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RE: Another (partial) literature review
-----Original Message-----
From: Les Crable
yes, these just came up also. Jim, if we want to see these articles, we
will sign on the Radiation Science and Health Listserv. You post them
all
there don't you? We all know how to run a pubmed search. Should we all
post abstracts every time a new radiation related article appears on pub
med?
<Les, While these aren't lit review papers, a couple are interesting.
I'll try to find the papers in the next few days. At first cut, the
first seems to just be creative hypotheses built on hypotheses, finally
using a-bomb survivor thyroid cancer (??) as a basis to "correlate" with
H4-RET damage, with no consideration of the damage-repair processes at
low vs. high doses (for chromosome aberrations, much less cancer
induction). They don't address natural variations vs. doses, or thyroid
cancer here, but maybe in the paper. It's been a while since I saw the
'94 a-bomb survivor solid-cancer data (Rad Res) but it's unlikely to
show effects at low doses, unless the increase beyond 35 years has a low
dose component?
The second seems to be just another weak case-control study that doesn't
seem to have the data to produce a credible result.
The Curtis paper looks interesting, and potentially useful.
The discussion of Field's paper seems complete, but I haven't read it
and should.
Darby/Doll seems just a "defending/proliferating the faith" paper to the
Oncologists. Sarah Darby's last paper on radon studies wasn't very
credible.
The same of Frumpkin/Samet, in spades. "...radon IS the second leading
cause
of lung cancer," even though there was none before smoking. In Eastern
Europe there was negative correlation even then with radon (per Werner
Schuttmann, the East German medical authority and campaigner against
excess radon exposure to miners in the service of the Soviet uranium
mining/production).
The RSH list isn't open. When we did we lost some of the senior around
the world scientists who wouldn't put up with the nonscience and
beligerent reponses that comprise the "debate." :-)
I recommend that you/all post credible papers that are reasonably judged
to be relevant to the science, and perhaps the policy, of the issue. It
contributes beyond the simple rhetoric of opinions.
Regards, Jim
============
Radiat Environ Biophys 2001 Sep;40(3):191-7
On target cell numbers in radiation-induced H4-RET mediated papillary
thyroid cancer.
Radivoyevitch T, Sachs RK, Nikiforov YE, Nikiforova MN, Little MP.
Department of Epidemiology and Biostatistics, Case Western Reserve
University, Cleveland, OH 44106, USA. radivot@hal.cwru.edu
Radiation-induced human papillary thyroid cancer (PTC) is associated
with
chromosomal inversions that involve the genetic loci H4 and RET on
chromosome 10. Recently, experimental data has shown that these loci lie
in
very close spatial proximity in a high proportion of adult human thyroid
cells. Applying the generalized formulation of dual radiation action to
this
H4-to-RET geometric distance data, we predict here the radiation
dose-response of H4-RET induction. The predicted H4-RET dose-response
has a
linear-to-quadratic transition dose of approximately 7 Gy, suggesting
the
validity of linear risk extrapolations to very low doses for H4-RET
mediated
radiation-induced PTC. In conjunction with A-bomb survivor data, the
predicted H4-RET dose-response yields estimates of the number of PTC
target
cells that are of the order of approximately 10(6) to approximately
10(7)
cells, i.e. considerably less than the total number of follicular cells
in
the thyroid gland.
--------------
PubMed Identifier
11416777
Authors
Lagarde F. Axelsson G. Damber L. Mellander H. Nyberg F. Pershagen G.
Institution
Institute of Environmental Medicine, Karolinska Institutet, Stockholm,
Sweden.
Title
Residential radon and lung cancer among never-smokers in Sweden.
Source
Epidemiology. 12(4):396-404, 2001 Jul.
Abstract
In this study, we attempted to reduce existing uncertainty about the
relative risk of lung cancer from residential radon exposure among
never-smokers. Comprehensive measurements of domestic radon were
performed
for 258 never-smoking lung cancer cases and 487 never-smoking controls
from
five Swedish case-control studies. With additional never-smokers from a
previous case-control study of lung cancer and residential radon
exposure in
Sweden, a total of 436 never-smoking lung cancer cases diagnosed in
Sweden
between 1980 and 1995 and 1,649 never-smoking controls were included.
The
relative risks (with 95% confidence intervals in parentheses) of lung
cancer
in relation to categories of time-weighted average domestic radon
concentration during three decades, delimited by cutpoints at 50, 80,
and
140 Bq m(-3), were 1.08 (0.8--1.5), 1.18 (0.9--1.6), and 1.44
(1.0--2.1),
respectively, with average radon concentrations below 50 Bq m(-3) used
as
reference category and with adjustment for other risk factors. The data
suggested that among never-smokers residential radon exposure may be
more
harmful for those exposed to environmental tobacco smoke. Overall, an
excess
relative risk of 10% per 100 Bq m(-3) average radon concentration was
estimated, which is similar to the summary effect estimate for all
subjects
in the main residential radon studies to date.
--------------------------------
: Phys Med 2001;17 Suppl 1:157-60
The role of promotion in carcinogenesis from protracted high-LET
exposure.
Curtis SB, Luebeck EG, Hazelton WD, Moolgavkar SH.
Fred Hutchinson Cancer Research Center, Seattle WA 98109, USA.
Recent analysis of epidemiological studies using the two-stage clonal
expansion (TSCE) model has shown that radiation-induced promotion
dominates
radiation-induced initiation for protracted exposures to radon. This
strong
promotion effect (i.e. enhanced proliferation of already-initiated
cells)
causes a pronounced 'inverse dose-rate effect', but by a mechanism
completely different from those usually discussed in this connection.
This
rather startling result is discussed along with implications to extended
space missions that include a significant amount of high-LET radiation.
It
is suggested that the effect might be caused by a 'Bystander Effect' by
which normal cells in the vicinity of initiated cells are hit by alpha
particles and send out signals that modify the cell kinetics of the
already-initiated clones.
----------------------
: Rev Environ Health 2001 Jul-Sep;16(3):151-67
A review of residential radon case-control epidemiologic studies
performed
in the United States.
Field RW.
College of Public Health, Department of Epidemiology University of Iowa,
Iowa City, Iowa 52242, USA. bill-field@uiowa.edu
Lung cancer is the leading cause of cancer death in the United States
for
both men and women. Although most lung cancer deaths are attributable to
tobacco usage, even secondary causes of lung cancer are important
because of
the magnitude of lung cancer incidence and its poor survival rate. This
review summarizes the basic features and major findings from the
published
U.S. large-scale residential radon case-control studies performed in New
Jersey, Iowa, and Missouri (two studies). The methodology from an
unpublished study covering Connecticut, Utah, and Southern Idaho is also
presented. Overall, the higher categorical risk estimates for these
published studies produced a positive association between prolonged
radon
exposure and lung cancer. Two studies (Missouri-II and Iowa) that
incorporated enhanced dose estimates produced the most compelling
evidence
suggesting an association between prolonged residential radon exposure
and
lung cancer. The prevailing evidence suggests that the statistically
significant findings may be related to improved retrospective radon
exposure
estimates. The general findings from the U.S. studies, along with
extrapolations from radon-exposed underground miners, support the
conclusion
that after cigarette smoking, prolonged residential radon exposure is
the
second leading cause of lung cancer in the general population
---------------
Ann Oncol 2001 Oct;12(10):1341-51 Related Articles
Radon: a likely carcinogen at all exposures.
Darby S, Hill D, Doll R.
Clinical Trial Service Unit, University of Oxford, UK.
sarah.darby@ctsu.ox.ac.uk
BACKGROUND: Radon is a well-established lung carcinogen that has been
extensively studied. Very high concentrations can occur in some
underground
mines. Concentrations also tend to build up in homes. MATERIALS AND
METHODS:
Epidemiological studies of radon-exposed miners and of residential radon
and
lung cancer are reviewed. Quantitative estimates of the risk of lung
cancer,
based on the experience of the miners, are applied to residential radon
exposures in the United Kingdom. Strategies for the prevention of lung
cancer induced by residential radon are discussed. RESULTS: Estimates
are
uncertain, but residential radon is probably responsible for about 2000
lung
cancer deaths per year in the United Kingdom, or around 6% of the total,
making it the second biggest cause after smoking. Over 80% of the deaths
are
estimated to occur at ages less than 75 and over 80% in smokers or
ex-smokers. Around 90% of radoninduced deaths in the United Kingdom
probably
occur as a result of exposures to radon concentrations below the
currently
recommended action level of 200 Bq m(-3). CONCLUSIONS: Further work is
needed to obtain more reliable estimates of the risk of lung cancer
associated with residential radon and on the cost-effectiveness of
various
intervention strategies before the most appropriate policies can be
developed for managing exposure to this natural carcinogen.
-----------------
CA Cancer J Clin 2001 Nov-Dec;51(6):337-44, 322; quiz 345-8
Radon.
Frumkin H, Samet JM.
Department of Environmental and Occupational Health, Rollins School of
Public Health, Emory University, Atlanta, GA, USA.
Residential and occupational exposure to radon is the second leading
cause
of lung cancer after cigarette smoking. As many as eight million homes
in
the US have elevated radon levels according to Environmental Protection
Agency estimates. High exposure levels in homes are largely a result of
radon-contaminated gas rising from the soil. This makes it an unusual
indoor
air pollutant in that it has a natural source. This study examines the
synergism between smoking and radon, what levels are considered safe,
and
what to do to safeguard against overexposure to radon.
-\------------------\
>From: "Jim Muckerheide" <jmuckerheide@cnts.wpi.edu>
>Reply-To: "Jim Muckerheide" <jmuckerheide@cnts.wpi.edu>
>To: <radsafe@list.vanderbilt.edu>
>CC: <rad-sci-l@ans.ep.wisc.edu>
>Subject: Another (partial) lliterature review
>Date: Sun, 13 Jan 2002 03:11:31 -0500
>
>For some reason this just came up on PubMed (indexed 1/10/02). I had
>thought Biogerontology had been indexed, but maybe not. A number of
>informative papers on aging with in vivo results demonstrating
>biopositive effects of radiation and other stressors have been pub'd in
>this journal, esp. by Rattan in the Netherlands.
>
>Work funded by NRC! Black hole? Rad protectionists suck in everything
>with mass? NRC funded NCRP-136. Could expect NCRP to address the data
>(as directed by the Chairman following our presentations in 1996). NCRP
>suppressed the data. Only zero-mass science and "the ether" get out!
>:-)
>
>Regards, Jim
>==========
>
>Biogerontology 2000;1(4):309-19
>
>The effects of gamma rays on longevity.
>
>Calabrese EJ, Baldwin LA.
>
>Department of Environmental Health Sciences, Morrill Science Center,
>School of Public Health, University of Massachusetts, Amherst, MA
01003,
>USA. edwardc@schoolph.umass.edu
>
>A number of animal model studies have assessed the capacity of
long-term
>whole body gamma rays to affect life span. The initial goal of such
>studies was to establish the equivalent of a no observed adverse
effects
>level (NOAEL) that would provide a toxicological foundation for
deriving
>an acceptable worker exposure standard. In the course of initial
studies
>to establish such a 'tolerance threshold', data emerged suggesting that
>low dose rates/cumulative doses enhanced longevity in mice and guinea
>pigs of both sexes. Extensive large scale follow-up investigations with
>other mouse strains and rats revealed what appear to be
>inter-strain/species differences in response with some models providing
>strong evidence for a low dose increase in longevity. The subsequent
>positive studies in mouse models were generally well designed, well
>conducted and used extensive numbers of mice. In all experiments that
>displayed enhanced longevity the average life span was enhanced by
>10-30% but not the maximum life span potential. The underlying
>mechanisms affecting the apparent enhancement in longevity are believed
>to result from the stimulation of hematopoietic and immune systems
>following an initial low level chronic injury to the bone marrow.
>
>
>
>***********************************************************************
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