| Copyright © 2009. National Academy of Sciences. All rights reserved. Terms of Use and Privacy Statement |
Below are the first 10 and last 10 pages of uncorrected machine-read text (when available) of this chapter, followed by the top 30 algorithmically extracted key phrases from the chapter as a whole.
Intended to provide our own search engines and external engines with highly rich, chapter-representative searchable text on the opening pages of each chapter.
Because it is UNCORRECTED material, please consider the following text as a useful but insufficient proxy for the authoritative book pages.
Do not use for reproduction, copying, pasting, or reading; exclusively for search engines.
OCR for page 168
AppendE~c B
Responses to Selected Comments by the Public
This section provides responses to various questions
and comments posed to the subcommittee at the public meeting
held in Spokane, Washington, in June 1999.
Comment: Differences in terrain were not included in the
fallout model, and there were great differences in mountains
and plains in that area.
Response: Major terrain effects are indirectly accounted for in
the HEDR dose mode! even though the computer code
assumed a flat terrain for the entire area being modeled. The
terrain was implicitly taken into account in the meteorologic
projections of where the ]3~{ pane went and to a lesser extent
in a "surface roughness parameter". The hourly meteorologic
data from the 16 stations in the geographic area roughly reflect
the effects of the Cascade range, the Blue Mountains south of
WalIa Walla, and the Bitterroot Mountain range east of
Spokane, Coeur d'A1ene, and Lewiston. The modeling of
terrain effects in a more detailed manner is impeded by the
severe limitations of the meteorologic data that are available
for the mode] for 1944-1947, the period of greatest interest.
168
OCR for page 169
Append['x B
169
Comment: The Spokane area has had a historically high
thyroid disease incidence due to lack of iodized salt or other
sources of iodine. Were the data corrected for the high
incidence in the Spokane area in the 1940s and 1950s?
Response: iodized salt was widely available by the 1940s, so
low dietary iodine might have been an issue only in some
unidentified and probably small subset of children in that era.
Development of thyroid disease related to iodine deficiency
typically takes a number of years of low iodine intake. The
children in this study, born when iodized salt had already been
introduced, were probably much less subject to iodine-
deficiency disease than were their parents and grandparents.
However, one potential impact of low iodine in a
subset of the children might have been to increase the uptake of
|3~}, that is, to give iodine-deficient children more radioactive
iodine than they otherwise would have received. In the absence
of knowledge of which children were iodine-def~cient, it would
be impossible to factor this into the individual dose estimates.
Comment: The cohort studied should have been far larger, at
least 10,000 persons. More higher doses should have been
included in the cohort.
Response: The
calculations of
HTDS investigators performed initial
statistical power that showed excellent
statistical power for the set of assumptions that they used,
which at the time appeared plausible; and that made them think
that they did not need any more subjects. However, the NRC
subcommittee believes that their assumption that dose-
measurement errors were of a type ("Berkson error") that did
not adversely affect statistical power is unlikely to be valid.
There are several reasons to believe that the dose-measurement
errors did reduce statistical power. Hence, we agree that in
principle a larger study would have been very desirable.
OCR for page 170
170
Review of the HTDS Draft Final Report
Nevertheless, it seems unlikely that the number of
high-dose study subjects could have been increased
appreciably. it is preferable to study those who were young
children (less than 10 years old and preferably less than 5) at
the time of AT exposure, in that children, adolescents, and
adults are markedly less sensitive to radiation effects on the
thyroid than young children are. The HTDS investigators
apparently studied all possible young children in the high-dose
counties (Adams, Franklin, and Benton) unless there are other
high-dose counties that the subcommittee is unaware of. The
only other possibility would have been to increase the numbers
somewhat in the intermediate-dose category (for example,
WalIa Walla County), but this would probably have increased
the statistical power by only a small amount, and adding more
subjects from low-dose counties would likewise have only a
small effect on statistical power.
Comment: Increases in mortality and birth defects were high in
the area before and after the Hanford exposure period with no
explanation.
Response: Perinatal mortality (death rate during the first
month of life) and mortality due to birth defects (congenital
anomalies) were somewhat higher than national rates.
However, as the comment noted, they were higher in the area
both before and during the period of Hanford fallout exposures.
Therefore, it seems not very likely that the higher rates were
caused by the fallout. A more detailed study of birth defects in
Hanford downwinders found no increase in birth-defect rates,
except for a possible increase in neural-tube defects (Sever and
others, 1988~.
Comment: Risk analyses from other ]3~{ thyroid studies appear
different than this study.
OCR for page 171
Appendix B
171
Response: The Utah study of thyroid disease after Nevada Test
Site ~3~! fallout showed marginal excesses of thyroid cancer,
thyroid nodules, and both combined; but when dose
uncertainties were properly included in the risk estimates, the
results were not statistically significant. Furthermore, our
subcommittee shows in its report that the thyroid-cancer risk
estimates from the Utah and Hanford studies are probably
statistically compatible with each other.
A comparison with the Marshall islanders is
questionable because the doses were very high for children on
the islands studied and were mostly from short-lived forms of
radioactive iodine and gamma rays, rather than from Mar.
Two studies of ~3~T administered to young people
for diagnostic medical purposes have not shown statistically
significant excesses of thyroid cancer (Holm, 1991; Hamilton
and others, 1989~. The average thyroid doses in the two studies
were about 800 and 1500 mGy. However, most ofthe subjects
were adolescents at the time of }3~{ exposure, and the atomic-
bomb study and other studies show that radiation exposure in
adolescence causes much less thyroid cancer than the same
exposure in early childhood. Therefore, it is difficult to
interpret the negative results.
the Chernobyl studies In Ukraine and Belarus have
shown increases in thyroid cancer after the Chernobyl 13~}
releases. The risk per mGy is not well quantified at this point,
so it is not clear whether the Chernobyl and Hanford results are
statistically compatible.
a. a. . . . ~ . .
Comment: The study should have investigated synergism with
other environmental insults.
.
Response: The study did make some attempt to do so with
regard to radiation, the main known environmental risk factor
for thyroid disease. The HTDS investigators obtained a history
of diagnostic and therapeutic medical irradiation and
OCR for page 172
172
Review of the HTDS Draft Final Report
information on occupational radiation exposure, and they found
no synergism.
Other studies have found little evidence of
synergism of radiation and other environmental exposures in
causing thyroid cancer. For instance, one study that has
investigated this found no synergism of oral contraceptive use,
hormone-replacement therapy, and smoking (Shore and others,
19931.
Comment: A study of "clusters" should be done, particularly in
families in which no previous thyroid disease had been found.
Families with thyroid problems should be studied.
Response: At the various public-comment meetings, a number
of people who lived in downwind areas stated their belief that
they and their families had experienced more frequent thyroid
diseases than would have been expected in the population at
large. They could be right, and their disease could have been
the result of unusual fallout or ingestion patterns. However, it
is also true that thyroid disease tends to run in families, and the
particular occurrences could be related to genetic factors in the
families, chance, or even mistaken diagnoses. A compilation
and study of such clusters could have been undertaken, but that
would have been a special study and was not part of the HTDS
design.
Comment: Screening effects are a major unresolved issue that
needs evaluation.
Response: The HTDS investigators wanted to compare the rate
of thyroid cancer among the Hanford downwinders with that
found in an unirradiated general population. But to do so they
knew that they needed to take account of the fact that their
study population all had sensitive thyroid screening with
ultrasonography and palpation of the thyroid by expert thyroid
OCR for page 173
Appendix B
173
physicians. It is well known that many more thyroid cancers
and nodules are detected when there is intensive screening.
To address the inequity in thyroid-cancer or nodule
detection between the intensively screened population and the
general US population, the investigators chose an increase by a
factor of 3 in thyroid-disease rates due to screening on the basis
of an estimate in a 1985 publication (NCRP, 19851. However,
two studies since then have suggested different screening
factors, from 2.5 to about 7 for thyroid cancer and 17 for
thyroid nodules (Thompson and others, ~ 994~. Hence, we have
much uncertainty about the size of screening effects. That is
one of the reasons that it was more appropriate to compare
disease rates within the study population, in which everyone
underwent screening, than between this study population and
some other, mostly unscreened population.
Comment: Other health problems that could possibly result
from IT exposure should be included and not just thyroid
disease alone.
Response: IT concentrates in the thyroid, where it remains for
several weeks. The concentration and long residence time lead
to potentially large doses to the thyroid. Other organs receive
only about one-thousandth of the dose received by the thyroid,
and retain IT
or its
because they do not concentrate and retain CAST
radioactive metabolites. Except for the parathyroid glands, no
other organs could have received biologically significant doses
from the environmental releases from Hanford. The
parathyroid glands are intimately attached to the thyroid and
receive fairly high doses because of their proximity. Changes
in parathyroid function were screened for, and no changes
related to radiation injury were found; because no effects were
seen in the parathyroid glands, it is most unlikely that radiation
effects in other organs would have occurred and gone
undetected.
OCR for page 174
174
Review of the HTDS Draft Final Report
Comment: Doses were too low to detect any thyroid changes.
Only about 2 dozen in the study had estimated doses over 100
red.
Response: Many scientists believe that the bulk of evidence
suggests that even quite small doses can cause thyroid cancer.
For instance, a study in Israel of children who received x-ray
thyroid exposure of about 100 mGy (10 red) had clear excesses
of thyroid cancer and thyroid nodules (Ron and others, 19951.
In comparison, the average thyroid dose in the HTDS was
about I80 mGy (~8 red).
However, it is generally believed that nit is less
effective in causing thyroid disease than are x-rays, and this
might be especially true when the 13~{ doses are spread out over
several years (dose protraction tends to reduce the amount of
cell damage that cells cannot repair).
Comment: Effects of 13~ and x-rays should be considered
equivalent.
Comment: The AT dose-response relationship for thyroid
disease is not linear. There is a threshold for radiation effects
on the thyroid.
Response: Human data on thyroid cancer after gamma-ray
exposures (in the Japanese atomic-bomb study) or medical
studies of x-ray exposure are best fitted as a linear dose-
response association (Ron and others, 1989), although a
threshold at some low dose under 0.! Gy (10 red) cannot be
conclusively ruled out. There are no compelling biologic
reasons for the shape of the dose-response curve to differ
greatly for ]3~} exposure. in fact, the best study comparing the
effect of x-ray and HI exposure in rats found essentially the
OCR for page 175
Appendix B
175
same dose-response relationships for both (Lee and others,
1 982~. Furthermore, the largest body of data on thyroid cancer
after childhood exposure to IT the Chernobyl data-also
show a substantial excess of thyroid cancer in the estimated
dose ranges of 0.~-0.5 Gy (10-50 red) and 0.5-~.0 Gy (50-100
red), although there is a suggestion that ill} is only about 50°/0
as effective as gamma rays in inducing thyroid cancer (Jacob
and others, 1998~.
Representative terms from entire chapter:
thyroid disease