Charles M W
School of Physics and Astronomy, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK.
J Radiol Prot. 2007 Sep;27(3):253-74. doi: 10.1088/0952-4746/27/3/R02. Epub 2007 Aug 29.
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.
之前的一篇相关论文回顾了各种因素,这些因素构成了一系列假设链条,而这些假设对于支持所提出的人类氡暴露与皮肤癌之间的联系是必要的。总体而言,证据的平衡被认为不利于氡暴露与皮肤癌之间的因果联系。反对因果关系的一个因素是证据,特别是来自动物研究的证据,即毛囊和/或更深层的真皮以及毛囊间表皮需要有一定程度的暴露——超出自然产生的α粒子的范围。在此基础上,氡子体导致的任何皮肤癌风险仅归因于等效剂量的β和γ成分,它们比基底细胞层的α等效剂量小10 - 100倍。尽管得出了反对因果关系的结论,但还是进行了归因风险(ATR,即总人群中发生的病例中可由氡暴露解释的比例)的计算,计算基于保守假设,即靶细胞如通常所认为的那样位于表皮的基底细胞层。使用了基于数据源方差加权的超额相对风险数字。这个数字比通常使用的值低2.5倍。20年的潜伏期和10的相对生物效应系数(RBE)被认为比通常分别使用的10年和20更合理。这些假设导致在英国室内氡水平标称值20 Bq m(-3)时,归因风险约为0.7%(0.5 - 5%)。该范围反映了沉积的不确定性。之前不同作者的较高估计做出了更悲观的假设。有一些迹象表明,特别是由于降雨,户外的氡子体沉积可能会增加。尽管英国室外平均氡水平(约4 Bq m(-3))远低于室内平均水平,且户外停留时间平均约为10%,但这可能会使归因风险增加几倍。这需要大量进一步研究。英格兰西南部的生态流行病学数据没有提供证据表明在氡水平<100 Bq m(-3)时皮肤癌风险会升高。需要进行病例对照或队列研究来权威地解决这个问题。