A Geologically Based Indoor-Radon Potential Map of Kentucky

We combined 71,930 short-term (median duration 4 days) home radon test results with 1:24,000-scale bedrock geologic map coverage of Kentucky to produce a statewide geologically based indoor-radon potential map. The test results were positively skewed with a mean of 266 Bq/m3, median of 122 Bq/m3, and 75th percentile of 289 Bq/m3. We identified 106 formations with ≥10 test results. Analysis of results from 20 predominantly monolithologic formations showed indoor-radon concentrations to be positively skewed on a formation-by-formation basis, with a proportional relationship between sample means and standard deviations. Limestone (median 170 Bq/m3) and dolostone (median 130 Bq/m3) tended to have higher indoor-radon concentrations than siltstones and sandstones (median 67 Bq/m3) or unlithified surficial deposits (median 63 Bq/m3). Individual shales had median values ranging from 67 to 189 Bq/m3; the median value for all shale values was 85 Bq/m3. Percentages of values falling above the U.S. Environmental Protection Agency (EPA) action level of 148 Bq/m3 were sandstone and siltstone: 24%, unlithified clastic: 21%, dolostone: 46%, limestone: 55%, and shale: 34%. Mississippian limestones, Ordovician limestones, and Devonian black shales had the highest indoor-radon potential values in Kentucky. Indoor-radon test mean values for the selected formations were also weakly, but statistically significantly, correlated with mean aeroradiometric uranium concentrations. To produce a map useful to nonspecialists, we classified each of the 106 formations into five radon-geologic classes on the basis of their 75th percentile radon concentrations. The statewide map is freely available through an interactive internet map service

Lysophosphatidic acid and sphingosine-1-phosphate promote morphogenesis and block invasion of prostate cancer cells in three-dimensional organotypic models

Normal prostate and some malignant prostate cancer (PrCa) cell lines undergo acinar differentiation and form spheroids in three-dimensional (3-D) organotypic culture. Acini formed by PC-3 and PC-3M, less pronounced also in other PrCa cell lines, spontaneously undergo an invasive switch, leading to the disintegration of epithelial structures and the basal lamina, and formation of invadopodia. This demonstrates the highly dynamic nature of epithelial plasticity, balancing epithelial-to-mesenchymal transition against metastable acinar differentiation. This study assessed the role of lipid metabolites on epithelial maturation. PC-3 cells completely failed to form acinar structures in delipidated serum. Adding back lysophosphatidic acid (LPA) and sphingosine-1-phosphate (S1P) rescued acinar morphogenesis and repressed invasion effectively. Blocking LPA receptor 1 (LPAR1) functions by siRNA (small interference RNA) or the specific LPAR1 inhibitor Ki16425 promoted invasion, while silencing of other G-protein-coupled receptors responsive to LPA or S1P mainly caused growth arrest or had no effects. The G-proteins Gα12/13 and Gαi were identified as key mediators of LPA signalling via stimulation of RhoA and Rho kinases ROCK1 and 2, activating Rac1, while inhibition of adenylate cyclase and accumulation of cAMP may be secondary. Interfering with these pathways specifically impeded epithelial polarization in transformed cells. In contrast, blocking the same pathways in non-transformed, normal cells promoted differentiation. We conclude that LPA and LPAR1 effectively promote epithelial maturation and block invasion of PrCa cells in 3-D culture. The analysis of clinical transcriptome data confirmed reduced expression of LPAR1 in a subset of PrCa's. Our study demonstrates a metastasis-suppressor function for LPAR1 and Gα12/13 signalling, regulating cell motility and invasion versus epithelial maturation

Health implications of radon distribution in living rooms and bedrooms in U.K. dwellings – a case study in Northamptonshire

Environmental radon exposure of residents of domestic premises in the United Kingdom (UK) and elsewhere in Europe is estimated on the basis of the measured radon concentrations in, and the relative occupancies of, the principal living room and bedroom. While studies on radon concentration variability in the individual units in apartment blocks in various countries have been described, little data has been reported on variability in two-storey single-family dwellings, and the majority of extant studies consolidate living room and bedroom data early in the analysis. To investigate this further, detailed analysis was made of radon concentration data from a set of thirty-four homes situated in areas of Northamptonshire known to exhibit high radon levels. All homes were of typical UK construction of brick/block/stone walls under a pitched tile/slate roof. Approximately 50% of the sample were detached houses, the remainder being semi-detached (duplex) or terraced (row-house). Around 25% of the sample possessed cellars, while 12% were single-storey dwellings (bungalows), reflecting the typical incidence of this type of dwelling in England. In the two-storey homes, all monitored bedrooms were on the upper floor. Distribution of the ratios of bedroom/living room radon concentrations (BR/LR ratio) in individual properties was left-skewed (mean 0.67, median 0.73, range 0.05–1.05) with a tail extending to just above 1.0. The mean is consistent with the outcome of earlier extensive studies in England, while the variability depends principally on the characteristics of the property, and not on seasonal factors. In a small set of homes, the BR/LR ratio was anomalously low, (mean 0.3). BR/LR ratios in single-storey homes clustered around a value of 1.0, indicating that house design, rather than lifestyle, is the dominant factor in determining bedroom radon concentrations. Homes with higher mean annual radon concentrations showed lower BR/LR ratios, supporting our proposal that, in some homes, radon emanation from building materials may comprise a significant component of the overall radon level

Radon in air and water

Radon is a natural radioactive gas that you cannot see, smell, or taste and that can only be detected with special equipment. It is produced by the radioactive decay of radium, which in turn is derived from the radioactive decay of uranium. Uranium is found in small quantities in all soils and rocks, although the amount varies from place to place. Radon decays to form radioactive particles that can enter the body by inhalation. Inhalation of the short-lived decay products of radon has been linked to an increase in the risk of developing cancers of the respiratory tract, especially of the lungs. Breathing radon in the indoor air of homes contributes to about 15,000 lung cancer deaths each year in the United States and 1,100 in the UK (HPA 2009). Only smoking causes more lung cancer deaths