[ RadSafe ] EMS Meeting Abstract Related to LNT Controversy

[Scott, Bobby]

Dear Colleagues:

 

The abstract below has been accepted for the indicated upcoming meeting.
I thought that readers of the RadSafe Digest may find the abstract of
interest.  In addition, on Monday of this week I presented an in-house
seminar at our Institute entitled "Background radiation may be
protecting us from cancer and other diseases."  I have made a pdf
version of the seminar and would be happy to e-mail it to interested
researchers.

 

Sincerely,

Bobby R. Scott, Ph.D.

Senior Scientist

Lovelace Respiratory Research Institute

2425 Ridgecrest Drive SE

Albuquerque, NM 87108 USA

 

BASIC RESEARCH RESULTS THAT DO NOT SUPPORT THE BEIR VII REPORT
CONCLUSION REGARDING THE LINEAR-NO-THRESHOLD RISK HYPOTHESIS.  Scott RB,
Haque M, Di Palma J, Lovelace Respiratory Research Institute, 2425
Ridgecrest Drive SE, Albuquerque , NM.  Abstract for poster presentation
at 9th International Conference on Environmental Mutagens & 36th Annul
Meeting of the Environmental Mutagen Society, San Francisco, California,
September 3-8, 2005.

The BEIR VII Report (Phase 2) concluded that the empirical,
linear-no-threshold (LNT) hypothesis for low-dose extrapolation of
cancer risk is valid for low-linear-energy transfer (LET) radiation
exposure. This includes exposure to background radiation.  However,
there is growing evidence from basic research that low doses of certain
agents (e.g., low-LET radiation and genotoxic chemicals) can activate
protective processes that together lead to a reduction in mutations,
neoplastic transformation, and cancer below the spontaneous frequency.
However, after moderate or high doses, some of the protection appears to
be lost, leading to elevated risks for the indicated biological effects.
In this presentation, an existing dose-response model (NEOTRANS3) is
presented which attributes the low-dose protection to cooperative
protective processes: (1) presumed p53-dependent, high-fidelity DNA
repair/apoptosis and (2) a presumed p53-independent protective
apoptosis-mediated (PAM) process.  The indicated PAM process selectively
removes genomically compromised cells (e.g., mutants, neoplastically
transformed cells), is mediated via reactive oxygen and nitrogen
species, and for fibroblast, mediated by transforming growth factor beta
1 (TGF-b1).  Activation of the PAM process appears to require a
protective stochastic threshold, DPAM, which varies for different
individuals (in vivo), and also in vitro for different replicate
samples.  In addition, above a deleterious stochastic threshold, Doff,
the PAM process appears to be inhibited but not the high-fidelity,
presumed p53-dependent repair/apoptosis.  Because of the indicated
protective and deleterious stochastic thresholds, dose-response
relationships for mutagenesis, neoplastic transformation, and cancer
induction are predicted to be of the nonlinear hormetic type for
low-linear energy transfer (LET) radiation.  Our research results do not
support the general validity of the LNT hypothesis.  Rather, our results
indicate that use of the LNT dose-response function can lead to creating
phantom excess risks for stochastic radiobiological effects at low
doses, where in fact a reduction in risk occurs.  Research supported by
the Office of Science (BER), U.S. Department of Energy Grants
DE-FG02-03ER63671 and DE-FG02-03ER63657.