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1.
Radon is the second leading cause of lung cancer after smoking. Since the previous quantitative risk assessment of indoor radon conducted in France, input data have changed such as, estimates of indoor radon concentrations, lung cancer rates and the prevalence of tobacco consumption. The aim of this work was to update the risk assessment of lung cancer mortality attributable to indoor radon in France using recent risk models and data, improving the consideration of smoking, and providing results at a fine geographical scale. The data used were population data (2012), vital statistics on death from lung cancer (2008–2012), domestic radon exposure from a recent database that combines measurement results of indoor radon concentration and the geogenic radon potential map for France (2015), and smoking prevalence (2010). The risk model used was derived from a European epidemiological study, considering that lung cancer risk increased by 16% per 100 becquerels per cubic meter (Bq/m3) indoor radon concentration. The estimated number of lung cancer deaths attributable to indoor radon exposure is about 3000 (1000; 5000), which corresponds to about 10% of all lung cancer deaths each year in France. About 33% of lung cancer deaths attributable to radon are due to exposure levels above 100 Bq/m3. Considering the combined effect of tobacco and radon, the study shows that 75% of estimated radon-attributable lung cancer deaths occur among current smokers, 20% among ex-smokers and 5% among never-smokers. It is concluded that the results of this study, which are based on precise estimates of indoor radon concentrations at finest geographical scale, can serve as a basis for defining French policy against radon risk.  相似文献   

2.
This study is a comprehensive analysis of the latest follow-up of the Colorado uranium miners cohort using the two-stage clonal expansion model with particular emphasis on effects related to age and exposure. The model provides a framework in which the hazard function for lung cancer mortality incorporates detailed information on exposure to radon and radon progeny from hard rock and uranium mining together with information on cigarette smoking. Even though the effect of smoking on lung cancer risk is explicitly modeled, a significant birth cohort effect is found which shows a linear increase in the baseline lung cancer risk with birth year of the miners in the cohort. The analysis based on the two-stage clonal expansion model suggests that exposure to radon affects both the rate of initiation of intermediate cells in the pathway to cancer and the rate of proliferation of intermediate cells. However, in contrast to the promotional effect of radon, which is highly significant, the effect of radon on the rate of initiation is found to be not significant. The model is also used to study the inverse dose-rate effect. This effect is evident for radon exposures typical for mines but is predicted to be attenuated, and for longer exposures even reversed, for the more protracted and lower radon exposures in homes. The model also predicts the drop in risk with time after exposure ceases. For residential exposures, lung cancer risks are compared with the estimates from the BEIR VI report. While the risk estimates are in agreement with those derived from residential studies, they are about two- to fourfold lower than those reported in the BEIR VI report.  相似文献   

3.
Summary 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.  相似文献   

4.
A two-mutation carcinogenesis model was used to calculate the expected lung cancer incidence caused by both smoking and exposure to radon in two populations, i.e. those of the Netherlands and Sweden. The model parameters were taken from a previous analysis of lung cancer in smokers and uranium miners and the model was applied to the two populations taking into account the smoking habits and exposure to radon. For both countries, the smoking histories and indoor radon exposure data for the period 1910-1995 were reconstructed and used in the calculations. Compared with the number of lung cancer cases observed in 1995 among both males and females in the two countries, the calculations show that between 72% and 94% of the registered lung cancer cases may be attributable to the combined effects of radon and smoking. In the Netherlands, a portion of about 4% and in Sweden, a portion of about 20% of the lung cancer cases (at ages 0-80 years) may be attributable to radon exposure, the numbers for males being slightly lower than for females. In the Netherlands, the proportions of lung cancers attributable to smoking are 91% for males and 71% for females; in Sweden, the figures are 70% and 56%, respectively. The risk from radon exposure is dependent on gender and cigarette smoking: the excess absolute risk for continuous exposure to 100 Bq m-3 ranges between 0.003 and 0.006 and compares well with current estimates, e.g. 0.0043 of the International Commission on Radiological Protection (ICRP). The excess relative risk for continuous exposure to 100 Bq m-3 shows a larger variation, ranging generally between 0.1 for smokers and 1.0 for non-smokers. The results support the assumption that exposure to (indoor) radon, even at a level as low as background radiation, causes lung cancer proportional to the dose and is consistent with risk factors derived from the miners data.  相似文献   

5.
Radon is recognized as a public health concern for indoor exposure. Precise quantification derived from occupational exposure in miners is still needed for estimating the risk and the factors that modify the dependence on cumulated exposure. The present paper reports on relationship between radon exposure and lung cancer risk in French and Czech cohorts of uranium miners (n = 10,100). Miners from these two cohorts are characterized by low levels of exposure (average cumulated exposure of less than 60 WLM) protracted over a long period (mean duration of exposure of 10 years) and by a good quality of individual exposure estimates (95% of annual exposures based on radon measurements). The modifying effect of the quality of exposure on the risk is analyzed. A total of 574 lung cancer deaths were observed, which is 187% higher than expected from the national statistics. This significantly elevated risk is strongly associated with cumulated radon exposure. The estimated overall excess relative risk per WLM is 0.027 (95% CI: 0.017-0.043, related to measured exposures). For age at exposure of 30 and 20 years since exposure, the ERR/WLM is 0.042, and this value decreases by approximately 50% for each 10-year increase in age at exposure and time since exposure. The present study emphasizes that the quality of exposure estimates is an important factor that may substantially influence results. Time since exposure and simultaneously age at exposure were the most important effect modifiers. No inverse exposure-rate effect below 4 WL was observed. The results are consistent with estimates of the BEIR VI report using the concentration model at an exposure rate below 0.5 WL.  相似文献   

6.
7.
Radon is a ubiquitous natural carcinogen derived from the three primordial radionuclides of the uranium series (238U and 235U) and thorium series (232Th). In general, it is present at very low concentrations in the outdoor or indoor environment, but a number of scenarios can give rise to significant radiological exposures. Historically, these scenarios were not recognised, and took many centuries to understand the links between the complex behaviour of radon and progeny decay and health risks such as lung cancer. However, in concert with the rapid evolution in the related sciences of nuclear physics and radiological health in the first half of the twentieth century, a more comprehensive understanding of the links between radon, its progeny and health impacts such as lung cancer has evolved. It is clear from uranium miner studies that acute occupational exposures lead to significant increases in cancer risk, but chronic or sub-chronic exposures, such as indoor residential settings, while suggestive of health risks, still entails various uncertainties. At present, prominent groups such as the BEIR or UNSCEAR committees argue that the ‘linear no threshold’ (LNT) model is the most appropriate model for radiation exposure management, based on their detailed review and analysis of uranium miner, residential, cellular or molecular studies. The LNT model implies that any additional or excess exposure to radon and progeny increases overall risks such as lung cancer. A variety of engineering approaches are available to address radon exposure problems. Where high radon scenarios are encountered, such as uranium mining, the most cost effective approach is well-engineered ventilation systems. For residential radon problems, various options can be assessed, including building design and passive or active ventilation systems. This paper presents a very broad but thorough review of radon sources, its behaviour (especially the importance of its radioactive decay progeny), common mining and non-mining scenarios which can give rise to significant radon and progeny exposures, followed by a review of associated health impacts, culminating in typical engineering approaches to reduce exposures and rehabilitate wastes.  相似文献   

8.
In order to evaluate the effect of indoor exposure to radon and thoron on the development of lung cancer in the population of two towns of Sverdlovsk Region, epidemiologic studies were conducted using a multifactarial method of analysis. Both towns, Pervouralsk and Karpinsk, are located within the geological area with the gamma-radiation exposure dose ranging from 5 to 12 mu r/hr, and are characterized by an increased cancer incidence rate--323.1 and 364.6 cases per 100,000 of population, respectively. The mean values of the voluminous indoor activity (VA) of radon in Pervouralsk and Karpinsk were 23 and 75 Bq/m3 (with maximal indices of radon VA being 395 and 739 Bq/m3), equivalent equilibrium concentrations (EEC) of residential radon and thoron were 0.6 and 2.5 Bq/m3 (maximal indices of EEC of thoron being 5 and 13 Bq/m3), respectively. The results of multifactorial analysis of 22 different lung cancer risk factors carried out using the pattern recognition method proved that the contribution of thoron and radon in the development of lung cancer in the population of Pervouralsk and Karpinsk was not significant--0.5 and 0.6%, respectively. The calculations performed in a monofactorial model of risk evaluation BEIR VI gave different results--11-16% and 35-52% for the towns of Pervouralsk and Karpinsk, respectively. The discussion of the results provides arguments for the reliability and adequacy of the application of multifactorial method of radiation risk evaluation as compared to the traditionally applied monofactorial method.  相似文献   

9.
10.

This study aimed to estimate (1) the number of avoidable lung cancer cases attributable to residential radon in Finland in 2017, separately by age, sex, dwelling type and smoking status, (2) the impact of residential radon alone and the joint effect of residential radon and smoking on the number of lung cancers and (3) the potential decrease in the number of radon-attributable lung cancers if radon concentrations exceeding specified action levels (100, 200 and 300 Bq m?3) would have been mitigated to those levels. Population-based surveys of radon concentrations and smoking patterns were used. Observed radon levels were contrasted with 25 Bq m?3 representing a realistic minimum level of exposure. Lung cancer risk estimates for radon and smoking were derived from literature. Lastly, the uncertainty due to the estimation of exposure and risk was quantified using a computationally derived uncertainty interval. At least 3% and at most 8% of all lung cancers were estimated as being attributable to residential radon. For small cell carcinoma, the proportion of cases attributable to radon was 8–13%. Among smokers, the majority of the radon-related cases were attributable to the joint effect of radon and smoking. Reduction of radon exposure to 100 Bq m?3 action level would eliminate approximately 30% of radon-attributable cases. Estimates were low compared with the literature, given the (relatively high) radon levels in Finland. This was mainly due to the lower radon levels and higher smoking prevalence in flats than in houses and a more realistic point of comparison, factors which have been ignored in previous studies. The results can guide actions in radon protection and in prevention of lung cancers.

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11.
12.
BackgroundThe objective of this study is to estimate the gap between smoking prevalence and lung cancer mortality and provide predictions of lung cancer mortality based on previous smoking prevalence.Materials and methodsWe used data from the Spanish National Health Surveys (2003, 2006 and 2011) to obtain information about tobacco use and data from the Spanish National Statistics Institute to obtain cancer mortality rates from 1980 to 2013. We calculated the cross-correlation among the historical series of smoking prevalence and lung cancer mortality rate (LCMR) to estimate the most likely time gap between both series. We also predicted the magnitude and timing of the LCMR peak.ResultsAll cross-correlations were statistically significant and positive (all above 0.8). For men, the most likely gap ranges from 20 to 34 years. The age-adjusted LCMR increased by 3.2 deaths per 100,000 people for every 1 unit increase in the smoking prevalence 29 years earlier. The highest rate for men was observed in 1995 (55.6 deaths). For women, the most likely gap ranges from 10 to 37 years. The age-adjusted LCMR increased by 0.28 deaths per 100,000 people for every 1 unit increase in the smoking prevalence 32 years earlier. The maximum rate is expected to occur in 2026 (10.3 deaths).ConclusionThe time series of prevalence of tobacco smoking explains the mortality from lung cancer with a distance (or gap) of around 30 years. According to the lagged smoking prevalence, the lung cancer mortality among men is declining while in women continues to rise (maximum expected in 2026).  相似文献   

13.
A combined analysis of three case-control studies nested in three European uranium miner cohorts was performed to study the joint effects of radon exposure and smoking on lung cancer death risk. Occupational history and exposure data were available from the cohorts. Smoking information was reconstructed using self-administered questionnaires and occupational medical archives. Linear excess relative risk models adjusted for smoking were used to estimate the lung cancer risk associated with radon exposure. The study includes 1046 lung cancer cases and 2492 controls with detailed radon exposure data and smoking status. The ERR/WLM adjusted for smoking is equal to 0.008 (95% CI: 0.004-0.014). Time since exposure is shown to be a major modifier of the relationship between radon exposure and lung cancer risk. Fitting geometric mixture models yielded arguments in favor of a sub-multiplicative interaction between radon and smoking. This combined study is the largest case-control study to investigate the joint effects of radon and smoking on lung cancer risk among miners. The results confirm that the lung carcinogenic effect of radon persists even when smoking is adjusted for, with arguments in favor of a sub-multiplicative interaction between radon and smoking.  相似文献   

14.
Relation between the risk of lung cancer and combined home and work indoor radon exposure was studied on the example of the population of Lermontov town (Stavropol Region, Russia). The town is situated in the former uranium mining area. Case (121 lung cancer cases) and control (196 individuals free of lung cancer diagnosis) groups of the study included both ex-miners and individuals that were not involved in the uranium industry. Home and work radon exposures were estimated using archive data as well as contemporary indoor measurements. The results of our study support the conclusion about the effect of radon exposure on the lung cancer morbidity.  相似文献   

15.
D T Wigle  N E Collishaw  J Kirkbride  Y Mao 《CMAJ》1987,136(9):945-951
Recently published evidence indicates that involuntary smoking causes an increased risk of lung cancer among nonsmokers. Information was compiled on the proportion of people who had never smoked among victims of lung cancer, the risk of lung cancer for nonsmokers married to smokers and the prevalence of such exposure. On the basis of these data we estimate that 50 to 60 of the deaths from lung cancer in Canada in 1985 among people who had never smoked were caused by spousal smoking; about 90% occurred in women. The total number of deaths from lung cancer attributable to exposure to tobacco smoke from spouses and other sources (mainly the workplace) was derived by applying estimated age- and sex-specific rates of death from lung cancer attributable to such exposure to the population of Canadians who have never smoked; about 330 deaths from lung cancer annually are attributable to such exposure.  相似文献   

16.
Radon is ubiquitous in indoor environments. Epidemiologic studies of underground miners with exposure to radon and experimental evidence have established that radon causes lung cancer. The finding that this naturally occurring carcinogen is present in the air of homes and other buildings has raised concern about the lung cancer risk to the general population from radon. I review current approaches for assessing the risk of indoor radon, emphasizing the extrapolation of the risks for miners to the general population. Although uncertainties are inherent in this risk assessment, the present evidence warrants identifying homes that have unacceptably high concentrations.  相似文献   

17.

Background

Tobacco smoking is a major risk factor for many diseases. We sought to quantify the burden of tobacco-smoking-related deaths in Asia, in parts of which men''s smoking prevalence is among the world''s highest.

Methods and Findings

We performed pooled analyses of data from 1,049,929 participants in 21 cohorts in Asia to quantify the risks of total and cause-specific mortality associated with tobacco smoking using adjusted hazard ratios and their 95% confidence intervals. We then estimated smoking-related deaths among adults aged ≥45 y in 2004 in Bangladesh, India, mainland China, Japan, Republic of Korea, Singapore, and Taiwan—accounting for ∼71% of Asia''s total population. An approximately 1.44-fold (95% CI = 1.37–1.51) and 1.48-fold (1.38–1.58) elevated risk of death from any cause was found in male and female ever-smokers, respectively. In 2004, active tobacco smoking accounted for approximately 15.8% (95% CI = 14.3%–17.2%) and 3.3% (2.6%–4.0%) of deaths, respectively, in men and women aged ≥45 y in the seven countries/regions combined, with a total number of estimated deaths of ∼1,575,500 (95% CI = 1,398,000–1,744,700). Among men, approximately 11.4%, 30.5%, and 19.8% of deaths due to cardiovascular diseases, cancer, and respiratory diseases, respectively, were attributable to tobacco smoking. Corresponding proportions for East Asian women were 3.7%, 4.6%, and 1.7%, respectively. The strongest association with tobacco smoking was found for lung cancer: a 3- to 4-fold elevated risk, accounting for 60.5% and 16.7% of lung cancer deaths, respectively, in Asian men and East Asian women aged ≥45 y.

Conclusions

Tobacco smoking is associated with a substantially elevated risk of mortality, accounting for approximately 2 million deaths in adults aged ≥45 y throughout Asia in 2004. It is likely that smoking-related deaths in Asia will continue to rise over the next few decades if no effective smoking control programs are implemented. Please see later in the article for the Editors'' Summary  相似文献   

18.
Putila JJ  Guo NL 《PloS one》2011,6(10):e25886

Background

Although strong exposure to arsenic has been shown to be carcinogenic, its contribution to lung cancer incidence in the United States is not well characterized. We sought to determine if the low-level exposures to arsenic seen in the U.S. are associated with lung cancer incidence after controlling for possible confounders, and to assess the interaction with smoking behavior.

Methodology

Measurements of arsenic stream sediment and soil concentration obtained from the USGS National Geochemical Survey were combined, respectively, with 2008 BRFSS estimates on smoking prevalence and 2000 U.S. Census county level income to determine the effects of these factors on lung cancer incidence, as estimated from respective state-wide cancer registries and the SEER database. Poisson regression was used to determine the association between each variable and age-adjusted county-level lung cancer incidence. ANOVA was used to assess interaction effects between covariates.

Principal Findings

Sediment levels of arsenic were significantly associated with an increase in incident cases of lung cancer (P<0.0001). These effects persisted after controlling for smoking and income (P<0.0001). Across the U.S., exposure to arsenic may contribute to up to 5,297 lung cancer cases per year. There was also a significant interaction between arsenic exposure levels and smoking prevalence (P<0.05).

Conclusions/Significance

Arsenic was significantly associated with lung cancer incidence rates in the U.S. after controlling for smoking and income, indicating that low-level exposure to arsenic is responsible for excess cancer cases in many parts of the U.S. Elevated county smoking prevalence strengthened the association between arsenic exposure and lung cancer incidence rate, an effect previously unseen on a population level.  相似文献   

19.
Summary Whereas lung cancer mortality surveys in French departments obviously demonstrate the effect of smoking or of living in strongly industrialized areas, the same survey does not give evidence of lung cancer deaths increases in the departments where the radon concentrations in dwellings are the highest.  相似文献   

20.
BackgroundLifestyle risk factors (tobacco smoking, alcohol consumption, overweight and obesity, unhealthy diet, and lack of physical activity) have been associated with increased risk of at least 20 types of cancer. We estimated the proportion of cancer cases and deaths that could be potentially avoided by eliminating or reducing lifestyle risk factors in Brazil.MethodsWe obtained the distribution of lifestyle risk factors by sex and age groups from recent representative health surveys in Brazil; relative risks from pooled analyses of prospective studies and meta-analyses; and cancer cases and deaths in 2012 from GLOBOCAN.ResultsWe found that 26.5% (114,497 cases) of all cancer cases and 33.6% (63,371 deaths) of all cancer deaths could be potentially avoided by eliminating lifestyle risk factors in Brazil. Plausible reductions in these exposures based on policy targets and cancer prevention recommendations could have potentially avoided 4.5% (19,731 cases) and 6.1% (11,480 deaths) of all cancer cases and deaths, respectively. Tobacco smoking accounted for most of the preventable cancer cases and deaths, followed by high body mass index and alcohol consumption. Larynx, lung, oropharynx, esophagus and colorectum cancer cases and deaths could be at least halved by eliminating these lifestyle risk factors.ConclusionFindings from this study may be useful to inform strategies for cancer prevention and control across Brazil.  相似文献   

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