Re: Epidemiology

[epirad@mchsi.com]

Jerry,



I would be glad to respond briefly, but would prefer you 

contact me directly if you want ot continue an extended 

dialogue.  I really do not have the time to respond to 

the 5 posts generated for each one of my posts to the 

list.  I also don't want to present my view merely to 

argue with others.  It really serves no purpose.  There 

are many more productive ways we could all be spending 

our time. 



In brief response to your points below:



1) I am not clear what you mean by "applying the 

approach" so really do not know how to respond to your 

comment.  I was talking a good bit in the past about 

cross-level bias so perhaps that is what you are 

referring to? Cross-level bias is generally not a 

problem with case-control studies, but usually occurs in 

ecologic studies like the one performed by Dr. Cohen.



2) Why is it up to the detractors to explain this?  I 

have explained this since 1998 in our HPJ Forum article 

and follow-up articles.  If you would have taken the 

time to read those papers the response in those papers 

would be evident.  Perhaps you can tell me what you 

specifically disagree with in our published articles on 

this topic?



Jay Lubin again gave a theoretical example again showing 

how an inverse assocaition can occur in a publication 

this month.  Have you taken the time to read it?  If so, 

perhaps you can tell me where Dr. Lubin is in error.



3) We have presented many mechanisms and Dr. Cohen feels 

they are inplauible.  Most others think they are very 

plausible.  The problem Dr. Cohen starts with is an 

inplausible LNT formula.  If one want to try to perform 

eecologic studies, they should start with a plausible 

LNT model on the individual level.  Unfortuntely, 

Cohen's model is not plausible.  Why should I have to 

explain his results in plausible terms (that meet his 

criteria of plausible) when he starts with an 

inplausible model?  Please see out HPJ papers for 

details why I believe his model is inplausible. 



4) Your 4th statement is not supported by the majority 

of scientific studies that have the power to examine the 

relationship between radon exposure and lung cancer.



Bill

-----------------------

R. William Field, M.S., Ph.D.

College of Public Health

Department of Epidemiology

Department of Occupational and Environmental Health

N222 Oakdale Hall

University of Iowa

Iowa City, Iowa  52242



319-335-4413 (phone)

319-335-4748 (fax)

mailto:bill-field@uiowa.edu 

Community of Science CV : 

http://myprofile.cos.com/Fieldrw



 

> Bill,

> In case my comments were too subtle and may have shot over you head,

> I'll try to explain the points I tried to make in simpler terms:

> (1) By applying the approach used in attempting to discredit Bernie Cohen's

> Radon studies, one could cast doubt on any or all epidemiological studies,

> including the one indicating that smoking causes cancer. In any such study

> there may be factors that we are unaware of causing or influencing the

> results.

> (2) In criticizing such work, the detractors at least ought to offer some

> plausable explanation of how or why these factors could have biased the 

> results.

> (3) Similarly, it would be helpful if those performing the study would

> suggest a mechanism that might account for the observed results. 

> Bernie did not suggest such a mechanism--other than to offer the 

> obvious conclusion that any presumption of LNT is bogus.

> (4) Perhaps it is presumptuous of me to do so, but I will suggest a

> mechanism to account for the observed results. Maybe, just maybe, 

> the  inverse correlation between radon levels and lung cancer 

> incidence  is due to hormetic effect of  radiation causing an increased 

> immunity to cancer. If hormesis is a valid concept (and I believe it is), 

> it would  readily explain the observed negative correlation between 

> radon levels and cancer incidence.     Jerry

> 

> 

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