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Cases and Controls
John,
As I recall, smoking reduces the radon concentration in ambiant indoor air
by increasing the attached fraction. Therefore, the alpha dose to the lung
in smokers would remain essentially constant, whereas the alpha dose to
non-smokers in the room would increase due smoke, and decrease due to
radon.
I do not buy the arguement for using smokers when studying correlations
between low order (potential) lung carcinogens. One can use smokers to
study a correlation between second-hand smoke and lung cancer, and obtain a
statistically correlation, probably even publishable. I (and probably most
other people), would question the project for not excluding such an
overpowering factor in the study.
I am indeed familiar with Kreuzer's contribution [Br J Cancer (2001) 84(1),
134-140].
This is what I've drawn from the study.
(1) The paper suggests that chemical carcinogens are the second leading
cause of lung cancer.
(2) The study breaks down radon concentration categories (in Bq/m^3) to:
<50, 50-79, 80-139, >140. Considering that the action level in Germany (I
believe) is 200 Bq/m^3 for new structures and 400 Bq/m^3 for existing
structures, I don't understand why the data was truncated at the U.S. EPA
action level. Why didn't the data grouping expand to test the higher
internationally used categories?
(3) In West Germany, there was a negative correlation between radon and
lung cancer. As a matter of fact, there were no lung cancers in people
exposed >140 Bq/m^3, where at least one would be expected based on East
Germany data. The whole correlation between lung cancer and radon in the
study depends on 5 lung cancers in people exposed to >140 Bq/m^3 from East
Germany.
(4) 47% (23 / 49) of the cases had radon levels in the lowest group (<50
Bq/m^3).
(5) 90% (44 / 49) of the cases had radon levels less than the EPA action
level.
(6) From the 5 cases with radon levels above 140 Bq/m^3 an odds ratio (OR)
of 2.0 was made on the overall data. An OR of 5.0 was made based on just
the East Germany data. I believe these OR would disappear if the data were
categorized to include the European action levels.
Frankly, I think this study supports my earlier post.
Regarding non-smoking studies in miners [Roscoe, R. et al., Lung Cancer
Mortality Among Nonsmoking Uranium Miners Exposed to Radon Daughters, JAMA,
Vol. 262, No. 5, 8/4/1989] found 14 lung cancers in 516 non-smoking miners.
None of the cases had radon levels less than 465 WLM.
Tom
John Williams wrote:
>
> Tom,
>
> There was no residual confounding noted in the Iowa Study. They
> checked for it.
>
> Multivariate analysis is a very powerful tool for adjusting for
> smoking. It does not require matched 1:1 case to control. In fact,
> such matching gets you away from your population based design of the
> study.
>
> The alpha particle exposure from polonium 210 is adjusted for as part
> of the smoking adjustment (pack-year rate). Tom, recall that the
> overall effective dose from radon is reduced when the radon progeny
> attach to particulates from the tobacco smoke.
>
> As far as specifics of their adjustment, I would ask the Iowa authors
> for those details on their analyses. They have kindly responded to
> all the questions I posed to them. In fact, if you check the archives
> Dr. Field himself spent many days discussing the study and responding
> to questions on this listserv. I have seen no other author of any
> case-control study do the same.
>
> As far as non smoking studies, Field refers to a positive German
> study in his debate and Becker. See Kreuzer article in Br. j. of
> Med. I have not had a chance to read it yet, have you?
>
> http://www.ntp.org.uk/951-TUD.pdf
>
> Sent by Law Mail
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--
Thomas Mohaupt, M.S., CHP
University Radiation Safety Officer
104 Health Sciences Bldg
Wright State University
Dayton, Ohio 45435
tom.mohaupt@wright.edu
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(937) 775-3761 (fax)
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