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. 2008;6(4):333-51.
doi: 10.2203/dose-response.07-005.Scott. Epub 2007 Sep 30.

It's time for a new low-dose-radiation risk assessment paradigm--one that acknowledges hormesis

Affiliations

It's time for a new low-dose-radiation risk assessment paradigm--one that acknowledges hormesis

Bobby R Scott. Dose Response. 2008.

Abstract

The current system of radiation protection for humans is based on the linear-no-threshold (LNT) risk-assessment paradigm. Perceived harm to irradiated nuclear workers and the public is mainly reflected through calculated hypothetical increased cancers. The LNT-based system of protection employs easy-to-implement measures of radiation exposure. Such measures include the equivalent dose (a biological-damage-potential-weighted measure) and the effective dose (equivalent dose multiplied by a tissue-specific relative sensitivity factor for stochastic effects). These weighted doses have special units such as the sievert (Sv) and millisievert (mSv, one thousandth of a sievert). Radiation-induced harm is controlled via enforcing exposure limits expressed as effective dose. Expected cancer cases can be easily computed based on the summed effective dose (person-sievert) for an irradiated group or population. Yet the current system of radiation protection needs revision because radiation-induced natural protection (hormesis) has been neglected. A novel, nonlinear, hormetic relative risk model for radiation-induced cancers is discussed in the context of establishing new radiation exposure limits for nuclear workers and the public.

Keywords: adaptive response; hormesis; radiation; risk assessment.

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Figures

FIGURE 1.
FIGURE 1.
Relative risk dose-response relationship for gamma-ray induced neoplastic transformation of HeLa x skin fibroblast human hybrid cells by brief high-rate exposure, based on in vitro data from Redpath et al. (2001).
FIGURE 2.
FIGURE 2.
Application of dose lagging (100 mGy) to the data in Figure 1. Analysis based on data from Redpath et al. (2001).
FIGURE 3.
FIGURE 3.
Odds ratio relative to controls for the neoplastic transformation data presented in Figure 1 for gamma-ray exposure of HeLa x skin fibroblast human hybrid cells.
FIGURE 4.
FIGURE 4.
Ratio of dose-interval-specific average odds for neoplastic transformation based on data in Figure 3. Ratio of average odds evaluated relative to the lowest dose group. The lowest dose group was plotted at dose = 0 mGy. Other data plotted at the midrange of the dose intervals are used.
FIGURE 5.
FIGURE 5.
Schematic representation of the hormetic relative risk model. The model is presented as a function of the total absorbed radiation dose D to allow for a two-dimensional representation. The dose scale ranges from hypothetical absolute zero natural background radiation dose (D = 0) to doses in excess of the current dose b from natural background. Doses D*, D** and D*** define the different dose zones indicated. The RR at absolute zero radiation is indicated by RR*. The exponential rise as dose decreases below b is supported by epidemiological data (Cohen 1995) for environmentally irradiated humans and is presumed to relate to reduced DNA repair capacity (Rothkam and Löbrich 2003), the loss of protective apoptosis (Scott and Di Palma 2007), and the loss of stimulation of immune functions (Liu et al. 1987).

References

    1. Azzam EI, de Toledo SM, Raaphorst GP, Mitchel RE. Low-dose ionizing radiation decreases the frequency of neoplastic transformation to a level below the spontaneous rate in C3H 10T1/2 cells. Radiat Res. 1996;146:369–373. - PubMed
    1. Bauer G. Elimination of transformed cells by normal cells: novel concept for the control of carcinogenesis. Histol Histopathol. 1996;11:237–255. - PubMed
    1. Bauer G. Reactive oxygen and nitrogen species: efficient, selective, and interactive signals during intercellular induction of apoptosis. Anticancer Res. 2000;20(6B):4115–4139. - PubMed
    1. Bond VP, Feinendegen LE, Sondhaus CA. Microdosimetric concepts applied to hormesis. Health Phys. 1987;52(5):659–661. - PubMed
    1. Boreham DR, Dolling J-A, Somers C, Mitchel R. The adaptive response and protection against heritable mutations and fetal malformation. Dose-Response. 2006;4(4):317–326. - PMC - PubMed

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