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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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