Radon ( 222Rn) gas produces decay progeny that emits high energy alpha (α)-particles. Epidemiological studies have shown that exposure to 222Rn is linked with elevated risk of developing lung cancer, however clear mechanisms leading to such effects have not been delineated. Cytokines play a critical role in inflammation and their dysregulated production often contributes to disease pathogenesis. In this study, Bio-plex multiplex technology was employed to investigate modulations of 27 pro-inflammatory cytokines following exposure of human monocytic cells to 1.5Gy of α-particle radiation. Concurrently, DNA damage was assessed by examining the formation of phosphorylated H2A histone family X (γ-H2AX) sites. Of the 27 cytokines assessed, 4 cytokines were shown to be statistically downregulated by ~2 fold relative to the untreated controls and included the interleukin (IL) family of proteins (IL-2, IL-15 and IL-17) and macrophage inflammatory protein 1 beta (MIP-1b). Interferon-inducible protein-12 (IP-12), vascular endothelial growth factor and regulated on activation normal T cell expressed and secreted (RANTES) were shown to be high expressors and upregulated. Cells irradiated with α-particles ranging from 0.27 to 2.14Gy showed statistically significant, dose-dependant increases in γ-H2AX formation. These data suggest that α-particle radiation causes dysregulation in the production of a number of pro-inflammatory cytokines and results in significant DNA damage.

Additional Metadata
Keywords Alpha radiation, Cytokine secretion, DNA damage, Monocytic cells, Radon gas, THP-1
Persistent URL dx.doi.org/10.1016/j.ijheh.2011.11.002
Journal International Journal of Hygiene and Environmental Health
Citation
Chauhan, V. (Vinita), Howland, M. (Matthew), Kutzner, B. (Barbara), McNamee, J.P. (James P.), Bellier, P.V. (Pascale V.), & Wilkins, R.C. (2012). Biological effects of alpha particle radiation exposure on human monocytic cells. International Journal of Hygiene and Environmental Health, 215(3), 339–344. doi:10.1016/j.ijheh.2011.11.002