AW: AW: [ RadSafe ] Re: Exposed "had lower incidences of all cancers - "Environmental -

[Rainer.Facius at dlr.de]

Don,

if indeed continuous irradiation at the chronic exposure rates typical for the Taiwan sample population did suppress carcinogenesis by (i) accelerated cellular damage repair, (ii) by enhanced apoptosis of irreparable cells, (iii) by enhanced tissue homeostatic control due to a bystander effect and (iv) by raising the defences of the immune system due to as yet enigmatic mechanisms then - after approach to a stationary equilibrium level - you would expect what the earlier report claims to have seen. You would also expect that the thereby reduced cancer rate approaches again (from below) the normal cancer incidence rate after cessation of such a protective radiation exposure - what appears to be compatible with the later report. Given that and the data(!) of the later report one might muse whether one had done better to let these people continue to live in their flats - with the exception of the most highly exposed and of school children.

Unfortunately both reports present insufficient information to assess what other reasons might contribute to their discrepancy. The earlier lacks adequate data for me to assess technical aspects of epidemiology, the second only presents parameter fit values to support its claim but no data to assess the fit quality (Chisquare statistics and the like for me are only sufficient if you are estimating the parameters of an analytical model WELL founded in theory or first principles - and even then I would insist to see the scatterplot of the residuals if the result had any impact on my own work). So without proper methods (Chen 2004) and proper/complete data (Hwang 2006) the door remains wide open for speculations of any kind.

Your conclusion about follow-up studies of course remains appropriate! 

Kind regards, Rainer


Dr. Rainer Facius
German Aerospace Center
Institute of Aerospace Medicine
Linder Hoehe
51147 Koeln
GERMANY
Voice: +49 2203 601 3147 or 3150
FAX:   +49 2203 61970

-----Ursprüngliche Nachricht-----
Von: Don Higson [mailto:higsond at bigpond.net.au] 
Gesendet: Dienstag, 23. Januar 2007 00:09
An: Facius, Rainer; crispy_bird at yahoo.com; radsafe at radlab.nl
Cc: rad-sci-l at WPI.EDU
Betreff: Re: AW: [ RadSafe ] Re: Exposed "had lower incidences of all cancers - "Environmental - 

John, Rainier

Bearing in mind:

- the earlier report from Chen, Luan et al that a dramatic reduction of cancer incidence apparently took effect almost immediately, and
- the fact that there is still plenty of time for increases in the incidence of solid tumours due to the exposure to radiation from Co-60,

do you find it conceivable that there might have been short-term hormesis, followed by carcinogenesis in the longer-term? Follow-up studies certainly appear to be essential.

Don Higson

----- Original Message -----
From: <Rainer.Facius at dlr.de>
To: <crispy_bird at yahoo.com>; <radsafe at radlab.nl>
Cc: <rad-sci-l at WPI.EDU>
Sent: Tuesday, January 23, 2007 12:01 AM
Subject: AW: AW: [ RadSafe ] Re: Exposed "had lower incidences of all cancers - "Environmental -


John,

regarding the "reduced cancer incidences" the message of table III is equally clear. Concentrating on the pooled incidences for men and women the data say:
all cancers:       95/114.9 -> SIR95%=(0.67, 0.83, 1.01) : non-significant

all w/o leukaemia: 88/111.6 -> SIR95%=(0.63, 0.79, 0.97) : formally significant

all solid cancers: 82/109.5 -> SIR95%=(0.60, 0.75, 0.93) : formally significant

In my view, for the purely statistical evaluation of a putative beneficial association the same criteria should be applied as for the appraisal of a putative detrimental association, i. e., these data at best can serve as a justification to continue such epidemiological investigations. Hence, I would hesitate to claim the above 'positive' associations as proof for a beneficial action of those exposures.

However, such - by controlled, truly low dose and dose-rate laboratory work - well established phenomena like induced radiation resistance, adaptive response, non-monotonous dose response functions for several cancer related radiobiological endpoints at all levels of biological organization yield some plausibility to the assumption that biological mechanisms do exist which indeed might CAUSE the above association. My present bet
(prejudice) is that eventually the mechanisms behind these laboratory observations will be sufficiently elucidated so that the inference of a causation of the statistical observations will be justified.

Regarding the "consideration of all studies and not just one report" I would urgently invite you to quote the one or two studies which you consider as presenting the most compelling evidence that low dose and dose-rate exposure to low LET ionizing radiation below say 500 mSv causes cancer.

Kind regards, Rainer