[ RadSafe ] Calculated Health Impacts of Reducing Natural Background Ionizing Radiation

[Scott, Bobby]

Related to writing a chapter entitled "Radiation Hormesis and the
Control of Genomic Instability" for a Nova Science Publishers, Inc. book
with the tentative title "New Research on Genomic Instability," I now
have some new modeling results that led to the following conclusions: 

 

1.  Reducing current natural background ionizing radiation to near zero
would be expected to lead to significant increases in cancer and other
genomic instability associated diseases as well as increased mortality
from these diseases.  

 

2. A significant reduction in life expectancy would therefore be
expected to be associated with reducing natural background ionizing
radiation to near zero. 

 

I recognize that it may not be possible to reduce natural background
ionizing radiation to near zero; however, carrying out calculations of
the expected health consequences can be quite informative, especially in
light of the widely circulated claims by some (largely in the US) that
any amount of ionizing radiation is harmful (linear, no-threshold [LNT]
hypothesis).

 

Our modeling research shows that at current natural background radiation
levels and at lower levels, the risk of radiation-induced cancer should
be governed by the degree to which a system of protective biological
processes (normal DNA repair/apoptosis, presumed related to the p53
protein; an auxiliary apoptosis process that selectively removes
genomically unstable cells and is presumed to be independent of p53; and
immune system stimulation) is activated. This system of transient
protection against harm is activated by low doses of low-LET radiation
including natural background low-LET radiation.  Dose somewhat above
natural background radiation also activate the protection.  We call this
form of low-stress activated protection "adapted protection."  Our
dose-response models for low-dose radiation-induced stochastic
biological effects are called "adapted protection models".  Adapted
protection is a form of hormesis, thus our models are also called
hormetic models.  

 

Natural background radiation doses above a stochastic threshold (which
varies for different individuals) probably over and over activates the
indicated system of protection, which is transient.  Background low-LET
radiation (including gamma rays associated with radon progeny) doses
accumulated over a few weeks may be sufficient for activating the
transient protection.  High-LET alpha radiation by itself appears not to
activate the protection, based on limited data for neoplastic
transformation. Each of us likely has a different threshold for
activating the indicated protection.  Below the minimum threshold, no
protection from the indicated system is expected in anyone.  Low
fidelity DNA repair which is error-prone may operate below the threshold
but it is also possible that no repair would occur.  Above the maximum
threshold, each of us are expected to have the system of protection
activated, but not if the doses are too high where a second stochastic
threshold comes into play and inhibits a significant amount of
protection.  This second threshold however appears to be quite large in
comparison to natural background radiation and probably depends on dose
rate (increasing as dose rate is reduced). These stochastic thresholds,
guarantee nonlinear dose-response curves for radiation-induced effects
such as mutations, neoplastic transformation, and cancer.

 

According to the LNT hypothesis, reducing a natural background radiation
(low- plus high-LET) dose of 0.05 mSv to 0.0000000005 mSv (eight-fold
lower) would be expected to reduce the risk of cancer by a factor of
100,000,000. In contrast our adapted protection modeling results
indicated that such a dose reduction would be expected to lead to the
loss of low-dose-radiation (low-LET component) induced adapted
protection leading any where from a modest to an astronomical increase
in cancers and other genomic instability associated diseases.  New
funded research is needed to reduce the indicated uncertainty.

 

The adapted protection indicated when activated by low-level, low-LET
radiation can reduce the cancer incidence to far below the spontaneous
level.  Many epidemiological and ecological studies have shown this.
Unfortunately, poorly designed epidemiological studies of nuclear
workers have apparently misinterpreted adapted protection to be a
healthy worker effect.  Such studies should be designed to allow
distinguishing between the healthy worker effect and adapted protection.
Funding agencies should insist on this for future nuclear-worker-based
studies that they fund.

 

In closing, our modeling results should bring pause to those who have in
the past not hesitated to make dire predictions of large numbers of
cancer deaths after low-level radiation exposures of large populations
based on the LNT hypothesis.  I thought that readers of the Radsafe
Digest would like to know about our new findings.  The calculations are
rather complicated and therefore are not presented here but are included
in the indicated chapter.  I will submit an e-mail to the digest when
the chapter is published for those who may have interest in reading it.

 

Sincerely,

Bobby R. Scott

Senior Scientist

Lovelace Respiratory Research Institute

2425 Ridgecrest Drive SE

Albuquerque, NM 87108 USA