[Date Prev][Date Next][Thread Prev][Thread Next][Date Index][Thread Index]
RE: Mechanisms are Needed to Explain Cohen's Data
Ken Bogen addressed the biological mechanisms, and showed that EPA's
environmental radon data by county for the US vs. women lung cancer
mortality 1950-54 (smoking prevalence 4% and 11% in two age groups)
confirms Cohen's data showing beneficial results at low doses. See,
e.g.:
http://www.belleonline.com/n3v72.html
See the two paragraphs under "Materials and Methods," and Fig 2a!
Another of the many substantial studies that confirm Cohen's results.
You have recommended that the LNT-defenders consider mechanisms to
support their position, but the very best of the science establishment
have spent a decade trying, and failing, to produce any plausible
mechanism to make the LNT theory "explain" the factual observations,
without just rationalizations parroted here, and producing poor science
and obfuscated data to support the LNT.
Regards, Jim Muckerheide
-----Original Message-----
From: Kai Kaletsch
Sent: Fri 11-Jan-02 2:21 PM
To: BERNARD L COHEN
Cc: RadSafe
Subject: Re: Mechanisms are Needed to Explain Cohen's Data
----- 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 11:09 AM
Subject: Re: Mechanisms are Needed to Explain Cohen's Data
> > > 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.
>
> --I thought the problem you raised was that the radon progeny are
> different for smokers and non-smokers.
3 separate mechanisms were proposed (all related to smoking): 1. The
presence of smokers systematically decreasing radon gas levels for
non-smokers. 2. The effect of smoking on the conversion between radon
gas
and WLM. 3. The effect of smoking on the conversion between radon gas
and
lung dose. (Numbers 2 and 3 deal with the conversion between a measured
quantity and a quantity of interest.)
> > You are trying to use the total amount
> > of radon in the county and divide it up between smokers and
non-smokers.
>
> --I am not trying to divide it up. I normally assume the same
> average radon levels for smokers and non-smokers. In special
treatments, I
> assume there to be differences and investigate the consequences.
It is the special treatments that I was referring to (latter part of
Section
D in your paper on treatment of confounding factors). I think these
special
treatments are necessary for any study that tries to investigate the
link
between lung cancer and anything else. Especially, if the "anything
else" is
systematically related to smoking.
> --My treatments of plausibility of correlation are based on the
> assumption that there is no strong direct mechanism,
If everything but radon concentration and lung cancer is random and if
your
sample is big enough, everything "comes out in the wash". The question
is
what is a "strong" direct mechanism. The argument being made by others
is
that small systematic mechanisms (they call them biases) can have a
large
effect on the shape of your graph. My position is that they must
identify,
or at least propose, those mechanisms before I buy the argument.
Best Regards,
Kai Kaletsch
************************************************************************
You are currently subscribed to the Radsafe mailing list. To
unsubscribe,
send an e-mail to Majordomo@list.vanderbilt.edu Put the text
"unsubscribe
radsafe" (no quote marks) in the body of the e-mail, with no subject
line. You can view the Radsafe archives at
http://www.vanderbilt.edu/radsafe/