Radon exposure is rising steadily within the modern North American residential environment, and is increasingly uniform across seasons
Fintan K. T. Stanley, Jesse L. Irvine, Weston R. Jacques, Shilpa R. Salgia, Daniel G. Innes, Brandy D. Winquist, David Torr, Darren R. Brenner & Aaron A. Goodarzi
https://www.nature.com/articles/s41598-019-54891-8 03 December 2019
Abstract
Human-made buildings can artificially concentrate radioactive radon gas of geologic origin, exposing occupants to harmful alpha particle radiation emissions that damage DNA and increase lung cancer risk. We examined how North American residential radon exposure varies by modern environmental design, occupant behaviour and season. 11,727 residential buildings were radon-tested using multiple approaches coupled to geologic, geographic, architectural, seasonal and behavioural data with quality controls. Regional residences contained 108 Bq/m3 geometric mean radon (min < 15 Bq/m3; max 7,199 Bq/m3), with 17.8% ≥ 200 Bq/m3. Pairwise analysis reveals that short term radon tests, despite wide usage, display limited value for establishing dosimetry, with precision being strongly influenced by time of year. Regression analyses indicates that the modern North American Prairie residential environment displays exceptionally high and worsening radon exposure, with more recent construction year, greater square footage, fewer storeys, greater ceiling height, and reduced window opening behaviour all associated with increased radon. Remarkably, multiple test approaches reveal minimal winter-to-summer radon variation in almost half of properties, with the remainder having either higher winter or higher summer radon. This challenges the utility of seasonal correction values for establishing dosimetry in risk estimations, and suggests that radon-attributable cancers are being underestimated.
Introduction
Lung cancer is the 6th leading overall cause of death and the foremost cause of cancer death in the world. It is understood to be predominantly triggered by chronic inhalation of tobacco smoke and/or radioactive radon (222Rn) gas, often coupled with underlying genetic predispositions1,2,3,4,5,6. Radon is a primary cause of lung cancer in never smokers and the second leading cause in smokers, encompassing an estimated 3–20% of lung cancer deaths worldwide7,8. Gaseous radon isotopes arise from decaying uranium, thorium and radium-containing minerals in bedrock, surficial materials and groundwater that are prevalent globally1,9. First order estimations of radon potential have been classified previously based on radiometric data derived from uranium and thorium radionuclide content of bedrock lithology, surficial materials, groundwater, structures and anthropogenic activity10,11. There are positive correlations in uranium (ppm), estimated from airborne radiometric and direct indoor measurements, that additionally account for permeability factors in the assessment of radon mobility in surficial materials (i.e. groundwater history)12. Although arising naturally, radon and radon-derived ‘daughters’ (including 214Po, 218Po) can concentrate within the built environment to levels typically not observed in nature. Thus, hazardous radon exposure is largely an anthropogenic environmental health issue.
Radon synergizes with lung carcinogens such as tobacco smoke to multiply lung cancer risk13,14. However, unlike tobacco use, radon inhalation is not addictive and effective testing and mitigation techniques exist15. Thus, radon exposure represents a readily preventable cause of the most lethal and common cancer type, and is a priority area of public health intervention and cancer prevention. Decaying 222Rn emits alpha particle ionizing radiation, severely damaging DNA in such a way that is almost impossible for our cells to repair without introducing genetic errors16. Such errors trigger ‘genomic instability’, a self-propagating cycle of DNA alteration that drives cancer formation2. Further to this, approximately 1 in 30 adult humans display radiation sensitivity, meaning that (compared to the average) they over-respond to ionizing radiation exposure leading to moderate to severe health effects including morbidities, mortality and/or increased risk of cancer17,18,19,20. The International Agency for Research on Cancer lists radon as a category 1 carcinogen, meaning it is unequivocally known to cause human and animal cancers1. Ionizing radiation such as alpha particle radiation is measured in Becquerels (Bq) that represents one radioactive decay event per second. A 16% increase in relative lifetime risk of lung cancer is measurable per ≥100 Becquerel/m3 (Bq/m3) chronic radon inhalation1,21,22.
Historically, radon exposure is thought to be increased in cold climate regions where populations predominantly occupy closed indoor air environments long periods of the year to avoid adverse meteorological conditions. However, climate change and growing adoption of air conditioning across all regions may alter this 20th century norm. It is estimated that the average North American spends 86.9% of their lives indoors23, meaning that analyzing the modern built environment is crucial for understanding exposure to many carcinogens. There are many regions of high radon potential on Earth, although this does not mean that all buildings in those areas contain unsafe radon levels8,15. Indeed, there are three factors needed to incur hazardous radon exposure: (i) a rich geologic source and pathway (upwards) for radon, (ii) environmental design metrics that actively draw up and concentrate radon and (iii) essential or elective human behaviour that prolongs exposure or increases radon concentrations. These latter two variables are potentially modifiable and are of interest in terms of exposure reduction.
Establishing historic and ongoing radon exposure represents significant ‘exposome’ information, similar to documenting smoking history24. Such information is important for early cancer detection programs, harm reduction25 and is also of interest to define best practice within scenarios such as business licensing, rental leasing, real estate transactions or home inspections. Thus, establishing the contextual (geographic, seasonal and environmental) effectiveness of distinct radon testing method(s) for decision-making is also important. Motivated by this, we measured household radon across a large North American area of high radon potential encompassing ~5.45 million humans spread across 1,313,748 km2. Radon dosimetry data was coupled to geospatial analysis, an interrogation of how built environment metrics and associated behaviours correlate with radon levels and, within a subset of regional buildings, an evaluation of multiple modalities of radon testing.
Results
Radon potential and domestic exposure in North America
Geochemical composition of glacial tills (including outwash deposits, lacustrine clays, conglomerates, etc.) and derived soils can closely compare with local bedrock units and, as such, allows radon potential assessment26. Using this, we analyzed the radon potential of the Western North American Prairie Region using the US Geological Survey Data Series 424 as a base27. This method indicated the majority of the survey area contained geologies with greater than 300 Bq/kg of radon generating radionuclides (Fig. 1A). Thus, based on population density, survey region residents predominantly occupy areas of uniformly high geologic radon potential. The total radon dosimetry dataset encompasses 11,727 residential long term alpha track radon tests conducted between 2010–2018 in Alberta (AB) and Saskatchewan (SK), of which 55% (n = 6,257) were ≥100 Bq/m3 and 17.8% (n = 2,086) were ≥200 Bq/m3, the maximum tolerated exposure limit for Canada (Fig. 1B,C). The geometric mean for all tests was 108 Bq/m3 (arithmetic mean 146 Bq/m3), equivalent to 2.92 pCi/L (a non-SI unit commonly used in the USA) or, based on ICRP calculations, an annual adult lung equivalent radiation dose of 5.07 mSv/year. The median test duration was 103 days and 91% were deployed from October-April. Comparison to global radon levels recently compiled by Gaskin et al.9 (and accounting for other studies28) indicates the 1,313,748 km2 survey region encompasses one of the most radon-exposed large populations mapped to date (Fig. 1D). Concurrent duplicates confirmed test precision, with r2 = 0.962 for duplicates placed <10 cm apart and r2 = 0.808 for duplicates located in a different room but within the same building (Fig. 1E). Tests exposed to known quantities of radon demonstrate accuracy, with r2 = 0.996 (Supplementary Fig. 1A). There were no significant differences in radon levels reported by different room types (F (3, 5046 = 1.67, p < 0.17)) (Supplementary Fig. 1B). There were no significant differences in mean radon by the study year of testing (Supplementary Fig. 1C). Radon levels were statistically higher when the test device was placed on the basement/cellar level (F (4, 5063 = 8.20, p < 0.0001)), as compared to the main/ground and/or upper floors, encompassing a ~13% reduction in mean radon when comparing basement level to any upper floor (Fig. 1F). These data permitted the calculation of a test floor correction value of 1.2 between basement/cellar and any upper level. Applying this to normalize all readings to the lowest floor of testing, the overall level for the region was a geometric mean of 111 Bq/m3 (arithmetic mean = 150 Bq/m3).
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