[ RadSafe ] The Role of Low-Dose Radiation in the Maintenance of Life

[Scott, Bobby]

John:

Thanks for your interest in our low-dose radiation research. For
clarification, we are not monitoring irradiated humans.  Our research
mainly focuses on researching, interpreting, and reporting research data
(molecular, cellular, tissue/organ, and systemic levels) obtained by
other scientists.  That low doses of low-LET radiation can protect
(sometimes called adaptive response and sometimes called hormesis)
against stochastic effects such as mutations, neoplastic transformation,
and cancer is now becoming widely published.  Doses as low as 0.02 mGy
of ionizing photon radiation induce protection (suppressed spontaneous
mutations) in animal studies.  Low-dose data from numerous
epidemiological and ecological studies of radiation-induced cancer show
evidence for radiation suppressing cancer rather than increasing cancer.
The data involve a wide range of doses and dose rates. A paper (Chuck
Sanders is first author) has been submitted for publication which
discusses much of the indicated data showing cancer suppression by low
doses and dose rates or low-LET radiation or combinations of low and
high-LET radiation.  The paper relates to a presentation given at the
2006 International Hormesis Society Conference.

Increase cancer risk after low doses of low-LET radiation (or
combinations of low and high-LET radiation) is essentially created by
using an in appropriate risk modeling assumption for characterizing the
risk at low doses.  The most popular but incorrect assumption used is
that any amount of ionizing radiation, including low-LET radiation, is
harmful, and that cancer increases linearly with dose. This model
assigns increased risk even for natural internal irradiation of our
bodies (e.g., associate with potassium-40).  High-dose-rate and
high-dose data usually determines the slope of the caner risk
dose-response curve (e.g., data from Hiroshima and Nagasaki). Risk at
low doses and dose rates are then projected based on reducing the slope
of the high-dose-rate dose-response curve by a fixed amount (low-dose
and dose-rate effectiveness factor, DDREF).

Please note that the claim by experts that any amount of radiation is
harmful led to more than 100,000 lives being lost via abortions
(radiation-phobia driven) following the Chernobyl accident, while fewer
than 10 cancer deaths (thyroid cancer) have been so far attributed to
low-dose radiation exposure in associated with the Chernobyl accident.
Tens to hundreds of thousands of cancer deaths were predicted by some
experts shortly after the accident. 

Radiation-phobia driven casualties (LNT-related) are the current main
risks in association with low doses of ionizing radiation in the event
of a radiological terrorism incident involving a large population and
low-level, low-LET radiation exposure.

Regarding the question as to whether low-dose radiation provides a weak
or strong cancer-suppression benefit, in some cases it has been a weak
and in other cases a strong benefit.  Weak benefits seem to be
associated with low doses of low-LET radiation delivered at a high rate.
Strong benefits seem to be associated with low and moderate doses of
low-LET radiation delivered at a low rate over years.  Such data are
discussed in the cited submitted paper with Chuck Sanders as first
author.

Our research results indicate that the cancer suppressive effects of low
doses of low-LET radiation depend on age, increasing with age. Thus, the
very young may benefit much less from protection than the elderly.
Further, we have not found evidence for a purely alpha-radiation source
inducing protection against stochastic effects.  In addition, our
research has led us to conclude that each person likely has a different
(stochastic) low-LET radiation threshold for activating the protective
processes that suppress cancer occurrence.  Thus, for a given low dose
of low-LET radiation, a person selected at random may have a higher
threshold and in such cases would therefore not be expected to benefit
from the protection.  Thus, we do not claim that a specified low dose of
radiation is necessarily beneficial to all (although it may be
beneficial to most, depending on dose and dose-rate histories).  In
addition, each person is thought to have a higher deleterious stochastic
threshold that inhibits at least some or the protection (e.g.,
suppression of immunity).  The indicated protective and deleterious
stochastic thresholds lead to nonlinear dose-response relationships. 

For readers of the Radsafe Digest who have interest in stochastic
thresholds and their expected impact on dose-response curve shape, you
may find the following publication to be a useful reference:

Scott BR. Stochastic thresholds: A novel explanation of nonlinear
dose-response relationships for stochastic radiobiological effects.
Dose-Response 3:547-567, 2005.

An upcoming book chapter may also be of interest to some Radsafe Digest
readers:

Scott BR. Natural Background Radiation-Induced Apoptosis and the
Maintenance of Mammalian Life on Earth. Chapter 1 in: New Cell Apoptosis
Research, L.C. Vinter (Editor), Nova Science Publishers, Inc.
https://www.novapublishers.com/catalog/product_info.php?products_id=4948
&osCsid=432f071849b59bb26326e99721f8335a


Sincerely,
Bobby R. Scott
 

-----Original Message-----
From: John Jacobus [mailto:crispy_bird at yahoo.com] 
Sent: Friday, October 27, 2006 2:51 PM
To: Scott, Bobby; radsafe at radlab.nl
Subject: RE: [ RadSafe ] The Role of Low-Dose Radiation in the
Maintenance of Life 

Dr. Scott,
Yes, I have heard the old saw too many times.  I
prefer caveat emptor.

Of course dose rate is important.  That is the basis
for fractionation of radiation therapy.  So does the
end point of the study.  Exactly what doses and dose
rates above background are you talking about?  Are the
effects seen in humans?  And what effects are you
monitoring.  If you monitor the blood of a patient and
find an increase of some cellular component, this may
indicate that the response is due to cellular damage
and of or the cytokines being released from the
affected cells.  If the immune cells attack the
damaged cells and not the undamaged tumor cells, what
is the consequence?  Does the tumor survive?  

If radiation is recognized as a weak carcinogen, is it
also a weak benefactor?
--- "Scott, Bobby" <BScott at lrri.org> wrote:
 (http://www.yahoo.com/preview)