Imaging

Technology in Cancer Research &

Treatment
Does Imaging Technology Cause Cancer? 2016, Vol. 15(2) 249–256
ª The Author(s) 2015

Debunking the Linear No-Threshold Reprints and permission:

sagepub.com/journalsPermissions.nav
DOI: 10.1177/1533034615578011
Model of Radiation Carcinogenesis tct.sagepub.com

Jeffry A. Siegel, PhD1 and James S. Welsh, MS, MD, FACRO2

Abstract
In the past several years, there has been a great deal of attention from the popular media focusing on the alleged carcinogenicity of
low-dose radiation exposures received by patients undergoing medical imaging studies such as X-rays, computed tomography
scans, and nuclear medicine scintigraphy. The media has based its reporting on the plethora of articles published in the scientific
literature that claim that there is ‘‘no safe dose’’ of ionizing radiation, while essentially ignoring all the literature demonstrating
the opposite point of view. But this reported ‘‘scientific’’ literature in turn bases its estimates of cancer induction on the linear
no-threshold hypothesis of radiation carcinogenesis. The use of the linear no-threshold model has yielded hundreds of articles, all
of which predict a definite carcinogenic effect of any dose of radiation, regardless of how small. Therefore, hospitals and
professional societies have begun campaigns and policies aiming to reduce the use of certain medical imaging studies based on
perceived risk:benefit ratio assumptions. However, as they are essentially all based on the linear no-threshold model of radiation
carcinogenesis, the risk:benefit ratio models used to calculate the hazards of radiological imaging studies may be grossly inaccurate
if the linear no-threshold hypothesis is wrong. Here, we review the myriad inadequacies of the linear no-threshold model and
cast doubt on the various studies based on this overly simplistic model.

Keywords
radiation carcinogenesis, linear no-threshold model, low-dose radiation exposure risk, CT scans, cancer

Abbreviations
BEIR, biological effects of ionizing radiation; CT, computed tomography; EPA, Environmental Protection Agency; ERR, excess
relative risk; LNT, linear no-threshold; LT, linear threshold; LSS, Life Span Study; PAG, Protection Action Guides; RERF, Radiation
Effects Research Foundation; UNSCEAR, United Nations Scientific Committee on the Effect of Atomic Radiation.

Received: December 17, 2014; Revised: February 03, 2015; Accepted: February 22, 2015.

Introduction and dose rates (<100-200 mSv acute or chronic exposures). A

Intensive media attention aimed at the general public regarding
the alleged cancer-inducing potential of the low-dose radia-
tion exposure associated with medical imaging can provoke
anxiety and even unnecessarily scare patients. In a vicious
circle, the recent increased media hype may have caused indi-
vidual physicians, hospitals, and even professional medical
societies to create policies that unnecessarily limit radiologi-
cal imaging studies. Additionally, because of a perceived
need to reduce radiation dose, suboptimal imaging that does
not yield a definitive diagnosis might result in the need for
additional or repeat imaging studies, ironically increasing the
overall radiation dose required to establish a diagnosis.
Although radiation is known to cause cancer at high doses
and high-dose rates, no data have ever unequivocally demon-
strated the induction of cancer following exposure to low doses
hypothetical model must be therefore applied to high-dose data
to estimate what the presumed carcinogenic effects of low-dose
radiation might be. The most commonly employed model is the
linear no-threshold (LNT) model wherein dose-effect data at
high doses are simply extrapolated linearly downward to zero
dose with no threshold. The LNT model, although being
1
Nuclear Physics Enterprises, Marlton, NJ, USA
2
Department of Radiation Oncology, Stritch School of Medicine Loyola
University-Chicago, Maywood, IL, USA
Corresponding Author:
James S. Welsh, MS, MD, FACRO, Department of Radiation Oncology, Stritch
School of Medicine Loyola University-Chicago, 2160 S 1st Ave, Maguire
Center, Rm 2932, Maywood, IL 60153, USA.
Email: james.welsh@lumc.edu
250 Technology in Cancer Research & Treatment 15(2)

heavily promoted by scientific advisory bodies around the

world and serving as the established paradigm used by radia-
tion regulators, is of questionable validity, utility, and applic-
ability for estimation of cancer risks resulting from low-dose
radiation exposures.1-3 We will provide compelling evidence
that the dose–effect relationship at low doses is not linear and
there is an obvious threshold demonstrating the existence of the
body’s adaptive protective responses.

The LNT Model of Radiation Carcinogenesis

is Likely Incorrect
Figure 1 illustrates the dose–response relationship for solid
cancer incidence using data from 1958 to 1998 in the Life
Figure 1. Dose–response relationship for solid cancer incidence using
Span Study (LSS) atomic bomb (A-bomb) survivor popula- data from the Life Span Study (LSS) A-bomb survivor population.4 As
tion as presented in the Radiation Effects Research Founda- stated on the Radiation Effects Research Foundation (RERF) Web site,
tion (RERF) Website (http://www.rerf.jp) and as reported by the thick solid line is the fitted linear sex-averaged excess relative risk
Preston et al.4 The LSS data have been considered by many (ERR) dose response at age 70 after exposure at age 30. The thick
to be the most important data for estimating radiation effects dashed line is a nonparametric smoothed estimate of the dose category-
in humans and have traditionally been used to justify the specific risks and the thin dashed lines are 1 standard error above and
below this smoothed estimate.
existence of adverse health effects due to low-dose radiation
exposure.
According to the RERF, the dose–response relationship in
Figure 1 ‘‘appears to be linear, without any apparent threshold
below which effects may not occur.’’ It is also noted, how-
ever, that there has been no statistically significant increase in
the observed cancer frequency in survivors who were exposed
to radiation doses of 150 mSv or less. Based mainly on these
LSS data, the National Academy of Sciences Biological
Effects of Ionizing Radiation (BEIR) VII Committee5 con-
cluded that the ‘‘current scientific evidence is consistent with
the hypothesis that there is a linear, no-threshold dose–
response relationship between exposure to ionizing radiation
and the development of radiation-induced solid cancers in
Figure 2. Graph of excess risk versus dose using only low-dose data
humans.’’ However, this report does not conclude that the
(0.2 Gy) as presented in Figure 1.
LNT theory is correct and it does not rule out the possibility
of a threshold. In contrast to BEIR VII, the French Academy
of Sciences report6 came to very different conclusions regard- not exhibit a threshold is to constrain the fit through the
ing the LNT model. The French report raised doubts about the origin, but there is no scientific basis for such an action.
validity of using the LNT model to estimate carcinogenic Thus, even using this paragon of A-bomb survivor data, the
risks at doses less than 100 mSv, recognizing the abundant LNT model still does not correctly represent the data, par-
evidence for radiation adaptive response in terms of protec- ticularly at low doses.
tion and lack of evidence for harm below this dose level. Figure 2 is a graph of excess risk versus dose using the LSS
An independent analysis of these LSS A-bomb survivor data from Figure 1, but only showing, for the first time, the
population data (using all data except the last 2 data points) portion of the curve in the low-dose region that consists of the 8
based on linear regression (ie, a linear dose–response data points for doses ranging from 0 to  0.2 Gy (illustrated by
model) indicated an excellent correlation coefficient (r ¼ the solid rectangles). For illustrative purposes, this portion of
.98), but with an apparent threshold at approximately 45 mGy.1 the curve below 0.2 Gy will be referred to as ‘‘the box.’’ It is
The 95% confidence interval for this threshold was deter- apparent from the graph that at these low doses the dose–
mined to be 37 to 55 mGy, consistent with a linear thresh- response is not linear.
old (LT) model, under the assumption that the dose– Three curve fits are presented and characterized in Figure 2
response is linear. Consistent with this result, others have illustrating the analyses, based only on a linear dose–response
determined that a threshold as high as 60 mSv may be model, reflecting thinking both ‘‘inside’’ and ‘‘outside’’ the box:
present for cancer from these Japanese data.7,8 It appears
then that the data in Figure 1 are not consistent with the 1. Using only risk versus dose data for doses ranging from
LNT model; the only way the data fit would be linear and 0 to  0.2 Gy, also known as thinking inside the box.
Siegel and Welsh
The solid line is a linear fit to these 8 data points (solid
rectangles), constrained to go through the origin, and as
can be seen, the dose–response relationship is very poor
(r2 ¼ .25), indicating a linear fit is inadequate. If the fit
is unconstrained, there is an obvious threshold, but the
data fit is still poor. So, excess risk data at low doses
does not conform to the LNT model; in fact, any ade-
quate dose–response model would have to exhibit a
threshold to describe these data.
2. Using all data in Figure 1 except the last 2 data
points, that is, a wider dose range from 0 to approx-
imately 2.2 Gy. The dotted line is an unconstrained
linear fit to these data and this fit exhibits a threshold
of approximately 0.045 Gy (45 mGy) as discussed
previously. Therefore, an LT model is more appropri-
ate than use of an LNT model. The correlation coef-
ficient is better but this is because of use of data
‘‘outside the box.’’ Note that the linear fit to the data
points 0.2 Gy is still very poor, again indicating
the lack of a linear relationship at low doses, even
though the correlation coefficient for the wider dose
range is good (r ¼ .98). The slopes of these 2 linear
fits are significantly different (0.52 vs 0.34, respec-
tively) illustrating that an extrapolation of what to
expect at low doses (dotted line) rather than what has
been observed (solid line) yield significantly different
results.
3. Using all data in Figure 1 except the last 2 data points,
but this time constraining the linear fit to pass through
origin. The dashed line is the constrained linear fit and
has essentially the same slope and correlation coeffi-
cient as the unconstrained fit. Note again that the use of
the LNT model to characterize what happens at low
doses using only low-dose data (solid line) or to predict
what might happen at low doses based on an extrapola-
tion (dotted and dashed lines) both yield poor results in
the low-dose region. So the actual low-dose data are not
adequately characterized by applying the LNT model to
only these low-dose data, ranging from 0 to 0.2 Gy,
nor are they adequately predicted based on extrapolated
results from higher doses.
Thus, based on data from 1958 to 1998 in the LSS A-bomb
survivor population, analyses performed either ‘‘inside the
box’’ or ‘‘outside the box’’ demonstrate that there is not a
linear, no-threshold relationship between excess risk and
radiation dose at low doses (0.2 Gy or 200 mSv), so other
dose–response models need to be utilized. Linearity at low
doses does not exist; rather, it is forced by the high-dose
extrapolation of the LNT model. If high-dose data did not
exist and only the low-dose data were known and analyzed, it
is obvious and inescapable that the LNT model is inadequate
to describe the reported low-dose LSS data. Furthermore, a
threshold is rendered invisible by the preconceived assump-
tion that none exists—a self-fulfilling prophecy. If no such
251
assumption is made to begin with and an unconstrained fit is
then used, the data force the acceptance of a threshold.
Recent Evidence Further Contradicting the LNT
Model—A Hormetic Model Perhaps?
A recent update to the LSS data reported by Ozasa et al9
indicated that the new dose–response data for cancer mortal-
ity at low doses are more consistent with a linear-quadratic
dose–response model because a significant upward curvature
is exhibited. Further, according to a 2013 revision of this
update (explanatory material available at http://www.rerf.jp),
‘‘The linear dose–response relationship provided the best fit
for the ERR data across the entire dose range, but a concave
curve was the best fit for data restricted to dose <2 Gy. This
resulted because risk estimates for exposure to around 0.5 Gy
were lower than those in the linear model.’’ It is important to
note that zero dose was reported to be the best estimate of the
threshold, but this may be unjustified as the model used for
their formal dose-threshold analysis restricted excess relative
risk (ERR) values from extending into negative values. Use of
a more generalized model employing multiple linear regres-
sion indicated the presence of a nonzero dose threshold and in
addition, when a correction was applied to these data for a
likely bias in the baseline cancer rate,10 it provided possible
evidence of radiation hormesis, that is, ERR values were neg-
ative for all doses below approximately 0.6 Gy. This is indi-
cative of a beneficial or cancer preventative effect such that
low-dose radiation would reduce rather than increase cancer
risk. Finally, another recent reanalysis of the LSS cohort of A-
bomb survivors using a nonparametric statistical procedure
has exhibited a threshold at low dose (<0.2 Sv or 200 mSv)
which is manifested as negative ERR, again consistent with a
radiation hormesis model.11
Such conclusions are consistent with the existence of an
adaptive response, which serves to protect organisms follow-
ing low-dose radiation exposure. These findings are in agree-
ment with the experimental evidence of, for example, DNA
double-strand break repair as has been reported after patient
low-dose radiation exposure from computed tomography
(CT) scans.12 Thus, overall, these data are more consistent
with a radiation hormesis model than the LNT model, para-
doxically indicating that low-dose radiation is beneficial, not
harmful, from both mechanistic and epidemiological
considerations.8
Based on the above-mentioned revisions to, and analyses
of, the LSS data since the BEIR VII report, the atomic bomb
survivor data no longer support the LNT model, but rather
a hormetic model exhibiting a negative ERR at low doses
(<200 mSv). This hormetic concept is further supported by
a large body of evidence indicating that low-dose radiation
has the opposite effect of high-dose radiation exposure.13
Although any damage that may occur after exposure to low-
dose radiation exposure may occur in a linear fashion (ie, the
dose-damage response may be linear), the dose–response at
252
this dose level is not linear because of the body’s demon-
strated response to mitigate/eliminate this damage.
The LNT Hypothesis is Not
Biologically Plausible
When viewing radiation carcinogenesis from an exclusively
molecular biological perspective or when only considering in
vitro cellular experiments, it is easy to get lulled into an LNT
mindset. It is true that any dose of ionizing radiation is capa-
ble of inducing a mutation and there is a finite probability that
such mutations could be deleterious or transform normal cells
into a malignant phenotype. However, when considering a
broader, organismal-level perspective, the pitfalls of the LNT
hypothesis of radiation carcinogenesis become apparent. For
example, the average human body has a spontaneous back-
ground mutation rate that has been estimated to be 2  105
mutations per cell per day thanks to thermal insults and oxi-
dative metabolism.14 This spontaneous rate of DNA altera-
tions absolutely dwarfs the DNA alteration rate due to
background radiation (10-100 DNA alterations per cell per
cGy per year). To put things in perspective, the natural back-
ground radiation mutation rate, assuming an average back-
ground exposure rate of 3 mSv per year in the United
States, would be 3 to 30 DNA alterations per cell per year,
which is almost 2.5 million times lower than the spontaneous
mutation rate. The point is that the normal body effectively
deals with these numerous spontaneous mutations through a
set of mechanisms collectively called the adaptive response;
the small excess conferred by a low dose of radiation, even if
LNT were true, is unlikely to overwhelm the system.
The observed threshold and negative ERRs are in agree-
ment with experimental evidence for the induction of adaptive
protection against cancer, such as antioxidant production,
apoptosis, immune system-mediated effects, and repair of
DNA double-strand breaks that have been shown to occur
even after patient exposure to the low-dose radiation from
CT scans. 12 DNA damage response mechanisms defend
against exogenous and endogenous DNA damage and
enhance both survival and maintenance of genomic stability
(which is critical for cancer avoidance).
The vast majority of human cancers are not simply the end
products of a single (or even multiple) driver mutations. Such
mutations may be necessary, but they are not sufficient to
produce cancer. Modern understanding of the role of the
immune system in the development of clinically overt cancers
has led to a replacement of the outdated ‘‘one mutation ¼ one
cancer’’ model. In fact, evasion from immune system detec-
tion and escape from destruction have emerged as one of the
newer ‘‘hallmarks of cancer.’’15 Supporting this concept is the
observation that in immunocompromised patients (eg,
patients with HIV/AIDS and organ transplant recipients),
vastly increased cancer rates have been reported.16 Thus,
there is far more than the simple accumulation of mutations
in the creation of a clinically overt cancer.
Technology in Cancer Research & Treatment 15(2)
Additionally, the LNT hypothesis is illogical from the per-
spective of evolutionary biology.17 The early Earth was far
richer in natural background radionuclides than it is today.18
Much of our planet’s primordial radionuclide endowment
such as 40K has decayed and in fact the ‘‘neptunium series’’
or 4n þ 1 series has long been extinct in nature due to the
relatively short half-lives of the radioactive isotopes involved.
The bottom line is that life emerged and evolved in an envi-
ronment several-fold higher in background radiation than the
levels of today. It is likely that powerful adaptive responses
developed thanks to this high radiation background and it
would be overly simplistic to assume that organisms have
‘‘forgotten’’ how to cope with low-level radiation damage.
Mechanisms of action are unique for low-dose radiation
exposure. Processes activated by low doses are related to
protective responses, whereas high-dose responses are asso-
ciated with extensive damage, such as cell killing, tissue dis-
ruption, and inflammatory diseases.19 Furthermore, low-dose
radiation exposure is known to boost the immune system
causing a reduction in cancers.20 Intriguingly, low-dose radia-
tion exposure might paradoxically be invaluable in radiation
therapy of cancer thanks to recently uncovered immunomo-
dulatory effects on tumor-infiltrating macrophages and on
regulatory T-cells (Tregs).21-23
Thus, there are different mechanisms of action at high and
low doses indicating that the LNT-based assumption of, or
‘‘belief’’ in, an excess cancer risk at low doses is erroneous.
High-dose effects cannot be extrapolated down to accurately
predict effects at low doses, that is, ‘‘what happens at high
doses, stays at high doses.’’ Paracelsus, a 16th century Renais-
sance physician, took an anti-LNT stance before it was even
known or fashionable to do so when he said, ‘‘Poison is in
everything, and no thing is without poison. The dosage makes
it either a poison or a remedy’’ (http://www.brainyquote.com/
quotes/authors/p/paracelsus.html).
Recent Epidemiological Studies Do Not
Provide Evidence of Radiation Carcinogenesis
at Low Doses
There are 2 recently published epidemiological studies sug-
gesting increased cancer risks at low radiation doses associated
with pediatric CT scans24,25 and a third large record-based
case–control study indicating an excess risk of childhood leu-
kemia associated with natural background radiation expo-
sure.26 However, significant concerns have been raised in a
2013 United Nations Scientific Committee on the Effect of
Atomic Radiation (UNSCEAR) report that serve to invalidate
these risk estimates.27 The putative CT-caused cancers may
have been caused by the medical conditions prompting the
CT scans and may have nothing to do with the radiation expo-
sure involved (reverse causation—CT scans aren’t causing can-
cers and cancers are causing CT scans). Further, there is a huge
uncertainty associated with the assigned radiation doses as
individual dosimetry was not performed. Since the 2 pediatric
Siegel and Welsh
CT studies do not provide evidence that low doses are causally
associated with cancers in children, direct estimation of the
health impact of CT radiation exposure remains imprecise.
Further large-scale epidemiological studies with more accurate
dosimetry and assessment of potential biases and uncertainties
are needed. The ‘‘Epidemiological study to quantify risks for
pediatric computerized tomography and to optimize doses’’
(EPI-CT) was set up to enroll approximately 1 million patients
in 18 centers located in 11 countries to investigate these issues
(http://epi-ct.iarc.fr); results are expected in 2015.
According to the UNSCEAR report, the study indicating
natural background-associated cancers ‘‘should be interpreted
with caution because of the large uncertainties associated with
using an ecological measure of dose.’’ Radiation doses in this
study were based on estimated mean exposure levels for the
county district in which the mother resided at the child’s birth;
thus, there is a huge uncertainty associated with these assigned
radiation doses as individual dosimetry was not performed.
Further, although the authors conclude that substantial bias is
unlikely, the study provides no information on potential con-
founding factors other than measures of socioeconomic status.
Background Radiation and Definitions of a
‘‘Low Dose’’ of Radiation
There are perhaps 2 realistic definitions of a low dose of radia-
tion. One is a dose below which it is not possible to detect
adverse health effects (<100 mSv, according to the Interna-
tional Commission on Radiological Protection and the Health
Physics Society). The second is the level of radiation that we
are exposed to annually from natural background radiation, a
dose range spanning 2 orders of magnitude depending on where
in the world you live, from a few mSv to as high as 260 mSv in
Ramsar, Iran.28
The high end of the range, corresponding to high natural
background levels in regions including Ramsar, Iran, Yang-
jiang County of the Guangdong Province in China, and Kerala,
India, are fascinating because of the very high background
radiation but no apparent increased incidence of cancer. In fact,
1 in vitro study demonstrated a significantly reduced frequency
of chromosome aberrations in lymphocytes following a chal-
lenge dose of 1.5 Gy of g rays from people living in high
background versus those living in normal background areas
in and near Ramsar.28 These data are consistent with an adap-
tive response to low-dose chronic radiation exposure.
Irrespective of the level of background exposure to a given
population, to date no associated health effects have been docu-
mented anywhere in the world. In fact, people in the United
States are living longer today than ever before, likely due to
always improving levels of medical care, including even more
radiation exposure from diagnostic medical radiation (eg, life-
saving X-ray and CT imaging examinations) which are well
within the background dose range across the globe. Therefore,
a low dose of radiation can be considered to be a dose less than
100 to 200 mSv.
253
Overestimating Radiation Risks—The
Fukushima and Chernobyl Accidents
Use of the LNT model to illegitimately and unjustifiably pre-
dict low-dose effects (risk assessment) is not only wrong, it is
not even conservative. Conservative is an ambiguous word and
we wish to clarify its meaning here since it can mean conser-
ving either life or resources; concepts that may be in opposi-
tion. In the case of Fukushima, for example, as discussed
subsequently, the use of the LNT model and its derived policies
was intended to be conservative with respect to protecting lives
(ie, minimizing loss of life, a good thing), but despite the inten-
tions, the outcome was quite different due to the actions taken
(eg, forced evacuations), resources used, and number of actual
lives lost. More thought should be given to policy decisions
(risk management) based on the LNT model. Current regula-
tory dose limits should certainly be raised as they are somewhat
arbitrary and well below the level at which adverse health
effects have been demonstrated in humans.1 Overestimating
radiation risks using the LNT model may be more detrimental
than underestimating them, as this approach has resulted in
unnecessary loss of life due to traumatic forced evacuations,
suicides, and unneeded abortions after the Fukushima nuclear
accident. Fear of radiation in this case may have been more
harmful than the radiation itself as official figures indicate that
well over 1000 deaths (http://www.world-nuclear.org/info/
Safety-and-Security/Safety-of-Plants/Fukushima-Accident/)
have been reported due to the forced evacuations. These avoid-
able and unnecessary ‘‘disaster-related deaths’’ were caused by
fear of radiation resulting from LNT-derived policies that are
directly attributable to ICRP recommendations. According to
the UNSCEAR (http://www.unis.unvienna.org/unis/en/press-
rels/2013/unisinf475.html), ‘‘Radiation exposure following the
nuclear accident at Fukushima-Daiichi did not cause any
immediate health effects. It is unlikely to be able to attribute
any health effects in the future among the general public and
the vast majority of workers.’’
Following the Fukushima accident, the ICRP convened
Task Group 84 to collate lessons learned in a memorandum29;
for the record, the ICRP has noted that the material contained in
this memorandum does not reflect their official view. Never-
theless, it is instructive to note some of the conclusions of this
memorandum, such as ‘‘Following exposure to low radiation
doses below about 100 mSv an increase of cancer has not been
convincingly or consistently observed in epidemiological or
experimental studies and will probably never be observed
because of overwhelming statistical and biasing factors. In sum,
theoretical cancer deaths after low-dose radiation exposure
situations are obtained by inappropriate calculations based
on the LNT model and misuse of the collective dose concept.
Any effects—if they occur at all—will be so small that they
would fall within the ‘ noise’ (scatter) of the ‘spontaneous’ can-
cer of unexposed people.’’ It should therefore be patently obvious
that the ICRP needs to immediately raise its recommended
dose limits, as adherence to the LNT model will cause more real
deaths than the imaginary ones the model purports to save.
254
With respect to Chernobyl, 1 study examined cancer inci-
dence (1986-2008) and mortality (1986-2011) among the
Estonian cleanup workers in comparison with the Estonian
male population.30 The cohort of 4810 men worked in the
contaminated area for a median duration of 92 days and were
exposed to an average radiation dose of approximately 10 cGy
(certainly a low radiation dose). The conclusion of the article
states, ‘‘ . . . our study suggests that after a quarter century of
follow-up of the Estonian cohort of Chernobyl cleanup work-
ers, there is an increase risk of alcohol-related cancers, and of
suicide. No definite indication of health effects directly attri-
butable to radiation exposure was found.’’
Medical Imaging and Low-Dose Health Effects
First and foremost, any discussion of risks related to radiation
dose from medical imaging procedures must be accompanied
by acknowledgment of the benefits of the procedures. Radia-
tion exposure is considered by many to be the only risk
involved in medical imaging applications. The more signifi-
cant and actual risks associated with not undergoing an ima-
ging procedure or undergoing a more invasive exploratory
surgery are generally being ignored in both the scientific lit-
erature and the popular media.31 The LNT model and the
philosophy behind it are more concerned with the extremely
small number of very long term and only theoretically pre-
dicted cancer deaths attributed to radiation exposure rather
than the much larger numbers of actual deaths that are certain
to occur without imaging.
One group has even gone so far as to predict that CT scans
will cause at least 29 000 cases of cancer and 14 500 deaths
in the United States each year.32 This prediction was based
on the LNT model, that is, by a simple multiplication of the
unproven and theoretical cancer risk associated with the
small radiation dose involved by the estimated number of
CT scans performed in 2007 (the authors referred to this
simple and trivial prediction as a ‘‘detailed’’ calculation).
This type of calculation and result appears to be condoned
by Brenner and Hall33 who have stated that, ‘‘although CT
risks are small, a small risk multiplied by many millions of
scans may translate into a public health concern some years
in the future . . . ’’ These types of inappropriate calculations
based on the LNT model are at the very least misleading;
they are in fact absolutely wrong and should be firmly crit-
icized as being alarmist and not founded in scientific reality.
According to ICRP Publication34 103 and others,29,35 the
LNT hypothesis should not be used to calculate the hypothe-
tical number of cancers that might be associated with small
radiation doses received by large numbers of people.
Radiation is a weak carcinogen. In considering a strategy
of risk reduction (for radiological imaging as well in the
aftermath of a radiological event), it is critical for the general
public and public health officials to understand that lifetime
risk of developing cancer for an individual is not exclusively
related to unnecessary or accidental exposure to radiation but
is dependent on several factors including age at the time of
Technology in Cancer Research & Treatment 15(2)
radiation exposure and other variables such as genetics, and
voluntary and involuntary exposures to carcinogens, such as
cigarette smoke.36 For example, in the United States, the
lifetime risk of developing cancer in the absence of radiation
exposure is already quite high, that is, *41% of the popula-
tion is likely to develop cancer during their lifetimes from
factors other than radiation exposure.37 This high baseline
rate of developing cancer in the absence of radiation expo-
sure poses a challenge in the determination of probability of
causation of cancer in an individual.
There is no question that risk:benefit analysis and risk
communication are keys to how the public will respond. A
reasonable summary risk (for high radiation doses) for an
exposed general population has been reported to be 6% per
Sv,36 based on the increased excess lifetime cancer risk as
reported by the ICRP.34 Given that a single CT examination
is associated with a radiation dose of approximately 10 mSv,
this corresponds to a 0.06% fatal cancer risk based on the
LNT model. A fatal cancer risk of 0.06% means that 99.94%
of patients so exposed are not expected to get cancer due to
this low radiation dose exposure. The average lifetime risk of
dying from cancer in the United States is approximately
21%. 37 A CT examination would theoretically add only
another 0.06% to the lifetime risk of cancer death, bringing
the LNT-based calculated risk to 21.06%. Put this way, the
LNT-based risk of cancer due to a CT scan can be seen as
miniscule. Importantly, as minute as this purported risk is,
since it is an LNT-derived hypothetical estimate, it is in
actuality likely much lower, probably nonexistent and most
likely inversely correlated. The 10-mSv CT dose is a factor of
10 lower than the average radiation dose of 10 cGy received
by the Chernobyl cleanup workers, a dose that caused no
observable health effects, as noted previously.
If it turns out that the responses to low radiation doses
are more consistent with the hormetic model than the LNT
model, there may be no risk at all, and instead there may be
a benefit. In this case, the risk:benefit idea would give way
to the benefit:benefit paradigm for radiological imaging
and adherence to firmly entrenched ‘‘as low as is reason-
ably achievable’’ regulatory policies would no longer have
any validity.
It is of course important to minimize radiological imaging
studies that are not clinically warranted, as should be the case
for any medical procedure.35 Nevertheless, according to the
American Association of Physicists in Medicine, ‘‘Risks of
medical imaging at effective doses below 50 mSv for single
procedures or 100 mSv for multiple procedures over short
time periods are too low to be detectable and may be non-
existent.38 Predictions of hypothetical cancer incidence and
deaths in patient populations exposed to such low doses are
highly speculative and should be discouraged. These predic-
tions are harmful because they lead to sensationalistic articles
in the public media that cause some patients and parents to
refuse medical imaging procedures, placing them at substan-
tial risk by not receiving the clinical benefits of the pre-
scribed procedures.’’
Siegel and Welsh
The LNT Model Contradicted by
Environmental Protection Agency Policies
Apparently, the carcinogenic risk associated with radiological
imaging, as discussed previously, has not been given much
weight by the US Environmental Protection Agency (EPA)
as provided in their Protection Action Guides (PAG) manual.39
For example, according to the EPA PAG Manual, the decision
to shelter-in-place or evacuate should begin at 10 mSv, that is, a
dose level corresponding to a single CT scan and an associated
hypothetical risk of no more than 0.06%. Given this negligible
risk, it is likely that real deaths may occur—not due to radiation
exposure but rather due to forced unnecessary evacuations.
It is important to note that although the EPA strongly asserts
that LNT is the most suitable basis for assessing radiation risks
at low doses, LNT was not used in the setting of its radon
mitigation requirements.40 The EPA has set 0.15 Bq L1 as
the action level above, which it recommends that a homeowner
take corrective measures to mitigate radon exposure and below
which no action is needed. This action level represents a de
facto ‘‘acceptable’’ level, as well as a de facto threshold, that
presents the same lung cancer risk as having 200 chest X-rays
per year (equivalent to an annual dose of 20 mSv). In the EPA’s
response to a critique of this policy by Stabin and Siegel,41 EPA
noted this action level was not chosen on a health-risk basis, but
it was rather driven by technical feasibility, thereby admitting
LNT played no role. It would thus be contradictory of EPA
policy and therefore need to be so noted, each and every time
LNT is applied for any lesser exposures (such as may result
from a medical radiological imaging procedure, such as a CT
scan); such doses should just be associated with ‘‘acceptable
risk’’ or represent a risk that is so low as to be of no concern.
Conclusion
Low-dose radiation exposure (<100-200 mSv) is likely bene-
ficial, not harmful. The LNT model does not account for the
body’s response (ie, repair) of any radiation-induced damage
and assumes that all outcomes are linear across the range of
high- and low-dose exposures; an assumption that is likely
false. The use of the LNT model is not conservative and there-
fore should be abandoned; otherwise, more people may be
inadequately diagnosed and treated and perhaps even die unjus-
tifiably should they refuse a needed imaging study. The cause
of death would not be radiation, but rather ‘‘radiophobia,’’ due
to misguided LNT-driven policies at a cost to tax payers
amounting to billions of dollars of wasteful spending. It may
be time for radiation protection policies to adopt a different
paradigm that would also not compromise public health and
safety or the environment. There is a need for national policy
discussions. In light of limited health care resources, it is
increasingly important that policies serve not only to protect
society from real hazards but also be based on realistic projec-
tions of the severity and likelihood of risks, as well as on
consideration of the actual financial and other costs to patients,
radiation workers, and society.
255
Declaration of Conflicting Interests
The author(s) declared no potential conflicts of interest with respect to
the research, authorship, and/or publication of this article.
Funding
The author(s) received no financial support for the research, author-
ship, and/or publication of this article.
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