Molecular and cellular studies have demonstrated that ionizing radiation emitted from the radioactive decay of radon and its decay products, primarily alpha particles, can cause cytogenetic damage, chromosome aberrations, and gene mutations [18]. Animal models suggest a potential link between radon and mammary tumors [19]. At the cellular level, alpha particles in the presence of estradiol were associated with increased cell proliferation and altered morphology in MCF-10F human breast cancer cells [20]. Moderate levels of radon (100 to 1200 μGy) have been associated with increased proliferation of MCF-7 human breast cancer cells [21, 22].
Although there is biological plausibility that radon exposure could influence breast carcinogenesis, few epidemiologic studies have been conducted. Increased breast cancer incidence was observed among former female employees of a Missouri school with elevated radon levels [23]. Ecologic studies showed no association between county-level radon levels and breast cancer incidence in the U.S. [24, 25]. A prospective analysis showed no association between radon exposure and breast cancer-related mortality [26]. Female breast cancer incidence was higher among residents of high-temperature geothermal areas characterized by radon-containing water in Iceland compared to residents of non-geothermal areas [27]. However, to date, no prospective epidemiologic study of breast cancer incidence has been conducted. The objective of this study was to examine the association between environmental radon exposure and breast cancer incidence in a prospective cohort of non-occupationally exposed U.S. women.
Published online 2017 Sep 7. doi: 10.1186/s12940-017-0305-6
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5590193/
US National Library of Medicine
National Institutes of Health
Radon and radon decay products have been predicted to deliver radiation doses to breast tissue [15, 16]. Although most inhaled radon gas is subsequently exhaled, the majority of the radon-related radiation dose to humans is from the radon decay products polonium-218 and polonium-214 [13]. Decay products are primarily deposited on the surface of the respiratory tract, decaying in the lung due to their relatively short half-lives (<1 s-3 min) before being cleared by absorption into blood or particle transport to the gastrointestinal tract [12, 13]. Inhaled radon and decay products are predicted to deliver radiation doses to various tissues by virtue of irradiation by alpha particles emitted from radon decay products [13]. Alpha particles are particularly harmful, classified as having a high linear energy transfer (LET), reacting more readily with DNA and generating oxidative stress via radiolysis [17]. As radon gas is fat soluble, female breast tissue and red bone marrow receive high doses relative to other tissues [15]. The estimated annual radiation dose to the breast from inhalation of radon gas and decay products (i.e., polonium-218, lead-214, and bismuth-214) assuming a radon gas concentration of 200 Bq/m3 is 0.42 mSv and 0.02–0.15 mSv (depending on blood clearance rates), respectively, as compared to 1.2 mSv and 35.8–159 mSv for the lung [15]. Although these levels are low, the National Academy of Sciences’ Committee on Health Risks of Exposure to Radon (BEIR VI) report notes the possibility of radon-related DNA damage occurring at any level of radon exposure as a single alpha particle can cause substantial genetic damage to a cell [13].
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International and national geographic variation in breast cancer incidence suggests that environmental exposures may play a role in breast carcinogenesis .