J Radiol Prot. 2007 Sep;27(3):231-52. Epub 2007 Aug 29.

Radon exposure of the skin:I. Biological effects.

Charles MW

School of Physics and Astronomy, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK.

Radon progeny can plate out on skin and give rise to exposure of the superficial epidermis from alpha emitters Po-218 (7.7 MeV, range approximately 66 microm) and Po-214 (6 MeV, range approximately 44 microm). Dose rates from beta/gamma emitters Pb-214 and Bi-214 are low and only predominate at depths in excess of the alpha range. This paper reviews the evidence for a causal link between exposure from radon and its progeny, and deterministic and stochastic biological effects in human skin.Radiation induced skin effects such as ulceration and dermal atrophy, which require irradiation of the dermis, are ruled out for alpha irradiation from radon progeny because the target cells are considerably deeper than the range of alpha particles. They have not been observed in man or animals. Effects such as erythema and acute epidermal necrosis have been observed in a few cases of very high dose alpha particle exposures in man and after acute high dose exposure in animals from low energy beta radiations with similar depth doses to radon progeny. The required skin surface absorbed doses are in excess of 100 Gy. Such effects would require extremely high levels of radon progeny. They would involve quite exceptional circumstances, way outside the normal range of radon exposures in man.There is no definitive identification of the target cells for skin cancer induction in animals or man. The stem cells in the basal layer which maintain the epidermis are the most plausible contenders for target cells. The majority of these cells are near the end of the range of radon progeny alpha particles, even on the thinnest body sites. The nominal depth of these cells, as recommended by the International Commission on Radiological Protection (ICRP), is 70 microm. There is evidence however that some irradiation of the hair follicles and/or the deeper dermis, as well as the inter-follicular epidermis, is also necessary for skin cancer induction. Alpha irradiation of rodent skin that is restricted to the epidermis does not produce skin cancer. Accelerator generated high energy helium and heavy ions can produce skin cancer in rodents at high doses, but only if they penetrate deep into the dermis. The risk figures for radiation induced skin cancer in man recommended by the ICRP in 1990 are based largely on x and beta irradiated cohorts, but few data exist below absorbed doses of about 1 Gy. The only plausible finding of alpha-radiation induced skin cancer in man is restricted to one study in Czech uranium miners. There is no evidence in other uranium miners and the Czech study has a number of shortcomings.This review concludes that the overall balance of evidence is against causality of radon progeny exposure and skin cancer induction. Of particular relevance is the finding in animal studies that radiation exposure of cells which are deeper than the inter-follicular epidermis is necessary to elicit skin cancer. In spite of this conclusion, a follow-on paper evaluates the attributable risk of radon to skin cancer in the UK on the basis that target cells for skin cancer induction are the cells in the basal layer of the inter-follicular epidermis-since this is the conservative assumption made by international bodies such as the International Commission on Radiological Protection (ICRP) for general radiological protection purposes.

J Radiol Prot.2007 Sep;27(3):253-74. Epub 2007 Aug 29

Radon exposure of the skin: II. Estimation of the attributable risk for skin cancer incidence.

Charles MW

School of Physics and Astronomy, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK.

A preceding companion paper has reviewed the various factors which form the chain of assumptions that are necessary to support a suggested link between radon exposure and skin cancer in man. Overall, the balance of evidence was considered to be against a causal link between radon exposure and skin cancer. One factor against causality is evidence, particularly from animal studies, that some exposure of the hair follicles and/or the deeper dermis, as well as the inter-follicular epidermis, is required-beyond the range of naturally occurring alpha particles. On this basis any skin cancer risk due to radon progeny would be due only to beta and gamma components of equivalent dose, which are 10-100 times less than the alpha equivalent dose to the basal layer. Notwithstanding this conclusion against causality, calculations have been carried out of attributable risk (ATR, the proportion of cases occurring in the total population which can be explained by radon exposure) on the conservative basis that the target cells are, as is often assumed, in the basal layer of the epidermis. An excess relative risk figure is used which is based on variance weighting of the data sources. This is 2.5 times lower than the value generally used. A latent period of 20 years and an RBE of 10 are considered more justifiable than the often used values of 10 years and 20 respectively. These assumptions lead to an ATR of approximately 0.7% (0.5-5%) at the nominal UK indoor radon level of 20 Bq m(-3). The range reflects uncertainties in plate-out. Previous higher estimates by various authors have made more pessimistic assumptions. There are some indications that radon progeny plate-out may be elevated out of doors, particularly due to rainfall. Although average UK outdoor radon levels ( approximately 4 Bq m(-3)) are much less than average indoor levels, and outdoor residence time is on average about 10%, this might have the effect of increasing the ATR several-fold. This needs considerable further study. Ecological epidemiology data for the South West of England provide no evidence for elevated skin cancer risks at radon levels <100 Bq m(-3). Case-control or cohort studies would be necessary to address the issue authoritatively.