[ RadSafe ] Research shows CT and nuclear imaging tests during pregnancy do not boost the risk of childhood cancer
garyi at trinityphysics.com
garyi at trinityphysics.com
Mon Oct 4 21:28:48 CDT 2010
Doll et all (yuk yuk :)
wrote that selection bias was not proven, and that Mole showed such bias was unlikely based
on twin studies.
Doll OUGHT to have shown selection bias could NOT account for the measured mortality
increase. Evidence from Mole seems weak, based on small study size (70 twin lukemias, 91
twin cancers). Further, near the end of that paper, Mole attempts to reconcile the significant
difference in results between atomic bomb survivors and the OSCC data, essentially by
assuming hormesis. Here's a quote:
On the other hand, the basic assump- tions underlying these comparisons may be in
error. It is not in fact the case that increasing radiation dose always leads to an
increased frequency of induced malignancy (Mole, 1973). It is the general rule, both
in experimental work and in observations on man, that there is an optimum radiation
dose and that for larger exposures the frequency of induc- tion per unit dose
decreases. There is an elementary radiobiological reason for this. Whatever the
mechanism of cancer induction, there must be a multiplication of the transformed cell
or cells before the cancer can become clinically evident. Ionizing radiation can kill
cells and can sterilize them so that, though viable for a time, they cannot reproduce.
Thus, the observed frequency of induced malig- nant disease after doses in the
cell sterilizing range will always be less than the frequency expected from the induc-
Maybe I'm reading that wrong, but it kinda sounds like the ABS had fewer fatal cancers from
antenatal irradiation because they got more dose.
Abstracts from at least one of Mole's later works (after the twins study) suggest that he did
not accept the LNT model. (Br J Radiol. 1987 Jan;60(709):17-31.)
Clonal hypotheses predict that there will be a virtual threshold for polycystic (non-
stochastic) forms of radiation damage. It may be misguided to adopt a linear dose-
response relationship for deriving risk estimates for the practical purposes of
radiological protection unless some mechanism for production of clinically evident
harm can be advanced which provides a plausible reason for expecting linearity.
If he felt the twins study was so strong, why would he later write something like that? Also, I
see the error bars on most of the studies in the Doll paper extend to relative risk values less
Two animal studies cited in the Doll study:
Rats exposed in utero to 266 cGy, vs exposure at 3 and 9 mos. Per the abstract, the higher
sensitivity in utero was mainly in organogenesis, which we already knew. Besides, what is
this 266 cGy study supposed to tell us about medical imaging doses, or LNT? The other
animal study showed a "small increase in cancer" for beagles exposed in utero to 83 cGy, vs
a 16 cGy control group. I didn't actually read it or the abstract, but that doesn't sound like
great evidence for anything. If they had asked me, I would have told them before hand that
the 83 cGy group would have higher morbidity/mortality than the 16 cGy group. Duh.
What do they teach these kids now a days in school, hmm?
On 4 Oct 2010 at 17:06, Howard Long wrote:
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Otto, I support Bobby in this, with what info is available to me now.
No doubt, pregnancies with x-ray were more often followed by complications,
(Doll's study) but that is why the xrays were taken, --- expected complications!
I did pelvimetry in my office 50 years ago and remember that women with smaller pelvis had
poor nutrition -- one well known reason for fetal malformation.
On Oct 4, 2010, at 3:05 PM, "Otto G. Raabe" <ograabe at ucdavis.edu> wrote:
> At 12:51 PM 10/2/2010, Scott, Bobby wrote:
>> Research shows CT and nuclear imaging tests during pregnancy do not
>> boost the risk of childhood cancer
> As you surely already know, beginning in 1956 Alice Stewart and her followers have demonstrated a strong statistical association between pre-natal X-rays and childhood cancer in the Oxford Survey of Childhood Cancer OSCC . These data and positions received considerable prestige with the review of the data by Doll and Wakeford (The British Journal of Radiology, Vol 70, Issue 830 130-139,1997)
> Risk of childhood cancer from fetal irradiation
> R Doll and R Wakeford
> Imperial Cancer Research Fund Cancer Studies Unit, Radcliffe Infirmary, Oxford, UK.
> The association between the low dose of ionizing radiation received by the fetus in utero from diagnostic radiography, particularly in the last trimester of pregnancy, and the subsequent risk of cancer in childhood provides direct evidence against the existence of a threshold dose below which no excess risk arises, and has led to changes in medical practice. Initially reported in 1956, a consistent association has been found in many case-control studies in different countries. The excess relative risk obtained from combining the results of these studies has high statistical significance and suggests that, in the past, a radiographic examination of the abdomen of a pregnant woman produced a proportional increase in risk of about 40%. A corresponding causal relationship is not universally accepted and this interpretation has been challenged on four grounds. On review, the evidence against bias and confounding as alternative explanations for the association is strong. Scrutiny
of the objections to causality suggests that they are not, or may not be, valid. A causal
explanation is supported by evidence indicating an appropriate dose-response relationship
and by animal experiments. It is concluded that radiation doses of the order of 10 mGy
received by the fetus in utero produce a consequent increase in the risk of childhood cancer.
The excess absolute risk coefficient at this level of exposure is approximately 6% per gray,
although the exact value of this risk coefficient remains uncertain.
> Prof. Otto G. Raabe, Ph.D., CHP
> Center for Health & the Environment
> University of California
> One Shields Avenue
> Davis, CA 95616
> E-Mail: ograabe at ucdavis.edu
> Phone: (530) 752-7754 FAX: (530) 758-6140
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