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UNSCEAR is indeed a high-grade scientific organization,
not (one assumes) given to distorting information. I would look elsewhere
for the source of apparent contradictions.
In
this case, based on the information given below I don't see the
contradiction. The UNSCEAR statement about elevated thyroid cancer appears
to be supported by the referenced paper, as quoted in Jerry's email further down
the thread?
Jeremy
Whitlock
Can it be that UNSCEAR distorts scientific
information?
The scientists who authored the study [F13]
stated clearly that there was a decrease in overall cancer incidence and
mortality. How can UNSCEAR state in Para. 265 that the risk is
elevated? What else did they distort?
And I thought UNSCEAR is a high-grade scientific
organization.
Jerry Cuttler
265. Two recent studies [F13, R17] found an elevated risk of
thyroid cancer mortality following adult 131I treatment for
hyperthyroidism, which is in contrast to previous studies of hyperthyroid
patients [H14] or patients examined with 131I [H6]. The reason for
referral, i.e. the underlying thyroid disorder, could have influenced the
risk, since the highest risk was seen less than five years after exposure. The
thyroid dose (60-100 Gy) received
by most hyperthyroid patients had previously been considered as having a
cell-killing rather than a carcinogenic effect.
----- Original Message -----
Sent: Tuesday, February 03, 2004 6:27 AM
Subject: Re: My letter to NN, Jan 2000, Re: Dose-response
follow-up for nuclear medicine I-131 therapies
Dear Jerry,
You may be interested in seeing how skilfully the
consultant of UNSCEAR distorted the information from the Birmingham
study. See paragraph 265, in page 497, Annex J, UNSCEAR Report
2000.
Best wishes,
Zbigniew
----- Original Message -----
Sent: Saturday, January 31, 2004 12:40
AM
Subject: My letter to NN, Jan 2000, Re:
Dose-response follow-up for nuclear medicine I-131 therapies
Jim, see my letter to Nuclear News of 2000 Jan
31:
When I think about the linear no-threshold (LNT) hypothesis of
radiation carcinogenesis, I am reminded of the famous quotation: "The great tragedy of science is the
slaying of a beautiful hypothesis by an ugly fact."2 How can the LNT hypothesis continue
to be an exception to this fundamental requirement of science? Are political, social and economic
considerations preventing us from opening our minds to a different
hypothesis?
The University of Birmingham study of radioiodine treatment of
hyperthyroidism, recently published in The Lancet,3 provides yet
another of the hundreds and hundreds of ugly facts that contradict the LNT
hypothesis.4 This
study of 7414 adult patients, treated in Birmingham UK between 1950 and 1991
with a mean cumulative dose of 308 MBq of iodine-131, identified 638 cancer
diagnoses and 448 cancer deaths in 1971-91 among the treated patients. This was compared with National
Statistics data on cancer incidence and mortality for England and Wales,
specific for age, sex and period: 761 and 499. The standardized incidence ratio is
0.83 [95% confidence interval 0.77-0.90] and the standardized mortality
ratio is 0.90 [0.82-0.98].
"There were increases in incidence and mortality for cancers of the
small bowel and thyroid, although the absolute risk of these cancers was
small." The scientists
concluded, "The decrease in overall cancer incidence and mortality in those
treated for hyperthyroidism with radioiodine is reassuring."
It certainly is reassuring when we realize that a dose of 308 MBq
corresponds to ~280 mSv (or 28 rem) to the whole body.5 This is more than ten times
the average dose of 15 mSv (or 1.5 rem) received by the evacuees from the
30-km zone around the Chernobyl disaster.6 According to the radiation hormesis
model,4 a dose below the NOAEL point stimulates a protective
response and results in overall beneficial effects. If the dose is above this point,
defense mechanisms are weakened and overall adverse effects result.
I just can't get over the irony of this
situation. We design, build and
operate each of our nuclear plants to keep its likelihood of a severe
accident below once in a million years. And if this event actually did
occur, the doses to people outside the plant would likely be
beneficial! Yet we continue to
use the LNT hypothesis, and most people associate every nuclear activity and
incident with their likelihood of getting a cancer, and they are just
terrified of cancer.
Can we expect the prospects for nuclear power to improve as long as
LNTH continues to thrive?
Sincerely,
Jerry Cuttler
References:
2.
Huxley TH (1825-95), "Collected Essays 1893-94
Biogenesis and Abiogenesis."
3.
Franklyn JA, Maisonneuve P, Sheppard M, Betteridge J and
Boyle P, "Cancer incidence and mortality after radioiodine treatment for
hyperthyroidism: a population-based cohort study," The Lancet 353, 1999 June 19, pp
2111.
4.
Calabrese EJ, Baldwin LA. "Radiation hormesis: origins,
history, scientific foundations," BELLE Newsletter 8:2, University of Massachusetts,
School of Public Health, Amherst, MA 01003, 1999 December. See also
http://www.belleonline.com/home82.html
5.
Eisenbud M, "Environmental Radioactivity, 2nd
Edition," Academic Press, New York, 1973, pp 421-425.
6.
"Chernobyl - ten years on: radiological and health
impact," an appraisal by the NEA Committee on Radiation Protection and
Public Health, Nuclear Energy Agency, Organisation for Economic Co-operation
and Development, 1995 November, pp 47.
-----------------------------------------
----- Original Message -----
Sent: Friday, January 30, 2004 11:05
AM
Subject: Dose-response follow-up for
nuclear medicine I-131 therapies
Friends,
Please review
the following abstract for the significance of measured acute and late
effects, as chromosomal damage, of I-131 therapies.
What are dose
conversion estimates (whole body, not thyroid) for 300-3700
MBq doses?
This study is
one of the very few studies that have been conducted to measure human
biological responses in the 10s of millions of patients that are exposed
to nuclear medicine procedures. (The primary interest is in diagnostic
procedures. I have not distributed various papers on P-32 for polycythemia
vera because it is fundamentally high-dose therapy. I-131 is also,
but the high dose is to the thyroid with a low to moderate dose to the
whole body - with epi follow-up as reported in our early studies by
Rosalyn Yalow and others, primarilty from work by Las-Erik Holm and others
from Swedish data.)
The failure to conduct dozens of such studies to follow human
biological responses from injection and ingestion of radionuclides in the
face of the "LNT debate" is unfortunate, if not unforgivable. I invited
Dr. Carretta, as past president of the SNM, to address this in our
Nov 2000 sysmposium on medical applications, but he then did not do
so.
Do you know of
any other such studies that are being conducted?
I do not have
access to this journal. I would appreciate a copy and any comments on the
significance of this study to the assessment low-dose
response.
Thank
you.
Regards, Jim
Muckerheide
====================
Eur J Nucl Med Mol Imaging. 2004 Jan 28 [Epub ahead of print]
Iodine-131 treatment and chromosomal damage: in
vivo dose-effect relationship.
Erselcan T, Sungu S, Ozdemir
S, Turgut B, Dogan D, Ozdemir O.
Department of Nuclear
Medicine, Cumhuriyet University School of Medicine, P.K. 806, Sivas,
Turkey.
Although it is well known that radiation induces
chromosomal aberrations, there is a lack of information on the in vivo
dose-effect relationship in patients receiving iodine-131 treatment, and
the results of previous studies are controversial. In this study, the
sister chromatid exchange (SCE) method was employed to investigate acute
and late chromosomal damage (CD) in the peripheral lymphocytes of 15
patients who received various doses of (131)I (259-3,700 MBq), either for
thyrotoxicosis (TTX) or for ablation treatment in differentiated thyroid
cancer (DTC). The SCE frequencies in cultured peripheral lymphocytes were
determined before treatment (to assess basal SCE frequencies), on the 3rd
day (to assess acute SCE frequencies) and 6 months later (to assess late
SCE frequencies). The basal, acute and late SCE frequencies (mean+/-SD)
were 3.19+/-0.93, 10.83+/-1.72 and 5.75+/-2.06, respectively, in the whole
group, and these values differed significantly from each other (
P<0.001). In order to perform a quantitative evaluation of the present
data and a comparative analysis with the results of previous studies
reported in the literature, we defined acute and late effects using a
"damage ratio" (DR) and a "recovery ratio" (RR), based on the basal, acute
and late data for individual patients. No statistically significant
difference was found in the DR between DTC and TTX patients (76.4%+/-11.5%
vs 67.6%+/-9.0%), while the mean RR was higher in TTX patients than in the
DTC group (75.2%+/-24.4% vs 36.8%+/-13.7%). The DR on the 3rd day was not
related to the administered (131)I dose in the whole group, but a negative
correlation was found between the (131)I dose and the RR at the 6th month
( r=-0.60, P=0.04). The best fit for this relationship was obtained by a
linear-quadratic model, as y=104.89 x-28.4 x(2)+38.1 ( R(2)=0.51, P=0.04).
On the other hand, comparative analysis with the results of previous
studies with comparable sampling times revealed that the best fit for the
relationships between the administered dose of (131)I and DR and RR were
obtained with a linear-quadratic model ( Y=alpha D+beta D(2)) rather than
a linear one. However, there was an interesting difference in comparison
with in vitro studies, in that we found the coefficient beta to have a
negative value, suggesting the disappearance of damaged lymphocytes from
the peripheral circulation in a dose-dependent manner following (131)I
treatment. Further studies are therefore needed to clarify the effect of
the negative beta value on the biological dosimetry approach in continuous
internal low LET radiation, as in the case of (131)I treatment.
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