Do low dose-rate bystander eVects in uence domestic radon risks?

exposure (NCRP 1987) . For a variety of reasons, Purpose : Radon risks derive from exposure of bronchio-epithelial however, direct epidemiological assessment of the cells to high-linear energy transfer (LET) a-particles. a-particle risks from domestic radon exposure is diYcult, exposure can result in bystander eVects, where irradiated cells resulting in risk estimates with wide conŽ dence interemit signals resulting in damage to nearby unirradiated bystander vals (Lubin et al. 1995b). Consequently, domestic cells. This can result in non-linear dose–response relations, and inverse dose-rate eVects. Domestic radon risk estimates are radon risk estimates are currently based on extrapolacurrently extrapolated from miner data, which are at both higher tion of data from miner studies, largely at considerdoses and higher dose-rates, so bystander eVects on unhit cells ably higher radon exposures and exposure rates. At could play a large role in the extrapolation of risks from mines present, a linear extrapolation of the risks from high to homes. Therefore, we extend an earlier quantitative mechanto low radon exposures is generally considered to istic model of bystander eVects to include protracted exposure, with the aim of quantifying the signiŽ cance of the bystander have the strongest biophysical rationale (NRC 1999) . eVect for very prolonged exposures. At an average home radon concentration, few Materials and methods : A model of high-LET bystander eVects, potential target cells in the bronchial epithelium of a originally developed to analyse oncogenic transformation in vitro, home resident will be struck or traversed by an ais extended to low dose-rates. The model considers radiation particle in, say, 1 year (NRC 1999)—and this obserresponse as a superposition of bystander and linear direct eVects. It attributes bystander eVects to a small subpopulation of hypervation remains true even at high domestic radon sensitive cells, with the bystander contribution dominating the levels (Ž gure 1). direct contribution at very low acute doses but saturating as This inhomogeneous energy deposition by a-parthe dose increases. Inverse dose-rate eVects are attributed to the ticles is of potential relevance to the radon problem replenishment of the hypersensitive subpopulation during because there is convincing evidence, at least in vitro, prolonged irradiation. Results : The model was Ž tted to doseand dose-rate-dependent that irradiated cells can send out signals that can radon-exposed miner data, suggesting that one directly hit target result in damage to nearby unirradiated ‘bystander’ bronchio-epithelial cell can send bystander signals to about 50 cells. The evidence is particularly strong for highneighbouring target cells. The model suggests that a na ṏ ve linear LET radiation, with a broad variety of endpoints extrapolation of radon miner data to low doses, without account(summarized, for example, by Sawant et al. 2001b) ing for dose-rate, would result in an underestimation of domestic radon risks by about a factor of 4, a value comparable with the including chromosomal damage and oncogenic transempirical estimate applied in the recent BEIR–VI report on formation. Some recent results suggest that bystander radon risk estimation. eVects can be induced by high-LET radiation even Conclusions : Bystander eVects represent a plausible quantitative when the bystander cells have been previously and mechanistic explanation of inverse dose-rate eVects by highexposed to low doses of low-LET radiation (Sawant LET radiation, resulting in non-linear dose–response relations and a complex interplay between the eVects of dose and exposure et al. 2001a). time. The model presented provides a potential mechanistic underpinning for the empirical exposure–time correction factors applied in the recent BEIR–VI for domestic radon risk estimation. 1.2. Modelling the bystander e Ú ect Brenner et al. (2001) suggested a model for acute