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Re: Mechanisms are Needed to Explain Cohen's Data
IMHO, this whole radon-LNT gig is getting tiresome, and should be classified as much sound and fury signifying nothing. Furthermore, the participants
seem confined to a few individuals, which is a strong indication that my opinion is NOT an outlier.
I thus respectfully request that the participants take their debate to another forum.
BTW, it may be healthier for those involved to switch to a more worthwhile activity, e.g., watching sitcoms.
The opinions expressed are strictly mine.
It's not about dose, it's about trust.
Bill Lipton
liptonw@dteenergy.com
Kai Kaletsch wrote:
> ----- Original Message -----
> From: "BERNARD L COHEN" <blc+@pitt.edu>
> To: "Kai Kaletsch" <info@eic.nu>
> Cc: "RadSafe" <radsafe@list.vanderbilt.edu>
> Sent: Friday, January 11, 2002 8:40 AM
> Subject: Re: Mechanisms are Needed to Explain Cohen's Data
>
> > --This reopens the old question of whether we should measure radon
> > gas or radon progeny in homes. There was a general consensus that it
> > should be radon gas because factors that influence radon progeny also
> > influence unattached fraction in a way that compensates, so we should not
> > neasure radon progeny unless we also measure unattached fraction and that
> > would be a very difficult and expensive proposition.
>
> That leaves you open to a possible cross confounding effect with smoking.
>
> > Note that your suggestion would also affect every other study that
> > has ever been done on radon vs lung cancer, including all the case-control
> > studies.
>
> I am not trying to explain case control studies of radon in homes. There is
> nothing to explain. The error bars are too big and the results are too
> random at the very low levels that we are interested in. Your data is strong
> enough to deserve an explanation.
>
> (As for the old miner studies, I think the dosimetry there has bigger
> problems than a small correlation between dose and smoking, even if some of
> the measurements were for radon gas.)
>
> > --Are you suggesting that a treatment is needed for non-smokers
> > living in houses where there are smokers? That would be very difficult in
> > any study.
>
> Actually, I was looking for some reassurance (perhaps by a mathematical
> exercise) that this could not bias your results by much.
>
> > In case-control studies, they don't ask whether there are other
> > people in the house who smoked.
>
> They don't have to. They actually measure the radon concentration of the
> house and assign it to the occupants. You are trying to use the total amount
> of radon in the county and divide it up between smokers and non-smokers. I
> am saying that your formula for dividing the dose may be wrong. Your table 4
> might address my mechanism by varying a correlation coefficient between x
> and r. I'm not sure.
>
> > > I meant the use of filtration units that is causally related to smoking.
> I
> > > think in most cases the combination of smoking and filtration will
> result in
> > > a higher number of attachment sites than the combination of not smoking
> and
> > > no filtration.
> >
> > --This depends on the type of filtration. I have tested filtration
> > and precipitation instruments that drastically reduce the number of
> > attachment sites.
>
> Even a 100 % efficient filtration unit running 100% of the time can only
> cause an exponential decay in the number of attachment sites in the room,
> because the cleaned air is immediately mixed with the old air. The smokers
> that I know only turn on their filters once you can no longer see your hand
> in front of your face.
>
> > > I don't see how one can judge the plausibility of the correlation, if
> one
> > > does not consider the underlying mechanism. For example, you deal with
> > > migration in your papers and conclude that it cannot explain the
> observed
> > > radon - lung cancer relationship. Would that conclusion still hold if
> the
> > > following mechanism was to be confirmed?:
> > >
> > > High radon in the interior of the US causes precursor to lung cancer
> > > conditions in people . These precursor conditions make the dust, pollen
> and
> > > cold air of the interior unbearable and these people move to the coast,
> > > where radon levels are low. There the precursor conditions develop into
> lung
> > > cancer.
> >
> > --I think most people would consider this to be very highly
> > implausible
>
> That was my point: plausibility of the correlation depends on the
> plausibility of the mechanism.
>
> > > I would be glad to write a letter to the Editor saying that these 20 or
> 30
> > > mechanisms must be disposed.
> >
> > --That would be fine with me but they should be problems that do
> > not apply to case-control studies. Also, I could not respond to 20-30
> > mechanisms, so I would much prefer if you could specify a few that are
> > most important in your list.
>
> I don't have a list. My original post was intended to challenge the people
> who want to save LNT to come up with specific mechanisms for cross level
> biases rather that use generic arguments like "Cohen's effect is caused by
> cross level biases". I gave a few possible examples to start them thinking.
>
> Best Regards,
> Kai Kaletsch
>
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