Re: Mechanisms are Needed to Explain Cohen's Data

[BERNARD L COHEN <blc+@PITT.EDU>]

On Tue, 8 Jan 2002, Kai Kaletsch wrote:



> Of course, it is also interesting to test a better model than BEIR IV.

> Therefore, we could also test a model that correlates lung cancer to lung

> dose. This is a separate issue.



	--See Sec.M of my 1995 paper. I would be delighted to do my

analysis with another model (eg BEIR-VI) if I could get it published. It

would be a lot of wasted effort if I couldn't get it published. If someone

would suggest this in a letter to the Editor, that would open the door for

me to do the analysis and get it published, at least briefly.



> 1.    The first mechanism that I want to propose is the possibility of an

> incorrect smoking to radon relationship on the county level. Homes with

> smokers have on average 0.9 times the radon concentration of homes where no

> one smoked.

> It is not a trivial matter to take the known relationship that homes with

> smokers have on average 0.9 times the radon concentration of homes where no

> one smoked and move this to the county level. How was this done in the

> analysis of Cohen's data?



	--See my forthcoming paper on "Treatment of confounding factors in

an ecological study" which is posted on my web site

	www.phyast.pitt.edu/~blc

This problem is treated in the latter part of Section D and in Table 4

>

> 2.    The second mechanism deals with the influence of smoking on the

> Equilibrium factor F.



	--This is effectively a difference in radon exposure for smokers

and non-smokers, which is treated in the reference above, Sec D and Table

4.



 There are competing factors that affect the

> Equilibrium factor in smokers' houses (increased ventilation reduces F,

> increased aerosol concentrations increase F, air cleaners reduce F .). I

> have no idea which one would be dominant



	--When considering air cleaners, it is vital to include their

effect on unattached fraction. Air cleaners can easily reduce the WLM, but

they also increase the unattached fraction and the two effects normally

cancel each other fairly closely. That is why air cleaning is not

generally regarded as a cheap and easy way to solve the radon problem.



> 3.    The third mechanism deals with the influence of smoking on the number

> of unattached radon progeny in the air. This becomes important if we want to

> test the data against an "improved" BEIR model, one that uses lung dose as

> the suspected carcinogen, rather than WLM. Unattached radon progeny are said

> to deliver larger lung doses than attached radon progeny.



	--Again this is essentially a difference between radon exposures

for smokers and non smokers, covered in the above reference





> :) ] The point is that the mechanism is all-important. Every observation

> must have an explanation, whether the observation is on an individual level

> or an aggregate level. If you are not looking for a mechanism, you are not

> doing science!



	--In any large data set such as mine (nearly a million data

entries) there are innumerable correlations. I use these to give

perspective on what sort of correlations are plausible. But I don't see

why it is necessary to explain them. "Doing science" is largely testing

theories, and if the test fails, it is only necessary to find a not

implausible reason for the failure if the theory is to survive. In my

studies, I have not been able to find such a not implausible explanation

that could save LNT.



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