[ RadSafe ] Untold Radiation Protection Story

[Scott, Bobby]

I thought readers of the Radsafe Digest may find the radiation
protection story that follows to be of interest.  Our research relates
to stochastic biological effects of exposure of mammalian cellular
communities to low doses of ionizing radiation.  These effects include
induced genomic instability, mutation, neoplastic transformation, and
cancer in organisms.  What we have learned about exposure to low doses
and dose rates of low-LET radiations such as X and gamma rays is that
doses above varying thresholds (for different individuals) appear to
activate a system of transient protective processes that include high
fidelity (efficiency) DNA repair, an auxiliary selective apoptosis
process (called the PAM process), and the immune system.  The high
fidelity repair when activated likely includes repair of spontaneously
occurring DNA double-strand breaks and competes with normal apoptosis
(cell suicide, when severely damaged).  The abbreviation PAM stands for
"protective apoptosis mediated".  The PAM process, which involves an
auxiliary apoptosis mechanism, when activated removes existing
genomically unstable cells (spontaneous and other) that arise from
misrepair of DNA damage (e.g., mutant and neoplastically transformed
cells). 

 

Natural background ionizing radiation (sparsely ionizing low-LET forms)
appear to over and over activate the transient system of protection.
Doses just above natural background radiation likely most efficiently
activate the system of protection. This radiation-induced protection we
called "adapted protection".  Adapted protection is a form of hormesis.
Progressively reducing doses to below natural background levels is
expected to lead to a progressive loss of adapted protection.  Whether
or not adapted protection is missing at a given dose depends on the
individual and their specific threshold for activating the protection.
Also for a single individual, different thresholds may apply to the
different components of the protective system.

 

Related to adapted protection associated with the PAM process and immune
system stimulation, our modeling results lead to a cancer relative risk
(RR) relationship given by:

 

RR(S) = S + [(1-S)/(1-PROFAC)].          (1)

 

Equation 1 applies only to very low radiation doses (at, below, and
slightly above natural background levels). The variable S (explained
shortly) can range from 0 to 1.  The protection factor (PROFAC) gives
the proportion of spontaneous cancers that are avoided due to induced
adapted protection (not including activated high-fidelity DNA repair)
and therefore also takes on values from 0 to 1.  We have modeled
protection associated with DNA repair as not influencing the PROFAC
parameter but influencing another parameter not discussed here which
comes into play at higher doses than are being considered here. The
variable S is called the stochastic effects normalized dose and takes on
a value of 1 at the minimum absorbed low-LET radiation dose for which
the indicated system of protection is fully activated for each person in
the irradiated population.  S appears to take on a value of one at a
low-LET dose on the order of about 0.01 mGy.  RR is set to one at the
absorbed dose for which S=1.  Above this dose, the RR appears to remain
fairly constant for a rather large range of values of S.  Thus, Equation
1 does not apply to this higher dose range. As S decreases below 1, RR
increases (opposite of LNT hypothesis) as indicated by Equation 1,
approaching the limiting value of 1/(1-PROFAC). 

 

At moderate and high absorbed radiation doses D, protection is lost and
RR then appears to increase linearly as a function of the absorbed
radiation dose D for a range of doses.  This corresponds to the absorbed
dose range where the LNT (linear-no-threshod) function has been applied
in epidemiological, ecological, and laboratory animal studies.

 

We have validated Equation 1 using available ecological data for cancer
induction for average monthly natural background radiation doses in the
range 0.02 to 0.08 mSv (total low- and high-LET radiation dose).
Equation 1 therefore allows evaluation of the minimal impact of reducing
natural background radiation to near zero on cancer RR. Minimal impact
applies here since only loss of protection associated with the PAM
process and immune system stimulation are accounted for with Equation 1.
For chronic exposure over years at a low rate, PROFAC can be > 0.5 and a
value as large as 0.86 has been derived for protecting against lung
cancer by chronic low-level gamma irradiation.  Using a value of 0.5 for
PROFAC, at least a doubling in cancer cases would be expected with
removal of natural background ionizing radiation.  Taking into
consideration that high-fidelity DNA repair may also be lost (i.e. not
activated to protect from spontaneous genomic instability) the factor of
2 could increase by orders of magnitude.

 

High-LET alpha particles do not by themselves seem to activate the PAM
process.  However, for combined exposure of Mayak workers to low doses
and dose rates of alpha plus gamma radiations, the gamma-ray component
seems to activate the PAM process and suppress lung cancer induction by
alpha radiation and cigarette smoke 

( http://www.radiation-scott.org/Los_Alamos_Seminar_Nov_05_B_Web_ver.pdf
).

 

Thus, there is an untold radiation protection story:  low doses and dose
rates of low-LET ionizing radiation protect against cancer via
activating a system of protective processes (i.e., adapted protection).
Similar protection is also expected against spontaneous noncancer
diseases that are associated with genomic instability.  Reducing natural
background radiation would be expected to lead to increases in cancers
and other diseases associated with genomic instability.  Excessive
cleanup of radionuclide contaminated sites may not provide any added
protection from cancer.  Instead, some radiation induced adapted
protection against genomic-instability-associated diseases could be
lost.  For persons (e.g., heavy smoking adults) exposed to low-level
radioactive fallout from the Chernobyl accident, cancers cases may
decrease rather than increase.  The chronic low-level radiation exposure
may suppress lung cancer associated with smoking.  Diagnostic X rays
(chest X ray and CT scans) appear to activate the system of transient
protective processes discussed and may be contributing in a small way to
the suppression of cancers and other genomic-instability-associated
diseases.

 

Bobby R. Scott

Lovelace Respiratory Research Institute

Albuquerque, New Mexico USA

 

Related Publications:

 

Scott BR, Stochastic thresholds:  A novel explanation of nonlinear
dose-response relationships for stochastic radiobiological effects.
Dose-Response (in press).

 

Scott BR, Radiation hormesis and the control of genomic instability.
Book Chapter, in New Research on Genomic Instability, Nova Science
Publishers, Inc., Hauppage, NY (accepted).

 

Scott BR et al., Biological basis for radiation hormesis in mammalian
cellular communities.  International Journal of Low Radiation
(accepted).

 

Scott BR, A biological based model that links genomic instability,
bystander effects, and adaptive response.  Mutation Research
2004;568:129-143.

 

Scott BR, Low-dose radiation risk extrapolation fallacy associated with
the linear-no-threshold model.  BELLE Newsletter 13(2), Part 2; December
2005:22-27. http://www.belleonline.com/newsletters/volume13/vol13-3.pdf