Summary
NCRP Committee 1 has misrepresented the scientific data to support its
false premise that low-dose radiation (LDR) might be harmful. But the data say otherwise. The Committee:
1. Produced voluminous irrelevant
and misleading data to support the linear no threshold (LNT) premise.
2. Selectively misrepresented and
obfuscated data that do provide highly statistically significant
and consistent evidence of LDR benefits, and null dose-response effects, that
contradict the LNT.
3. Failed to consider the
voluminous scientific literature, submitted to them by the scientific
community, including RSH, that consistently contradicts the unsupported LNT
premise.
The NCRP’s position
leads to extreme radiation protection policies requiring enormous public
expenditures for no public health benefit. This will be challenged before the Federal
agencies that would be misled; before authorities that assess scientific
misconduct, and the Office of Scientific Integrity; and before the Congress,
and the courts.
Overview
1. The Committee has primarily compiled
material that is not relevant to health effects dose-response:
·
Data from
irradiated cells, without anti-mutagenic functions, falsely imply effects to
living organisms
·
Other high
dose, high-dose-rate, data from conditions that overwhelm the body’s natural
defenses
·
Japanese bomb
survivors (‘instantaneous’ doses; neutrons; poor dosimetry; major confounders)
·
Uranium
miners and other extreme conditions (diesel fumes; silica dust; poor dosimetry;
smoking)
2. The Committee virtually ignores the
vast body of low-dose radiation research data:
·
Human and
animal data that show beneficial effects, with no harmful effects where LNT
‘predicts’ effects
·
Laboratory
data and analysis that reveal the many molecular and cellular stimulatory
mechanisms
·
Successful
treatment of cancer and other diseases in humans and animals
3.
Falsely
presents data from credible studies that show statistically-significant
benefits from LDR:
·
Nuclear
Shipyard Workers Study (24% lower overall mortality; 99.9+% confidence level)
·
Canadian
fluoroscopy study (statistically-significant reduced breast cancer, called an
“anomaly”)
·
The many
population radon studies (consistent decreases in lung cancer with increasing
radon)
4. Inappropriately applies the fact that
initial damage to DNA is linearly proportional to dose:
·
Initial damage from radiation is trivial
compared to that from normal metabolism
·
LDR
stimulates anti-mutagenic systems, so persistent mutations are reduced
overall
4.
Misleads
about a higher percent of double-strand breaks (DSBs), that are harder to
repair, from radiation
·
There are
still 1000 times more DSBs produced by metabolism than by background radiation
·
LDR enhances
error-free enzymatic repair of all DSBs, which are mostly produced by
metabolism
5.
Misleads about
the fact that radiation can linearly increase chromosomal damage
·
Chromosome
aberrations do not cause adverse health effects
Relevant
data and concerns about such flaws were provided to the Committee. Our data
presented to the NRC in 1996 caused Chairman Jackson to formally require the
NRC staff to inform the NCRP that such deficiencies must be avoided – and
specifically to consider all relevant data.
These admonitions were ignored.
In the March 1999 NRC review of the October 1998 draft, the Committee
again committed to the NRC to consider all of the relevant data. Despite this
official warning, the NRC effectively rescinded Chairman Jackson’s direction,
by indicating that NRC, and its Advisory Committees, would not hold the
Committee accountable.
Initial Comments
[more comprehensive comments being developed]
Following doggedly in the
path of its predecessors, NCRP Committee 1-6 reported on its six-year
evaluation of low-dose radiation health effects as predicted by the linear
non-threshold (LNT) premise. The Committee
asserts (p.6) “it is
important to note that the rates of cancer in most populations exposed to
low-level radiation have not been found to be detectably increased, and that in
most cases the rates have appeared to be decreased.”
Despite this proven fact, the Committee concludes that radiation
protection policy and regulations should continue on the false “biophysical”
premise (NCRP 121, p.45) that any amount of radiation, no matter how small, is
hazardous and should therefore be reduced to “as low as reasonably
achievable.” The Committee does not
claim that this premise is shown to be valid.
They merely state that the possibility “cannot be excluded.” But this possibility falls if the overwhelming contrary scientific
evidence is considered.
Less than two pages, plus a
few scattered phrases, of this 287-page report discuss hormesis, the basic
biological principle cited by Paracelsus in 1540: “Nothing is poison, but the dose makes it so.” This hormetic principle has been
demonstrated in hundreds of studies at the level of cells, tissues, and
organisms. LDR is shown to prevent and cure cancer, other diseases and adverse
health conditions. Biological response mechanisms are stimulated by LDR: Immune
cells and functions; genes and adaptive responses that enhance system-wide DNA
damage control; and hormones and other physiological responses.
By this principle,
radiation, like selenium and other toxic metals and minerals that are
nutritional supplements, is harmful at high doses but beneficial, and probably
essential, at low doses. The Committee
concedes (p.8) that the data they use “come primarily from observations at
moderate-to-high levels of exposure.” But there is no important
dispute over moderate-to-high level dose-response data. Far better had the
Committee devoted most of the other 285 pages to the abundant LDR human and
biological data, showing that populations exposed to LDR show, if and when
anything, beneficial, not detrimental, health effects.
The Committee’s mutagenesis
review (pp.36-49) omits hundreds of significant biological studies of molecular
anti-mutagenic cell functions and their responses. Also unmentioned are oxidative
free radicals and associated reactive oxygen species (ROS), the principal cause of DNA damage
produced by both ionizing radiation and oxygen metabolism. DNA damage from metabolism exceeds that from
1 mGy per year background radiation by a factor of more than 100 million. The anti-mutagenic system of DNA damage
control evolved to cope with this relentless onslaught of metabolic damage. There are three effective components of
cellular DNA damage control: prevention by anti-oxidant scavenging of ROS; enzymatic repair of damaged
DNA; and removal of persistent damage by apoptosis and the immune system.
Double-strand breaks in DNA
(DSBs) are a thousand times more likely to have errors in repair than simple
single-strand breaks; and they occur in
2% of radiation-induced DNA damage, but only in 0.000001% of metabolism-induced
DNA damage. However, DSBs from metabolic
damage still exceed those from background radiation by a factor of 1000. But, LDR
stimulates all three components of the anti-mutagenic system.; (High-dose radiation, on the other hand, suppresses them.) High dose, high dose-rate, radiation
mutagenesis is linearly proportional to doses that are sublethal to cells. In contrast, hormetic LDR decreases mutagenesis. This effect has
been shown to slow aging, and to decrease mortality from cancer and other
causes. This generally results in longer
mean lifetimes of LDR-exposed populations.
The Committee’s primary
failure, like its predecessors, is to ignore most
of the vast body of data that show no
harm from low-level radiation, and show stimulatory responses that produce
health benefits. E.g., they cite RSH’s
“Data Document” (but only 1998, though they received the 1999 and 2000
updates), but they do not assess the several hundred science literature data
sources there that contradict the LNT.
The Committee disingenuously refers to a magazine article that has no
references (Muckerheide 1995), while ignoring the actual data sources
provided. They cite a one-page editorial
comment by Pollycove, but not his comprehensive, data-filled papers; and cite
Cohen’s 1995 radon health effects paper, but not his many papers that refute
the unsubstantiated disparaging comments that they use to simply dismiss,
rather than assess, his many studies.
They especially fail to assess Cohen’s joint paper with Colditz (1994),
a renowned Harvard epidemiologist, that finds Cohen’s data and analyses
epidemiologically valid. Nor do they
mention independent confirmatory studies by Bogen (1998) and others.
Instead of scientific
scrutiny, the Committee dismisses such studies, using
generic comments with no
assessment of their application to the study.
In fact, most credible science authors carefully avoid such pitfalls, or
analyze their significance. The
Committee did not show that results were invalidated by such generic
concerns. They only state (p.136) “Given the intrinsic problems with analyses of
ecological data described above, such data cannot be regarded as trustworthy,” and conclude (p.49): “Under some experimental conditions the
adaptive response can protect cells against the mutagenic effect of ionizing
radiation; however… the response seems unlikely to have a significant impact on
radiation effects in human populations.” This statement is not
compatible with its assertion (p.6 quoted above) that “cancer in most populations… have not been
found to be detectably increased, and that in most cases the rates have
appeared to be decreased.”.
After dismissing studies on
large populations irradiated by radon in homes, or Co-60 at work, or living in
high natural radiation areas, or receiving medical treatment with
low-to-moderate radiation doses, the Committee states “in vitro studies have yielded the most
reliable dose-response data.” This is true for pounding on
cells in a Petri dish, but it has no direct relevance to radiation health
effects in whole organisms.
Since in vitro tissues and cells do not have capable
immune systems, nor enzymatic and hormonal responses, nor apoptotic removal
capabilities, etc., they do not indicate how whole organisms respond.
Biologists know that cells in culture are laboratory artifacts; that cell experiments
help elucidate mechanisms, but they can not indicate how an organism will respond. Renato Baserga
states in “The Molecular Basis of Cell Cycle and Growth Control,” (Ed. Stein,
Baserga, et al., Wiley-Liss, 1999): “If
you wish to study the cell cycle of the lining epithelium of the small
intestine in mice, there is only one way to study it, and that is in a mouse.
But if your concern is about mechanisms, gene expression, growth factors and so
on, then yeasts and other cells in culture are the best choice. One only has to
be very careful in avoiding extrapolations… the environment of cells in culture
resembles the environment of cells in vivo no more than a zoo resembles
an African habitat. The Petri dish is a hostile environment, and when cells are
asked to grow in that environment, they pull out all the stops and start
expressing all kinds of genes they do not express in the adult animal.”
On the page-and-half that
“cover” hormesis (pp. 196-197), only two of the studies that clearly show
beneficial responses to LDR were “addressed.”
First: a study by Miller et al. (1989) of Canadian
women TB patients who were
periodically examined by fluoroscopy.
Breast cancer incidence vs. radiation dose shows a clear, statistically
highly significant, cancer deficit in the 100 to 300 mGy range vs. the
lowest-dose controls. Contradicting NCRP
member E.W. Webster’s analysis of this study in his 1992 Lauriston S. Taylor
Lecture at the Annual NCRP meeting, published by NCRP September 1, 1992, the
Committee claims that the deficit is not statistically significant, and falsely
states that “a simple
linear dose-response curve provided an adequate fit to the data.” A
1996 “update” by Howe and McLaughlin is used instead. But it is well known that this study grouped
the 10 to 490 mGy data into a single dose point. It is reasonable to presume that this is to
hide this hormetic effect by burying the 53 deaths in the hormetic range (of
about 79 “expected”) with deaths above and below this range. They then state
that “the most recent report by Howe
(2001-to be published)… found that a simple linear model fit the data better
than a pure quadratic model… Thus the alleged deficit… should be regarded as a
statistical anomaly that has now disappeared.”
Adding to the obvious effort
to suppress the actual data, this sleight-of-hand raises other questions: Does the Committee intend that failure to fit
a quadratic model automatically proves a linear model? In fact, since entirely different biological
processes take place during low-dose irradiation from those occurring at high
doses, a single linear fit to both ends of the data is precluded. And is “Howe (2001-to be published)” on which
the Committee relies, the same as “Howe (1998-in press)” used in this same
context in the October 1998 draft SC 1-6 report (was this falsely claimed to be
“in press”?) still not accepted for publication? The Committee does not even summarize the
methods and results of this “new study,” unlike its expositions on other much
less significant unpublished studies. The history of the effort to transform
this study from clearly demonstrating statistically significant beneficial
effects of LDR, into a study “consistent with” linearity, is being
documented. The significance of the
Committee’s misrepresentation of data is readily apparent in their use of this
well-known obfuscated data in Section “9.3.4 Breast Cancer” (p.162), Tables 9.9
and 9.10.
Secondly: the Committee
discusses the Nuclear Shipyard Worker Study, clearly the best and strongest epidemiological
study of nuclear workers ever conducted.
This 10 million dollar, 10-year study (1978-1987) was directed by
Congress in response to allegations of adverse health effects in shipyard
workers. It was done for the US
Department of Energy by the Johns Hopkins Department of Epidemiology. The Technical Advisory Panel was headed by
Dr. Arthur Upton, who was concurrently BEIR-V Committee Chairman, and is now
also Chairman of this NCRP Committee to supposedly “review” those pre-ordained conclusions.
This study population (about
70,000 workers) was taken from more than 700,000 workers that include 108,000
radiation-exposed workers. Thus, the study was able to match
unirradiated-worker control groups to exposed-worker groups, by age, under the
same health plan, doing the same work under identical working conditions, except
for exposure to Co-60 irradiation. In
this way, the study, concurred in by its Technical Advisory Panel, was able to
eliminate the “healthy worker effect.”
All irradiated workers wore film badges, under a rigorous program
compared to other early nuclear workers; and since the significant radiation
source was external Co-60, they had the most accurate radiation dose data.
As shown in the Figure to the left, there
is a highly-significant decrease in mortality from “All Causes,” by 16 standard
deviations (SDs). Deaths from “All
Malignant Neoplasms,” that is, All Cancers, not “just for radiosensitive
cancers” (p. 196) were more than 4 SDs below controls (p<0.001). This was apparently not the result expected
or desired. These dramatic effects are explained by the Committee as, “This interpretation ignores the likelihood of
occupational selection factors that led some to qualify for radiation work
while others did not."
However, this had already
been addressed by the study authors.
They determined that this selection affected only a handful of nuclear
workers out of nearly 30,000, and could not affect the results.
DOE published an abstract in
1993, but neither DOE nor the Principle Investigator has submitted a paper for
publication, even though a contract with the Principal Investigator to support
this study was continued in 1994. Most
egregiously, DOE’s Summary of Findings reported only a few statistically
insignificant "radiosensitive cancers", not the most important result
- the "All Malignant Neoplasms" endpoint. When DOE finally made the report available
with a brief news release in 1991, the large, highly significant decrease in
mortality from “All Causes” was explained away as a "healthy worker
effect". This duplicitous
explanation was recently repeated in DOE's comments on the June 30, 2000 GAO
Report on this subject, even though this has been documented and acknowledged
many times as a misrepresentation, including by UNSCEAR 1994.
This study was excluded by
the BEIR V Committee, which again were both chaired by the same chairman. That study was also excluded by the DOE-funded
IARC “study of nuclear workers in three countries” (Cardis 1995); and today is
again being excluded in the on-going IARC “study of 600,000 nuclear workers.”
The Committee makes a few
fleeting references about genetic effects of radiation. It would have been forthright
to confirm, at least, the long-standing conclusion that ‘no heritable genetic
effects are observed in several generations of irradiated humans; nor in
massive animal studies at doses below 250 mGy.’
In view of the public fear of the possibility of creating mutant
off-spring, exemplified by an estimated 100,000 “preventive” abortions after

The Committee
misrepresents volumes of data, especially by using high-dose data to project effects to zero dose,
and using figures that substantially conceal low dose data. The Committee has figures and tables with
multiple data sources that exclude highly significant studies. E.g., for lung cancer, Section 9.3.5 (p.166)
does not include the well-known analysis of studies by Harald Rossi and Marco
Zaider in their 1997 comprehensive assessment of lung cancer caused by external
radiation. (Their “Figure 1” is
above.)
Rossi and Zaider state: “A critical review of the
literature leads to the conclusion that at the radiation doses generally of
concern in radiation protection (< 2 Gy), protracted exposure to low linear
energy transfer (LET) radiation (x- or gamma-rays) does not appear to cause
lung cancer. There is, in fact, indication of a reduction of the natural
incidence.”
In addition to
selective inclusion of data, and misrepresentation of data, the Committee also
suppresses voluminous LDR dose-response data from biology and medicine. Animal and human studies consistently show
bio-positive responses to LDR, with lower cancer and disease rates, and
successful treatment of some established cancers and other diseases.
LDR effectiveness in clinical medicine has shown significant results in
combating inflammations and infection.
The Committee acknowledges these in its statement (p.124-125): “…where the mean survival time of lightly irradiated animals
has significantly exceeded that of the controls, the differences have generally
been attributable to radiation-induced reduction in the rate of mortality from intercurrent
infectious diseases…”


This same immune system also controls cancer. This is shown by hundreds of studies,
and current anti-cancer research.
One example, from a study of 24 patients with
non-Hodgkin's lymphoma, is shown in the Figure to the right (from Takai,
1992). LDR stimulation of the immune
system by “half-body” X-ray (by 2 or 3 exposures / week, of 150 or 100 mGy, for
5 weeks, for 1.5 Gy total exposure) was sufficient to eliminate this nasal
tumor at the base of the skull. These CT
images were obtained one week before, and one week after, the LDR series. Blood tests and tumor tissue examinations
confirmed the role of the enhanced immune system in destroying the tumor. These studies, and much more data on immune
system stimulation by LDR, were provided to the Committee. They chose to ignore, and thereby
misrepresent, the data.
The suppression of the relevant data by this Committee, and
its predecessors, on behalf of extreme radiation protection standards,
regulatory agencies, and funding, inhibits serious research and applications
that could have prevented millions of unnecessary early deaths from cancer and
other diseases. The Committee stated the
significance of its conclusions as follows (p.205):
Although it is
widely acknowledged that adaptive responses may underlie some of the observed
[data]…there is no firm evidence thus far that such responses can be expected
to operate effectively enough to protect completely against the mutagenic and
carcinogenic effects of low-level radiation.
Thus, in spite of some suggestions to the contrary… the data are
generally interpreted not to exclude the linear non-threshold model and thus to
provide insufficient grounds for rejecting the linear non-threshold
dose-response model as a basis for assessing the risks of low-level ionizing
radiation in radiation protection (ACRP, 1996; NRPB, 1995; UNSCEAR, 1994).
To achieve even this weak
conclusion, the Committee had to select biased data, and cite for support their
kindred policy bodies whose reports are similarly biased, rather than
substantial scientific sources.
This report, constructed by
NCRP, a full member of the tight-knit North America-Europe radiation protection
‘family,’ evokes the words of Army prosecutor Joseph N. Welsh at a hearing of
Senator Joseph McCarthy’s Committee for the Investigation of Un-American
Activities:
“Have you no sense of decency, Sir, at long
last? Have you no sense of decency?”