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The fluorspar mines of Newfoundland : their history and the epidemic of radiation lung cancer
John Martin tells the history of Newfoundland's fluorspar mines from their founding to the last shipment of fluorspar in 1990 and declaration of bankruptcy a year later. He focuses on the health hazards experienced by the miners, and how the mining companies, workers, governments, and health services came to terms with the unfolding human tragedy. He also covers such matters as the improvement of methods for dust quantification and radiation surveillance in the mines, battles for compensation, and the influence of the St Lawrence case on the development of labour law in the province.
Book
Global Estimate of Lung Cancer Mortality Attributable to Residential Radon
Radon is the second most important cause of lung cancer, ranked by the World Health Organization as the fifth leading cause of mortality in 2010. An updated database of national radon exposures for 66 countries allows the global burden of lung cancer mortality attributable to radon to be estimated.
Our goal was to estimate the global population attributable burden of lung cancer mortality in 2012 from residential radon.
Estimates of the population attributable risk (PAR) of lung cancer mortality from radon were determined using the attributable fraction approach, using three models for excess relative risk of lung cancer from radon.
The estimates of the median PAR of lung cancer mortality from residential radon in 2012 for the 66 countries having representative national radon surveys were consistent, as 16.5%, 14.4%, and 13.6% for the exposure-age-concentration (EAC) model (BEIR VI), the Hunter model, and the Kreuzer model, respectively. The mean PAR using the EAC model ranged from 4.2% (95% CI: 0.9, 11.7) for Japan, to 29.3% (95% CI: 22.9, 35.7) for Armenia, with a median for the 66 countries of 16.5%. Radon-attributable lung cancer deaths for all 66 countries totaled 226,057 in 2012 and represent a median of 3.0% of total cancer deaths.
Consistent findings between the three models used to estimate excess relative risks of lung cancer from radon, and between the attributable fraction methodology and the life table analysis, confirm that residential radon is responsible for a substantial proportion of lung cancer mortality worldwide. https://doi.org/10.1289/EHP2503.
Journal Article
Experimental Setups for In Vitro Studies on Radon Exposure in Mammalian Cells—A Critical Overview
Naturally occurring radon and its short lived progeny are the second leading cause of lung cancer after smoking, and the main risk factor for non-smokers. The radon progeny, mainly Polonium-218 (218Po) and Polonium-214 (214Po), are responsible for the highest dose deposition in the bronchial epithelium via alpha-decay. These alpha-particles release a large amount of energy over a short penetration range, which results in severe and complex DNA damage. In order to unravel the underlying biological mechanisms which are triggered by this complex DNA damage and eventually give rise to carcinogenesis, in vitro radiobiology experiments on mammalian cells have been performed using radon exposure setups, or radon analogues, which mimic alpha-particle exposure. This review provides an overview of the different experimental setups, which have been developed and used over the past decades for in vitro radon experiments. In order to guarantee reliable results, the design and dosimetry of these setups require careful consideration, which will be emphasized in this work. Results of these in vitro experiments, particularly on bronchial epithelial cells, can provide valuable information on biomarkers, which can assist to identify exposures, as well as to study the effects of localized high dose depositions and the heterogeneous dose distribution of radon.
Journal Article
Human Health Impacts of Residential Radon Exposure: Updated Systematic Review and Meta-Analysis of Case–Control Studies
This study investigated the impact of residential radon exposure on human cancers (i.e., lung cancer and childhood leukemia) through a systematic review and meta-analysis of case–control studies. A total of 9724 articles obtained from electronic databases were assessed; however, only 55 case–control studies were eligible after manually screening and eliminating unnecessary studies. The causal associations were addressed by determining the meta-analysis’s estimated size effects (i.e., ORs/RRs) of the meta-analysis. Residential radon was revealed to significantly increase the incidence of lung cancer and childhood leukemia with pooled ORs of 1.38 [1.19; 1.60] (I2 = 90%; p < 0.00001) and 1.43 [1.19; 1.72] (I2 = 0% and p = 0.51), respectively. In addition, subgroup analyses were performed to reduce the heterogeneity of the initial meta-analyses. The results provided strong evidence that inhaling radon in the indoor environments is closely associated with the development of lung cancer and childhood leukemia in patients living in Europe and areas with high radon levels (≥100 Bq/m3).
Journal Article
Radon in homes and risk of lung cancer: collaborative analysis of individual data from 13 European case-control studies
Abstract Objective To determine the risk of lung cancer associated with exposure at home to the radioactive disintegration products of naturally occurring radon gas Design Collaborative analysis of individual data from 13 case-control studies of residential radon and lung cancer. Setting Nine European countries. Subjects 7148 cases of lung cancer and 14 208 controls. Main outcome measures Relative risks of lung cancer and radon gas concentrations in homes inhabited during the previous 5-34 years measured in becquerels (radon disintegrations per second) per cubic metre (Bq/m3) of household air. Results The mean measured radon concentration in homes of people in the control group was 97 Bq/m3, with 11% measuring > 200 and 4% measuring > 400 Bq/m3. For cases of lung cancer the mean concentration was 104 Bq/m3. The risk of lung cancer increased by 8.4% (95% confidence interval 3.0% to 15.8%) per 100 Bq/m3 increase in measured radon (P = 0.0007). This corresponds to an increase of 16% (5% to 31%) per 100 Bq/m3 increase in usual radon—that is, after correction for the dilution caused by random uncertainties in measuring radon concentrations. The dose-response relation seemed to be linear with no threshold and remained significant (P = 0.04) in analyses limited to individuals from homes with measured radon < 200 Bq/m3. The proportionate excess risk did not differ significantly with study, age, sex, or smoking. In the absence of other causes of death, the absolute risks of lung cancer by age 75 years at usual radon concentrations of 0, 100, and 400 Bq/m3 would be about 0.4%, 0.5%, and 0.7%, respectively, for lifelong non-smokers, and about 25 times greater (10%, 12%, and 16%) for cigarette smokers. Conclusions Collectively, though not separately, these studies show appreciable hazards from residential radon, particularly for smokers and recent ex-smokers, and indicate that it is responsible for about 2% of all deaths from cancer in Europe.
Journal Article
Chronic radon exposure is associated with developmental alterations to neural and behavioral indices of cognitive control
•Environmental exposures have been linked to neurocognitive dysfunction.•Home radon exposure’s impact on cognitive function has not been well characterized.•We examined links between radon exposure and dynamics of cognitive control in youth.•Youths with greater exposure showed aberrant oscillations with attentional control.•Radon exposure modulated expected neural and behavioral developmental trajectories.
Radon is a prevalent, naturally occurring gas which contributes to radiation within the environment and is the second-leading cause of lung cancer worldwide. Although many environmental toxins have been linked to maladaptive neurodevelopmental outcomes in children and adolescents, radon has seldom been examined for its effects on the developing brain. This study aimed to investigate the effects of chronic home radon exposure on top-down neural processes of cognitive control in youths. Fifty-nine participants (aged 6–14 years) completed a Simon interference task during magnetoencephalography (MEG), and radon levels were measured in their homes. MEG data were transformed into time-frequency space and significant oscillatory responses relative to baseline were imaged condition-wise and then subtracted to isolate the Simon interference effect (i.e., Simon-control). Whole-brain linear regressions indicated that children with greater radon exposure exhibited aberrant oscillatory activity in widespread networks related to attentional control. We also found that radon exposure moderated the developmental trajectory of theta and gamma oscillations underlying selective attention in frontoparietal cortices and other regions. Further, mediation analyses showed that the neural interference effects within cerebellar and extended motor cortices mediated the relationship between radon exposure and behavioral outcomes. Additionally, we found the mediating effects of neural interference within the left superior frontal gyrus and precuneus on the relationship between age and task accuracy were dependent on radon exposure. These data are among the first to demonstrate radon-related disruptions to the normative development of the neural substrates supporting cognitive control processes. Further, these disruptions have direct implications on observable behavior.
Journal Article
A Novel Strategy for the Assessment of Radon Risk Based on Indicators
Among the physical pollutants affecting indoor air, the radioactive gas radon may turn out to be the most hazardous. Health effects related to radon exposure have been investigated for several decades, providing major scientific evidence to conclude that chronic exposures can cause lung cancer. Additionally, an association with other diseases, such as leukemia and cancers of the extra-thoracic airways, has been advanced. The implementation of a strategy to reduce the exposure of the population and minimize the health risk, according to the European Directive 59/2013/Euratom on ionizing radiations, is a new challenge in public health management. Starting from an understanding of the general state-of-the-art, a critical analysis of existing approaches has been conducted, identifying strengths and weaknesses. Then, a strategy for assessing the radon exposure of the general population, in a new comprehensive way, is proposed. It identifies three main areas of intervention and provides a list of hazard indicators and operative solutions to control human exposure. The strategy has been conceived to provide a supporting tool to authorities in the introduction of effective measures to assess population health risks due to radon exposure.
Journal Article
Environmental/Occupational Exposure to Radon and Non-Pulmonary Neoplasm Risk: A Review of Epidemiologic Evidence
Although Radon (Rn) is a known agent for lung cancer, the link between Rn exposure and other non-pulmonary neoplasms remains unclear. The aim of this review is to investigate the role of Rn in the development of tumors other than lung cancer in both occupational and environmental exposure. Particularly, our attention has been focused on leukemia and tumors related to brain and central nervous system (CNS), skin, stomach, kidney, and breast. The epidemiologic literature has been systematically reviewed focusing on workers, general population, and pediatric population. A weak increase in leukemia risk due to Rn exposure was found, but bias and confounding factors cannot be ruled out. The results of studies conducted on stomach cancer are mixed, although with some prevalence for a positive association with Rn exposure. In the case of brain and CNS cancer and skin cancer, results are inconclusive, while no association was found for breast and kidney cancers. Overall, the available evidence does not support a conclusion that a causal association has been established between Rn exposure and the risk of other non-pulmonary neoplasms mainly due to the limited number and heterogeneity of existing studies. To confirm this result, a statistical analysis should be necessary, even if it is now not applicable for the few studies available.
Journal Article
Consequences of changing Canadian activity patterns since the COVID-19 pandemic include increased residential radon gas exposure for younger people
The COVID-19 pandemic has produced widespread behaviour changes that shifted how people split their time between different environments, altering health risks. Here, we report an update of North American activity patterns before and after pandemic onset, and implications to radioactive radon gas exposure, a leading cause of lung cancer. We surveyed 4009 Canadian households home to people of varied age, gender, employment, community, and income. Whilst overall time spent indoors remained unchanged, time in primary residence increased from 66.4 to 77% of life (+ 1062 h/y) after pandemic onset, increasing annual radiation doses from residential radon by 19.2% (0.97 mSv/y). Disproportionately greater changes were experienced by younger people in newer urban or suburban properties with more occupants, and/or those employed in managerial, administrative, or professional roles excluding medicine. Microinfluencer-based public health messaging stimulated health-seeking behaviour amongst highly impacted, younger groups by > 50%. This work supports re-evaluating environmental health risks modified by still-changing activity patterns.
Journal Article
Characterization of DNA Methylation Episignatures for Radon-Induced Lung Cancer
Radon (Rn) exposure has a strong association with lung cancer risk and is influenced by epigenetic modifications. To investigate the characterization of DNA methylation (DNAm) episignatures for radon-induced lung cancer, we detected the specific changes in DNAm in blood and lung tissues using reduced representation bisulfite sequencing (RRBS). We identified the differentially methylated regions (DMRs) induced by radon exposure. The bioinformatics analysis of the DMR-mapped genes revealed that pathways in cancer were affected by radon exposure. Among them, the DNAm episignatures of MAPK10, PLCG1, PLCβ3 and PIK3R2 were repeated between lung tissue and blood, and validated by the MassArray. In addition, radon exposure promoted lung cancer development in the genetic engineering mouse model (GEMM), accompanied by decreased MAPK10 and increased PLCG1, PLCβ3, and PIK3R2 with mRNA and protein levels. Conclusively, radon exposure significantly changes the genomic DNAm patterns in lung tissue and blood. The DNAm episignatures of MAPK10, PLCG1, PLCβ3 and PIK3R2 have a significant influence on radon-induced lung cancer. This brings a new perspective to understanding the pathways involved in radon-induced lung cancer and offers potential targets for developing blood-based biomarkers and epigenetic therapeutics.
Journal Article