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.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Program Projects (P01)
Project #
2P01CA049062-07
Application #
6237039
Study Section
Project Start
1997-02-01
Project End
1998-01-31
Budget Start
1996-10-01
Budget End
1997-09-30
Support Year
7
Fiscal Year
1997
Total Cost
Indirect Cost
Name
Columbia University (N.Y.)
Department
Type
DUNS #
167204994
City
New York
State
NY
Country
United States
Zip Code
10032
Wu, Jinhua; Hei, Tom K (2018) Focus small to find big - the microbeam story. Int J Radiat Biol 94:782-788
Wu, Jinhua; Zhang, Qin; Wuu, Yen-Ruh et al. (2017) Cytoplasmic Irradiation Induces Metabolic Shift in Human Small Airway Epithelial Cells via Activation of Pim-1 Kinase. Radiat Res 187:441-453
Liao, Wupeng; Hei, Tom K; Cheng, Simon K (2017) Radiation-Induced Dermatitis is Mediated by IL17-Expressing ?? T Cells. Radiat Res 187:454-464
Wu, Jinhua; Zhang, Bo; Wuu, Yen-Ruh et al. (2017) Targeted cytoplasmic irradiation and autophagy. Mutat Res 806:88-97
Domogauer, Jason D; de Toledo, Sonia M; Azzam, Edouard I (2016) A Mimic of the Tumor Microenvironment: A Simple Method for Generating Enriched Cell Populations and Investigating Intercellular Communication. J Vis Exp :
Chen, Hongxin; Chong, Zhao Zhong; De Toledo, Sonia M et al. (2016) Delayed activation of human microglial cells by high dose ionizing radiation. Brain Res 1646:193-198
Azzam, Edouard I; Colangelo, Nicholas W; Domogauer, Jason D et al. (2016) Is Ionizing Radiation Harmful at any Exposure? An Echo That Continues to Vibrate. Health Phys 110:249-51
Hei, Tom K (2016) Response of Biological Systems to Low Doses of Ionizing Radiation. Health Phys 110:281-2
Gong, Xuezhong; Ivanov, Vladimir N; Hei, Tom K (2016) 2,3,5,6-Tetramethylpyrazine (TMP) down-regulated arsenic-induced heme oxygenase-1 and ARS2 expression by inhibiting Nrf2, NF-?B, AP-1 and MAPK pathways in human proximal tubular cells. Arch Toxicol 90:2187-2200
Ivanov, Vladimir N; Hei, Tom K (2015) Regulation of viability, differentiation and death of human melanoma cells carrying neural stem cell biomarkers: a possibility for neural trans-differentiation. Apoptosis 20:996-1015

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