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RE: Radon-Stirring the Pot



Good morning all,



I read again the following reference



1.Lubin, and J. Boice Jr., “Lung cancer risk from 

residential radon: Meta-analysis of eight epidemiologic 

studies,” J. Natl. Cancer Inst. 89, 49-57 (1997).



Fig 1 in the paper shows a wide dispersion of relative risk vs Radon

concentration around the no effect line. Confidence intervals for all

Relative Risk points, with 2 exceptions, include 1.  From the graph

itself it is impossible to detect an effect, either way.  The authors

say that the combined trend for all RR is 0,03, p=0.03, significantly

different from zero.



Could someone explain the statistical or practical meaning of "trend" in

that context and give references?  Plain English explanation would be

welcome.  In the few textbooks I checked trend refers generally to time

trends. 



Thank you in advance 



Philippe Duport

International Centre for Low-Dose Radiation Research

Institute of the Environment

Universirty of Ottawa

555 King Edward Ave.

P.O. Box 450, Stn. A

Ottawa, Canada, K1N 6N5

Tel: (613) 562 5800, ext. 1270

pduport@uottawa.ca

 



-----Original Message-----

From: owner-radsafe@list.vanderbilt.edu

[mailto:owner-radsafe@list.vanderbilt.edu] On Behalf Of epirad@mchsi.com

Sent: September 19, 2002 2:38 PM

To: radsafe@list.vanderbilt.edu

Subject: Re: Radon-Stirring the Pot



The basis for the BEIR VI risk estimates are derived 

mainly from extrapolations from radon-exposed miners.  I 

think both BEIR IV and BEIR VI provides the evidence to 

suggest prolonged radon progeny exposure is the second 

leading cause of lung cancer, but as you know this is a 

seemingly never ending debate. 



Regarding direct evidence - Residential Radon Studies.



Analytic epidemiologic studies (not ecologic) are used 

to infer whether causal associations are appropriate or 

not.



The main factors that must be considered in determining 

causality from epidemiologic studies are: consistency of 

results from case-control studies, chance (how likely 

are the findings from all positive studies due to 

chance?), bias (has potential sources of bias been 

identified), strength of association, dose response, 

temporality (disease occurs within a biologically 

reasonable time period after exposure), and biological 

plausibility (the association makes sense in light of 

what is known biologically).



These factors should all be considered in making causal 

inferences from analytic epidemiologic studies.  In many 

cases, lack of consistency among studies can be 

explained when there are good explanations for 

inconsistencies in studies such as small sample size or 

poor retrospective exposure assessment.   For example, 

the more rigorous recent case-control studies (see 

below) have consistently shown a positive association 

between residential radon exposure and lung cancer, even 

in non smokers. 



Also, see debates elsewhere: 

http://www.ntp.org.uk/951-TUD.pdf



1.Lubin, and J. Boice Jr., “Lung cancer risk from 

residential radon: Meta-analysis of eight epidemiologic 

studies,” J. Natl. Cancer Inst. 89, 49-57 (1997).



2. L. Kreienbrock, M. Kreuzer, M. Gerken, G. Dingerkus, 

J. Wellmann, G. Keller, G. and H.E. Wichmann, “Case-

control study on lung cancer and residential radon in 

western Germany.” Am. J. Epidemiol. 153, 42-52 (2001).



3.S. Darby, E. Whitley, P. Silcocks, B. Thakrar, M. 

Green, P. Lomas, J. Miles,  G. Reeves, T. Fearn, and R. 

Doll, “Risk of lung cancer associated with residential 

radon exposure in South-West England: a case-control 

study,” Brit. J. Canc. 78, 394-408 (1998).



4. Z. Wang, J.H. Lubin, L. Wang, S. Zhang, J.D. Boice 

Jr, H. Cui, S. Zhang, S. Conrath, Y. Xia, B. Shang, et 

al., “Residential radon and lung cancer risk in a high-

exposure area of Gansu Province, China,” Am J Epidemiol, 

155, 554-64 (2002). 



5.D. Krewski, J. Lubin, J. Zielinski, M. Alavanja, V. 

Catalan, R.W. Field, J. Klotz, E. Létourneau, C. Lynch, 

J. Lyon, D. Sandler, et al., “A combined analysis of 

North American studies of lung cancer and residential 

radon exposures,” American Statistical Association 

Conference on Radiation and Health, Deerfield Beach, 

Florida, (2002).



6. M.C. Alavanja, J.H. Lubin, J.A. Mahaffey, and R.C. 

Brownson, “Residential radon exposure and risk of lung 

cancer in Missouri,”  AJPH, 89, 1042-8 (1999).



7. R.W. Field, D.J. Steck, B.J. Smith, C.P. Brus, J.S. 

Neuberger, E.L. Fisher, C.E. Platz, R.A. Robinson, R.F. 

Woolson, and C.F. Lynch, “Residential radon gas exposure 

and lung cancer: the Iowa radon lung cancer study,” Am. 

J. Epidemiol. 151(11), 1091-1102 (2000).



8. M. Kreuzer, M. Gerken, L. Kreienbrock, J. Wellmann, 

and H.E. Wichmann,  “Lung cancer in lifetime nonsmoking 

men - results of a case-control study in Germany.” Br. 

J. Cancer 84(1) 134-40 (2001).



9. F. Lagarde, R. Falk, K. Almren, F. Nyberg, H. 

Svensson, G. Pershagen, “Glass-based radon-exposure 

assessment and lung cancer risk,”  J. Expo. Anal. 

Environ. Epidemiol. 12, 344-54, (2002).



Bill Field

bill-field@uiowa.edu

> Ruth Weiner wrote:



> Epidemiological studies do not "prove," or even show, causality; they

show 

> correlations, and correlation is not causality.  I belive that at

least part 

> of the epidemiological basis for this statement is the "Iowa Study" of

Field 

> et al.  I wouldn't draw this conclusion from the Iowa Study, but then

I am 

> not an epidemiologist either.

> 

> I would like to see both Bill Field 's and bernie Cohen's response to

these 

> questions.

> 

> Ruth.

> 

> Ruth Weiner, Ph. D.

> ruthweiner@aol.com

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