CYTOGENETICS--ALPHA PARTICLE INDUCED CHROMOSOMAL CHANGES

将主要的电离辐射危害归因于人类 由于氡是基于气体的普及性质而感知的 生物功效负责任的高LETα粒子。当它 早就认识到，高LET的辐射可能更多 在生物破坏性的情况下，在许多情况下， 最有效的LET。确定阿尔法的有效性 在LET与氡相关的范围内的粒子将允许更大的 人类风险评估的精确性。这一点尤其适用于 环境中的氡水平，主要的细胞伤害来自于 一个且只有一个氡子体是α粒子。要解决的问题 与计划项目的主要总体目标有关，即 提供有关单个a粒子影响的信息； 对RBE的评估：让关系对质量因素做出贡献 估计；并寻找a=-粒子的特征“指纹” 曝光。染色体的变化已被证明与细胞有关 死亡、突变和癌症及其定量评估是关键 此项目的PIN，并提供与此项目的其他项目的链接 计划项目。 每个细胞核中只有一个或多个α粒子所产生的影响 将微束与均值(泊松)的效果进行比较 分布)a粒子的数量在同一定义字母在正常人中 支气管上皮细胞和成纤维细胞。前者构成了 主细胞类型受到氡子体a粒子照射的威胁。 定义的高Leta粒子引起的染色体变化将是 与X射线诱发的改变相比。变化将是数量上的 正常人支气管上皮细胞在不同时期的评价 细胞周期，包括所有变化和特定于染色体的变化 用鱼。我们将比较染色体间和染色体内交换比率 对于a粒子与X射线的对比，以寻找a粒子的依赖结果- 粒子辐射。 获得的信息将被分析并合并到一个综合的 生物数据和风险估计的建模(项目1) 提供更可信的风险评估和可能的手段 准确归因于阿尔法粒子(氡)引起的变化。

Attribution of the principal ionizing radiation hazard to humans as being due to radon is based on the pervasive nature of the gas and perceived biological efficacy of the responsible high LET alpha particles. While it has long been recognized that radiation of high LET may be more biologically damaging, there is in many instances a decline past an optimally effective LET. Ascertainment of the effectiveness of alpha particles over the range of LET's relevant to radon will allow for greater precision in human risk estimates. This is particularly pertinent for environmental levels of radon where the principal cellular insult is from one and only one radon progeny a-particle. The issues to be addressed relate to the primary overall goals of the program project, namely the provision of information on the effects of single a-particles; to assessments of RBE: LET relations to contribute to quality factor estimates; and to seek a characteristic "fingerprint" for a=-particle exposure. Chromosomal changes have been shown to be associated with cell death, mutation and cancer and their quantitative evaluation is the linch pin of this project and provides links with the other projects of this program project. The effects of exactly one or more a-particles per cell nucleus delivered by microbeam will be compared with the effects of mean (Poisson distributed) numbers of a-particles at the same defined LET in normal human bronchial epithelial cells and fibroblasts. The former constitute the principal cell type at risk from radon progeny a-particle exposure. Chromosomal changes induced by defined high LET a-particles will be compared with X-ray induced changes. Changes will be quantitatively evaluated in normal human bronchial epithelial cells in different stages of the cell cycle, both for all changes and for chromosome specific change using FISH. Inter versus intrachromosomal exchange ratios will be compared for a-particles versus X-rays in a search for a dependent consequence of a- particle radiation. Information gained will be analyzed and incorporated into an integrated modeling of biological data and risk estimation (Project 1) with the intent of providing both a more credible assessment of risk and possible a means of accurately attributing alpha particle (radon) induced change.