1,200 Bq/m3 and 95 Bq/m3, respectively. The estimated mean for the whole area was 370 Bq/m3. The concentrations 2,000 Bq/m3 and 800 Bq/m3 were exceeded in 32 and 90 houses, respectively. The present lung cancer incidence does not differ significantly from the national mean.
A sandlike residue from uranium mills widely used as construction fill material since 1951 in Western Slope counties of Colorado was recently reported to be carcinogenic. We studied county-specific mortality statistics for cancer in Colorado through 1967 and found no trends attributable to this residential exposure to radiation. Continued monitoring of the population for radiation effects is needed.
In a retrospective study, we investigated lung-cancer mortality from 1951 to 1976 in 1415 Swedish iron miners exposed to short-lived radioactive daughters of radon gas at concentrations leading to annual doses close to the currently accepted occupational limit. Fifty deaths from lung cancer were observed, as compared with 12.8 expected; expected rates were determined by a smoking-specific analysis based on data from a random sample of the Swedish male population. Among nonsmokers 18 deaths were observed, as compared with 1.8 expected; among current smokers and recent exsmokers 32 deaths were observed and 11.0 were expected. The effects of smoking and exposure to alpha radiation from radon daughters were nearly additive. Comparison of lung-cancer risk coefficients from this study and from other cohort studies of underground miners showed good agreement. Exposure to radon daughters is a major medical problem is underground metal mining, but our results also indicate that exposure to radon daughters at home accounts for an appreciable number of cases of lung cancer in the general population.
The expectation of elevated 222Rn levels in modern homes that have low air interchange rates with the out-of-doors caused us to survey both solar and conventional homes in northeastern New York State. The solar homes as a group have three times the 222Rn levels of the conventional homes, and specific problems exist that are introduced or exaggerated by modern construction. For example the highest two levels of radon in the solar homes give radiation doses over 30 yr that are known to produce lung cancer in 1% of uranium miners. Summer readings in more than half of the cases are different from winter ones by a factor of two or more, so that year-round measurements are necessary for precise dosimetry. The track etching technique is ideally suited for such measurements.
The distribution of 222Rn has been measured in the sixteen counties of Maine, U.S.A. by liquid scintillation counting of water samples from more than two thousand public and private wells. Three hundred and fifty of these wells have been characterized for geology and hydrology. Airborne radon has been measured in seventy houses with grab samples and in eighteen houses for 5-7 days each with continuously recording diffusion-electrostatic radon detectors. Concentrations of radon in water ranged from 20 to 180,000 pCi/l. Granite areas yielded the highest average levels (mean = 22,100 pCi/l.; n = 136), with considerable intra-granite variation. Metasedimentary rocks yielded levels characteristic of the lithology for metamorphic grades ranging from chlorite to andalusite. Sillimanite and higher-grade rocks yielded higher 222Rn levels, probably due to the intrusion of uranium-bearing pegmatites in these terranes. Airborne 222Rn in homes ranged from 0.05 to 210 pCi/l. At the high end of this range, doses will exceed recommended industrial limits. In some homes only a small fraction of the airborne 222Rn was due to the water supply. Average 222Rn levels in domestic water supplies for each of the 16 counties, calculated by areally averaging rock types and their associated 222Rn levels, were found to be significantly correlated with rates for all cancers combined and rates for lung and reproductive cancers in the counties. Although numerous factors other than cancer induction by indoor daughter exposures may be responsible for the observed correlations, these have not been investigated in detail.
The effects of low-dose radiation have been a matter of controversy over the years, and the epidemiologic results have been conflicting. A couple of recent studies have indicated a possible impact on lung cancer mortality from exposure to indoor levels of radon and radon daughters. In this study, selected mortality rates, ie, lung cancer, pancreatic cancer, breast cancer (females only), leukemia, and multiple myeloma were correlated for the counties of Sweden with estimates of average background radiation exposure in these areas. Significant correlations were obtained for lung cancer (males, r = 0.46; females r = 0.55) and pancreatic cancer (males, r = 0.59; females, r = 0.40) , and there was a borderline correlation (r = 0.36; p = 0.04) for leukemia in males. In all, there were positive correlations for eight out of the nine computations made. Since background radiation correlates with urbanization and therefore with smoking, air pollution, etc, the correlations might be spurious due to confounding; on the other hand confounding is a reciprocal phenomenon which suggests that background radiation should to be taken into consideration when widespread risk factors like smoking, coffee drinking, general air pollution, etc, are studied.
Iowa towns of 1000-10,000 population, whose water came solely from wells of over 500 feet (152 meters) in depth and was not treated by a process that would remove radioactivity, were identified. Age-adjusted, sex-specific, cancer incidence rates were determined for these towns for the years 1969-1978 (excluding 1972) and related to the mean level of radium-226 in the municipal water supply. Incidence rates of cancers of the lung and bladder among males and of cancers of the breast and lung among females were higher in towns with a radium-226 level in the water supply exceeding 5.0 pCi/l. A gradient of increasing cancer incidence associated with rising radioactivity level for three time periods was also seen for lung cancer among males. The associations between cancer incidence and radioactivity of water supply could not be explained by smoking patterns, water treatment factors, other water quality measurements, or known socio-demographic features.
Confidence intervals for the attributable risk in various epidemiologic study designs are obtained, via a transformation, from the confidence interval for the natural logarithm of the product of the probability of being exposed to the risk factor, and the risk ratio minus one. When the estimated attributable risk is between .21 and .79, the width of the logarithmic transformation (LT)-based interval is less than that for a maximum likelihood (ML)-based interval. This simple sufficient condition applies to all three well-known epidemiologic study designs. Computer simulation results further demonstrate the superiority of the LT-based interval to the ML-based one when the sufficient condition is satisfied.
Phosphate mining is a major industry (52 x 109kg in the U.S. in 1977) and the deposits plus their mining and milling involve large amounts of uranium, radium and radon and associated radiochemical pollution, including the release of 222Rn (Ro73). The amount of uranium contained in the processed phosphate rock is approximately equal to that mined as uranium ore. The data presented in this paper raise the possibility that phosphate mining and processing lead to increased lung cancer. Clearly it is possible that other, presently unrecognized factors are responsible for the observed excess of coincidences between sites where phosphates are mined and processed and where lung cancer is high. If a cause and effect relationship exists, then unworked phosphate deposits are not hazards, but the processing of phosphates can be. The fact that the correlations are generally similar for men and women and the existence of the coincidences in counties adjacent to those with phosphate mills both raise the possibility that relatively widespread environmental problems are more probable than localized occupational ones. Some epidemiological possibilities are discussed.