1991
DOI: 10.1097/00004032-199109000-00004
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Radon Exposure System for Mammalian Cells in Culture

Abstract: A novel system for Rn gas exposure of mammalian cells in culture has been designed, constructed, and used to directly assess both the magnitude and the nature of chronic, low-dose Rn/Rn daughter toxicity of exposed vital lung cells isolated from normal pulmonary tissue, propagated and exposed in vitro. Direct correlations between atmospheric Rn concentrations, alpha-particle fluences, and macro- and microdoses of absorbed radiation doses by lung cells provide for a heretofore unavailable assessment of critical… Show more

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Cited by 4 publications
(2 citation statements)
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“…Mathematical details are given in the Appendix. In terms of notation and relations previously described (Bogen 1997), new assumptions used for the present study were: (1) dose rate (E) in cGy y -1 to surface (secretory) cells in lobar/segmental bronchi was estimated to be 3.3 and 4.4 cGy WLM -1 for residents and miners, respectively (NRC 1991); (2) excess relative risk was modeled as s × E (unitless) for S→P and P→M transitions; (3) k r was modeled as E/D 0 with D 0 taken to be the approximate mean (35 cGy) of published D 0 values for alpha-induced killing of human lung cells in vitro (Seed et al 1991;Simmons et al 1996;Søyland and Hassfjell Nonlinearity in Lung Cancer Risk 2000); (4) d Q was modeled as b Q -g[1 + c(b R b -1 -1)]; and (5) R→Q and Q→M transitions were presumed to occur at a background rate per cell division of w × m (vs. the rate m assumed for S→P and P→M transitions). Other CD2 parameters were assigned biologically plausible values (see Appendix).…”
Section: Cancer Risk Modelmentioning
confidence: 99%
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“…Mathematical details are given in the Appendix. In terms of notation and relations previously described (Bogen 1997), new assumptions used for the present study were: (1) dose rate (E) in cGy y -1 to surface (secretory) cells in lobar/segmental bronchi was estimated to be 3.3 and 4.4 cGy WLM -1 for residents and miners, respectively (NRC 1991); (2) excess relative risk was modeled as s × E (unitless) for S→P and P→M transitions; (3) k r was modeled as E/D 0 with D 0 taken to be the approximate mean (35 cGy) of published D 0 values for alpha-induced killing of human lung cells in vitro (Seed et al 1991;Simmons et al 1996;Søyland and Hassfjell Nonlinearity in Lung Cancer Risk 2000); (4) d Q was modeled as b Q -g[1 + c(b R b -1 -1)]; and (5) R→Q and Q→M transitions were presumed to occur at a background rate per cell division of w × m (vs. the rate m assumed for S→P and P→M transitions). Other CD2 parameters were assigned biologically plausible values (see Appendix).…”
Section: Cancer Risk Modelmentioning
confidence: 99%
“…The rate k r (y -1 ) of induced reproductive death was modeled as E/D 0 , with D 0 taken to be the approximate mean (35 cGy) of published D 0 values for alphainduced killing of human lung cells in vitro (Seed et al 1991;Simmons et al 1996;Søyland and Hassfjell 2000). Mutation rates m T (y -1 ) were modeled as bTm i (1+sE) or bTm i ′(1+sE), where the corresponding mean background mutation rates per cell division, m i and m i ′ (i=1 for T= S or R, i =2 for T= P or Q, prime only for T= R or Q), were estimated in terms of (unitless) parameters m and w under assumptions that m 1 = m 2 = m and m 1 ′ = m 2 ′ = w m. Alpha-induced interphase (as opposed to reproductive) cell death was not modeled explicitly.…”
Section: Bogenmentioning
confidence: 99%