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Hormesis and Cancer Risk Assessment Models

Theoretical/Empirical Question Since the LNTs negate any protective response at low dose rates, what is the appropriate science policy to overcome this limitation  [Pg.198]

Corollary Question Since the J-shaped hormetic (or biphasic) cancer dose-response model yields empirically demonstrated protective (stimulatory) effects at low doses in one or more species, is biologically plausible, and describes a damaging relationship at higher dose that is consistent with the LNT, which of the two is the logical and prudential default model  [Pg.198]

The LNT-based dose-response model for cancer, being a cumulative distribution function, begins at zero and is proportional to doses (i.e., is linear at low doses, resulting in the LNT hypothesis). The early form of the LNT model is the one-hit model  [Pg.199]

In this model, Pr(T)) is the lifetime probability of cancer death from lifetime exposure to dose D (often expressed in units of mg/kg-day, consistent with animals exposures). [Pg.199]

Cellnlar division into a normal or premalignant cell, (a carcinogen [Pg.200]


See other pages where Hormesis and Cancer Risk Assessment Models is mentioned: [Pg.198]    [Pg.199]    [Pg.201]   


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