Abstract

Purpose

Natural radiation is the major source of human exposure to ionizing radiation. About 52% of the total dose received from the high natural background radiations (HNBR) areas are due to inhalation dose from radon (²²²Rn)/thoron (²²⁰Rn) and their progenies. Hence, we reviewed the biological effects of ²²²Rn/²²⁰Rn and their progenies on lung tissue, and the possible role of lung stem cells in salvaging the damage caused by ²²²Rn/²²⁰Rn and their progenies.

Materials and Method

We have extensively reviewed articles among several hits obtained in PubMed, Scopus, and Elsevier databases with keywords ‘Radon/Thoron’ OR Thoron progeny/Radon progeny OR ‘Thoron/Radon inhalation and lungs’, and proceed for further analysis. Also, databases related to oxidative damage to lung stem cells by radiation and the repair mechanisms involved by the lung stem cells were also included.

Results

Based on the existing epidemiological data on radon in residential buildings, we found that evidence exists on the association of radon induced lung carcinogenesis, but the data regarding the role of thoron induced lung damage is very limited and inconclusive. We also found that limited information has been provided based on ecological designs, leading to poor documentation of health statistics, in particular, organ-specific cancer rates. Finally, we tried to elucidate the possible mechanisms of lung injury induced by thoron inhalation and the probable role of lung stem cell toward the redemption of such oxidative damages.

Conclusion

Existing epidemiological data on thoron inhalation and associated health outcomes are limited and inconclusive. Further, in vivo experiments, with respect to radon/thoron inhalation dose rate ranges corresponding to the HNBR areas will be helpful in understanding the cellular and molecular effects.

中文翻译：

---

ron虫后代对肺的损伤与肺干细胞可能对损伤的挽救：一个观点。

摘要

目的

自然辐射是人体暴露于电离辐射的主要来源。从高自然本底辐射（HNBR）区域接收的总剂量中约有52％是由于ra（²²² Rn）/ ron（²²⁰ Rn）及其后代的吸入剂量所致。因此，我们综述了²²² Rn / ²²⁰ Rn及其后代对肺组织的生物学作用，以及肺干细胞在挽救²²² Rn / ²²⁰ Rn及其后代造成的损害中的可能作用。

材料与方法

我们已经广泛审查了PubMed，Scopus和Elsevier数据库中一些关键词为“ Radon / Thoron”或Thoron子代/ Radon子代或“ Thoron / Radon吸入和肺”的命中文章，并进行了进一步分析。此外，还包括与辐射对肺干细胞的氧化损伤和肺干细胞所涉及的修复机制有关的数据库。

结果

根据现有居民住宅中ra的流行病学数据，我们发现存在有关induced诱导的肺致癌作用的证据，但是关于tho诱发肺损伤的作用的数据非常有限且无定论。我们还发现，根据生态设计提供的信息有限，导致健康统计资料记录不佳，尤其是特定器官的癌症发生率。最后，我们试图阐明由吸入ron气引起的肺损伤的可能机制，以及肺干细胞可能在赎回这种氧化损伤中的作用。

结论

现有的关于吸入和相关健康结果的流行病学数据是有限的，也没有定论。此外，关于experiments / to气吸入剂量率范围对应于HNBR区域的体内实验将有助于理解细胞和分子效应。