The Cellular and Molecular Carcinogenic Effects of Radon Exposure: A Review

International Journal of Molecular Sciences

Aaron Robertson²  James Allen²  Robin Laney¹ 

[1] Clinical Oncology, Sunrise Centre, Royal Cornwall Hospital, Truro, Cornwall TR1 3LJ, UK; E-Mail:;Clinical Photobiology, European Centre for Environment and Human Health, University of Exeter Medical School, University of Exeter, Knowledge Spa, Royal Cornwall Hospital, Truro, Cornwall TR1 3HD, UK; E-Mails:

关键词: radon;    carcinogenesis;    cytogenetics;    DNA damage;    alpha particles;    bystander effect;    chromosome aberrations;    micronuclei;    linear;    no-threshold;    hormesis;   

DOI  :  10.3390/ijms140714024

来源: mdpi

【 摘 要 】

Radon-222 is a naturally occurring radioactive gas that is responsible for approximately half of the human annual background radiation exposure globally. Chronic exposure to radon and its decay products is estimated to be the second leading cause of lung cancer behind smoking, and links to other forms of neoplasms have been postulated. Ionizing radiation emitted during the radioactive decay of radon and its progeny can induce a variety of cytogenetic effects that can be biologically damaging and result in an increased risk of carcinogenesis. Suggested effects produced as a result of alpha particle exposure from radon include mutations, chromosome aberrations, generation of reactive oxygen species, modification of the cell cycle, up or down regulation of cytokines and the increased production of proteins associated with cell-cycle regulation and carcinogenesis. A number of potential biomarkers of exposure, including translocations at codon 249 of TP53 in addition to HPRT mutations, have been suggested although, in conclusion, the evidence for such hotspots is insufficient. There is also substantial evidence of bystander effects, which may provide complications when calculating risk estimates as a result of exposure, particularly at low doses where cellular responses often appear to deviate from the linear, no-threshold hypothesis. At low doses, effects may also be dependent on cellular conditions as opposed to dose. The cellular and molecular carcinogenic effects of radon exposure have been observed to be both numerous and complex and the elevated chronic exposure of man may therefore pose a significant public health risk that may extend beyond the association with lung carcinogenesis.

【 授权许可】

CC BY   
© 2013 by the authors; licensee MDPI, Basel, Switzerland