The Unreasoned Fear of Radiation English

THE UNREASONED
FEAR OF RADIATION
THE UNREASONED
FEAR OF RADIATION
THE UNREASONED
FEAR OF RADIATION
Arun Kumar Nayak

Department of Atomic Energy, Mumbai, India
Ratan Kumar Sinha

Department of Atomic Energy, Mumbai, India
Samyak Sanjay Munot

Homi Bhabha National Institute, Mumbai,
India
Published By
Department of Atomic Energy
Title:
The Unreasoned Fear of Radiation
Authors
Arun Kumar Nayak, Ratan Kumar Sinha and Samyak Sanjay Munot
Copyright @ Department of Atomic Energy
All rights reserved. No part of this book may be reproduced or

transmitted in any form or by any means, electronic or mechanical
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and retrieval system without permission, in writing, from the
publisher.
Published by:
Department of Atomic Energy
Anushakti Bhavan,
C.S.M. Marg,
Mumbai – 400 001.
Maharashtra, India.
Printed by:
M/s. Sundaram Art Printing Press
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Naigaum X Road, Wadala,
Mumbai – 400 031.
Edition:
First Print: 2023
ISBN No:
978-81-907216-7-7
Contents
Foreword by Anil Kakodkar ix

From Chairman’s Desk by K. N. Vyas xi
From Director’s Desk by Ajit Kumar Mohanty xiii
Message by R. Chidambaram xv
Executive Summary xvii
1. What is ionising radiation? 1
1.1. Discovery of ionising radiation 1
1.2. Discovery of fission and its consequences 2
2. More about nuclear weapons programme 5
2.1. The aftermath of Hiroshima and Nagasaki
bombing 5
2.2. Further analysis of atom bomb radiation
effects in Japan 7
2.3. Evidence of longer lifespan of some people
who were heavily irradiated by ionising radiation 9
2.4. A-bomb survivor's lifespan was statistically
shortened 9
2.5. More analysis of atom bomb explosion 10
2.6. Trans-generational effects of radiation 11
2.7. Nuclear test participants exposure 12
3. Civil nuclear reactor accidents – the effects of
radiation leak 15
3.1. Risk of nuclear power 15
3.2. Major accidents in civil nuclear power reactors
and their consequences 17
3.3. Inferences from the nuclear reactor accidents 22
3.4. Unnecessary evacuations: mis-governance
out of fear of radiation 23
3.5. Contamination levels in Fukushima 25
3.6. Further studies on health effects of radiation
released from nuclear power plant accidents 26
3.7. Summary of radiation effects from three
civilian nuclear reactor accidents 31
4. Case studies on effects of Low-Dose Radiation (LDR) 33
4.1. Biological effects of Low-Dose Radiation (LDR) 42
4.1.1. Effects of LDR on Inflammation diseases 43
4.1.2. Effects of LDR on Arthritis and Retinitis
Pigmentosa 46
4.1.3. Effect of LDR on Infections 47
4.1.4. Effect of LDR on Cardiovascular-related
chronic diseases 51
4.1.5. Summary of Chinese studies 52
4.1.5.1. Low-Dose Radiation effect on Immune
system 52
4.1.5.2. Effect of LDR on Tumour cells 53
4.1.5.3. Effect of LDR on Diabetes 57
4.1.5.4. Stochastic effects of LDR 60
4.2. Medical occupational exposure 61
4.3. Radiation-based medical procedures exposure 67
4.3.1. Diagnostic irradiation 68
4.3.2. Low-Dose Radiotherapy 69
5. Then why do people fear radiation? 73
6. History of Linear No Threshold (LNT) theory 75
6.1. What does the LNT model ignore? 81
6.2. Muller’s deception and Russell’s mistake 83
6.3. So, the debate Hormesis vs Harm – Limitations
of LNT theory 88
6.4. Adaptive responses or hormesis acquired
through evolutionary history 89
6.5. Biological basis of hormesis as a homeostatic
defence mechanism 91
6.6. Theory to explain thresholds by homeostatic
defence mechanisms 93
7. Dose Limits by UNSCEAR 95
8. The solid evidence of LNT inapplicability -
Misleading scientific research’s contribution to
fear of radiation and collateral damage 99
8.1. A scientific scandal of the last two centuries 100
8.2. LNT is not based on solid data 103
8.3. The enforcement of LNT for radiation
dose limits 104
9. Impact of Dose vs Dose rate of radiation 105
10. Closure 109
References 117
Index 163
About the Authors 167
Foreword
The book “The Unreasoned Fear of Radiation” being brought out
by the Department of Atomic Energy is, in my view, an important
contribution to resolve the dilemma between perceptions of safety
(nuclear being among the safest of various energy alternatives) and
disaster syndrome (for example images of Hiroshima - Fukushima in
public mind) in the context of large-scale deployment of nuclear
energy. This is a crucial matter particularly for the developing world (in
particular India) which is still suffering from a significant development
deficit while the climate change has created an existential threat for the
humanity as a whole. Large scale use of nuclear energy has become
inevitable in the context of minimising the development deficit while
realising the net zero carbon-di-oxide emission goals. While there can
be no justification of the large-scale adverse impact in public domain
and nuclear technology has continuously improved to minimise such a
possibility, it is clear that the unfounded fear of nuclear radiation leads
to distress relocation of a disproportionate number of people in case of
a severe nuclear accident. Adverse impact including health effects
arising out of such distress relocation is often significantly larger than
the consequences of radiation exposure involved. The authors, Arun
Kumar Nayak, Ratan Kumar Sinha and Samyak Sanjay Munot must be
richly complimented for preparing this exhaustive review of scientific
literature in this domain that establishes the need to be more objective
in this regard.
The Linear No Threshold (LNT) hypothesis, which is the basis of

contemporary radiation protection framework, while has enabled
exemplary safety performance of nuclear applications including
nuclear power, has become a major cause of public trauma resulting
from large scale distress relocation of people around nuclear plants at
TMI, Chernobyl and Fukushima when they suffered a severe accident.
Evidence suggests that the psycho-somatic health effects have much
outweighed the radiation related health effects in the public in these
cases. The book has comprehensively examined available data on
effects of radiation including low level radiation and how the evolution
of LNT hypothesis misses the available evidence on existence of a
threshold and also the hormesis effects of low-level radiation. This has
Page ix
cost humanity dearly in terms of slow-down of nuclear power
deployment. A situation humanity can ill afford in the face of the need
for enough clean energy to support development aspirations of much
of the world. It is clear that India (and may be other similarly placed
countries) cannot become a developed nation without a significant
contribution of nuclear energy in a net zero world.
India has been one among the few countries that have carried
out large-scale epidemiological studies to look at effects of low-level
radiation. This was done in high natural radiation background areas
along the Kerala coast. This study has found no evidence of additional
cancer risk in these areas. While these studies have been published in
scientific literature, we have been less than vocal, in our advocacy at
international level, for a more rational view and having right standards
for management of evacuation following a severe accident. An
international consensus in this matter would go a long way in reducing
the public trauma that results following a severe accident in a nuclear
plant. This book would certainly help bridging the gaps that are
relevant and important, at least to an extent.
This is a larger public policy matter. One needs opinion makers

and larger public to be fully informed about the issues involved in
addition to the experts from diverse domains involved in matters
related to nuclear energy. This book should become a significant
resource in this context. I would strongly recommend ensuring that the
book is available in numbers that would be able to reach the broad
spectrum of potential readership.
The world is at crossroads today in terms of the risks of

underdevelopment in the context of both climate change threat as well
as depleting earth resources on one side and large-scale deployment of
nuclear energy that can alleviate the risk on the other. Clearly, we need
a more objective and rational approach. I hope this book would help
define the way forward.
Anil Kakodkar
Former Chairman, Atomic Energy Commission
x Page
From Chairman’s Desk
Nuclear power, undoubtedly, offers a clean energy option for
coping with global warming, energy crisis and associated challenges.
As early as 1960s, Dr. Homi Jehangir Bhabha had envisioned the need
to develop technologies for nuclear power, which initiated R&D
programmes in various sectors. Today, Department of Atomic Energy
has demonstrated unparallel progress, from development stage to
deployment stage, for nuclear technologies in several power and non-
power applications. These include generation of almost 6780 MWe
from 22 reactors and supply of radioisotopes produced from research
reactors in India for healthcare, food security, industry, etc.
While doing so, it becomes paramount to address the people’s

perception regarding the nuclear energy and radiation levels. In this
regard, this book serves as an important resource in spreading
awareness and addressing the radiation concern amongst the common
public. This book summarises the evidences of reduced cancer
mortalities and increased lifespan of not only the atomic bomb
survivors in Japan, but also that in the civilians and servicemen
associated with various nuclear weapon tests during the cold war
regime. In addition, the inferences from the three nuclear reactor
accidents have evidences of very low amount of release of radioactivity
in public domain, which has very insignificant effect on health and
lifespan of the public in comparison to the damages caused by the
relocation of public by the authorities out of fear of radiation. This book
also provides several evidences of benefits of low-dose radiation for
curing various life-threatening diseases and infections, including
neurodegenerative diseases. In spite of the above, the public feels
radiation is carcinogenic and leads to death, irrespective of dose and
dose rate. This book has addressed this aspect through detailed
analysis from literature on the root cause of the fear of radiation. I must
recommend that the future scientific community must explore the
scientific aspects of radiation on health and finding out the threshold
above which the radiation is detrimental and below which it improves
the health and cures many critical diseases. This will also help in
reducing the number of additional barriers in the nuclear plants which
results in increased cost and public fear.
Page xi
I must say that this book is an excellent scientific resource, which
would be of great interest to a broad and diverse audience. I must
compliment the authors of the book, Dr. A. K. Nayak, Dr. R. K. Sinha and
Mr. S. S. Munot for putting in hard efforts for writing this book.
I wish all the readers an enjoyable journey through this book.
K. N. Vyas
Chairman, Atomic Energy Commission
&
Secretary, Department of Atomic Energy
From Director’s Desk
Worldwide, there is a growing concern for the ever-increasing
carbon footprint and its damage to the environment. There is no
denying the fact that nuclear power will play a vital role as a clean
energy source for decarbonising the energy sector and move towards a
green future. This will also aid in achieving the Government of India's
goal for balanced and sustainable socio-economic development of the
nation.
Additionally, today, nuclear radiation and isotopes find its

applications in many non-power industries including food irradiation,
medical diagnostics and cancer treatments. Use of radiations in these
applications are found to be advanced and life without radioisotopes is
almost impossible today. Particularly for the medical industry, use of
nuclear radiation and isotopes in diagnostics and treatment purposes
have become imperative.
Having known all the above beneficial effects about the nuclear
radiation and its uses, the much-required expansion of the nuclear
industry is still facing a societal unacceptance due to the phobia
amongst the common public that "nuclear radiation is carcinogen".
The public's association of cancer with radiation is the leading case for
fear. Perhaps this is the most misrepresented science presented as a
fact despite glooming evidence against it.
This book provides a summary of the several hundreds of studies

on the radiation hormesis, especially at low dose for curing several
diseases including cancer. It is well known that, the three, major
civilian nuclear accidents released very small amount of radiation dose
to the public, in spite of that there was large evacuation of the public
which caused more panic and non-radiological deaths. Also, there are
plenty of evidences from the atomic bomb survivor data that the life
span of the exposed population to the radiation had increased as
compared to those unexposed. Similarly, the servicemen involved in
nuclear weapon programs had lesser cancer incidences and relatively
longer life as compared to the general population. This book has tried
to explain the root cause of fear of radiation in spite of several
Page xiii
evidences which show low dose radiation is beneficial to health. To
explain the origin and evolution d the fear of radiation, the authors
provide historical evidence of development of LNT model, its
inapplicability for low dose conditions against the radiation risks, and
its incorporation into the policy of regulatory bodies.
This book will definitely benefit the scientists, engineers and

students in every field in addition to the common public to overcome
the fear of radiation. It is a must read for professionals engaged in
nuclear safety field and for students and researchers in this multi-
disciplinary domain.
I must compliment the authors of the book, Dr. A.K. Nayak, Dr. R.
K. Sinha and Mr. S.S. Munot. I wish all the readers an enjoyable journey
through this book.
Ajit Kumar Mohanty

Director, Bhabha Atomic Research Centre
Unreasoned fears are common. People in England were at
time afraid of automobiles on road when they were introduced for
the first time, but such fears disappear with familiarity and
experience.
The same has already happened with radiation, which people

have realized is an important accompaniment of an essential
energy source (Nuclear Power), and that it has also many unique
medical uses.
R. Chidambaram
Chairman(Honorary), School for Advanced Studies in Nuclear
Science & Technology, BARC
Former PSA to Govt. of India and Former Chairman, AEC
Page xv
Executive Summary
In this book, we have endeavoured to bring out the historical
evidence of health effects of ionising radiation through a large
literature review without any personal bias. Since the discovery of X-
ray, efforts have been made to study the use of radiation in various
applications including medicine. A major breakthrough in the field of
radioactivity and radiation occurred with Enrico Fermi demonstrating
existence of radioactive elements produced by neutron irradiation,
which further led to the discovery of fission. With the first self-
sustaining nuclear fission chain reaction demonstrated at Chicago Pile
(CP-1) in 1942, the immediate application was the development of
atomic bomb and nuclear power reactors. The USA tested the two atom
bombs at two Japanese cities in 1945, which led to a large-scale
devastation and shock not only to the Japanese people but also to the
entire world.
Following the devastating nuclear bombings at the two cities,

nuclear radiation phobia developed in common people without
understanding the main cause of the prompt fatalities. In the absence
of radiation measuring devices at the time of the bomb explosions, the
actual extent of radiation exposure to the individuals was not known.
The long and short term effects of radiation on health of humans were
also unknown. Indeed, several scientists in USA and Japan worked for
almost six decades to create dosimetry systems for estimating the
doses. Only the simulation tests and computations could reveal the
dose which the affected Japanese people might have encountered, and
the risk due to atomic radiation in the form of death and cancer could
be scientifically studied only thereafter. It may be noted that, the doses
received due to the atomic bomb explosions ranged from lethal (for
those living nearer to the epicentre) to infinitesimal for those living
away or shielded by buildings or terrains. Further investigations into
the impact of the atomic bombs on Japan showed that the energy of A-
bombs was made up of roughly 35% thermal energy (heat and light),
50% blast energy (pressure shock waves), and 15% radioactive
radiation (5% prompt and 10% residual, which consists of minor
induced radioactivity and major fallout). The majority of the
immediate deaths, were therefore, caused by heat and blast energy,
Page xvii
which the general population, even today, is the least aware of. The
threat of cancer persists in the public consciousness even today. Data
from the Life Span Study (LSS) of survivors of the Japanese atomic
bomb reveal a threshold dosage range of 100 to 200 mSv, below which
no detectable risk of cancer has been observed. In reality, compared to
normal Japanese population, it was found that the "average life span"
was enhanced and the "average death rate" was decreased for those
exposed to such low dose radiation. Furthermore, even 62 years later,
the offsprings of those who were exposed to the atomic bombs
dropped on Hiroshima and Nagasaki, show no signs of having negative
health impacts. Thousands of military and servicemen who
participated in nuclear weapon tests in the UK, Australia, USA, and
USSR, have been the subject of numerous research on the health
implications of low dosage radiation exposure. No significant effects
were reported on the mortality or subsequent risk of cancer and other
fatal diseases among these people.
Apart from atomic weapons, the nuclear energy was used for
commercial electricity production in atomic power reactors. Many
countries including the USA, Canada, USSR, UK, France, Germany,
Japan, South Korea and other European countries constructed several
atomic power reactors during 1970 to 1980, which is termed as the
golden era of nuclear power, until the first nuclear accident at TMI-2
occurred in 1979. The accident led to significant melting of uranium
fuel and release of radioactive gases. However, due to robust
construction of nuclear reactors with several layers of safety
protection against radioactivity release, only 0.01% of fission products
escaped to environment (only 10 Ci was released in 16 hrs. and ~ 70 Ci
of Iodine was released in the next 30 days). Out of fear of radioactivity,
the Governor of Pennsylvania ordered evacuation of people. Several
studies confirmed that no significant rise in rates of cancer incidence in
and around the area was observed since the accident occurred. The
other nuclear accident was the Chernobyl reactor core melt down and
damage of structural materials, which released a large amount of
radioactive gases to the environment. This accident was more severe
than the TMI-2 accident. The then Soviet administration overreacted
by forcibly evacuating a large number of people without warning. This
caused enormous panic and social dislocation among the public, which
xviii Page
caused more deaths than the accident. The dose received by people in
Chernobyl region showed that the liquidators received a maximum
dose of 100 mSv only. There is no evidence of them having cancer.
Abundant wildlife populations in the Chernobyl Exclusion Zone, today,
has made it a magnificent nature preserve. The recent accident at
Fukushima nuclear power plants also caused large panic in
Government and public, even at a release dose of 1 mSv. The public
evacuation was ordered even at such a meagre release, causing more
stress and deaths. The hazard of the evacuation outweighed any
potential risk of radiation exposure, especially for the elderly. Instead
of protecting human health, the evacuation actually created more risk
than radiation could make. The mortality risk of nursing home
residents who left after the Fukushima accident was 2.7 times higher
than it was for those who stayed. Obviously, the stress of leaving their
abodes was significantly more dangerous than radiation.
In general, it can be emphasised that the public is exposed to low

levels of radiation, of the order of a few mSv, with the exception of a
small number of individuals who were specifically exposed to high
levels of radiation during the atomic bomb explosions, as shown by the
data from survivors of atomic bombs as well as accidents in civil
nuclear power reactors. Therefore, we focused our study on other
simulated trials and the consequences of low-dose radiation on human
health. In this regard, we have presented the case studies on effects of
low-dose radiation on health of human beings. In Taipei City (capital of
Taiwan), nearly 10,000 residents were living in houses made with
recycled steel structures and re-informcements polluted with Cobalt-
60 radioactive material. The studies revealed that they experienced
comparatively less cancer deaths than the general Taiwanese
population. Similar results were reported from inhabitants living in
High-Level Natural Radiation Areas (HLNRA) of Karunagapally, Kerala.
There are several thousands of publications available in open

literature (we have referred around 400 manuscripts here) supporting
the health benefits of low-dose radiation (LDR) or radiation hormesis.
LDR is found to cure several diseases such as gas gangrene, pneumonia,
bronchitis, tuberculosis, diphtheria, dermatitis, HIV/AIDS, etc. and
non-infectious ones such as cancer, Alzheimer's disease, vascular
Page xix
disease, heart disease, Type 2 diabetes and painful degenerative
disorders (spondylitis, arthritis, asthma, fibromyalgia, multiple
sclerosis, psoriasis, ulcers, etc.). A large number of studies were
conducted by Chinese researchers supporting the above results
particularly the effects of low-dose radiation on tumour cell growth,
diabetes, stochastic effects, etc. The health effects of low-dose radiation
in cohorts of physicians and technical personnel, show that the overall
mortality rate and cancer mortality rates are substantially reduced as
compared to those who were not exposed.
Having said so much on the beneficial effects of radiation on

human health, cure of life threatening diseases, enhancement of life
span, there is a big question “Why do people fear radiation ?”
The answer is: when people think about nuclear, they don't think
about electricity, medicine, or food shelf-life enhancement, or cure of
diseases including cancer, increase in life span due to direct or indirect
applications of radiation; they think about nuclear warheads,
Hiroshima and Nagasaki, Chernobyl, Fukushima, and finally, cancer. It
may be emphasised that the public perception about nuclear radiation
as a carcinogen; is more political, scientific misinterpretation and
“cherry-picking” than the actual science, as pointed out by Sacks,
Meyerson and Siegel in their studies published in 2016. In particular,
governments used fear of radiation as an effective weapon during the
Cold War period. Ultimately, it resulted in collateral damage to public
morale about radiation. The fear of radiation is linked to the concept of
Linear No Threshold (LNT) hypothesis, which means no matter
howsoever small the radiation dose is, it has the potential to induce
cancer. The history of LNT goes to the discovery of X-ray-induced
mutations, which suggest that cosmic/terrestrial radiation-induced
mutations provide the principal mechanism of the driving force for
evolution. Subsequently, the German scientist, Muller performed
studies on mutation in fruit-flies at a very high dose of 1000 to 4000 R
and he suggested a linear dose response for ionising radiation-induced
mutations and extrapolated to “zero” R dose. He assumed that the LNT
dose relationship with genetic damage was proportional to the energy
absorbed. In his 1946 Nobel Prize lecture, Muller tried to impress his
personal bias and announced to the world that radiation harms
xx Page
linearly down to zero doses, regardless of dose rate. It may be noted
that Muller's experiments on fruit-flies was conducted at very high
doses of 1000 to 4000 R to get quickly the significant mutations;
however, the subsequent studies by others showed that doses <50 R or
about 500 mGy, did not increase the mutation rate when given
continuously over a 21-day period. In fact, the results were dose rate
dependent. In the process, Muller ignored and withheld data that
showed that he was wrong. In fact, more recent studies on fruit-flies
have shown that X- and γ-ray doses as low as 200 mGy to eggs
significantly increased adult fly longevity, whether given as an acute or
chronic dose.
The LNT approach was eventually expanded to include chemical

carcinogen risk assessment and is now utilised by regulatory and
public health organisations all over the world. The general consensus
was that if ionising radiation can cause mutagenesis in fruit flies, it can
also cause cancer in people. Muller and other prominent members of
the radiation genetics community were ardent supporters of the LNT
model for genomic alterations and the development of cancer, despite
the fact that many others did not continue to maintain major support
for it.
The LNT model was suggested by the U.S. National Academy of

Sciences (NAS) Biological Effects of Atomic Radiation (BEAR) - I
Committee's Genetics Panel (GP), and it was quickly adopted by all
governments and regulatory organisations throughout the world
except France. The NAS Genetics Panel did not check thoroughly the
human genetic risk to radiation exposures. Others who supported the
LNT theory, based their arguments on the incorrect information of
delayed cancer deaths among Hiroshima and Nagasaki blast survivors.
Using simple linear extrapolation and statistics, the risk versus dose
line was stretched from 1 Gy to "zero" Gy (100 to 0 R) without any
statistical evidence utilising the cancer data of atomic bomb survivors
who had an immediate exposure in the high dosage range from 1 to 10
Gy (100 to 1000 R).
Page xxi
What does the LNT model ignore? Low-doses of radiation have
proven to improve the health of people with hundreds of proofs given
in this manuscript. Radiation, at large doses, can be deadly, however it
is false to say that radiation at any dose is harmful. The authors who
support the LNT model believe that zero dose is the best estimate for a
dose threshold for solid cancer mortality. Other researchers
discovered that they had neglected the negative risk values of low-dose
radiation (atomic bomb survivor data), which indicated the errors in
their analysis.
In conclusion, despite the vast amount of published scientific

material that demonstrates thresholds and the positive effects of low-
dose ionising radiation, every regulatory agency in the world, with the
exception of France, bases its regulations on the LNT. While, the LNT
dose response model is highly conservative with regard to the
radiation risk to the public, however, it has created the radiation phobia
in the public consciousness. Today, the LNT has broad implications for
nuclear and diagnostic medicine, radiography, nuclear power, nuclear
waste management, food irradiation, and home radon. The societal
cost of radiophobia and fear mongering is exorbitant. The cost of
implementing and upholding radiation laws does not increase the
safety of plants or people's health; rather, it results in the loss of tens of
thousands of lives each year across the globe because of depriving
them from the benefits of low dose radiation, as indicated by
Parthasarthy in his study published in 2016. Sticking to As Low As
Reasonable Achievable (ALARA) principles add fear, cost and difficulty
to implement.
On June 12, 1956, the National Academy of Sciences (NAS)

Biological Effects of Atomic Radiation (BEAR) committee's Genetics
Panel (GP) approved LNT. The 500 mGy/y upper limit dosage for
nuclear workers, in effect since 1934, was abolished. The next day, the
front page of the New York Times, reported that radiation is dangerous.
Other media did the same. This choice was imposed, as being
motivated by an ideology and not on facts.
xxii Page
The LNT model, which assumes that carcinogenic
hazards are proportional to radiation exposure for all
radiation doses without taking dose rates and
threshold into account, is the basis of today's radiation
safety laws. Growing evidence suggests that the
current, excessively strict radiation protection
regulations are not the most effective means of
safeguarding the general public's health. Therefore,
there are already enough factors for policymakers to
think about . Re-evaluating the International
Commission on Radiological Protection (ICRP) dosage
standards is necessary in order to allay public radiation
fears as well as concerns among policymakers related
to nuclear power plants. While numerous studies show
that low-dose radiation has beneficial impacts on
people's lives and health (increase in life span, cure of
several diseases, reduction in cancer cases, etc.), more
focused research must be done to assess the threshold
doses against various diseases, to maximise the
curative effects of low-dose radiation.
Page xxiii
What is ionising radiation?
1
Energy emitted from a source is known as radiation. The sun's
heat or light, microwaves from an oven, X-rays from an X-ray tube,
gamma rays from radioactive materials, etc. are a few examples.
Radiation comes in a variety of forms that merely vary in frequency and
wavelength. Longer wavelength and lower frequency waves such as
heat and radio waves have less energy than shorter wavelength i.e.,
higher frequency waves like X rays and gamma rays. With its energy, the
high frequency region of the electromagnetic spectrum, which includes
X rays and gamma rays, ionises or charges an atom by displacing irmly
bound electrons from its orbit. This means that all electromagnetic
(EM) radiation, with the exception of the high frequency region of the
electromagnetic spectrum does not result in ionising radiation. In
addition to X-rays and gamma rays, atoms' nuclei also emit alpha and
beta rays, which are categorised as ionising radiations. UV radiation, on
the other hand, does not ionise matter.
1.1. Discovery of ionising radiation

In the latter half of the 19th century, tremendous progress was
made in the study of radiation and
atomic structure. The periodic system
of elements was irst proposed by
Dmitri Mendeleev in 1869. Wilhelm
Roentgen accidentally discovered the
fundamentals of X-rays in December
1895 while taking an X-ray image of his
wife's hand. This sparked additional
research into the characteristics of
ionising radiation and the potential
use of radiation in medicine. Henri
Becquerel announced the discovery of
X-ray image of Wilhelm
radioactivity in 1896. He was under
Roentgen's wife's hand
(December 1895) the impression that he was exploiting
the sun's energy to create X-rays.
Page 1
THE UNREASONED FEAR OF RADIATION
He exposed potassium uranyl sulphate to sunlight for the

experiment. He then placed it on photographic plates wrapped in black
paper, believing that the Uranium absorbed the sun's energy and
emitted it as X-rays. His theory was refuted in 1896, as his experiment
"failed" in Paris due to the overcast. Becquerel made the decision to still
develop his photography plates. To his surprise, the images were
powerful and distinct, demonstrating that uranium could produce
radiation without the need for an outside energy source like the sun
[1], [2]. As they were emanated from uranium, Becquerel referred to
them as "uranic rays" [2]. Marie and Pierre Curie in Paris started
investigating the peculiar uranium rays in 1898. On July 18, 1898, they
jointly announced the discovery of a brand-new element that they
termed polonium [3]. For the irst time, the word "radioactive" was
used in a scienti ic paper [3], and "uranic rays" were renamed as
"Becquerel rays." They made other radioactive discoveries, including
radium, polonium, and thorium. The new rays were soon labelled as
alpha, beta, and gamma radiation by Ernest Rutherford. Rutherford
and Frederick Soddy conducted experiments in 1902 to demonstrate
the concept of radioactivity, which they de ined as the spontaneous
transformation of one element into another through the emission of
radiation [4], [5]. In 1903, Becquerel and the Curies were awarded the
Nobel Prize for their research on radiation.
1.2. Discovery of fission and its consequences

Enrico Fermi's demonstration of the presence of new radioactive
elements [radioisotopes] created by neutron radiation and his
subsequent discovery of nuclear reactions caused by slow neutrons,
marked the next major advancement in the ields of radioactivity and
radiation. Following Fermi's research, radio-chemists Meitner, Hahn,
and Fritz Strassmann carried out more experiments in 1938 by
bombarding neutron-beam on uranium. Unexpectedly, Hahn and
Strassmann discovered barium isotopes among the decay products.
Meitner developed the nuclear ission theory with the aid of her
physicist nephew, Otto Frisch [6]. Other scientists rapidly noticed that
secondary neutrons are also released during this ission event.
2 Page
WHAT IS IONISING RADIATION?
At the University of Chicago, Fermi and his colleagues

established the irst self-sustaining nuclear ission chain reaction in
1942 in Chicago Pile (CP-1) reactor [7]. It is recognised as the single
most signi icant scienti ic development in the atomic power industry
including nuclear warhead. The development of nuclear warheads
made a grand, devastating, and painful entrance into the public
perception against nuclear energy when two cities, Hiroshima and
Nagasaki, were decimated to the ground by enormous explosions of the
two atom bombs.
Schematic of the Fission Reaction
Page 3
4 Page
More about nuclear weapons
programme
2
The United States made the decision to create nuclear weapons
in the wake of World War II, after successful demonstration of nuclear
ission chain in CP-1 (Chicago Pile) reactions. The Manhattan project,
which aimed to create the atomic bomb, was carried out at Los Alamos
Laboratory during the war under the leadership of Professor
Oppenheimer. He is regarded as the "father of the atomic bomb."
However, prior to the detonation, nothing was known about the deadly
effects of the nuclear bombs. On August 6, 1945, the "Little Boy" atomic
bomb was detonated on Hiroshima, and three days later, on August 9,
the "Fat Man" atomic bomb was dropped on Nagasaki, Japan. The
scientists working on the Manhattan project were shocked including
the rest of the world after the explosions which decimated the two
cities.
The "Little Boy" atomic bomb was detonated on Hiroshima and the "Fat
Man" atomic bomb was dropped on Nagasaki, Japan
2.1. The aftermath of Hiroshima and Nagasaki bombing

Following the devastating nuclear bombings, many people lost
life. For a comprehensive understanding of how radiation affects
people, a huge database of atomic bomb survivors was generated [8].
However, calculating the actual doses received by the population was a
dif icult undertaking because there were no radiation measuring
devices available at the time of the explosion. Radiation Effects
Research Foundation (RERF) and Atomic Bomb Causality Commission
conducted extensive studies to determine the precise dose that the
Page 5
public in both the cities received [9]. The doses received by the
survivors ranged from lethal to in initesimal depending the distance of
the public from the bomb's epicentre (the point directly below it). For
more than 60 years, many scientists in Japan and the U.S. worked to
develop dosimetry devices for the measurement of radiation doses
accurately.
Retrospective radiation dose measurements were conducted

utilising special simulation tests and techniques. Together with the Los
Alamos National Laboratory (LANL) and Oak Ridge National
Laboratory (ORNL), many tests were conducted as part of Operation
Teapot at the Nevada Test Site (NTS) in 1955, which signi icantly
improved understanding of radiation ields [10]. Tentative 1957
Dosimetry (T57D), the irst dosimetry system, was created in the
1950s. Based on measurements made during Operation Plumb Bob
utilising two model homes, T57D gave streamlined estimates of
shielding. The system's primary law was the absence of
characterisation of radiation source terms, which eventually resulted
in limited estimates of shielding. The Tentative 1965 Dosimetry
(T65D) system was created in the 1960s as an upgrade to T57D. Based
on calculations of gamma ray and neutron transmission coef icients
using data on survivors' shielding at the time of the bombing, T65D
provided methods for coping up with various types of external
shielding [10]. The Later Dosimetry System 1986 (DS86) was created
employing the most up-to-date computing techniques and the best
current understanding of the source term, radiation transport, and
shielding. In contrast to T57D and T65D, DS86 took a comprehensive
characterization of radiation into account rather than the empirical
results of dosimetric measurements [11]. In 2003, a revised dosimetry
system known as DS02 was approved and put into use to study atomic
bomb survivors using data from the Radiation Effects Research
Foundation (RERF). This was done after a thorough re-evaluation of
bomb source terms, radiation transport calculations, and experimental
errors in the activation measurement [11].
6 Page
MORE ABOUT NUCLEAR WEAPONS PROGRAM
2.2. Further analysis of atom bomb radiation effects in Japan

Japan is the only nation that has endured a nuclear assault.
About 200,000 individuals were instantly killed by the 1945 A-
weapons [12]. The energy of A-bombs comprise 35% thermal
radiation (heat and light), 50% blast energy (pressure shock waves),
and 15% nuclear radiation [13]. In reality, the majority of
instantaneous fatalities, particularly in the bomb's centre, could be
attributed to heat and blast energy (85%) and not due to radiation.
People tend to forget that victims of heat and blast were affected in a
moment or short period, whereas cancer induction has remained a
menace even to the present day. Table 1 and Table 2 show solid Cancer
and leukaemia incidences in the Hiroshima population.
Table 1 No. of deaths from Leukemia between 1950 and 2000 among
the survivors of Hiroshima and Nagasaki with measured doses [14]
According to data from the Life Span Study (LSS) of the Japanese
survivors of A-bomb, an acute dose for deaths due to Leukemia has an
effective threshold of 100 millisieverts, which can be considered as the
threshold. This threshold level can be viewed as the de ining marker
between the low dosage range and the intermediate dose range where
Page 7
Table 2 No. of deaths from solid cancers between 1950 and 2000
among the survivors of Hiroshima and Nagasaki with measured
doses [15]
the effect is too small to even be quanti iable. The deaths due to
leukaemia data indicate that the threshold even could be as high as 200
millisieverts, although using 100 millisieverts is more conservative.
Most importantly, there is no evidence in this or any other study that a
single dose below this threshold carries a discernible risk of cancer.
From the analysis [14] of the impacts of A-bomb survivors on

lifespan and cancer incidence it can be inferred that the low-dose
radiation from A-bombs has increased survivor lifespan and decreased
cancer mortality, on average, against the control individuals who did
not live in these cities. It is true that A-bomb survivors who received
large doses showed shorter lifespans and higher cancer mortality, but
they only made up a small portion of the local population. The indings
indicate that overall "average cancer mortality" was decreased and
"average lifetime" was prolonged. Similar indings for deaths due to
solid cancers was observed, where for radiation doses less than 200
millisieverts the extra risk due to radiation is negligible or even
negative i.e., have positive health effects. Hence the threshold dose for
deaths from solid cancer can be considered to be 200 millisieverts.
8 Page
2.3. Evidence of longer lifespan of some people who were

heavily irradiated by ionising radiation
Mr. Tsutomu Yamaguchi, the unhappiest man in the world, was
A-bombed at Hiroshima. Later, he moved to Nagasaki, where he
managed to survive the second A-bombing [16]. He was the only
survivor of the two A-bomb bombs, and he may be the happiest man
alive because more than 70 people were killed while being evacuated
from Hiroshima to Nagasaki except him. More astonishingly, the two A-
bombs did not shorten his life; he passed away at the age of 93.
Sunao Tsuboi, Chairman of the Japan Confederation of A-Bomb

and H-Bomb Sufferers Organizations, was chosen as an honorary
citizen of Hiroshima city, according to a report by the Nikkei Shimbun
on April 5, 2018. He was only 1.2 km away from the epicentre of the A-
bomb explosion. In 2018, he turned 93 years of age. In order to support
initiatives to ban nuclear weapons, he spoke with then-US President
Obama[17], [18].
Shigeaki Mori was injured after being blown away due to the
explosion of atom bomb into a riverbed from a bridge, located 2.5 km
away from the epicentre. He was born in 1937 and has lived longer than
most Japanese men [17], [18].
For Japanese men and women, the average life expectancy (for
remaining life) at the age of 80 is 8.61 and 8.19, respectively [12].
Therefore, it was shown from above studies that the A-bomb survivors
lived much older than 88. It could be argued that the A-bomb survivor
life span was higher due the Japanese government's high- quality
healthcare services. This may have played a role to some extent, but
low-dose radiation boosts human biological defence mechanisms, thus
that appears to be another major component that has an impact [12].
2.4. A-bomb survivor's lifespan was statistically shortened

Cologne and Preston investigated the longevity of 120,321 A-
bomb survivors [19]. They came to the conclusion that their "median
life expectancy reduced at a rate of around 1.3 years per Gy with
increasing radiation dose but declined more rapidly at high doses. The
Median loss of life among cohort members receiving estimated doses
Page 9
under 1 Gy was around 2 months, whereas it was 2.6 years among the
few cohort members receiving estimated doses of 1 Gy or more.
Their model also showed that people with dosage exposed more
than zero, experienced a median loss of life of roughly 4 months. In
view of the above, the readers might have the apprehension that
ionising radiation from A-bombs was hazardous and it had shortened
A-bomb survivors' longevity to a greater or lesser degree. However, the
evidences of longer lifespan of the A-bomb survivors, show that the
model was unable to account for known and unknown factors which
actually had caused the reverse, i.e., increase in lifespan at low doses
[19].
2.5. More analysis of atom bomb explosion

As stated earlier, the energy of a typical atomic bomb can be
broken down into three different types of energy: 50% blast (pressure
shock wave), 35% thermal radiation (heat and light), and 15% nuclear
radiation (5% prompt and 10% residual [13], [20]). Of the 15, 5% are
initial radiation released within 30 seconds, and 10% are residual
radiation, which includes substantial fallout and moderate induced
radioactivity [21]. Thermal radiation either burned or scalded plants,
animals, including people, homes, and other organic materials in
Hiroshima and Nagasaki. A sizable amount of water evaporated from
Hiroshima's numerous canals, contributing to the mushroom cloud.
After rising into the sky, the vapour condensed to produce raindrops
that contained soot and other debris. This "black rain" began to fall 20
to 30 minutes after the explosion. Black rain might have included twice
as much radiation as the initial radiation, as a result which was neither
measured nor known through simulated test including the test in the
Nevada desert which never had black rain. However, the radiation
doses were thought to be the initial radiation (5%). Thus, despite
several years of research, it should be highlighted that precise estimate
of exposure doses from residual radiation is rather inconclusive. The
radiation dosage maps near the explosion's epicentre are therefore
inconsistent and unreliable even until today [22].
10 Page
The mushroom clouds created during the bombing at Hiroshima

and Nagasaki
According to a report, the area west of the epicenter has a higher

cancer risk than other places, indicating a negative impact of black rain
[23]. Although harmful health effects cannot be totally ruled out, but
according to another investigation, exposure to rain soon after the
atomic explosions of Hiroshima and Nagasaki is unlikely to raise cancer
risk [24].
2.6. Trans-generational effects of radiation

Contrary to popular belief, radiation does not have trans-
generational consequences. There were no signs of harmful health
effects after 62 years of A-bomb explosions in the Japanese cities,
according to a recent epidemiological study on the risk of death among
children of atomic bomb survivors [25]. The writers claimed,
“…models of the trans-generational effects of radiation

exposure predict more genetic disease in the children of
people exposed to radiation. However, children of people
exposed to the atomic bombs in Hiroshima and Nagasaki had
no indications of deleterious health effects even after 62
years of bombing [25].”
Page 11
2.7. Nuclear test participants exposure

Follow-up research on the health of servicemen and citizens who
participated in nuclear weapon tests offered more details on the
impacts of low-dose radiation exposure. There were no discernible
impacts on mortality or the probability of developing cancer and other
fatal diseases in the cohort of
participants who took part in
atmospheric nuclear weapon
tests in the United Kingdom in
the 1950s to 1960s (n = 22347)
[26], [27]. Standard Mortality
Ratios (SMR) were 1.01 for all
causes and 0.96 for all neoplasms
in participants compared to
unexposed control populations
[26]. Signi icant differences in
mortality were seen for a number
of cancer types. Leukaemia and
multiple myeloma rates were
higher in the participants,
whereas prostate and kidney
malignancies were more
common in the controls. The
An image of an active site of the differences were primarily
nuclear weapon test site in United
attributed to chance by the
Kingdom
authors, but some were thought
to be the result of smoking
behaviours of cohort rather than radiation. During a subsequent 7-year
follow-up, participants' death rates for all causes, leukaemia and
multiple myeloma were lower than expected based on national rates
(SMRs: 0.86, 0.85, 0.57, and 0.46, respectively), and they were also
lower than those of controls (RRs: 0.99, 0.96, 0.57, and 0.57,
respectively) [27]. When mortality risk for participants was compared
to that of controls for periods longer than 10 years following the initial
involvement in the tests, it was discovered that it was comparable for
all causes (RR = 0.99) and all neoplasms (RR = 0.95). Following up on
mortality and cancer incidence in the same population, these indings
12 Page
were again con irmed [28], [29]. A cohort of Australians (n = 10983)

who took part in the British nuclear experiments in Australia did not
show any evidence of increased all-cause mortality [30]. Additionally,
no correlation was found between radiation exposure and any cancer
or excess cancer deaths, as well as with all-cause cancer incidence or
mortality. A retrospective cohort study of 12219 military veterans
from the Operation Plumbbob nuclear test series at the Nevada test site
revealed that they had a lower mortality rate than the US general
population and were suf iciently healthy even 53 years after exposure
[31].
In the Semipalatinsk (Union of Soviet Socialist Republics)

historical cohort (n = 19545) exposed to radioactive fallout during
nuclear testing in the vicinity of the Semipalatinsk Nuclear Test Site,
Kazakhstan, with a cumulative effective dose ranging from 20 mSv to 4
Sv [32], high rates of all-cause mortality and cancer mortality were
discovered. Based on the complete cohort data, the (Excess Relative
Risk) ERR/Sv for all solid tumours combined was 1.77 (95 percent CI,
1.35-2.27). This cohort also had a high prevalence of cardiovascular
mortality [33] (The Excess Relative Risk is de ined as the rate of disease
in an exposed population divided by the rate of disease in an unexposed
population, minus 1.0). No signi icant dose-response connection for
any cardiovascular illness, heart disease, or stroke could, however, be
shown when baseline rates in exposed and unexposed groups were
compared.
Page 13
14 Page
Civil nuclear reactor accidents
– The effects of radiation leak 3
A lot of nuclear reactors were constructed during the Cold War to
produce fuel suitable for use in weapons, creating a negative
perception against nuclear among the general populace. Additionally, a
lot of industrialised nations built nuclear power reactors after realising
the sustainability of nuclear energy. The Obninsk Nuclear Power Plant
in the Soviet Union became the irst nuclear power plant in history to
produce electricity on June 27, 1954 [34]. Many other nations followed
including the United States and the Soviet Union in developing nuclear
ission reactors for the production of electricity. In the majority of
developed nations, nuclear power became a standard component of
energy production. Nuclear power installed capacity increased quickly
from less than 1 GW in 1960 to ~100 GW in the late 1970s and more
than 300 GW in the late 1980s. Today nuclear power installed capacity
is around 392 GW, which is 10 % of the global electricity generation.
3.1. Risk of nuclear power

The 1960s and early
1970s were the golden era
of nuclear power with a lot
of promise of cheap
nuclear power. Numerous
orders for the building of
reactors with larger power
ratings were placed, and
hundreds of nuclear plants
were erected. However,
the risk to the public from
a nuclear power plant was
not quanti ied. The British
N-Regulator F. R. Farmer,
evaluated the risk for
NPPs, taking into account
a wide range of incidents,
not just the Maximum Risk due to a nuclear power plant [39]
Page 15
Credible Accident but also those of less signi icance and were
considerably likely.
When the USNRC was created in 1974, Prof. Rasmussen of MIT

undertook a study on "what is the risk of N-Power"? The WASH-1400
team set out to "identify every single accident sequence that matters
and its probability" and determine if the consequences would be core
damage, a release into the containment, or a release to an offsite
location. The PWR and BWR plants were chosen. Probabilistic Safety
Analysis at levels 1, 2, and 3 were conducted. The following factors
were taken into account for radioactivity emission from containment:
• Containment rupture due to steam explosion in Reactor
Pressure Vessel (RPV)
• Containment leak rate
• Containment rupture due to hydrogen burning
• Containment rupture due to over pressure
• Containment rupture due to melt through
Table 3 Early fatality due to various accidents [39]
Accident Type Total Nu mber for 1969 Approximate Individual Rise

Early Fatality Proba bility/yr (a)
Motor Vehicle 55791 3x10 -4
Falls 17827 9x10 -5
Fires and Ho t Substance 7451 4x10 -5
Drowning 6181 3x10 -5
Poison 4516 2x10 -5
Firearms 2309 1x10 -5
Machinery (1968) 2054 1x10 -5
Water Transp ort 1743 9x10 -6
Air Travel 1778 9x10 -6
Falling Objects 1271 6x10 -6
Electrocution 1148 6x10 -6
Railway 884 4x10 -6
Lightning 160 5x10 -7
Tornadoes 118 (b) 4x10 -7
Hurricanes 90 (c) 4x10 -7
All Others 8695 4x10 -5
All Accidents 115000 6x10 -4
Nuclear Acci dents (100 Reactors ) - 2x10 -10 (d)
(a) Based on total U.S. popula tion, except as not ed
(b) (1953 – 1971 avg.)
(c) (1901 – 1972 avg.)
(d) Based on a population risk of 15x10 6
16 Page
CIVIL NUCLEAR REACTOR ACCIDENTS – THE EFFECTS OF RADIATION LEAK
The WASH-1400 results, which provided an individual's

probability of early mortality due to different causes, were published in
1975 (Table 3). The danger resulting from 100 nuclear power plants
was found to be extremely low (~10-10/year) or insigni icant when
compared to even road accidents. This inspired a lot of trust in nuclear
reactor designers and suppliers .
3.2. Major accidents in civil nuclear power reactors and their
consequences
In less than 4 years after publication of WASH-1400, the core
melt accident occurred at TMI-2 on March 28, 1979. The fact that a
power reactor's core could melt and do it so fast surprised everyone in
the nuclear community. After the catastrophe, it was believed for
several years that just a small portion of the core had melted in TMI.
After removal of upper internals, it was found that at least half of core
had melted. Nearly 20 tons of fuel and other structural components
made it to the lower head. Less than half of the fuel had melted and gone
to the reactor coolant water in the reactor vessel, according to later
examinations in 1985 into the Three Mile Island accident.
The damaged core of the TMI-2

Page 17
Gaseous release during TMI Accident

When hydrogen formed due to the oxidation of the zirconium
fuel cladding, was leaked into containment via the open PORV (Pilot
Operated Relief Valve), it occasionally ignited locally and caused a 2 bar
pressure surge (within design pressure of containment of 5 bar). Since
a door was left open in the auxiliary building before it was shut, some of
the volatile ission products discharged from the core migrated to the
auxiliary building. Subsequently the ission products leaked to the
containment. However, only 0.01 percent of ission products leaked
into the environment in spite
of the fact that the auxiliary
building was not a leak-tight
structure [40].
Some radioactive gases
also discharged into the
environment, however it was
quite small (only 10 Ci in 16
hours and about 70 Curies of
Iodine in the following 30
days). But the accident had no
negative consequences on
health. An emergency was
declared 180 minutes after
the event began. Radiation
discharge took place on March
Evacuation of the Public from the 30 (after two days of the
Pennsylvania province
18 Page
disaster), from midnight until 8:00 in the morning. The governor of

Pennsylvania advised providing shelter for those who lived nearby (10
miles). Pregnant women and schoolchildren who lived within ive
miles were evacuated at 12:30 PM, ultimately, 144,000 people were
evacuated [40].
The public's fear of radiation increased despite multiple

epidemiological studies [41] conforming that there hasn't been a
statistically signi icant increase in the rate of cancer in the area since
the disaster happened.
A more serious catastrophe happened at one of Chernobyl's

nuclear power plants in 1986, a few years after the TMI-2 tragedy [42].
The Chernobyl reactor was a unique graphite moderated pressure tube
type BWR (RBMK) that the former USSR constructed and operated.
The accident was more serious than the TMI-2 because the
structural materials and core both melted and spilled onto the
basement. The Soviet administration's inability to handle the situation
only worsened the accident [42]. With the help of scienti ic, civilian,
and military troops, clean-up was accomplished. Number of immediate
deaths was small. The accident was put to an end by covering the
accident's core area with over 5000 tonnes of sand, clay, and material
containing boron carried by helicopter. All fuel bundles melted,
graphite burnt for at least seven days, releasing volatile ission
products. Fearing a steam explosion, the water in the pool was emptied
at the expense of two operators. The Soviet administration failed
immediately to provide iodine tablets and give out the required public
information. Later, it overreacted and abruptly relocated 116,000
residents forcibly, resulting in panic and social unrest [43]. More
people are likely to have died as a result of this than from radiation
itself.
The Chernobyl disaster dealt more blows to the ield of nuclear

science and, in particular, to the development of nuclear power. The
public was worried that a nuclear reactor may explode like an atom
bomb. Fission product emission at Chernobyl had a greater magnitude
than the Hiroshima bomb. Clean-up expenses were approximately 7
billion Rubles (that time Ruble was more expensive than dollar). Any
Page 19
new plant development and the operation of plants that were already
under construction were stopped due to widespread resistance and
fear of nuclear power growth. After 1986, there was a real stagnation
for nuclear power. Plant capital costs grew as a result of legal cases;
operating plants underwent intense inspection and assessment. All
these reduced capacity factor of plants from 50 to 70%; and resulted in
large cost of nuclear electricity.
Early international
assessments did not attempt to
dispute the overall risks to human
health; instead, they attempted to
document the radiation release
and contamination. Table 4 lists
the doses that the general public
and residents of the Chernobyl
region received. Liquidators
received a total dose of 100
millisieverts, according to the
statistics. But there is no proof that
they have illnesses like cancer.
In various administrative
districts of Belarus, Russia, and
The damage at the Chernobyl reactor
Evacuation of the Public due to Chernobyl accident
20 Page
Ukraine, the average effective doses for the general population in

"contaminated" areas accumulated in 1986–2005 were estimated to
be between 10 and 30 millisievert. The average exposure in places
under stringent radiological control was 50 millisievert or more.
Several hundred millisieverts were delivered to certain residents. It
should be emphasised that residents of the Chernobyl-contaminated
lands often received lower average doses than those who reside in
Kerala [44], which has certain areas with high natural background
radiation levels (100–200 millisievert in 20 years).
Table 4: Chernobyl dose received by people (excluding cases

of acute radiation sickness and thyroid cancer)[43]
Additionally, visitors to the site recently have expressed

astonishment. In contrast to what they had anticipated, they
discovered that despite the radiation levels, wildlife is surviving and
thriving in certain cases. Mary Mycio, an American journalist who is
originally from Ukraine, spent a lot of time there and wrote eloquently
about the lora and fauna she discovered. Similar indings were made in
a BBC documentary about Chernobyl that aired in July 2006. An expert
recorded
“Yesterday we spoke to an expert on the wildlife of the

Chernobyl zone, who surprised us by saying that animals did
not seem to be too bothered by the present level of radiation.
He said he had searched for rodents in the sarcophagus and
had not found any – but he put this down to the absence of
food rather than the presence of the reactor's highly
radioactive remains. Birds nested inside the sarcophagus, he
said, and did not appear to suffer any adverse effects.”
Page 21
Another signi icant setback to the expansion of nuclear power

happened in 2011 with the Fukushima tragedy. Following the
earthquake and tsunami, 3 on-site employees perished, while dozens
more sustained injuries. Radiation exposure has not been linked to any
fatalities. By 23rd May 2011, 7800 workers had been deployed and
received an average dose of 7.7 mSv, 30 had doses more than 100 mSv
and some of the latter might exceed doses of 250 mSv once internal
dose is taken into account. The fraction of the ission products release
to the atmosphere for 137-Cs (Cesium) and 131-I (Iodine), is estimated
to be 1.2 to 6.6 % and 1.1 to 7.9 % respectively. Nearly all 133-Xe
(Xenon) gaseous ission product might have been discharged into the
atmosphere. Additionally, the contaminated water which leaked into
the sea, was carrying around 16 % of the 137-Cs inventory [40]. More
than 200,000 people had to evacuate the region around the site and
other possibly affected locations. Due to the lack of a clear plan for
allowing displaced residents to return to their homes, tens of
thousands of individuals are still residing in temporary housing
without knowing when they can return. There were nearly 600 non-
radiological deaths that were indirectly caused by fatigue or
aggravation of chronic illness due to the disaster and mandatory
evacuation. TEPCO estimates that the whole cost of clean-up, including
victim compensation and resettlement, might be as high as US$ 125
billion [40]. Other sources' estimates even as high as US$ 250 billion
over the next few years, including US$ 54 billion to buy up and
decontaminate all land within 20 km of the Fukushima plant, US$ 8
billion for compensation payments to local residents whose jobs or
home lives have been affected, and up to US$ 188 billion to scrap the
plant's reactors [40].
3.3. Inferences from the nuclear reactor accidents

The local agricultural community at Chernobyl was compelled to
leave and relocate in distant and unfamiliar accommodation. This was
to blame for the serious social harm brought on by inadequate public
awareness and overly cautious radiation regulations. This resulted in a
misperception of danger levels and generated great dejection and
suffering. Reports [43] show that this dislocation has implications.
Even in distant places like Greece, the tragedy caused an increase in
abortions of approximately 2,000 due to the psychological
repercussions of radiation [45].
22 Page
The accident of the Fukushima Daiichi nuclear power plant
Fukushima also sustained devastation on a similar scale. The

accident at the Fukushima Daiichi nuclear power plant is a prime
illustration of a policy-made catastrophe as opposed to radiation-
induced harm. Even though, the dose to the public was estimated to be
low, and health effects were not of concern [46]; nevertheless, the fear
of radiation caused the massive relocation of people in the surrounding
area [47]. The evacuation and prolonged separation of local
inhabitants from their houses as a result of the accident, has increased
mortality from numerous stress-related conditions [48]. Over 1600
people lost their lives as a result of the Fukushima crisis response, and
the elderly were particularly vulnerable to these effects [49].
Retrospective research revealed that the risk of the evacuation
outweighed any potential radioactive exposure risk especially for the
elderly. The evacuation did not protect human health but caused more
danger than radiation can ever do. As a result, the entire evacuation
effort turned out to be pointless and sounds unethical.
3.4. Unnecessary evacuations: mis-governance out of fear of

radiation
The Chernobyl disaster was the worst nuclear accident in the
nuclear history. However, the effects of radiation exposure have proven
minimal. The 116,000 evacuees did not die from radioactive exposure.
However, of the 134 ire ighters who were working to put out ires, 28
passed away in the irst four months from radiation sickness and other
Page 23
disorders [50]. They must be regarded as having been killed not by

radiation but by occupational orders. The other 106 people were
recovered, but 19 of them died during the next 20 years. Given that
there are around 1% of deaths per year from spontaneous causes,
these 19 may not be radiation victims: (106 × 20 × 0.01 = 21.2 > 19).
There have not been any credible indings indicating an increase in
leukaemia or solid tumours in highly contaminated regions of the
former Soviet Union. The biggest health issue is thyroid cancer. More
than 6000 cases were reported between 1991 and 2005, the majority
of which may be attributed to consuming milk that was contaminated
with Iodine (I-131), and 15 people died until 2005 [50]. Most thyroid
cancers are benign papillary thyroid carcinoma; 2000–3000 people
would have perished from them if they were malignant. The thyroid is
an organ that is radiation insensitive. Although its latent duration is not
known, it is around at least ten years.
In Fukushima, there are recent reports that the thyroid cancer

cases among children and teenagers under the age of 18 have increased
by about 30 times [51]. However, out of 367,687 cohort, only 110 cases
(0.00368 %) were found among the 298,577 examined. To understand
the implications of radiation better, the Fukushima Prefecture was
divided into three areas, i.e., the most contaminated area (subarea 1),
the moderately contaminated area (subareas 2-5), and the least
contaminated area (subareas 6-9). The cancer incidents were as low as
0.00195%, 0.00401%, and 0.00272% in these subareas respectively
[51]. In view of the above, it is dif icult to understand how a 30-fold
increase was arrived. This fear-mongering article was refuted more
recently [52]. In addition, it may be noted that, the average cancer sizes
were reduced before and after the Fukushima disaster (4.1cm vs
1.4cm). Large-scale and sophisticated screening could make it possible
to ind many thyroid malignancies in the children and teenagers of
Fukushima. The average age at surgery for thyroid cancer patients was
higher among those treated after the Fukushima disaster (age 17.4 vs.
11.9 years), suggesting that the disease had already begun to develop
before radiation exposure. In any event, there are no compelling
arguments in favour of believing that the nuclear accident is to blame
for the cancer cases. Newspapers reported on October 21, 2015, that a
welder who developed leukaemia after being exposed to 15.7 mSv
24 Page
while working at the

Fukushima Daiichi Nuclear
Power Plant (FDNPP) from
November 2011 to
December 2013, had inally
received government
compensation. Additionally,
some media outlets
expressed concern that low
dose radiation may cause
cancer. The public exposure
limit was set at 5 mSv/y
beginning in 1976, and any
person who had exceeded
that level and developed
cancer after one year or
l a te r we re e l i g i b l e fo r
workman's compensation.
However, Leukaemia is very
Evacuation during the Fukushima Nuclear unlikely to be caused by the
accident nuclear accident based on
exposure dose and time
since the accident [52].
3.5. Contamination levels in Fukushima

Cancer rates in Fukushima are not expected to rise, according to
of icial predictions from World Health Organisation (WHO) and United
Nations Scienti ic Committee on the Effects of Atomic Radiation
(UNSCEAR). Contrarily, the acute social and economic degradation of
the affected areas and the psychological issues that have resulted in
both the general population and emergency workers have had a
terrible toll [53]. In addition, long-term displacement and evacuation
led to grave healthcare issues, particularly for elderly residents [46]. In
Fukushima, there haven't been any radiation-related deaths. The
Chernobyl Exclusion Zone is now a spectacular ecological sanctuary
due to its large wildlife populations [54]. Although some anomalies in
butter lies caught near Fukushima have been noted [55], genetic
mutation cannot account for them [56].
Page 25
On March 21, 2011 [57], the International Commission on

Radiological Protection (ICRP) recommended for Fukushima that
reference values be set in the range of 20-100 mSv initially, and
afterwards in the range of 1-20 mSv/y once the radiation source is
under control. UNSCEAR estimated that the people in Okuma Town
would be exposed to the maximal radiation dose of 4.9 mSv during 1
year when evacuees return to their homes [58]. For the first four
months following the accident, the external dosages of 421,394
residents were examined. The results were 62.0 %, <1 mSv; 94.0 %, <2
mSv; and 99.4 %, <3 mSv. Other estimated doses in three areas of
Fukushima were 0.6-2.3 mSv/y in Tamura City, 1.1-5.5 mSv/y in
Kawauchi Village, and 3.8-17 mSv/y in Iitate Village [59]. These facts
suggest that Fukushima did not require evacuation. Out of all the
options available, the Democratic Party of Japan's administration at the
time, decided against following the ICRP's advice and used the
minimum dose of 1 mSv as the public dose limit for evacuation. This
decision induced tremendous human, social, and economic losses. The
mortality risk of residents in nursing homes evacuated after the
Fukushima accident was 2.7-fold higher than those who remained
there before the accident [60], which indicates that the stress of
evacuation caused loss more than that of radiation exposure. People
have been shown to lead active, healthy lives in places with far greater
natural background radiation than the radiation levels in Fukushima,
even in the absence of nuclear accidents [61].
3.6. Further studies on health effects of nuclear power plant

accidents
Despite the seriousness of the Three-Mile Island nuclear
accident, which resulted in the destruction of the plant, the average
radiation dose that exposed people (up to 20,00,000) received was
very low (approximately 1.7 mrem) [62]. It is now con irmed that, no
evidence of harmful health effects was found. Particularly, neither men
nor women experienced an increased risk of developing cancer
(Relative Risk = 1.00 and 0.99, respectively) [41]. Overall cancer
mortality was comparable to that of the local population in the long-
term follow-up of local inhabitants (n = 32,135) (Standard Mortality
Rate = 103.7 for men and 99.8 for women) [63].
26 Page
The Chernobyl disaster's long-term health effects have so far

been the subject of the most thorough research. Iodine-131 and
Cesium-137 radio-nuclides have greatly contaminated various areas of
Ukraine, Belarus, and South Russia as a result of this nuclear disaster.
During the spring and summer of 1986, 1,16,000 people were
relocated from the Chernobyl zone to uncontaminated areas; 2,20,000
more were relocated in the years that followed. The post-Chernobyl
radiogenic paediatric thyroid carcinoma is the unfavourable health
consequence of this event that is most frequently reported [64]. Iodine-
131 is a radio-nuclide with a relatively short half-life (8 days), it can
enter the body extremely fast through the air, vegetables, and milk that
have been contaminated. The thyroid gland is where most of the
Iodine-131 is located. The radiation doses are typically substantially
higher for children than for adults due to the smaller size of children's
thyroid glands and characteristics of their metabolism. High
contamination levels (no shielding, no food restrictions, and delayed
evacuation of contaminated populations) and high radio-iodine intake
of the thyroid gland (due to both iodine de iciency and lack of iodine
prophylaxis) resulted in high radiation doses to the thyroid gland in the
affected areas [65]. The thyroid gland received radiation doses that
were three to four orders of magnitude higher than those received by
other organs as a result of the Chernobyl accident [66]. The cumulative
doses were substantially larger, reaching several Gy or even several
tens of Gy.
Children, especially those between the ages of 0 and 5, saw a

sharp rise in the prevalence of new born thyroid carcinoma following
the accident [67]. Among the approximately 2 million heavily
contaminated patients who were children and adolescents at the time
of the disaster, more than 6000 thyroid cancer cases—15 of them with
fatal outcomes—had been identi ied by 2005. It has been assumed that
over the years exposure to Iodine-131 can cause a signi icant portion of
these thyroid tumours. Ecological studies revealed a link between
thyroidal Iodine-131 exposure and the risk of developing paediatric
thyroid cancer, and other case-control studies supported this inding
[68]. However, the dosage threshold for radiation-associated
paediatric thyroid cancer has not yet been established scienti ically
[69]. The above-described evidence may also be inconclusive due to
Page 27
thyroid cancer over diagnosis, as was earlier highlighted. The

complications of surgery can even be used to explain 15 fatal cases.
There was no rise in the incidence of other radiation-associated solid
tumours, leukaemia, or non-malignant illnesses in the exposed groups,
with the exception of the notable increase in thyroid cancer incidence
in children and young adults [70].
It should be noted that an increase in cancer incidence was seen

in the impacted areas even before the Chernobyl accident [64].
Furthermore, during the 1970s, a signi icant increase in the trend
incidence rate of thyroid cancer has been seen globally [71]. Therefore,
radiation exposure in and of itself cannot account for this tendency.
Another crucial issue is that, although radiation exposure itself was not
the cause of the accident's widespread psychological distress, fear of
radiation was the root cause. Such trauma may in luence the chance of
developing speci ic psychosomatic illnesses. According to a study [72],
the long-term effects of the Chernobyl accident, resulted in psycho-
emotional stress and societal instability, which had a much greater
negative impact on health than radioactive exposure. A "very traumatic
experience" was indeed had by the 3,50,000 persons who were forced
to leave their houses in the impacted areas as a result of the post-
accident evacuation. The "paralysing fatalism" that developed among
these people was the result of persistent misconceptions and
misunderstandings about the radiation threat. Another crucial fact in
this regard is that, in comparison to those exposed to background
radiation levels, the majority of emergency workers (liquidators) and
residents of polluted areas got relatively low doses of whole-body
radiation [73]. More speci ically, the mean effective dose for liquidators
(n = 2,40, 000) and evacuees from 1986 (n = 1,60,000) was 100 mSv
and 33 mSv, respectively [70], [74]. Most important, following the
Chernobyl accident, no overall carcinogenic consequences were seen
in people exposed to radiation doses under 100 mSv.
Nevertheless, despite such compelling counter arguments, a few

authors maintain that the Chernobyl accident has disastrous long term
radiogenic effects. For instance, Yablokov et al. [75] estimated through
a model analysis that from 1986 to 2004, Chernobyl accident was
responsible for 9,85,000 extra fatalities worldwide. This apparent
28 Page
ampli ication of potential negative impacts is undoubtedly caused by

the model's biased methodology. In further detail, the essay summarily
refutes the fundamental tenets of modern radiation epidemiology that
need evidence of radiation dose-effect connections. The selection of
articles is largely biased, and papers where radiation impacts were not
found are totally disregarded [76], [77]. Since direct dose
measurements were not used in the majority of the research cited by
Yablokov et. al. [75], an ecological approach was used instead. As a
result, it was unable to create a cohort or case-control design for
various research. Moreover, cancer incidence and death in the
impacted populations after 1986 were closely examined in an effort to
identify any changes that might be directly related to Chernobyl. As a
result, diagnostic and health screening services differed between
"clean" and "dirty" places, and variations in incidence and mortality
may not actually re lect disparities in health, but rather may be the
product of a systematic bias brought on by the screening effect [78],
[79]. In fact, it has been demonstrated that the intensity and types of
screening can signi icantly affect the apparent incidence of radiation-
associated thyroid cancers [78], [79]. For instance, in South Korea, the
apparent incidence of radiation associated thyroid cancer increased by
15 times in the subsequent years following the installation of screening
measures in the year 2000 [78], [79].
It is also clear that attempts to characterise patterns in health

indices across time have challenges. In the post-Soviet countries, the
economic slump that followed the dissolution of the Soviet Union in
1991 led to the collapse of the healthcare system and a dramatic rise in
mortality rates [80]. Notably, the Far East of Russia, which evidently
was not touched by the Chernobyl accident, saw a greater increase in
mortality [81]. Furthermore, it is impossible to discriminate between
the effects of low and high radiation doses in the majority of the studies
examined by Yablokov et al. [75]. The effects of radiation were
negligible at low doses in the studies that involved external radiation
doses. A study by Ivanov and colleagues [82]-[84] that looked at the
incidence of solid cancer in irst responders, who worked in the 30-km
radius around the Chernobyl nuclear power plant between 1986 and
1987 is one example. These employees were subjected to cumulative
Page 29
doses ranging from 1 to 300 mGy [82]. The results of this study showed
a hormetic dose-response relationship, with cancer risk rates in the
low-dose groups (mean dose of 79 mGy) being lower than those in the
general population (Standardized Incidence Ratio [SIR] = 0.87) as
opposed to higher risks (SIR = 1.27) in the high-dose groups (mean
dose of 194 mGy).
The International Nuclear Event Scale of the International

Atomic Energy Agency rated both the Chernobyl and Fukushima
Daiichi incidents as level 7, which is the worst level, but the actual
circumstances and levels of damage varied greatly [85]. Large amounts
of radioisotopes, including Iodine-131, were discharged in Fukushima
and the adjacent prefectures, similar to the Chernobyl accident.
However, radiation doses to the thyroid gland were signi icantly lower
in Fukushima, mostly because the Japanese government promptly
ordered food restrictions. With a maximum dose of 33 mSv to the
thyroid glands, the average individual exposure to the thyroid gland
was just 1 mSv. Therefore, it is not unexpected that during the course of
the ive years following the accident, no rise in the prevalence of clinical
thyroid malignancies was noted [86]. Later, an alarming 30-fold
increase in thyroid cancer incidence was discovered following
widespread screening of exposed children and teenagers (more than
3,00,000 people aged 18 and younger) using cutting-edge
ultrasensitive sonographic technology. In addition, sample screening
of cohorts of infants who had not been exposed (using the same tools
and protocol) also produced an increase of 10- to 60-fold [87]. As was
already mentioned, overdiagnosis is undoubtedly to blame for this rise
in incidence.
Chronic psychological stress and stress-related lifestyle

disorders, like obesity, hypertension, type 2 diabetes, and
dyslipidaemia in displaced people are likely to be the main public
health issues following the Fukushima accident. These conditions may
all increase a person's risk of cardiovascular disease in the future [88],
and should not be misinterpreted as the root cause of radiation
exposure.
30 Page
3.7. Summary of radiation effects from three civilian nuclear

reactor accidents
The three major accidents in the history of civilian nuclear
power reveal that the dose due to radiation leak is relatively small (a
few mSv) and additional risks due to radiation leakage on human life
are almost non-existent. The primary risk is the inancial loss of the
company owning the plants. The Government is to blame due to
"evacuation of public out of the fear of radiation," and the most
important the “psychological risks in the public mind against
radiation.” Whether it is a nuclear accident, chemical risks, war, or a
natural disaster like a lood, tsunami, storm, etc., "public evacuation" is
a poor taste for the people to accept. Nobody loves to leave their home
or possessions, and in the event of a nuclear accident, there is
additional radiation fear apart from the need to evacuate.
Page 31
32 Page
Case studies on effects of
Low-Dose Radiation (LDR)
4
The previous studies have shown that low dose radiation (a few
mSv) is found to bene it the health and life span of Japanese atomic
bomb survivors of Hiroshima and Nagasaki. In addition, it was also
found that the dose received by the residents living around the three
damaged nuclear power plants (TMI, Chernobyl and Fukushima) is
only a few mSv, which is found to have insigni icant effects on the health
and life span of the exposed residents. In view of this, we have
concentrated in this chapter to understand more through case studies
for the effect of low dose radiation on human health, especially on their
life span and cancer incidence.
The building made with recycled steel polluted by waste cobalt-60

source in Taipei City, Taiwan
The development of life on earth has been marked by natural

background radiation since its commencement roughly 4.5 billion
years ago [89]. Exposure of human beings to ionising radiation (IR)
from natural sources is inevitable and perhaps even necessary [90].
According to current estimates, humans receive an effective dosage of
2.4 mSv annually on average, with a range of 1–10 mSv depending on
Page 33
geographical location[91]. All other exposures are added to this as the

baseline and are then compared.
There are numerous case studies in literature that discuss

ionising radiation's advantageous health impacts [92]. For instance,
recycled steel polluted by waste cobalt-60 source was utilised to build
180 structures, including around 1700 lats, as public and private
schools and small businesses, in Taipei City and surrounding counties
in Taiwan. Over a period of 9 -20 years, about 10,000 people occupied
these buildings and received an average radiation dose of 400 mSv.
Legal action against the Taiwanese government has resulted from this
incident [93]. As opposed to the general Taiwanese population,
inhabitants in the contaminated region had a 3% decrease in cancer
fatalities. Additionally, the prevalence of congenital abnormalities was
reduced to about 7% of the general population's prevalence [92]. This
data implies that even if aggregated to a high yearly dose, chronic
whole-body low-dose-rate radiation exposure may be bene icial to
human health. However, it is common to see "cherry-picking of facts" in
numerous articles that are based on the same case study [94].
The coastal region of Karunagappally, Kerala, India
Another illustration comes from research on the coastal region

of Karunagappally, Kerala, India, which is notorious for having high
background radiation (HBR) due to monazite sand that contains
34 Page
CASE STUDIES ON EFFECTS OF LOW-DOSE RADIATION (LDR)
thorium. The median outdoor radiation level is over 4 mGy/y, and the
outer radiation levels can reach as high as 70 mGy/y in some coastal
areas. The per capita average dosage for people residing in High-Level
Natural Radiation Areas (HLNRA) is 4 mGy/y, with annual absorbed
doses ranging signi icantly from ≤ 1 to ≥ 45 mGy [95]. The irregular
distribution of monazite in the beach sand is the cause of the wide
range of radiation dose. A comprehensive analysis of cancer risk was
conducted in the Karunagapally taluk (consisting of 12 panchayats),
located in the heart of the high-background-radiation belt in Kerala,
India [44]. (A panchayat is a local entity within a taluk; a taluk is an
administrative unit based on area and population.) A cohort of all
3,85,000 people living in the Karunagapally taluk was surveyed, with
an equal number of men and women. A baseline survey for socio-
demographic and lifestyle variables, food practices, cigarette and
alcohol use within the group was carried out between 1990 and 1997
[44]. A cancer registry was created concurrently, and the cohort's
cancer incidence was determined [96]. Radiation-risk analysis was
performed on a sub-cohort of 1,73,000 people, consisting of four
panchayats with high radiation doses (Alappad, Chavara, Neendakara,
and Panama) and two control panchayats (Oachira, Thevalakkam)
with low radiation doses. Statistical analysis was performed for 69,958
individuals, who were followed for 10.5 year on average. Indoor and
outdoor air kerma rates were measured and individual radiation doses
was estimated by incorporating sex- and age-speci ic occupancy
factors. By the end of 2005, a total of 736,586 person-years of
observation were accumulated and a relatively large average
cumulative dose of 161 mGy was estimated [44].
1,349 cases of cancer in total were found, with oropharyngeal,

lung, and breast cancers being the most prevalent types. Leukaemia
cases totalled 30, with ten of the cases being CLL (chronic lymphocytic
leukaemia). Data were analysed using Poisson regression, strati ied by
sex, achieved age, and additional covariates like follow-up interval,
socio-demographic characteristics, and smoking. For leukaemia and
solid tumours, cumulative dosages were lagged by 10 and 2 years
respectively. The indings indicated that the HLNRA cohort's cancer
incidence is comparable to those of other parts of India. There was no
extra cancer risk associated with exposure to terrestrial gamma
Page 35
radiation. In contrast to leukaemia, all malignancies had an Excess

Relative Risk (ERR) of 0.13 per Gy (95% Con idence Interval [CI]),
which was not substantially correlated with background radiation.
Leukaemia and other cancer sites were not substantially correlated
with cumulative radiation dosage in site-speci ic analyses [44], [95]
[97], [98]. Nishad et al. [98] discovered that several proteins involved
in various biological processes, such as DNA repair, RNA processing,
chromatin modi ications, and cyto-skeletal organisation, showed
distinct expression in HLNRA individuals, suggesting both recovery
and adaptation to low-dose radiation [99], [100].
Forgotten radiation source was taken from an abandoned hospital

location, which led to the Goiânia accident in Brazil
On September 13, 1987, a forgotten radiation source was taken

from an abandoned hospital location, which led to the Goiania accident
in Brazil. It was referred to as "one of the world's worst radiological
incidents" by the International Atomic Energy Agency (IAEA) [101]. It
was subsequently handled by many people, resulting in four deaths.
249 out of approximately 1,12,000 people, were found to be
contaminated. Only four people who were exposed, died from acute
radiation sickness rather than cancer [101].
36 Page
Some of the highest natural radiation levels on earth can be

found in Ramsar, a city in north Iran that is situated on the Caspian Sea
coast [102]. In this region, high amounts of Radium 226 and its decay
products are present, and they are brought to the surface of the earth
by sulphurous hot springs as the water lows through young,
uraniferous igneous rocks [103]. The anoxic nature of the groundwater
prevents uranium from dissolving. Travertine, a calcium carbonate
mineral, also contributes to the high radiation levels as the
groundwater rises to the surface. Hot springs can have Radium 226
concentrations as high as 146 kBq m-3, which results in yearly internal
doses of 2.5 mSv to 72 mSvfrom Radium 226 [104]. In control zones,
the average effective doses vary between 0.6 and 1.5 mSv with a mean
value of 0.7 mSv, whereas the average effective doses to the general
population range from 0.6 to 131 mSv with a mean value of 6 mSv
[105]. In this region, Ramsar City has a population of ~60,000,
although only about 1000 people live in High Level Natural Radiation
Area (HLNRA). The majority have lived in the area for many
generations. Studies conducted in Ramsar, Iran have provided some of
the earliest evidences of in vivo radio-adaptive responses [106], [107].
In an early investigation, 3000 people of the Ramsar zones with the
highest radiation levels were examined for cancer-related morbidity
between 1998 and 2001 [108]. In comparison to the national rates,
neither the Standard Mortality Rates nor the Standard Incidence Rates
demonstrated a statistically signi icant difference. However, because it
was an ecological study, similar to the ones done in Brazil, it was unable
to determine the risk of cancer due to radiation exposure.
Initial cancer mortality statistics were generated in

retrospective surveys between 1970 and 1978 in the Yangjiang High
Level Natural Radiation Area (HLNRA) of China. Cancer mortality
between 1979 and 1995 was examined by Sun et al. (2000) [109], who
found an Excessive Relative Risk (ERR) of 0.11 per Sv (95% Con idence
Interval) [109]. In 1979, the HLNRA created a cancer registry. A cohort
of 31,604 people (16,045 men and 15,559 females), aged 30-74, were
monitored for cancer and non-cancer disorders between 1979 and
1998. Tao et al. (2012) [110] compiled and published data for 7,36,842
person-years at risk. 4525 fatalities from non-cancer diseases and 956
deaths from cancer in total (including 15 instances of leukaemia) were
Page 37
recorded. Here, too, indoor and outdoor air kerma rates were assessed,
sex- and age-speci ic occupancy factors were included to estimate
individual radiation doses, and individuals aged 30 y and above were
excluded from statistical analysis, similar to the study carried out for
cohort from the HLNRA of Kerala [97]. The cumulative external
radiation dose, lagged by 2 years for leukaemia and 10 years for all
cancers excluding leukaemia, was 84.8 mGy for High Level Natural
Radiation Area (HLNRA) and 21.6 mGy for Normal Level Natural
Radiation Area (NLNRA) (control) areas. The ERR for all malignancies,
except leukaemia, was estimated by Poisson regression analysis and
found to be 1.01 per Gy (95% Con idence Interval), which is
statistically insigni icantly negative. A site-speci ic study revealed an
inverse relationship between cumulative exposure and death from
liver cancer. It is well known that liver cancer has a signi icant viral
aetiology, and Guangdong province is said to have one of China's
highest hepatitis B virus prevalence rates. Accurate diagnosis is also
challenging due to the dif iculty in differentiating between liver
cirrhosis and liver cancer. Excessive Relative Risk [ERR] was
determined to be 0.25 per Gy (95% Con idence Interval), with no
statistically signi icant correlation to radiation exposure. The ERR for
all cancers excluding leukaemia and liver cancer was calculated to be
0.19 per Gy (95% Con idence Interval). As a result, the investigation on
total mortality did not uncover any elevated cancer risk associated
with gamma radiation exposure [110]. These indings corroborated an
earlier prospective mortality study by Zou et al. (2005) [111] that
studied 125,079 participants from 1979 to 1998 [Relative risk (RR) =
1.00; 95% Con idence Interval ].
In addition, the study by Tao et al. (2012) [110] determined that

4525 deaths from non-cancer diseases and 524 deaths from external
causes occurred in HLNRA, China [110]. The cumulative radiation
exposure has no discernible relationship with the mortality from non-
cancer disorders. With increased cumulative exposure, the death rates
from infectious diseases (ERR per Gy is 2.88, 95% CI) and tuberculosis
(ERR per Gy is 4.05, 95% CI) dramatically decreased. However, liver
disorders accounted for the majority of the mortality from digestive
diseases, which had an ERR per Gy of 5.02 (95% CI) [110]. An earlier
study by Zou et al. [111] over the years 1979-1998 found a statistically
signi icant RR of 1.06 when comparing non-cancer mortality in the
38 Page
HLNRA with that in the Control Area (CA) (95% CI). However, as the
excess only affected people under the age of 50, cumulative radiation
was not the cause [111].
In the early 1900s, radioactive luminous paint was used to make

the igures on the faces visible in the dark. Because it was common
practice to lick the paintbrush tip to achieve ine detail, the employees
hired to paint these dials got contaminated. Because of this, the alpha-
emitting radium accumulated in their bones, the activity continuously
administers a whole-life dose. It is anticipated to increase the chance of
developing bone cancer. Only 46 occurrences of bone cancer were
found among the 191 workers with whole-of-life exposures more than
10 Gy, according to data on the dial painters provided by Rowland et al.
[112]. There were no cases of bone cancer among the 1,339 workers
who had cumulative doses under 10 Gy. These therefore support the
advantageous effects for low radiation dosages.
Dr. Don Wiles, Emeritus Professor of Chemistry at Carlton

University in Canada, once spent 16 months beginning in 1947
extracting radium from uranium ore. Radium in a glass tube was
utilised as a cancer treatment alternative to cobalt by embedding it in
the cancerous tissues. Marie Curie utilised a crystallisation method
that, in comparison to today's standards, appears to be rather loose
and crude: encapsulation was carried out with bare hands. Rubber
gloves were not worn by the workers because they were slippery. At the
daily check, radiation badges became black even behind the lead
shield. Due to the chemical similarities between radium and calcium,
radium appears to have accumulated in Dr. Wiles' bones. He was born
in 1925, and at the age of 88, he exhaled
radon, a by-product of radium, roughly
25 times more than what was permitted.
He might have been gravely infected, one
might think. He stated “About 65 years
later, I am still healthy”[113].
Ian Soutar, when he was younger, used

a friend's Geiger counter to play in the
Ian Soutar wearing Uranium Ranwick Uranium Mine near Sault Ste.
glass beads
Page 39
Marie, Canada, and collected radioactive samples. Until 1960, he slept

with radioactive rocks under his pillow and on the nightstand. He
contacted every youngster he had known growing up who had played
at the Ranwick Uranium Mine in 2011. Everyone had been warned to
anticipate issues as a result of their radiation exposure later in life.
Rather, Ian discovered that they were all in good health and none had
cancer. Soutar used pendants and mudpacks from Night Hawk
Minerals that emit radiation between 3 and 85 Gy/h, as well as pure
thorite crystals from Thailand, Czech glass beads, and other materials.
The irst Czech beads, which contain 2% natural uranium, were created
around 1840 [114]. Due to self-irradiation, an allergy that had
developed to his cat, fully vanished and never reappeared. Pain from
plantar warts and arthritis could be effectively relieved by the
mudpack [115].
Leslie Corrice, a
member of Scientists for
Accurate Radiation
Information (S.A.R.I.),
h a d wo r n a u ra n i u m
stone necklace from Night
Hawk Minera ls for 5
years; Corrice claims that,
since then, he never had
any colds or upper
respiratory tract
Uranium stone necklace from night hawk infections. He said: “I
minerals irmly accept that if
everyone wears one of
these, we will have a signi icantly healthier society”.
Low doses of low-Linear Energy Transfer (LET) radiation can
also boost biological defences against DNA damage and cancer
immunity, as mentioned by Sakai and colleagues in Japan and by Liu
and colleagues in China [116], [117]. Also, this can eradicate pre-
existing cancer cells [118]. This suggests that low-dose radiation may
be used in cancer therapy (either alone or in combination with other
drugs, such as those that block cancer cell survival signaling pathways)
[119].
40 Page
Thus, contrary to popular belief, not all radiation exposure is

dangerous. The evidence is unequivocal that relatively low ionising
doses extend life and have other positive health effects. Lorenz started
keeping track of life expectancy during the early stages of the
Manhattan Project in World War II. He noticed that mice exposed to 1.1
mGy/day lived longer than those who weren't. In rodents, this
observation has frequently been made. In 1980, Luckey coined the
term "radiation hormesis" to describe this bene icial impact. Botanists
and entomologists who use ionising radiation in their research are well
aware of and accepting the positive bene its of the radiation. In an
animal model of accelerated ageing brought on by a mutation in the
klotho gene, low-dose-rate gamma rays dramatically delayed the rate
of ageing [120].
Meadow voles bene ited from ongoing low-dose gamma

radiation exposure at levels 50–200 times higher than background
values [121]. Exposure to Low Dose Radiation (LDR) has been found to
lengthen the lives of bacteria, plants, seeds, fungi, insects (including the
lour beetle, house ly, codling moth, cricket, and mosquito),
invertebrates, vertebrates,
mammals, and humans [122]. A tiny
dosage of ionising radiation seems
to be bene icial for all living things.
Buettner [123] listed nine

factors that he believed signi icantly
in luenced lifespan, including diet,
moderate exercise, alcohol and food
intake, outlook, lifestyle, love and
faith. Buettner travelled the world
for National Geographic to ind
"blue zones," where residents lived
noticeably longer than expected,
based on their genes than those
l i v i n g n e a r b y. A c c o r d i n g t o
Buettner, most people can live an
Residents of Blue Zone having additional 12 years by using these
noticeably longer life span elements, but not through
Page 41
medication or surgery [123]. In the island of Ikaria, which is 30 miles

off the coast of Turkey, he discovered one of the world's longest living
community. Compared to any other region in Europe or even the USA,
where the average life expectancy is currently around 81 years for
females and 76 years for males [124] , the island has ten times as many
siblings over the age of 90. The islanders bath and live in a radon and
radium-rich environment.
Health bene its from low-dose radiation exposure have

been documented in about 4000 publications, there is
clear evidence for effects of “radiation de iciency” similar
to “nutrition de iciency” on health and the optimum dose
is about 60 mGy/year [125].
Luckey even suggested building meeting rooms with a

dosage rate of 1 mGy/day near nuclear power plants and
using monazite for radon rooms intended for therapy and
prevention [125]. The most effective dosage rate
recommended for the prevention of in lammatory-
related disorders was continuous 25 μGy/h, or almost
100 times the average background radiation level seen in
the entire world [126].
4.1. Biological effects of Low-Dose Radiation (LDR)

Research on LDR's biological impacts irst started in 1970s. In
his monograph "Hormesis with Ionizing Radiation," Luckey was the
irst to come to the conclusion that LDR bene itted animal growth and
development, health, and lifespan. He called these effects "radiation
hormesis." [127], [128].
When pre-exposed to LDR, cultured human cells can develop a

resistance to the chromosomal abnormalities caused by subsequent
High Dose Radiation (HDR), according to research by Olivieri et al. in
1984 [129]. They called these effects as an adaptive response (AR)
[129]. The "bystander effect" of LDR was more recently characterised
as the exposure of a cell population to LDR resulting in signi icant
cytotoxic and geno-toxic consequences in the population's non-
42 Page
irradiated cells [130]. The biological impacts of LDR, including

hormesis, AR, and the bystander effect, have drawn a lot of attention
from researchers over the past few decades.
4.1.1. Effects of LDR on In lammation diseases

Sokoloff published his irst study on pain alleviation in arthritic
patients in 1898, using X-rays that were commonly used in clinical
settings [131]. Super icial cancers were successfully treated with
external beam X-rays in 1899 [132]. Pusey wrote on cell stimulation
and the effective management of a few chronic in lammatory diseases
in 1911 [133]. As a reimagining of standard medical practice from 1920
to 1945, the use of LDR for active therapy of in lammatory and
proliferative illnesses is currently experiencing a rebirth. Radium γ-
rays and X-rays at doses between 0.5 and 2.0 Gy were successfully used
to treat a wide spectrum of infectious and in lammatory disorders
throughout the 1930s [126]. Simple math will demonstrate that
adopting LDR therapy to prevent and treat in lammatory diseases
at a small fraction of present prices results in little to no morbidity
and an yearly saving of millions of lives worldwide [126].
Chronic in lammation is a key factor in both infectious diseases

and non-infectious conditions such as cancer, Alzheimer's disease,
peripheral vascular disease, heart disease, and type 2 diabetes, which
impact more than a billion people worldwide today. The processes
causing chronic in lammation for each of these disorders may be
extremely diverse, despite the fact that in lammation is frequently a
common starting component in the aetiology of these illnesses.
Chronic in lammation markedly represses p53 functions, one of which
is acting as a suppressor of in lammation, helping to keep it within safe
limits [134] .
Numerous therapeutic approaches may weaken or impair the

immune system, undermining the LDR-stimulated natural healing
mechanisms. In conventional radiotherapy for cancer, both the disease
and the nearby normal, healthy cells receive a very high radiation dose.
LDR applied only to healthy cells will initiate the adaptive response
which will protect (precondition) normal cells from the large
therapeutic dose. Most in lammatory disorders can be effectively
Page 43
treated with LDR without any negative side effects and at a low cost.
LDR expedites the healing of wounds, the prevention of

infections, the treatment of cancer, and the management of other
excruciating in lammatory diseases [135], [136]. The LDR method uses
a broad-based immune system strengthening and a variety of anti-
in lammatory treatments to target in lammation linked to key disease
categories. Chronic and complex disorders with a major in lammatory
component may be prevented, controlled from progressing, and
treated with a tiny dosage of low-Linear Energy Transfer (LET)
ionising radiation delivered continuously or over a long period of time.
Asthma, ibromyalgia, multiple sclerosis, psoriasis, scleroderma,
ulcerative colitis, and carpal tunnel syndrome are among the painful
degenerative conditions for which LDR has been demonstrated to be a
bene icial treatment [137]. Ionising radiation proved a successful
treatment for asthma in 1926 [138]. Application of low-dose ionising
radiation, especially in the case of patients with persistent diseases;
may cause reduction in pain, stopping or slowing the progression of the
disease, and recovery from the diseases [139]. Asthma, diabetes,
hypertension, hepatitis, Parkinson's disease, Alzheimer's disease,
neuralgia, spondylitis, bursitis, amyotrophia, tenosynovitis,
osteoporosis, and allergic and atopic eczema are among the illnesses
listed by Hattori as being treated by LDR [140]. Post-operative large
unsightly keloids, pterygium (a web that grows across the pupil of the
eye obstructing vision), plantar wart, hidradenitis scalp dissecting
cellulitis, and acne conglobata were found to be successfully treated
with radiation therapy, according to Scientists For Accurate Radiation
Information (S.A.R.I.) members, who received radiation or as
physicians who treated patients [131]. These local exposures were not
known to cause cancer.
Ioni s ing radiation and the immune system interact in a

complicated, multi factorial manner that is dependent on the radiation
dose, quality, and immune cell types under investigation. In general,
higher doses of X-ray irradiation (such as single doses of ≥2 Gy) have
pro-in lammatory effects and cause in lammatory processes as a
common radiation therapy toxicity [141]. Contrarily, Low-Dose
Radiation Treatment (LD-RT) (single doses <1 Gy) modulates a
44 Page
number of in lammatory processes and clearly demonstrates anti-

in lammatory characteristics [142]. The underlying molecular
mechanisms of LD-RT, despite being clinically used for decades to treat
non-cancerous in lammatory and degenerative diseases [143], [144],
are still far from being fully understood, in part due to their prominent
discontinuous dose dependency and putative non-DNA targeted
properties.
As an alternative to opioid narcotic addiction and its side effects

(constipation, disorientation, drowsiness, and nausea); the pain
relievers frequently need to be taken every few hours. And hence,
radiation treatment for pain management becomes more acceptable
and signi icant. High radiation doses have been used to treat bone pain
from cancer (8 Gy) and nerve pain from tic douloureux or trigeminal
neuralgia (75 Gy) (these are among many diseases being treated as
given in Table 5). In the 1930s, treatment schedules and doses in
clinical treatment of the diseases (Table 5) were empirically
established, with single doses of 0.3-1.0 Gy in 4-5 fractions for acute
and 1-3 fractions for chronic diseases per week to total doses of 3-5 Gy
and 12 Gy, respectively [145]. Due to bone marrow disorders at high
doses, Low-Dose Radiation Treatment (LD-RT) is unpopular in some
nations [146], [147]. The development of powerful non-steroidal and
steroidal medications also supported the shift away from LD-RT. These
treatments (non-steroidal and steroidal medications) also have a lot of
negative effects, and many patients do not respond to them.
Table 5 Treatment of mostly painful in lammatory and ibrotic

conditions by moderate-dose radiation therapy in Germany
In lammatory disease Number of patients References

Plantar fasciitis 7947 [148]
Gonarthrosis 5046 [149], [150]
Heel spur syndrome 130 [151]
Periarthritis of the shoulder 141 [152]
Dupuytren's contracture 135 [153]
Plantar ibromatosis 24 [154]
Calcifying tendonitis of
the shoulder joint 102 [154]
Page 45
Typical dose schedules gave 0.5–1.0 Gy in 1–5 fractions

for a total dose of 3–5 Gy over a week or more. Most
common responses to patients were pain relief and
improved mobility as reported by Rodel [136].
4.1.2. Effects of LDR on Arthritis and Retinitis Pigmentosa

It has been demonstrated that low-dose radiation is quite
successful at treating and managing arthritis [157]. For painful
degenerative illnesses, radiotherapy with fractions of 0.3–1.0 Gy and a
total dose of 3–12 Gy had anti-in lammatory and analgesic effects
[157]. As an effective and less harmful alternative to steroids and low-
dose chemotherapeutic medications, relatively low-dose radiation for
joint in lammation has been used to treat arthritis and a range of other
chronic painful disorders [137], [143], [145], [158][166].
Von Pannewitz conducted a number of researches on animals to

determine how low dose ionising radiation affected osteoarthritis in
the early 1930s. He noted a reduction in the pain, swelling, and clinical
signs of arthritis in animal models treated with X-rays or gamma rays.
Pannewitz failed to ind any impact on structural integrity or
degenerative alterations [158]. Inactivated Mycobacterium TB or
papain was injected intra-articularly into rabbit knees to cause acute
arthritis. Five weekly portions of 1.5 or 1.0 Gy in these rabbits
decreased the swelling of the joints and in lammatory proliferation of
the synovial cover cells [167]-[169].
Low-dose-rate γ-irradiation is found to suppress collagen-

induced arthritis by reducing pro-in lammatory cytokines, auto
antibody production and up-regulating T cells [170], [171]. Frey
investigated the effects of (Low-Dose Radiation Therapy) LD-RT on
rheumatoid arthritis using a transgenic mice model. In this paradigm,
transgenic mice produce the human cytokine TNF- α, and by the time
they are 4-6 weeks old, exhibit chronic polyarthritis, which is
characterised by bone erosion, cartilage degradation, and synovial
in lammation. When mice were irradiated at the onset of the disease
with 0.5 Gy in ive fractions over the course of a week, it was found a
considerable temporal improvement of the clinical progression of the
disease in terms of grip strength and joint swelling [172] .
46 Page
In 2004 a patterns-of-care study performed in Germany was

published with 37,410 patients treated for degenerative or hyper-
proliferative disorders like impingement of the shoulder joint (rotator
cuff syndrome), tennis/golfer's elbow, plantar fasciitis (painful heel
spur), osteoarthritis, and Dupuytren's disease. Concerning the most
important clinical end point of pain relief, complete response and
longtime analgesic effects, LDR resulted in a 33–100%, a 47–100%,
and a 12–89% ef icacy, respectively [159], [160], [173]-[175]. A rise in
the acceptance of this treatment was seen in a patterns-of-care
research conducted in 2010 with 4500 patients who had osteoarthritis
of the knee (95 % of whom were referred for radiation) [176].
Blindness may result from the genetic degenerative eye

condition retinal pigmentosa, which affects the retinal pigment
epithelium. Right now, there is no treatment. In animal studies of
retinitis pigmentosa, a dose of 650 mGy was discovered to be useful
[177].
4.1.3. Effect of LDR on Infections

The value of X-rays in treating infections linked to gas gangrene,
pneumonia, bronchitis, tuberculosis, staphylococcus infections,
diphtheria, ulcerative dermatitis, otitis media, and mastoiditis was
recognised by doctors more than 115 years ago [178]. More recently,
the potential of the X-rays for treating HIV/AIDS and other viral
diseases were also reported. Roentgen radiation was used in 1896 by
Professor William Shrader of Missouri State University to study how
diphtheria bacilli responded in guinea pigs. One of the injected animals
was exposed to the rays for four hours in a wooden box and was still
alive and free of disease eight weeks later. Within 28 hours of the
injection, another animal which had not been exposed to the rays
perished and its death was caused by diphtheria germs, according to
the post-mortem examination [131], [179]. Under the epidermis of
both rabbit ears, Freund administered injections of cholera, TB,
diphtheria, or typhus bacteria in 5 cc saline. When "uranium" rays were
exposed to one ear, no in lammation developed there [180]. The
attenuation of guinea pig tuberculosis infections by roentgen rays was
demonstrated by Lortet of Lyon, France, in which the animals' injected
areas underwent daily X-ray exposure. The animals that had not been
Page 47
exposed showed ulcerous lesions and weight loss, while the opposite
was found with the exposed animals who gained weight and showed no
signs of ulceration [181]. In addition, the lifespan of tuberculosis-
inoculated irradiated guinea pigs was longer than that of controls
[182].
A number of infections were effectively treated using X-rays

prior to World War II [183], [184]. When compared to unexposed
controls in the same location, the death rate from parasitic and
infectious diseases was 66% lower in exposed workers using X-rays at
the Savannah River Plant [185], while workers at shipyards had 14%
decrement[186], [187].
In the US, otitis media affects more than 2.2 million people each
year. Tympanic membrane perforation characterises otitis media, a
chronic inner ear infection. Antibiotics and inner ear draining are the
usual treatments. Otitis media with eardrum perforation can result in
mastoiditis, an infection of the mastoid bone. Antibiotics and/or
mastoidectomy are used as treatments. If untreated, intracranial
problems may develop. This is a signi icant issue in emerging nations.
Massively swollen lymph nodes in the neck that are associated

with tonsillitis, dental infections, otitis media, mastoiditis, the mumps,
in luenza, and other paediatric illnesses are the characteristics of
cervical adenitis. X-rays were used to treat the irst cervical adenitis
case in 1902. Without requiring surgery, 75–90% of patients
experienced clinical success by using X-rays, which showed rapid and
noticeable relief in the patients [188], [189]. 10–20 % of the skin
erythema dose (SED) was historically thought to be the dose for
treating in lammatory disorders. Mastoiditis was resolved after
receiving X-ray treatment without causing any bone loss. Within 24
hours of the treatment, symptoms such as temperature rise,
discomfort, pus discharge, and insomnia disappeared. LDR stopped
the development of osteomyelitis into mastoiditis with 20–25 R of
dose. Up until the mid-1940s, therapy was still supported by medicine.
The most common way to administer the cumulative dosages of X-rays
was as a single exposure, which ranged from 75 to 200 R. In cases of
otitis media, treatment was successful in 85% of cases. Mastoiditis
48 Page
patients typically needed numerous (fractionated) X-ray exposures

[190].
Impaired hearing loss caused by throat in lammation and

nasopharyngeal lymphoid tissue development was treated with X-rays.
Within 1-2 days, X-rays signi icantly reduced the lymphoid mass. In
order to qualify them for service, some 25,000 submariners and airline
pilots received nasopharyngeal γ-rays from radium to treat their
hearing loss. Similar radiation therapy was also given to thousands of
children [191]. Decades later, epidemiological studies were unable to
detect a discernible rise in head and neck cancers.
As a result of tissue necrosis, Clostridium perfringens exotoxin-

producing gas results in gas gangrene. Most frequently, the infection
spreads throughout the body from the limbs. Currently, antibiotics and
hyperbaric oxygen are used for treatment (helpful since the pathogen
is anaerobic). The infection was successfully treated with X-ray doses
of 100–200 R [192]-[194] prior to World War II.
During the early part of the 20th century, bacterial (lobar and
bronchopneumonia) pneumonia was successfully treated with X-ray
therapy. Out of 15 investigations, 717 out of 863 pneumonia patients
who received approximately 50 R X-rays, survived (83 %) [195]. The X-
ray treatment for pneumonia works by inducing an anti-in lammatory
phenotype, which causes a quick reversal of clinical symptoms and
speeds up the healing process. The capacity of low doses of X-rays to
suppress in lammatory responses is a signi icant new concept with
widespread biomedical and therapeutic applications.
Low-dose X-rays were used from 1923 to 1948 to heal sinus

infections with an 80% cure rate by reducing swelling and promoting
tissue repair; the effective dose ranged from 30 to 70 R [196]. In 1916,
Osmond discovered that radiograms used to identify frontal sinusitis
removed pain in the forehead. He demonstrated in 1923 that sinusitis
symptoms vanished after 1-3 weeks of receiving two to three X-ray
treatments [197]. Around 40,000 to 50,000 patients were effectively
treated with X-rays for sinus infections by German doctors in the 1990s
[198]. LDR (with recommend dose of 10 cGy per day) was successfully
Page 49
utilised to treat periodontal disease, which is mostly brought on by

anaerobic bacteria that cause in lammation and ulceration of gingiva
tissues [199].
Serious Furuncles and carbuncles are frequently brought on by

Staphylococcus infections that affect the skin. A furuncle is an infection
or boil that begins in the hair follicle. A carbuncle is a skin lesion that
has developed an abscess and is dripping pus. If left untreated, they can
cause sepsis, which has a 10 to 20 percent fatality risk (pre-antibiotic
age). From 1920 to 1940, X-rays administered at 10–20% of the
erythema skin dosage (0.1–0.2 SED) were frequently used as a kind of
treatment, which was 75-200 R in value. Within 30 minutes, cells
within the lesions were destroyed by X-rays. A quick reduction in pain
due to the in lammatory components was made by the exposure [200].
In the struggle between antibiotic effectiveness and disease

management, there has been a surge in drug-resistant microorganisms
with altered genetic makeup. Based on historical experience before
1945, LDR was a viable treatment for TB, MRSA (Methicillin-Resistant
Staphylococcus Aureus), and other "resistant" infections.
In addition, it has been proven in numerous animal studies that

LDR has the ability to suppress viral infections. After 50 days of
infection, prion-infected mice were exposed to 4x500 mGy of Cobalt-60
γ-rays, given every other day at a dosage rate of 0.5 mGy/min [201].
This considerably increased the lifespan without any symptons. Mice
exposed to 1.5 mGy between 5 to 12 days following infection with
Friend virus, a type of murine AIDS, recovered, while all of the controls
(not exposed to radiation) died within 40 days [202]. LDR was also
useful for treating ulcerative colitis and dermatitis in mice [203]. Mice
infected with the retrovirus family member Friend leukaemia virus,
(which also includes HIV-1), were protected by radiation-induced
adaptation in immune cells [204]. Due to radiation-induced immune
defence mechanisms, low-dose TBI may be helpful in treating AIDS,
according to a few human studies [201], [202], [205]. There is strong
evidence that HIV/AIDS could be successfully treated with low-dose
radiation. It is reasonable to consider that the stimulating effect of low-
dose radiation will prevent the development of AIDS in people whose
50 Page
immune systems are deteriorating because AIDS is an immune

de iciency disease and because strong and enhanced immune
response has been successful in preventing full-blown AIDS in people
with HIV. Whole-body radiation therapy may be helpful in the
treatment of AIDS, according to human experiments that Del Regato
started [206].
According to studies on X-ray therapy for wound healing

conducted in the USA between 1900 and 1960 [207], low-dose
radiation can hasten wound healing by up to 50%. The ability of LDR to
activate the immune system, which can eliminate pre-cancerous cells,
cancerous cells, and tumour metastases, is now well established[208]-
[210]. Increased neutrophils and mononuclear cells linked to
in lammation are connected with infections. These cells can assist in
"capturing" and separating circulating tumour cells.
4.1.4. Effect of LDR on Cardiovascular-related chronic diseases

Low-dose cumulative radiation(<500 mGy) has been found to
not cause in lammation and chronic diseases including kidney,
cardiovascular, and related abnormal lipid pro iles and diabetes [211]-
[213]. There was no statistically signi icant associations of
cardiovascular disease in humans at cumulative radiation doses <500
mGy and at dose rates <10 mGy/day) [211]-[213]. Low-dose-rate γ-
irradiation has been found to prolong the lifespan of mice and inhibit
the development of type 2 diabetes by preserving insulin production,
maintaining normal lipid levels, and delaying the onset of nephropathy
[214]-[217]. Diabetes-prone mice were given total body radiation
doses of 50 mGy every other day for four weeks, or 25, 50, or 75 mGy for
four to eight weeks. These radiation doses markedly reduced lipid
pro iles, in lammation, and insulin resistance while also avoiding
nephropathy [214], [217], [218]. The most effective schedule and
radiation dose for shielding the kidney from the diabetes appears to be
whole-body LDR at 12.5 mGy every other day for 8 weeks [219].
Compared to unirradiated diabetic controls, mice with chemically
generated type 1 diabetes that underwent 25 mGy or 50 mGy whole-
body irradiation, did not develop diabetic cardiomyopathy and had
improved cardiac function, with less cardiomyocyte
hypertrophy[220].
Page 51
Forty percent of radiography exposure is given for cardiology

related issues. The average patient is exposed to about 50 chest X-rays
annually. The majority of the dose comes from nuclear cardiology (they
deliver the equivalent of 750 chest X-rays), cardiac electrophysiology,
percutaneous coronary intervention, and CT. Patients get mean skin
radiation doses of less than 10 cGy and maximum doses of more than
70 cGy during coronary angiography and percutaneous transluminal
coronary angioplasty, respectively. The usual lung dose is 25 mGy. Staff
members of cardiac catheterization laboratories who had received a
median cumulative radiation dose of 46 mGy [221], showed no
increased risk of cancer. In post-coronary artery bypass graft patients
aged 55–75 who had undergone coronary CT angiography, cancer risk
was decreased in comparison to the general population [222].
The well-known adaptive response, i.e., giving a low

conditioning radiation dose of 150 mGy a day before the high dose of
breast cancer treatment (2 Gy) is a good technique to prevent cardiac
damage from high-dose radiation. Low radiation doses activate
adaptive defence mechanisms that are bene icial to the healthy, normal
heart tissues but detrimental to the breast cancer cells that are
aberrant [135]. Cardiologists have a saying “everyone knows that
cardiologists do not get cancer” [135].
4.1.5. Summary of Chinese studies

There are more than hundred publications, on the bene icial
effects of low dose radiation for curing several diseases. A detailed
review has been performed by Ji et al [127]; a summary of that is
described below.
4.1.5.1. Low-Dose Radiation effect on Immune system

In Yangjiang, Guangdong Province, LDR hormesis was irst noted
in Chinese individuals who had been exposed to high background
radiation at a low dose rate of 1.96 mSv/y [223]. T- cells in this group
were much more reactive and capable of repairing DNA than those in
nearby low-background radiation locations. In a scenario where
Kunming mice were subjected to X-rays with whole-body irradiation
(WBI) of 25, 50, 75, 100, 200, 500, 1000, 2000, 4000, and 6000 mGy and
52 Page
a sham-irradiated control, Liu found that lymphocytes and related

functions presented a J- or inverted J-shaped dose-response curve
suggesting a hormesis effect (bene icial effects) at low dose [224]. It
was shown that the immune response was enhanced by LDR,
particularly for adaptive immunity. When doses of less than 0.2 Gy
were administered as WBI to male Kunming mice and in vitro
irradiated EL4 cells, Liu et al. found a signi icant decrease in the rate of
thymocyte apoptosis [225], [226]. In their research, pro-survival
molecules like Bcl-2 and Bcl-xl as well as the ratio of pro-survival to
pro-apoptotic molecules like Bcl-2/Bax and Bcl-xl/Bad had
considerably higher messenger RNA (mRNA) and protein expression
levels. As a result, proapoptotic molecules such as p53, Bax, Bad, FasL,
and Gadd45 dramatically decreased in both their mRNA and protein
expression levels. According to certain research, LDR may also
stimulate thymocytes by boosting their growth and development
through the cell cycle [227], [228].
The total number of thymocytes, the percentage of cells in the S

phase, and the proliferation of thymocytes in response to ConA
stimulation were all increased when Kunming mice were exposed to
LDR by WBI (75 mGy). LDR has been shown by Liu et al [229] to alter T-
helper differentiation and cytokine production. Interleukin 10 (IL-10)
mRNA and protein levels were both repressed while IL-12 expression
was simultaneously elevated in Kunming mice subjected to whole-
body LDR (75 mGy), which may have in luenced the immunological
response to promote Th1 differentiation [229], [230].
They proposed that the primary cause of this variation in

cytokine release and Th-cell differentiation may be the impact of LDR
on T-lymphocyte surface molecule expression and interactions with
antigen-presenting cells.
4.1.5.2. Effects of LDR on Tumour cells

In vitro tumour cell culture and animal models with tumours
have been extensively used by Chinese researchers to study the
biological effects of LDR on tumour cells.
Page 53
In vitro and in vivo experiments by Jiang et al. [232] showed that

LDR does not promote the growth of tumour cells. In their
investigation, scientists discovered that when exposed to LDR (25-200
mGy X-rays for cells and 75 mGy for tumor-bearing mice)[231], four
normal human cell lines—MRC-5, Hl7702, 293T, and 6550—had a
stimulating effect, but not all human tumour cell lines—K56, HL-60 ,
BEL7402, HCT-8, and HeLa and NCI-H446, U251 for mice. Jiang et al.
also showed that LDR does not cause an adaptive response (AR) in
tumour cells, either in vitro or in vivo [232].
Yu et al. [233] also found that there was a stimulating effect on

the normal cell line AG01522, but not the cancer cell line Lewis cells,
when they were exposed to LDR in vitro and in vivo. Additionally, they
observed a lack of LDR- induced AR in tumour cells in tumour-bearing
mice. Furthermore, they found a higher apoptotic effect and lower
expression of the antiapoptotic gene Bcl-2 in tumour cells of tumour-
bearing mice exposed to D1+D2 than those exposed to D2 alone [233].
In response to 20 to 75 mGy of X-rays, Liang et al. [234]

demonstrated that LDR can cause cell growth in the human embryonic
lung ibroblast cells 2BS but not in the lung cancer cells NCI-H446. They
also contend that LDR promotes cell proliferation in 2BS cells, but not
in NCI-H446 cells, through activating the MAPK/ERK and P13K/Akt
signaling pathways [234]. Through ataxia-telangiectasia mutated
(ATM) signaling, Yang et al. showed that LDR can generate unique
biological effects on HBE135-E6E7 normal lung epithelial cells and
A549 malignant human lung cells. In normal lung epithelial cells
(HBE135-E6E7), they discovered that LDR activated the
ATM/Akt/GSK-3b signaling pathway, nuclear accumulation of nuclear
factor erythroid 2-related factor 2, and the expression of antioxidant,
which can lessen cellular damage from excessive HDR-induced ROS
emissions. However, none of these effects were seen in A549 cells, and
the lack of activation of these pathways may account for the difference
in LDR responses between normal and cancer cells [235].
The converse phenotype, where LDR can produce radio-

resistance in cancer cells, has, however, been found in few
investigations. For instance, Chen et al. [236] demonstrated in human
54 Page
lung adenocarcinoma A549 cells, that exposure to 50 mGy radiation

can produce radio-resistance after exposure to 750 mGy particles
radiation. Additionally, they suggested that ROS rise in response to LDR
would encourage autophagy, Nrf2, and HO-1 while conferring radio-
resistance in A549 cells [236]. In cervical cancer cell lines Siha and
C33A, Yan et al [237] discovered that LDR can trigger p65-regulated
epithelial- mesenchymal transition, hence boosting cervical cancer
cells' invasiveness and metastasis [237].
According to some researchers, these inconsistencies could be

the result of various LETs, experimental time points, and cancer cell
lines [235]. Recent laboratory and clinical research have demonstrated
a strong correlation between immune suppression or malfunction and
the incidence of malignant tumours. As a result, it is thought that one of
the keyways to combat cancer is to successfully improve the immune
system of cancer patients. LDR has been shown to activate the immune
system's hormesis and ARs. Additionally, a lot of experts think LDR can
have different biological impacts on healthy and malignant cells.
Consequently, it has been suggested that LDR may have anticancer
effects in vivo. Chinese scientists have investigated this theory in great
detail for the past 30 years.
In 1995, Yin et al. [238] found that on day 12 following tumour

inoculation, tumour incidence was much lower in Kunming mice and
C57BL/6J mice that had received 50 mGy of radiation prior to tumour
inoculation (78.31%) than it was in mice which had not received any
radiation (91.7%). Tumour growth was slower and the tumour mass
was less in the LDR-irradiated group than in the control group, who
were not exposed to radiation [238]. Fu et al. [239] discovered that 14
days after Lewis lung cancer cells were inoculated into C57BL/6J mice
that had received 50 to 150 mGy of X-ray radiation, the mean number of
lung tumour nodules was considerably lower than in the LDR non-
irradiated tumour-inoculated mice. Additionally, the LDR group
considerably outperformed the non-irradiated tumour inoculation
group in terms of IL-2 secretion and NK cell activity [239]. In tumor-
bearing Kunming strain mice, Yu et al. showed that LDR (75 mGy)
signi icantly enhances erythrocyte immunological function and the
capacity to transport O2 [240].
Page 55
In Sprague-Dawley (SD) male rats, Wang et al. [241] showed that

low-dose splenic radiation can prevent the growth of liver tumours by
altering the functionality of CD4^CD25^T regulatory cells. Li et al [241]
observed that, in C57BL/6J mice subcutaneously transplanted with
S180 tumour cells were pre-exposed to 75 mGy whole-body LDR and
then irradiated with 10 Gy. The tumour growth rate was signi icantly
lower than in tumour-bearing mice which were exposed to 10 Gy
irradiation. The activity of natural killer and lymphokine-activated
killer cells was signi icantly higher in the spleen of the group pre-
exposed to LDR and then given 10 Gy as compared to the group just
given 10 Gy. In an experiment using C57BL/6J mice implanted with
Lewis lung cancer cells, Fu et al. discovered that pre-exposure to 75
mGy before mitomycin C systemic treatment dramatically increased
the impact of the chemotherapy. Analysing immunological markers at
the same time showed that treatment in the tumour-bearing animals
decreased the number of spleen cells, NK cell and cytotoxic T-
lymphocyte activity, phagocytosis by macrophages, and the responses
of splenocytes to ConA. When tumour-bearing mice were pre-exposed
to LDR before chemotherapy, all of the aforementioned immunological
markers outperformed the chemotherapy alone group [242] . In mice
suffering from S180 sarcoma, Yu et al. [243] demonstrated that LDR
can improve the anti-tumour effects of the chemotherapeutic drug
cyclophosphamide (CTX). In their investigation, Kunming mice bearing
S180 sarcoma cells were given 75 mGy of whole-body gamma
radiation, followed by an intra-peritoneal injection of 300 mg/kg CTX.
In the group treated to CTX along with LDR, tumour growth was found
to be greatly reduced and tumour cell apoptosis was found to be
signi icantly elevated. Compared to animals treated solely to LDR or
CTX, more cell-cycle arrest was seen in mice subjected to LDR or CTX.
Furthermore, BMC concentrations and proliferation were higher in
CTX + LDR mice than in untreated mice. LDR was therefore proposed to
greatly protect the bone marrow's hematopoietic activities, which may
be useful for adjuvant chemotherapy [243].
All the research mentioned above demonstrated that LDR may

have anticancer effects in vivo, which may be connected to
improvements in immune function or other LDR-induced functions.
These results suggest that LDR may be able to shield healthy tissues
56 Page
from radiation therapy while maintaining or improving the

effectiveness of tumour therapy.
4.1.5.3. Effects of LDR on Diabetes

Worldwide prevalence of diabetes mellitus, including types 1
and 2, has signi icantly increased [244]. This condition is characterised
by the death of beta cells, the pancreatic cells that produce insulin. It is
now understood that practically all pathogenic states of pancreatic
beta cells in diabetes are impacted by oxidative stress [245].
Ad d i t i o n a l ly, s e c o n d a r y ox i d a t ive s t re s s b ro u g h t o n by
hyperlipidaemia, in lammation, and hyperglycaemia in diabetics is a
major contributor to practically all diabetic complications [246]. The
question of whether LDR can stop the onset of diabetes and all of its
problems is brought up. In-depth research on this topic has been done
in China, particularly on the prevention of diabetic sequelae such as
diabetic nephropathy (DN), testicular damage from diabetes,
cardiomyopathy and skin ulcers.
One of the most common microvascular complications in people

with diabetes is diabetic nephropathy (DN). An essential factor in the
beginning of DN [247]-[249] is the systemic in lammation brought on
by hyperglycaemia and hyperlipidaemia, which causes renal oxidative
damage. Multiple exposures to LDR, according to Zhang et al. [250] can
lessen the effects of diabetes on the kidneys, including the suppression
of systemic and renal in lammation. In their investigation, diabetic
male C57BL/6J mice were subjected to whole-body 25 mGy X-rays,
which signi icantly reduced the degenerative and dysfunctional
alterations brought on by diabetes in the kidneys. The levels of TNF-α,
intercellular adhesion molecule-1 (ICAM-1), IL-18, monocyte chemo-
attractant protein-1 (MCP-1), and plasminogen activator inhibitor-1
(PAI-I) were also elevated in the serum and kidneys after several
exposures to LDR [250]. By enhancing Nrf2 expression activity and
promoting Akt-phosphorylation, Xing et al. [218] suggested that LDR
can prevent DN [218]. A single 75 mGy and cumulative 75 mGy have
both been demonstrated by Zhang et al [251] to promote SOD1
expression and activity; this may be one of the mechanisms preventing
DN [251].
Page 57
According to Shao et al. [214], type 2 diabetes-induced kidney

injury, which is characterised by renal dysfunction and pathological
alterations, can be signi icantly avoided by exposure to LDR (50 or 75
mGy). Additionally, they proposed that the reduction of dyslipidaemia
and the ensuing lipotoxicity-induced insulin resistance, in lammation,
and oxidative stress were the main causes of the protective
mechanisms of LDR [214]. Numerous studies conducted recently have
shown that diabetes adversely affects male fertility in various ways,
including erectile dysfunction, decreased sperm motility, and
decreased semen volume. In the testes of diabetic male SD rats, Cai et al.
[252] found a substantial increase in apoptotic cell death [252]. The
testes were reported to suffer genetic damage and cell death when
exposed to low-dose radiation (less than 100 mGy) [253]-[256]. As a
result, it was theorised that exposure to LDR could lessen the harm
diabetes causes to the testicles. In a type 1 diabetic experimental male
Wistar rat study, where diabetes was induced with a single injection of
streptozotocin (STZ), Zhao et al. [257] discovered that repeated
exposure to LDR signi icantly attenuates testicular apoptotic cell
death, decreases expressions of Bax mRNA and protein, and decreases
levels of serum sex hormones (testosterone, luteinizing hormone, and
follicle-stimulating hormone). Their indings show that increased
oxidative stress may be a mediator of diabetes-induced testicular cell
death, and that LDR protection from the cell death is most likely
mediated by maintenance of antioxidants [257].
Additionally, some research has looked at decreased wound

healing as a side effect of diabetes [258], [259]. Diabetes patients are
likely to experience slower wound healing due to a lack of cellular and
molecular signals needed for normal wound repair processes such as
angiogenesis, epithelialization, and remodelling [260], [261]. In a male
Wistar rat study of diabetes, Guo et al. [262] examined the biological
effects of repeated LDR exposure (75 mGy X-rays) on skin wound
healing. According to their indings, diabetic rats exposed to LDR
repeatedly, could heal skin wounds considerably faster than diabetic
rats not exposed to radiation. They also showed that increases in bone
marrow and circulating CD31 + CD34 + stem cells, vascular
regeneration, cell proliferation in the wound tissue, and the expression
of matrix metal loproteinases 2 and 9 were linked to the LDR-induced
58 Page
improvement in wound healing. They came to the conclusion that

stimulation of bone marrow stem cell proliferation and peripheral
mobilisation is linked to LDR-induced acceleration of wound healing in
diabetic rats [262]. Another serious complication of diabetes is diabetic
cardiomyopathy, which is characterised by cardiac remodelling,
including pro ibrotic alterations and ventricular hypertrophy linked to
cardiac dysfunction [263], [264]. The major characteristics of diabetic
cardiomyopathy are correlated with in lammation, oxidative stress,
and apoptosis brought on by diabetes [265], [266]. In a 2009 study
using a C57BL/6J mouse study of diabetes, Zhang et al. [267] looked at
the protective effects of recurrent LDR exposure on diabetes-induced
heart in lammation and damage. In their research, they found that
diabetes led to appreciable increase in cardiac in lammation, as seen
by rises in the mRNA and protein levels, IL-18, TNF-α, ICAM-1, PAI-1,
and MCP-1. Repeated exposure to LDR dramatically decreased the
cardiac expression of IL-18, TNF-α, MCP-1, and PAI-1 in diabetic mice
compared to non-irradiated diabetic mice. Additionally, diabetic mice
treated repeatedly to LDR showed less severe ibrosis, oxidative
damage, and cardiac histopathological abnormalities than controls
(not exposed to radiation). Their indings imply that LDR can reduce
myocardial in lammation and pathological remodelling brought on by
diabetes [267]. However, according to certain studies [268], [269],
considerable in lammation is typically shown in the short term rather
than the long term. Thus, the same team looked into whether LDR can
stop late-stage diabetic cardiomyopathy and whether this defence is
brought on by activating antioxidant and antiapoptotic pathways. In
the study, they discovered that whole-body LDR treatment for
C57BL/6J mice with STZ-induced hyperglycaemia can prevent
cardiomyopathy. Additionally, they noticed that this LDR-induced
protection was linked to Nrf2 activity, Akt activation increase, and p53
inactivation [220].
In summary from the studies by Chinese researchers mentioned

above, LDR may be a successful treatment for complexities brought on
by diabetes.
Page 59
4.1.5.4. Stochastic effects of LDR

The stochastic effect refers to the potential for cancer
development as a result of radiation-induced DNA damage and
alterations. It is still unknown if repeated exposure to LDR increases
the risk of carcinogenesis. In the high-background radiation areas of
Yangjiang, China, Tao et al. [270] assessed the cancer risk associated
with an LDR exposure of an average yearly effective dose of 6.4 mSv
[270]. They tracked 1,25,079 patients and recorded 10,415 deaths. Out
of the total number of deaths, 1003 were due to cancer between 1979
and 1995. They did not discover any evidence in their study that living
in a location with a lot of background radiation increased the risk of
cancer. On the other hand, they discovered that although not
statistically signi icant, the mortality of all malignancies was generally
lower in high background radiation areas than it was in the control area
(not exposed to radiation). Using a C57BL/6J mouse model, Yu et al.
[271] conducted research on the effects of several exposures to LDR on
carcinogenesis in 2009. Their indings suggested that a radiation dose
of 0.1 Gy does not enhance carcinogenesis even after many exposures
[271].
In Taiwan, Hwang et al. [272] evaluated the cancer risk in a

population that had undergone prolonged LDR for around 10 years as a
result of residing in a structure with Cobalt-60 contaminated steel.
Their indings suggested that prolonged LDR may increase the
incidence of cancer in the general population, particularly for
leukaemia [272]. However, as discussed in [92], [93] , as opposed to
the general Taiwanese population, inhabitants in the
contaminated region had a 3 % decrease in cancer fatalities.
Additionally, the prevalence of congenital abnormalities was
reduced to about 7% of the general Taiwanese population's
prevalence [92] .
The relative risk of getting various malignancies among medical

X-ray workers in China was calculated by Wang et al. [273] . They
discovered a link between the risk of cancer and the occupational
radiation component. Additionally, their indings indicated that
medical diagnostic X-ray workers may have a lung cancer risk higher
than that of the control group. Using a 64-slice multiple detector CT,
60 Page
Feng et al. [274] assessed the radiation exposure from computed

tomography (CT) scans in anthropomorphic phantoms in 2010 and
calculated the related cancer risk [274]. They came to the conclusion
that the effective doses from these routine paediatric CT scans varied
from 0.7mSv to 3.5mSv, and the cancer risks were discovered to be as
high as 0.16 % only, with particular organs of higher radio-sensitivity,
such as the breast, thyroid gland, colon, and lungs [274]. And the
studies mentioned above showed that there is still debate over
whether LDR causes any stochastic effect. This can be a result of the
small sample size. The danger of LDR is probably smaller than that of
HDR, and increasingly larger epidemiological studies are needed to
make a conclusive statement.
4.2. Medical occupational exposure

The majority of current studies
that provide information on the
health effects of low-dose radiation
exposure are carried out in groups
of medical professionals and
technical workers who are
regularly exposed to radiation. In a
series of studies to assess the
consequences of long-term
radiation exposure, mortality rates
among radiologists and radiologic
Impression of X-ray Imaging technologists were assessed. In the
early half of the 20th century,
radiologic technicians and radiologists were reported to have a
number of major health issues, including an elevated risk of skin cancer
and leukaemia as well as elevated cancer and all-cause mortality rates
[275]. For instance, elevated leukaemia-related mortality rates were
found in 8 historical cohorts of more than 2,70,000 radiologists and
radiologic technologists who worked before 1950, because these
professionals were exposed to very high doses of radiation (e.g., 30,000
mSv/y in 1902) [276]. However, excess mortality vanished once the
irst radiation protection recommendations (dose limit of 0.2 R/d,
corresponding to ~500 mSv/y) were put into place in the early 1920s
[276], [277]. For radiologists who began their careers after 1940 [278],
Page 61
the pattern of cancer mortality has drastically reduced. While among

the early entrants the mortality rates were higher in young radiologists
than those of other specialists, among the later entrants, Young
radiologists exhibited lower mortality rates.
Table 6 : Mortality rates in cohorts occupationally exposed to
radiation
(2,698)
(1,46,022)
(43,763) (64,990)
62 Page
(45,634) (64,401)
(46,970) (41,169)
(1,24,743)
(1,74,541)
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(1,20,000)
Abbreviations: CI, con idence interval; NA, not available.

a Male. b Female. c Male + female. d Relative risk for death.
64 Page
Matanoski et al. [278] hypothesised that radiologists might

experience protective effects from low-level radiation exposure based
on their analysis of the data. All-cause mortality among British
radiologists who irst registered with a radiological society in 1920 or
later was found to be signi icantly lower than that of the general
population (Berrington et al. [279] study). The number of cancer-
related deaths in this group was comparable to the sum of all medical
professionals (SMR = 1.04). Compared to other medical professional
groups, British radiologists who were registered after 1954 had
signi icantly reduced mortality rates; this was true for both cancer
mortality and other causes of death combined. On the basis of these
indings, Cameron [280] concluded that “British radiology data
show that moderate doses of radiation are bene icial rather than a
risk to health.”
In their investigation of a countrywide cohort of US radiologic
technologists (total n = 1,46,022), Mohan et al. [281] revealed indings
that were broadly in agreement with those of British radiologists.
Standard Mortality Rates (SMR) were discovered to be 24%
lower for all-cause mortality and 18% lower for cancer mortality in this
cohort (who were exposed to radiation) when compared to those in the
overall US population. Radiologic technologists who started working
before 1940 had greater relative risks (RRs) for breast cancer (RR =
2.92) and all malignancies (RR = 1.28) than those who started working
after 1960. In actuality, a lower risk of mortality was associated with
later employment [281], [289]. Similar indings showed that those who
started working before 1950 had higher rates of acute lymphocytic
leukaemia, acute and chronic myeloid leukaemia and other blood
cancers. In comparison to female radiologic technicians who began
their careers in 1970 or after, the adjusted breast cancer risks (RRs) for
those who began their careers before 1935, from 1935 to 1939, in the
1940s, 1950s, and 1960s were 2.9, 1.8, 1.0, 1.2, and 1.0, respectively
[290]. There was a higher risk of breast cancer for those women who
began their careers before 1935. It was observed that the breast cancer
risk was signi icantly reduced from 1935 to 1960. The RR was
signi icantly reduced because of low dose radiation. The RRs rose in
proportion to the total number of years worked before 1940 and were
signi icantly higher among those who began working before the age of
Page 65
17. On the other hand, the relative risks was found to have no
relationship to the number of years worked after 1940. It has also been
shown that occupational radiation exposure in the low- to moderate-
dose range increases the incidence of breast cancer in the US cohort of
radiologic technologists [291]. However, this was true for women born
before 1930 who began working before 1950 due to cumulative annual
doses (37 mGy). This dose was reduced signi icantly (1.3 mGy) due to
reduction in dose in later years. The most recent study by Kitahara et al.
[292] found no correlation between prolonged, low-to-moderate
radiation exposures (having cumulative mean absorbed brain dose of
12 mGy; in the range of 0-290 mGy) and malignant intracranial tumour
mortality in the US state-wide cohort of radiologic technologists [292].
In a further study by the same researchers [283], the total and cause-
speci ic death rates were compared in cohorts of doctors who
performed luoroscopy-guided interventional procedures (n = 45,634)
and psychiatrists (n = 64,401) across the country. Male and female
physicians who had been exposed to radiation had mortality rates for
both cancer and total mortality that were 20% lower (men: RR = 0.92;
women: RR = 0.83) than those of psychiatrists who were not exposed to
radiation. In addition, doctors' mortality rates from certain cancers
and circulatory conditions were comparable to those of psychiatrists.
In a different study by the same cohorts [282], male radiologists
showed lower all-cause mortality rates (RR = 0.94) and comparable
cancer mortality rates (RR = 1.00). It is also important to note that
these rates were driven by radiologists who inished their education up
to 1940. A nationwide prospective cohort of 90,957 US radiologic
technologists, who performed luoroscopically guided interventional
procedures from 1994 to 2008 showed an increased risk of brain
cancer mortality (hazard ratio [HR] = 2.55), as well as an increased
incidence of melanoma (HR = 1.30), breast cancer (HR = 1.16) [293],
and stroke (HR = 1.34) [294]. However, the authors pointed out that
these indings could potentially be in luenced by other unaccounted
non-radiation risk factors [293]. It has also been noted that American
radiologic technologists have a higher mortality risk from circulatory
disorders, but only for those who started their careers before 1950,
when occupational radiation exposure dosages were high [295]. The
risk of childhood cancer among 1,05,950 children born to US radiologic
technologists between 1921 and 1984 was assessed [296] because it
66 Page
has been suggested by various writers that parental pre-conceptional

irradiation can result in childhood cancer. However, this investigation
could not ind a statistically signi icant link between parental pre-
conceptional radiation exposure and increased risk of childhood
cancer in offspring. Data on cancer incidence and death among
radiologists and other groups of medical professionals who are
exposed to radiation were discussed by Brenner and Hall [297]. They
pointed out that radiologists could easily identify the radiation
concerns in the irst half of the 20th century. However, as more
stringent radiation safety regulations were put in place, radiation
impacts frequently dropped below the level at which they could no
longer be detected using modern epidemiological techniques. The
lowest cumulative radiation dose that may cause cancer is around 500
mSv, according to Tubiana's [298] assessment of the research indings
in this ield of study. It can be inferred from the whole of the evidence
(Table 6) that smaller doses have no effect at all or rather bene icial
effects.
4.3. Radiation-based medical procedures exposure

Patients receiving radiation therapy often receive low doses of
radiation (up to 0.1 Gy) to non-adjacent tissues while speci ic tumours
are typically exposed to high doses of radiation (~40-60 Gy) [299].
However, there are several problems with looking into the impacts of
such exposures because partial-body exposures plainly carry a
different risk than equal whole-body exposures.
Target organs are exposed to low amounts of radiation during

diagnostic X-rays and luoroscopy-guided interventional procedures,
which are becoming more common in clinical practise. The increased
radiation burden caused by these procedures is often not signi icant.
For instance, of the approximately 3 mSv yearly global per caput
effective dose in 2000, only 0.4 mSv came through diagnostic medical
exams and 2.4 mSv from natural background radiation [300].
Diagnostic radiation doses are often minimal, making it challenging to
study them using traditional epidemiologic methods. However, some
of these methods, like CT, can deliver signi icant cumulative doses to
the target tissues of the order of 100 mSv, making them an effective
Page 67
model for studying the effects of low-dose radiation on health [64].
4.3.1. Diagnostic irradiation

Modern patient screening procedures heavily rely on advanced
imaging technologies. However, numerous scholarly and popular
papers on the potential dangers of CT screens have been published
since 2000, raising significant public concern about this issue [301]. As
a result, imaging tests were postponed or cancelled in numerous
instances, putting patients at significantly higher risk than that
brought on by diagnostic radiation exposures [302]. In fact, the doses
used in CT typically range from 1 to 20 mSv, and for doses below 100
mSv, no extra malignancy has been seen.
After repeated chest luoroscopy treatments for persistent

tuberculosis or scoliosis, an increase of breast cancer was found in
women. A sample of 31,710 Canadian women who received
tuberculosis treatment between 1930 and 1952, showed an increased
breast cancer mortality (SMR = 1.36) [303]. A US cohort of 5,466
female patients with scoliosis who underwent repeated diagnostic
radiography examinations (mean cumulative radiation to the breast:
108 mGy; in the range: 0-1700mGy), also revealed an elevated breast
cancer mortality rate (SMR = 1.69) [304]. With an increase in the total
number of radiograph exposures and, thus, a rise in the cumulative
radiation dosage, the risk of breast cancer increased dramatically.
Breast cancer mortality was similarly signi icantly increased (SMR =
1.68) [305] in a more recent examination of a sample of 5,573 women
with scoliosis and other spine problems, who were subjected to
repeated diagnostic X-ray procedures. Surprisingly, mortality rates
from a few other malignancies were substantially lower than
predicted, particularly lung, cervical, and liver cancers (SMR: 0.77,
0.31, and 0.17, respectively). However, it should be remembered that
although single treatment doses are frequently minimal, many patients
may experience repeated treatments over time, which may eventually
result in relatively high cumulative doses. Due to the potential for
frequent diagnostic exams in studies like this, this factor is particularly
crucial. For instance, in the Boice et al. [306] study, women who
underwent X-ray luoroscopy examinations repeatedly and in whom
higher breast cancer incidence was noted underwent an average of 88
68 Page
times for such diagnostic procedures (observed/expected ratio = 1.29;

95 % CI, 1.1-1.5). Increased breast cancer incidence in this study was
unquestionably caused by high cumulative doses, averaging 790 mGy
and ranging from 10 mGy to 6,400 mGy. Tubiana [298] stressed that,
only cumulative doses more than 500 mGy have consistently been
shown to cause cancer excess while discussing these observations.
The risk of cancer brought on by diagnostic X-ray exposures

(such as CT scans) may have been lessened rather than increased,
according to Scott et al. [307]. This idea has been supported by results
from animal experiments that show low-dose radiation exposure can
reduce the growth of experimental cancers by encouraging the
elimination of preneoplastic cells and/or by preventing the metastasis
of pre-existing cancer [308]-[311]. Based on these indings, it is
hypothesised that doses currently associated with standard diagnostic
X-ray procedures (between 1 and 100 mGy) fall within the "hormetic"
zone for high-energy γ-ray photons and may therefore be protective
against cancer and a number of other diseases besides cancer [302],
[312].
Nevertheless, care must be taken when advising radiation-based

techniques for diagnostic purposes. This is particularly true for
expectant mothers because foetuses could be extremely sensitive.
Therefore, foetal radiation doses above 100 mGy may occasionally
cause serious developmental problems like pregnancy loss, growth
retardation, congenital deformities, and neurobehavioral defects
[313], [314]. However, the threshold levels for all of these side effects
are over 100 mGy to 200 mGy, and the risk is viewed as insigni icant at
50 mGy. Only very seldom are potentially dangerous doses possible
(for comparison, 100 mGy is equal to around 1000 conventional chest
X-rays) [313]. Therefore, the total of all maternal and foetal risks and
bene its should be taken into consideration when deciding whether to
perform such procedures [315, p. 2].
4.3.2. Low-Dose Radiotherapy

More than half of all cancer patients currently receive
radiotherapy, a form of cancer treatment that uses high doses of
ionising radiation to kill cancer cells [316]. However, the effectiveness
Page 69
of radiation therapy is severely constrained because the high (>2 Gy) or

intermediate (0.1-2.0 Gy) radiation doses that are frequently utilised in
modern radiotherapy , may harm healthy tissues, impair
immunological responses, and increase the likelihood of subsequent
neoplasms [317]. On the other hand, when low-dose radiation
exposures (≤100 mGy for acute exposure or ≤0.1 mGy/min dose rate
for chronic exposures) are used, these consequences are avoided.
Because low-dose radiation exposure offers tumour suppression with
hardly any hazardous side effects, several studies have proposed that it
is more successful than traditional radiotherapy protocols [318]-[320].
This belief is supported by evidence that suggests low-dose radiation
may boost antioxidant capacity, immunological responses, DNA repair,
and apoptosis, potentially leading to effective tumour control.
Particularly, it has been demonstrated that low-dose radiation causes
the activation of numerous anticancer pathways, including the
production of antibodies, the release of cytokines like interferon, and
the stimulation of natural killer activity [118]. As demonstrated in
numerous animal studies, these processes together can slow the
growth of tumours, reduce metastasis, and prevent the carcinogenesis
brought on by high-dose radiation. Paraswani et al. [321] studied the
effect of priming the human peripheral blood mononuclear cells
(PBMCs) with a low dose (100 mGy gamma radiation) and then, after
an 'adaptive window' of 4 hours, 'challenged' it with a high dose of (2
Gy). In comparison to non-primed cells, the results revealed a modest
(5.7 %) improvement in viability and a decrease in DNA strand breaks
in primed cells [321].
According to certain preclinical investigations, chemotherapy is

less likely to be successful in treating lymphosarcoma (non-Hodgkin
lymphoma) than low-dose radio-immunotherapy [319]. Results from
multiple clinical trials were consistent. Low-level total-body and
partial-body radiation therapy was employed by Harvard University's
clinical research teams to treat non-Hodgkin lymphoma. Four years
after the beginning of the trial, 70% of the low-dose irradiated patients
were still alive, while only 40% survived in the control group treated
with chemotherapy [322]. Similar to the above, low-dose irradiation
patients and chemotherapy-treated cancer patients saw the 4-year
survival rates of 74% and 52%, respectively [323]. Preclinical and
70 Page
clinical trials carried out at Tohoku University in Japan showed similar

indings [324]. In both the Harvard and the Tohoku clinical studies, the
typical irradiation doses were about 15 R administered twice weekly,
calculated to mid-pelvis for a total dose of about 150 R. More recently, it
has been demonstrated that low-dose radiotherapy is an effective
palliative treatment option for a variety of lymphoma types, including
marginal zone lymphoma [325]-[327], cutaneous B-cell and T-cell
lymphomas [328]-[330], and indolent non- Hodgkin lymphoma [331],
[332]. Additionally, low-dose pre-treatment has been suggested as a
viable radiation therapeutic strategy. When signi icant therapeutic
dosages are subsequently administered, such pre-treatment may
induce an adaptive response that could offer improved protection,
lowering the resulting harm and hence, the likelihood of recurrent
cancer [333]. Additionally, there is some preclinical experimental data
to support the use of low-dose radiation in the treatment of a number
of non-cancer conditions, including diabetes and diabetic
cardiovascular complications [214], [267], [334], [335], autoimmune
diseases [336], [337], and neurodegenerative diseases [177], [338].
Page 71
72 Page
Then why do people
fear radiation?
5
Having said so much bene icial effects of radiation on human
health, cure of life threatening diseases, enhancement of life span,
there is a big question “Why do people fear radiation?”
The answer is: When people think

about nuclear, they don't think about
electricity, medicine, or food, or about
improving one's quality of life or curing
diseases like cancer or enhancing life
expectancy as a result of direct or indirect
radiation exposure; instead, they think about
nuclear warheads, Hiroshima and Nagasaki,
Chernobyl, Fukushima, and inally, cancer. The Perception of Fear of
main cause of concern is the public link of Radiation
radiation to cancer. It may be emphasised that
“The public paradigm that “nuclear radiation
is a carcinogen” is a more political, scienti ic misinterpretation and
“cherry-picking” than actual science [339]. During the Cold War,
governments in particular used the fear of radiation as a weapon. As a
result, it caused collateral damage to the public perception of radiation.
The Linear No Threshold theory (LNT), which claimed that any amount
of radiation has the potential to cause cancer, was advocated by
regulatory organisations. This is possibly the most inaccurate science
[340] that has been promoted as fact [299] despite dire evidence to the
contrary [341].
Currently, International Commission on Radiological Protection

(ICRP) [342], recommends the use of the LNT model, yet there is no
empirical evidence that is statistically relevant to support the harmful
effects from low dose, low dose rate (LDDR) exposures [340] even
though several hundreds of studies on bene icial effects of low-dose
radiation as outlined above.
Page 73
74 Page
History of Linear No
Threshold (LNT) theory
6
After the discovery of X-ray-induced mutations, Olson and Lewis
[343] proposed that cosmic/terrestrial radiation-induced mutations
provide the principal mechanism of the driving force for evolution.
Genetic damage was considered to be proportionate to the amount of
energy absorbed in order for this concept to be generalised using the
LNT dosage relationship. The evolutionary concept was supported by
later research that indicated a linear dosage response for mutations,
brought on by ionising radiation [344], [345]. Based on an evaluation of
spontaneous and ionising radiation-induced mutation with
Drosophila iles, Muller argued that background radiation had a
negligible impact on spontaneous mutation, discrediting the ionising
radiation-based evolutionary hypothesis. Muller hypothesised that
ionising radiation from the environment might be a substantial
explaining element for genetic variation and might be what propels
evolution. The doses Muller used to induce mutation were exceedingly
high, surpassing background by nearly 2,00,000-fold, and caused
sterility or mortality in a signi icant number of the fruit lies tested
[346], [347]. As a result, Muller was hesitant in drawing a connection
between mutation and evolution.
However, a larger collection of mutation dose-response

observations served as a foundation for cooperation between
radiation geneticist Nicolai Timoféeff-Ressovsky and theoretical
physicists Max Delbruck and Gunter Zimmer. A biophysical model of
the gene, a theory of radiation-induced gene mutation targets, and the
single-hit hypothesis of radiation-induced mutation were established
by them. When they were integrated, these viewpoints supplied the
theoretical mechanism and mathematical foundation for the LNT
model. From the middle of the 1950s to the present, the LNT concept
has been acknowledged by radiation geneticists and endorsed by
national and international advisory bodies for risk assessment of
ionising radiation-induced mutational damage/cancer. The LNT
approach was eventually expanded to include chemical carcinogen risk
Page 75
assessment and is now utilised by regulatory and public health

organisations all over the world. Due to a slight loss of linearity at the
highest dose, the dose response was not linear but rather more like to a
square root function [346], [347]. It may have rami ications for an
explanation on how evolution works if the actual dose response for
ionising radiation-induced gene mutation was linear at low dose in
general.
On April 28, 1928, Axel R. Olson and eminent physical chemist

Gilbert N. Lewis of the University of California-Berkeley proposed in
Nature that natural radioactivity was probably a signi icant cause of
mutation that could generate variability from the parent generation
and affect the course of evolution [343]. This hypothesis was based on a
paper published in PNAS on January 1, 1928 by Goodspeed and Olson
on heritable alterations caused by X-rays in tobacco. The tests on
tobacco plants, according to these scientists, were speci ically
designed to enable a direct comparison of mutation rates between
synthetic X-rays and "naturally occurring radiations." It seems safe to
assume that the various rays will produce biological effects in
proportion to the ionisation which they cause, according to Olson and
Lewis (1928) [343], a perspective based on the emerging target theory
for radiation-induced biological effects put forth by leaders in the
physics community [348], [349].
A mutation estimate at a chosen natural background radiation

dose was then derived by Olson and Lewis (1928) [343], using a
straightforward linear mathematical model. They calculated the
annual number of variations (mutants) caused by natural radiation
using this method. It seems, therefore, not too outrageous to believe
that such changes that actually occur in nature are due to the
radioactivity of the environment, according to these authors. Muller
also independently advanced the viewpoint of Olson and Lewis (1928)
in a paper presented to the National Academy of Sciences on April 24,
1928 and released it on September 14, 1928. Muller's statement [350],
was primarily conceptual and lacked Olson and Lewis's (1928) [343]
speci ic formulation.
Babcock and Collins [351], [352] examined Olson and Lewis'

theory the following year (1928). They discovered a spot where the
76 Page
HISTORY OF LINEAR NO THRESHOLD (LNT) THEORY
ambient radiation was twice as high as it was in their Berkeley,

University of California, laboratory. They showed an increase in
mutation that matched in the same proportion as the difference in
background radiation using the clB strain sex-linked recessive
Drosophila test, supporting the proportionality theory.
Actual radiation levels and comprehensive experimental

procedures were never published. The idea that "natural radiation may
be responsible for the mutations that are the feed for natural selection
mill with the ensuing evolution of new forms," received more backing
in 1930 from Hanson and Heys. They came to their conclusions, based
on a research of fruit ly mutations in an old carnotite (or uranium)
mine. Initially, these views were backed up by other authors' remarks
[353]-[355]. By stating that natural radiation, which was present at
such low dose rates, could only be responsible for about 1/1,300 of the
gene mutations that naturally occurred in Drosophila melanogaster,
assuming a linear dose response [356], Muller and Rice University
physicist Mott Smith, challenged this LNT evolution perspective in
1930. The authors came to the conclusion that additional reasons are
required to account for the majority of spontaneous mutations.
Nevertheless, Oliver (1931) claimed in his dissertation, which was
under Muller's supervision, that cosmic and terrestrial radiations must
be responsible for a portion of the spontaneous mutations [357].
This result was supported by the idea that there is no threshold

for a mutation response and that the response is linear at low doses. It
was claimed that this link held true for all kinds of high-energy
radiation (e.g., gamma, beta, X-rays and probably ultra-violet rays).
Oliver (1931) came to the following conclusion: "By inference, it can be
stated that cosmic and terrestrial radiations likewise have the ability to
produce mutations in proportion to their ionisation power" [357].
O l ive r ( 1 9 3 1 ) a d d e d c h ro m o s o m a l i nve r s i o n s a n d
translocations to the concept of proportionality, strengthening his case
for the existence of a background radiation in luence [357]. Despite
this interpretation of environmental radiation-induced genetic
changes, Oliver (1931) concluded that “some other condition must,
therefore, enter in order to explain the difference in non-radiated
Page 77
material, between the frequency of gene mutation and that of the other
type of genetic changes” [357].
Muller [356] rejected the idea that exposure to natural radiation

might cause genetic novelty to result in evolutionary change, but he
continued to believe in the linear dose-response relationship based on
the research of Hanson and Heys [344], [358], and Oliver [345]. Even
though the Olson and Lewis (1928) [343] hypothesis did not enjoy
sustained support from the scienti ic community for a very long time,
Muller and other prominent members of the radiation genetics
community strongly supported the LNT model as a way to explain
genomic mutations and the development of cancer.
The LNT idea was therefore initially put forth to take

evolutionary change into consideration and afterwards, used for the
assessment of the risks for particular genetic diseases and the
incidence of cancer. Only a few research with acute effects and
extremely high doses provided the initial evidence that served as the
foundation for the LNT hypothesis. Within a decade, the single-hit
target theory was incorporated, giving the LNT dose-response model a
mechanistic basis. Radiation geneticists then used the LNT-single-hit
model, to frame the philosophical discussion surrounding the potential
harm from low-dose ionising radiation on the human genome. It
provided the basis for the recommendations of the US National
Academy of Sciences Biological Effects of Atomic Radiation (NAS BEAR
-I) committee in 1956 for the switch from a threshold to a linear dose-
response model for estimating ionising radiation-induced germ cell
mutation using the doubling dose concept. By the late 1950s and early
1960s, national and international bodies concerned with ionising
radiation had embraced the LNT single-hit model, which had quickly
been expanded to the process of cancer risk assessment. A probit
model-based approach for assessing cancer risk was proposed ive
years later by Mantel and Bryan (1961), researchers at the US National
Cancer Institute.
It was the Mantel and Bryan (1961) model that was proposed by
the FDA in 1973 for cancer risk assessment procedures, being replaced
78 Page
with a LNT model by the FDA in 1979, the same year that EPA applied
the LNT for the regulation of carcinogens (i.e. Trihalomethanes) in
drinking water Consequently, the LNT model and its single-hit
explanation/mechanism theory can be linked to the idea of radiation-
induced mutation target theory as put forth by Timoféeff - Ressovsky et
al. (1935), which was based on the proportionality rule of Muller
(1930), which itself had its roots in the 1928 paper of Olson and Gilbert
that created the LNT concept in response to Muller's (1927) seminal
indings that ionising radiation could induce mutation.
Excess Relative Risks at low doses [12]
The hypothesis of LNT is the result of numerous false

interpretations of scienti ic facts. Muller, who received the 1946 Nobel
Prize attempted to convey his personal prejudice through his lecture
[359], endorsed the LNT hypothesis. Muller declared to the world
during his award address in Stockholm that there was no way around
the fact that radiation effects accrue linearly with dose rate down to
zero doses [339]. The LNT model was suggested by the U.S. NAS BEAR I
Committee's Genetics Panel, and it was quickly adopted by all
governments and regulatory organisations throughout the world
Page 79
[360]. The NAS Genetics Panel engaged in scienti ic misconduct by

creating and misrepresenting its doctored estimates of the genetic
susceptibility of humans to radiation exposure before publishing them
in the journal Science [360]. On the other hand, other proponents of the
LNT theory depend on information of delayed cancer deaths among
Hiroshima and Nagasaki bombing survivors that they may link to the
radiation [361]. LNT theory is/was supported by the Life Span Study
(LSS) of atomic bomb survivors [362]. Based on linear extrapolation
and statistics, the line was stretched from 1 to "zero" grey (100 to 0 rad)
without any statistical signi icance utilising the cancer data of atomic
bomb survivors who had an immediate exposure in the high dosage
range from 1 to 10 grey (100 to 1000 rad). The figure (on the previous
page) shows the LNT model's inapplicability to low-dose radiations
[113]. The Excess Relative Risk (ERR for solid tumours) among
Japanese atomic bomb survivors is depicted in the figure (on the
previous page). In the igure's highlighted area in the high bottom, it is
shown that the 95% con idence intervals contain just one dot. The
huge scatter of these data is disregarded by many academics who
believe in the LNT theory [8].
This linear extension exceeded the expected rate of fatal

malignancies in the low dose range, which was understood by the
community involved in radiation monitoring and protection. However,
they defended it as a cautious theory adequate for safeguarding the
wellbeing of radiation workers. The low-level range was preserved
and employed the linear model (where it is dif icult to test due to
statistical errors). The main foundation for radiophobia was this
LNT idea - any dose above zero has a proportionate link to cancer,
which made the common public scared of radiation. In spite of
thousands of data show that low-dose radiation have bene icial
health effects, cure of diseases and increase in life span.
80 Page
6.1. What does the LNT model ignore?

Low radiation doses have been shown to bene it health of living
beings [362], [363]. Radiation at large doses can be deadly; however it
is false to say that radiation at any dose is harmful. Once Paracelsus
(1493-1541), a physician and a botanist, famously said, “Poison is in
everything, and nothing is without poison. The dosage makes it
either a poison or a remedy”. This quote very well applies to radiation.
Permanent movement vs. wind strength'
Depending on the dose, a medicine dose may have either a good

or bad effect. The above figure depicts permanent movement of a
structure depending on wind speed. It is illogical to consider the
permanent deformation at every wind velocity. Any engineer and
scientist will laugh at this. When a wind velocity is above a threshold,
then only damage occurs. The human immune system is similar to that
of above example, for ionising radiation below a threshold, even though
there are temporary cell damage, they can be recovered with time.
Permanent damage occurs after a threshold.
In reality, as discussed earlier, a number of studies have shown

that low doses of radiation can boost immunity. Radiation hormesis
refers to the bene icial effects of nuclear radiation doses. The Greek
word "hormaein," which meaning "to excite," is the source of the
English word "hormesis."
The overarching fallacy embodied in the LNT model is that it

ignores the fact that the body responds to radiation differently at high
versus low acute doses and dose rates, as many studies have shown:
Page 81
high-dose exposures are associated with inhibition of protective

responses and extensive damage to the organism, whereas low-dose
exposures are associated with the body eliminating the damage
through a variety of protective mechanisms, evolved in humans over
millennia of living in a world bathed in radiation.
Sacks et al. [365] stated, “Bathed in this sea of radiation

throughout their evolution, species of life forms have
been forced to adapt or become extinct. Only those that
have adapted through the development of protective
responses against damaging radiation have survived
this natural selection, whether they are bacteria, fungi,
plants, or animals.”
Solid cancer excess relative risk (ERR) estimates for the Techa River
cohort plotted against stomach dose. [366]
Additionally, linearity is just a calculation-related simpli ication

in any system, but notably in biological ones. One can anticipate a non-
linear relationship between the dose and risk given the intricate
interactions involved in biological systems and their interaction with
various forms of radiation.
82 Page
For instance, a review of the solid cancer data from the Techa
River Cohort [366] reveals that the ERR estimates for the two low-
dosage categories are lower than the controls with zero dose. This
reaction its the hormetic dose-response model (as shown in Figure on
previous page). The authors did not address it, though, other
researchers afterwards brought it up [367].
6.2. Muller's deception and Russell's mistake

Muller won the Nobel Prize in 1946 for demonstrating that fruit
ly mutation rates rose in direct proportion to the X-ray exposure.
Muller disregarded and hid information that would have proved him
wrong in the process. Muller's ly studies were supported by the
Rockefeller Foundation, which also gave funds totalling $991,000 for
genetic research in 1956 [368].
Additionally, Muller was paranoid and thought that his ideas

were being stolen by other researchers [369]. The world came to
believe that if mutagenesis from ionising radiation is true for fruit lies,
then it is also true for cancer in humans, which made his actions
extremely signi icant. Muller's scienti ic dishonesty was recently
exposed by Edward Calabrese, who also explained how the NAS had
misled the world over cancer risk assessment. Muller claimed to have
demonstrated a linear increase in mutations in irradiated fruit lies
(Drosophila) with increasing dose of X-rays in published investigations
conducted during 1927 [233]. The sex-linked recessive lethal test in
male lies was the mutation assay that was employed. The radiation
doses used by him to cause mutation in fruit lies, were high. Muller
made false claims in an effort to support the acceptance of the LNT
assumption for risk assessment from ionising radiation in his
acceptance speech for the Noble Prize on December 12, 1946. Muller
also wanted to exaggerate the health risk from low-level radiation
because he was opposed to aboveground nuclear weapon testing
[233].
In 1956, the NAS and Biological Effects of Atomic Radiation

(BEAR) Committee members adopted the LNT assumption, departing
from their prior view of a threshold due to the in luence of Curt Stern, a
well-known geneticist at the time [359]. Results from Caspari and Stern
Page 83
(1948) [370] showed that fruit lies have a dose-rate response. These
indings revealed both a threshold and dosage rate impact, similar to
those of Spencer and Stern (1948) [371]. Muller claimed that the
mutation rate was a linear function of dose down to zero with no
threshold in his 1946 Nobel address while his test doses ranged from
1000 R to 4000 R and he did not conduct tests below 1000 R. However,
Curt Stern (1948–1949) found that at doses <50 R or about 500 mGy
there was no increase in the mutation rate when given continuously
over a 21-day period. In fact, the results were dose rate dependent
[370], [372]. It is interesting that Muller found no linearity in the
incidence of mutations in fruit lies after exposure to UV light [373].
Before giving his Noble lecture, Muller was aware that Caspari
and Stern's [370] and Uphoff and Stern's [372] research had
shown a threshold of roughly 50 R for fruit ly mutations that
seriously questioned the LNT. According to data from Caspari
and Stern [370] and Uphoff and Stern [372], when the dose was
administered continuously for 21 days, there was a threshold
for sex-linked fruit ly mutations that followed 50 R. For one
group of lies, the dose rate was 13,000 times lower than the
high acute doses used by Muller and 80 times lower than the
highest dose used by Muller. Muller, however, bragged that a
threshold was no longer even a possibility. Over the entire dose
range, Muller claimed linearity. Additionally, he asserted that
dose rate had no bearing on his indings. In order to safeguard
his award and reputation and further his ideological aim of
linearity, Muller had falsi ied data on fruit ly mutations [374].
In a 1930 study, Muller noted that natural (spontaneous)
mutation rates are not caused by background radiation
exposures. He neglected to mention that the natural
background levels varied by a factor of several hundred [374].
In fruit lies, doses below 10,000 R had no in luence on

lifespan or the expression of genes permanently, according to
more recent research [375]. Only 200 mGy of radiation was used to
irradiate fruit ly spermatozoa, dramatically lowering the
frequency of mutations below that seen in control lies treated to
sham radiation [376]. Ogura later showed that a treatment of only
500 μGy [377] could considerably lower the prevalence of sex-
linked recessive fatal mutations in fruit lies. The threshold for
84 Page
fruit ly mutations was found to be 80 mGy by Shiomi [144], 800

mGy by Koana, [376] and >1000 mGy by Ogura [377]. Thus,
Calabrese thought that the NAS Genetics Panel's discussions
should be investigated for possible scienti ic misconduct and
intentional misrepresenting of the scienti ic literature in order to
advance their personal agenda [360], which led to consistently
false conclusions as a result [378].
In the 1920s, numerous experiments on irradiated insect

populations had revealed positive outcomes. Following radiation
exposures of 1–40 kR, lour beetles, mosquitoes, crickets, codling
moths, tsetse lies, house lies, and fruit lies all showed a 20–60%
increase in lifespan. When insects were exposed during the egg and
larval stages, their longevity was improved at much lower dosages,
usually between 10 and 100 R. More recent research on fruit lies has
revealed that, whether administered as an acute or chronic dose, X-
rays and γ-ray doses to eggs as low as 200 mGy dramatically boosted
adult ly longevity (as shown in igure below) .
Evidence for radiation hormesis in X-irradiated fruit flies[376]
Page 85
In 1996, the Department of Energy investigated allegations

about the now- accepted fact that the Oak Ridge National Laboratory
(ORNL) mega-mouse studies presented false data on genetic effects,
starting in 1951. The Genetics Panel and Biological Effects of Ionizing
Radiation (BEIR I) Committee of the 1972 NAS used Russell's mega-
mouse dose rate data to justify the adoption of the LNT for the
assessment of cancer and genetic risk [378].
Mutation frequency as a function of radiation dose
In an effort to stop Russell's dose rate approach from being

incorporated into risk assessment, Muller gave false information to the
ICRP (1964) [359], [379]. Russell, later acknowledged making a
mistake when counting the control mutation rate [380]. There was no
admission of fraud, but Russell did participate in a paper that quietly
revealed the error. Rod Adams, S.A.R.I. Selby discovered that lower-
dose rates reduced mutation rates by factors of 3 and 20 in germ cells of
male and female mice, respectively. As a result, genetic damage became
signi icantly dose rate dependent, contrary to earlier indings that
suggested it was only dose dependent. Based on Selby's indings
86 Page
[381], [382], a J-curve-hormesis model would have been a better it for

Russell's data. Selby's adjustment factor for underreporting of
mutations in Russell's control mice was validated by the overwhelming
body of scienti ic evidence. The data misrepresentations, according to
Selby, appeared to have been done on purpose [383]. Mice which were
given γ-rays for 90 days (0.0014 Gy/h) did not show an increase in
mutation frequency [384]. Doug Boreham also conducted a mutation
research on mice that received a total of 12 cGy over the course of 75
weeks, but he was unable to detect a rise in mutations [385].
International programmes are currently evaluating the possible
impacts of radiation for genetic illnesses using solely human data,
abandoning the fruit ly and mouse data (as shown in igure on
previous page).
Around the average mutation frequency, error bars are two

standard deviations wide (as shown in igure on previous page). Data
from Ogura [377] at 10 and 1 Gy and at 5 and 10 Gy, respectively, were
combined to create the data points at 0.3 Gy and at 7 Gy. In areas with
radiation doses below 1 Gy, mean mutation frequencies are noted to be
below the spontaneous (background) level (0.32 %) [135].
Japanese A-bomb survivors have been the subject of genetic

research for four decades, although no heritable effects on progeny
have been found [386]. Also residents who lived downwind of a 1957
Mayak nuclear waste tank experienced a reduction in cancer risk of
27–39%, and also those who lived close to a heavily contaminated river
along the Techa River did not see an increase in risk [366], [387].
Residents living close to the Techa River, those living in the vicinity of
the Kyshtym waste tank disaster, or the children of Mayak nuclear
employees have not shown any genetic impacts. Millions of individuals
who live in Ukraine and Belarus and were exposed to Chernobyl fallout
have not been reported to have more mutations or birth problems
[387]. Despite the dearth of human data, UNSCEAR recommended a
doubling dosage of 3.4–4.5 Gy for impacts on human genetics in 2001.
The doubling dose was even reduced by BEIR VII to 1.0 Gy despite the
absence of any human con irmation data. There was a tonne of
evidence of thresholds and radiation hormesis in the early
epidemiological studies of populations exposed to Chernobyl fallout,
Page 87
cleanup personnel, Mayak nuclear employees, downwinders of the

USSR nuclear tank accident in 1957, and Techa River residents [387].
The LNT was forced- itted in following studies using the ERR
methodology, and these researches frequently omitted to include
cancer risk estimates for each radiation dosage category in the
publications. Track the cash! Grants for ongoing research were only
awarded to individuals who could demonstrate increased risk and
those who demonstrated a threshold or hormesis were not eligible for
the grant.
6.3. So, the debate Hormesis vs Harm – Limitations of LNT

theory
The term "radiation hormesis" refers to the theory that ionising
radiation, when administered in amounts just above background
levels, may have positive effects by triggering the activation of defence
mechanisms against disease [95], [99], [321]. Ionising radiation-
induced harmful results in the activation of a number of compensatory
and reparatory mechanisms. These include enhancing antioxidant
defences, triggering apoptosis (which eliminates damaged cells that
can develop tumours), triggering enzymatic DNA repair systems, and
triggering the immune system to assist in identifying mutant cells at
risk of developing cancer [388]. In addition to mitigating the damaging
consequences of the modest dose of ionising radiation that activated
them, these repair mechanisms may also help to prevent disease owing
to exposure to additional risk factors [388]. There are numerous
instances of hormesis in nature; however, the most striking one might
be ischaemic pre-conditioning, in which exposure to brief periods of
sub-lethal ischaemia mitigates the harm caused by longer periods of
ischaemia. For instance, patients who report having angina in the 24
hours prior to an infarction have a signi icantly better prognosis than
those who do not [389]. A short-term, subtoxic generation of reactive
oxygen species—possibly similar to that brought on by low-dose
radiation—has an interesting pivotal role in the mechanisms initiating
ischemic pre-conditioning, according to the current animal and human
research [390]. This brief increase in oxidative stress would set off
defence mechanisms, such as the up regulation of antioxidant reserves,
guarding against a longer period of ischaemia. The mechanisms
triggering radiation exposure have been far less well studied than
88 Page
those triggering ischemic preconditioning, yet the similarities between

these two phenomena seem intriguing and stimulating. A more
dif icult question that cannot be answered with the evidence at hand is
whether the observations made by Russo et al. [391] re lect a
protective "pre-conditioning-like" phenomena as opposed to a
pathologically elevated cellular "fragility". The patho-physiology of
these events is incredibly complex [392], [393], and hormesis/pre-
conditioning and damage may be two sides of the same coin. Reactive
oxygen species are known to play a signi icant role in cardiovascular
disease. Whatever the response, we still need to strive to keep
occupational radiation doses at levels that are "as low as
reasonably achievable" and these considerations do not reduce our
obligation towards patients, our co-workers, and ourselves.
6.4. Adaptive responses or hormesis acquired through

evolutionary history
Typical examples of adaptive responses or hormesis if LNT is
used as a guide, even low radiation doses are considered dangerous.
Therefore, any proof of a positive outcome is suf icient to refute LNT. As
of February 28, 2016, a PubMed search produced 1336 hits for
hormesis and 33,134 inds for adaptive response[395]. A few typical
examples from the vast body of data on adaptive responses or hormesis
can be discussed here. Hormesis, or adaptive reactions, are present in
all biological things. A protozoan called Tetrahymena pyriformis
exhibits development retardation when exposed to lower radiation
levels, but growth enhancement when exposed to higher radiation
levels [394] (as shown in igure I, on next page). This is similar to the
previous discovery that at radiation levels 400 times lower at deep
underground from earth’s surface, bacteria could not thrive and
suppressed bacterial development [395]; and similar observations is
found with X-ray [396] and γ-ray [377] induced mutations with
hormesis and thresholds in D. melanogaster (as shown in igure II, on
next page). The dose-response relationship was J-shaped rather than
linear, demonstrating a hormetic effect brought on by 1 Gy or less.
These results are in direct opposition to Muller's indings and LNT.
Lifelong γ -ray irradiation at 1–10 mGy/day (365–3650 Gy/y),
200–2000 times higher than the natural radiation dosage, increased
the lifespan of mice [397] (as shown in igure III, on next page). The
Page 89
Examples of Adaptive response or Hormesis
90 Page
igure IV A, on previous page, shows that the cancer death rate in

villages northwest of Hiroshima was greater than that of "in-the-city
control" from 3 to 10 km from epicentre and that hormetic effects are
evident in solid cancer induction in atomic bomb survivors [398] (as
shown in igure IV B, on previous page). Cuttler [399] derived the
leukaemia incidence among Hiroshima Atomic Bomb survivors from
the original table [402] (as shown in igure V, on previous page). The
leukaemia incidence does not meet the LNT hypothesis (Line A). The
incidence is obviously lower (Line B) than the control at 0.02 Sv (D).
The data indicated hormesis by itting a J-shaped dose-response (Line
C). UNSCEAR [400] rejected this conclusion, claiming the dosimetry
data were inconclusive. The LNT model is incompatible with lung
cancer death rates as compared to average radon concentrations (as
shown in igure VI, on previous page) [401]. These examples of
hormetic effects clearly contradict LNT.
6.5. Biological basis of hormesis as a homeostatic defence

mechanism
According to a previous NHK TV investigation, rats found in the
Chernobyl Exclusion Zone didn't exhibit DNA damage or elevated DNA
repair mechanisms, but instead had higher levels of radical scavengers.
The level of glutathione, a radical scavenger, was shown to be raised in
birds of 16 different species that were collected in that area [402]. The
authors contend that the outcome exhibits a feature of hormetic
effects. Reactive Oxygen Species (ROS) and radicals, two of radiation's
main by-products, can be eliminated by animals and birds before they
can cause DNA damage.
Since the earth's formation 4.6 x 109 years ago, the primary
radio-nuclides related with ission, such as 238U, 232Th, 235U, and 40K, have
been present. Radiation exposure has aided the 3.8 billion years of
evolution of living things. Over the course of earth's evolution,
background radiation exposure is thought to have decreased roughly
from 7.0 to 1.35 mGy/y [403]. Living things would not exist if they were
unable to develop radiation defence mechanisms.
Water makes up 70 to 80 % of our body weight. Ionisation of

water to produce Reactive Oxygen Species (ROS) and/or radicals such
Page 91
OH, H2O2, and O2-, which are primary drivers of DNA damage, is the main
consequence of low-linear energy transfer radiation (LET).
Antioxidants and radical scavengers are hence the irst line of defence.
Before DNA damage occurs, animals and birds in the Chernobyl
Exclusion Zone make the most of antioxidants and radical scavengers.
By controlling the expression of a battery of more than 100
cytoprotective genes linked to glutathione metabolism, antioxidant
enzymes, drug detoxifying enzymes, and other processes, Nrf2 plays a
critical role in the oxidative stress response in mammalian cells.
Because ionising radiation activates Nrf2 and it can reduce the effects
of radiation and other oxidative stressors by restoring redox
equilibrium. The Keap1-Nrf2 stress response pathway is how Nrf2
works [404].
What is the perimeter of redox homeostasis defence? Daily

respiration results in 109 ROS/cell and 0.1 double strand breaks (DSB)
per cell, compared to that at 1 mSv which cause 0.0001 DSB per cell
[117]. The DSB ratio of 0.1: 0.0001 (1000:1) shows that 1 mSv occupies
only less than 1% of the defensibility, assuming that ROS produced by
daily respiration is within the range of defence capacity and that DSB
incidence represents the ratio of defensibility. In other words, 1 Sv is
defensible. According to LSS statistics, 0.4 to 0.6 Sv can be considered to
be hormetic. When radiation doses were underestimated by half, the
doses were actually 0.8–1.2 Sv. 1Sv is a threshold [as shown in igure II,
on page 90, (Section 6.4)]. 365-3650 Gy (Sv)/y doses increased the
lifespan of mice [as shown in igure III, on page 90 (Section 6.4)]. The
threshold for leukaemia induction by an atomic explosion is around 1
Sv [as shown in igure V, on page 90 (Section 6.4)].
Formation of reactive oxygen species (ROS) and their

elimination by enzymatic reactions.
DNA is harmed by radiation both directly and indirectly. The

majority of LETs, including background radiation and those from the
92 Page
Fukushima region, have an indirect effect on our bodies by ionising the

water there and creating ROS, which are easily squelched by redox
homeostasis systems. The majority of DNA damage caused by leaky
ROS is repaired. People who have weak repair systems are more likely
to develop cancer. DNA damaged cells stop cell division and wait for the
completion of repair. When cells fail to repair the damage, they die off
by apoptosis. The immune systems are ready to get rid of any tough
cells that manage to get past these defences and develop into cancer
cells. People who have immune system laws are more likely to develop
cancer. Adaptive response or hormesis must be based on these
numerous protective mechanisms. The neglect of these biological
mechanisms, which have evolved over 3.8 billion years, is what proves
the inapplicability of LNT.
6.6. Theory to explain thresholds by homeostatic defence

mechanisms
Because LNT assumes an excess risk of cancers from even the
smallest amount of radiation exposure, dose responses follow only a
rising straight line from bottom left to top right (Figure below, dashed
line) and never occur below the bottom line. Thus, the responses below
the bottom-line show that LNT is ineffective. The formation of ROS and
radicals, which are well-protected by effective defence systems, is the
main effect of low- to mild-dose radiation. The fundamental nature of
living organisms is incessant response to stimuli, one of which is
radiation that induces adaptive response or hormesis. Dynamic
reactions bring to mind Paracelsus' adage, "The dose makes it a remedy
or a poison,". Lower radiation doses are really advantageous; higher
amounts are dangerous [405].
Schematic illustration of the relation between LNT, thresholds, and

hormesis at chronic irradiation.
Page 93
94 Page
Dose limits by UNSCEAR
7
In order to determine the health impacts of low radiation doses,
UNSCEAR has created a variety of quantitative estimations that take
into consideration the available radiobiological and radio-
epidemiological data. The quantitative estimations from UNSCEAR are
summarised as follows:
¨ Epidemiological Estimates:
A) Lifetime mortality:
• 1.1% after exposure of 1000 mSv for leukaemia and
10.9 % for solid tumours (12% in total). For reference,
in UNSCEAR's 1988 report, the corresponding data was
1.0% for leukaemia and 9.7 % for solid tumours.
• Linear between 4000 mSv and 200 mSv (little evidence
at lower dose).
¨ Radiobiological Estimates:
• For low (chronic) radiation doses of around 1 mSv per year:
• Probability of an excess malignancy: 10-4 per year
• Lifetime probability: 0.5%
• Proportion of fatal concerns in the population that may be
attributed to radiation: approximately 1 in 40
¨ The above estimates are based on the following assumptions
and inferences:
• Cells in the human body: 10¹⁴ cells per individual
• Target stem cells: 10¹⁰ to 10¹¹ cells per individual
• Initiating event: single gene mutations in one of around
ten possible genes
• Induced mutation rate (per cell): 10-5 per 1000 mSv
• Excess probability of malignancy: approximately 10 %
• Interactions per cell: 1000 per 1000 mSv
Page 95
¨ Inferences:
• Excess malignancy: 1 per 10¹¹ to 10¹² target cells receiving
1000 mSv
• Rate of target gene deactivation: 10-4 per cell per mSv
• Probability that a single track will give rise to an excess
malignancy: 10-14 to 10-15
• Risk Estimates
¨ Risk of Malignancies:
• Lifetime probability of radiation induced fatal cancers:
• 5% per 1000 mSv in a nominal population of all ages
• 4% per 1000 mSv in a working population
¨ Risk of hereditary effects:
• (via doubling dose method)
• Probability of hereditary radiation effects for all
generations:1.2 % per 1000 mSv (or 1.2% per generation
for a continued exposure of 1000 mSv per generation)
• Probability of hereditary effects in the irst two
generations: 0.3% per 1000 mSv
• (via the direct method)
• Probability of hereditary effects (clinically important
disorders) in the irst generation: 0.2% and 4% per 1000
mSv
¨ Risk of effects on embryo:
• (for those exposed in uterus in the period between 8 and 15
weeks after conception)
• Downward shift of IQ distribution: 30 IQ points for 1000
mSv
• Dose required to shift from normal IQ to severely mentally
retarded: 1000 mSv or more
• Dose required to shift from low IQ to severely mentally
retarded: a few hundred mSv
96 Page
DOSE LIMITS BY UNSCEAR
The International Commission on Radiological Protection

(ICRP) has advised the use of total nominal risks from stochastic effects
of radiation for the following radiation protection reasons, taking into
account the estimates from UNSCEAR and adding an estimated harm
from non-fatal malignancies to them:
0.0073% per mSv for the whole population; and

0.0056% per mSv for all adult workers.
These have been the nominal risk factors used in developing the
new International Basic Safety Standards for Protection against
Ionising Radiation and for the Safety of Radiation Sources. As a result, it
is believed that radiation is a carcinogen and has a potential to cause
hereditary diseases, even at the smallest of the dose [406] .
Page 97
98 Page
The solid evidence of
LNT inapplicability
8
Misleading scienti ic research contribution to fear of
radiation and collateral damage
The linear no-threshold (LNT) model for radiation-induced
malignancies is still commonly employed despite the fact that a
signi icant quantity of published evidence contradicts it [363], [407],
[408].
For instance, several important reports, like the BEIR VII study
[299], used the data from those who survived the atomic explosion to
support the LNT concept. In fact, the authors of the most recent update
[361] to the atomic bomb survivor data assert that zero dose is the best
estimate for a dose threshold for solid cancer mortality, implying that
the LNT model is correct. However, other researchers have identi ied
weaknesses in their approach, with the primary criticism being the
limitation of potential functional forms of dose-response connection a
priori [409]. Additionally, some researchers noticed that they had
omitted the negative risk values (radiation hormesis) despite the fact
that eight of the ten lowest data points had con idence intervals with
negative values after evaluating their threshold analysis. Researchers
discovered the potential of a non zero threshold, when they included
those numbers [410]. The occurrence of a threshold dosage that varied
by organ, gender, and other characteristics was also discovered in a
recent arti icial neural network investigation of data from survivors of
the atomic bomb [411].
The 15-country study on radiation workers, which is cited in the

BEIR VII report, is yet another crucial piece of research [412]. A
reanalysis of the cancer mortality data of Canadian nuclear workers
contradicted the irst inding of the entire 15 nation radiation worker
research about cancer hazards from modest exposures of radiation
[413], [414]. Additionally, a Bayesian analysis of the data from the 15
country studies showed that there is insuf icient consistency in the
data to draw a irm conclusion about the cancer risk from low doses of
Page 99
radiation and that it is unjusti ied to discount the decline in overall

cancer rates among radiation workers [415].
Consequently, the BEIR VII report shouldn't be taken seriously. A

signi icant quantity of research supporting other (non-LNT) models
and radiation hormesis, has also been published after the BEIR VII
report [362], [416]. Unfortunately, the understandings gained from
these recent indings have been obscured by the continuous promotion
of the LNT concept of radiation-induced cancer risk.
This lack of knowledge related to the non-applicability of LNT

theory has far-reaching societal consequences, especially in terms of
radiation protection policies and public perceptions of radiation
danger.
Consider how poorly the Fukushima Daiichi accident was

handled to see the monumental failure of regulators and policymakers.
As Wade Allison suggested, possibly, As High As Relatively Safe
(AHARS) rather than As Low As Reasonably Achievable (ALARA),
should be used to regulate radiation safety. It is the responsibility of
groups like the ICRP to establish precise boundaries based on scienti ic
data rather than on false information. An appropriate scienti ic
investigation into the research works would reveal the bias in major
scienti ic reports as discussed and provide proper guidance to design
appropriate policies.
8.1. A scienti ic scandal of the last two centuries

Despite the vast body of published scienti ic literature that has
amply demonstrated thresholds and the positive effects of low dose
ionising radiation, every regulatory agency in the world, with the
exception of France, bases its regulations on the LNT. The LNT only
provides a mathematical treatment based on the assumption that low-
dose ionising radiation has proportionate health effects due to cancer..
Thus the theory is responsible for the loss of enormous amounts of
resources in terms of money and the quality and quantity of lives. It
does not address the Low-Dose Radiation (LDR) hormesis.
100 Page
THE SOLID EVIDENCE OF LNT INAPPLICABILITY
Phobia is a word that the Merriam-Webster dictionary

describes as an extreme, unjusti ied fear. Anxiety and
avoidance are the results of being afraid [417]. The LNT has
broad implications for nuclear and diagnostic medicine,
radiography, nuclear power, "dirty" weapons, nuclear waste
management, food irradiation, and home radon. The societal
cost of radiophobia and fear mongering is exorbitant, and
those that continue to promote it stand the most to gain. The
cost of implementation causes increase in electricity price from
nuclear (which becomes a burden on public) and prevents the
bene icial effects of radiation which could otherwise improve
the health and life span of human beings; it may be noted that
such implementation and carrying out radiation regulations
does not improve plant safety or personal health; it actually
costs tens of thousands of lives annually in the USA alone as
reported in reference [417].
Nuclear radiation is widely feared, however studies on the

biological consequences of radiation show that the level of panic is
much higher than the real risk. Although the dread of nuclear weapons
is at the basis of this "radiophobia," mishaps at nuclear power plants
have greatly reinforced and exacerbated it. More damage is done to
human health by radiophobia than by radiation from nuclear
accidents. In some cases, the harm results from disaster response. The
in luence of radiophobia on society's energy choices poses great
additional dangers [418].
In 1934, scientists studying radiation safety were aware of the

safe and hazardous radiation levels. In 1956, the US National Academy
of Sciences (NAS), based on large part on Muller's work on fruit ly
mutations, approved the LNT assumption from an assessment of
genomic risks related to ionising radiation. The LNT assumption was
extended to somatic cells and cancer risk assessment by the National
Council on Radiation Protection and Measurements (NCRP) in 1958
[419]. The LNT is not based on biological theories or mechanistic
biological research; rather, it is pragmatic, although thresholds and
hormesis, are con irmed by the majority of low-dose mechanistic
investigations at low radiation doses [387].
Page 101
During the Cold War era of extensive nuclear weapons testing, it

was the top physicists of the day who invented nuclear weapons and
created an exaggerated dread of small amounts irradiating healthy
tissues. Dr. Morgan (1907–1999) was a pioneer in radiation
protection. Morgan believed in a radiation dose threshold during
World War II, but afterwards changed his mind and irmly believed in
the LNT. He sided with anti-nuclear campaigners who made false
claims about the dangers of radiation, disregarded the evident
thresholds in radium dial painters and Japanese A-bomb survivors, and
instead supported LNT [420]. Morgan could not give any good evidence
for the LNT because it was theoretically impossible to do so [420].
The most insidious opponents are from the radiation safety

guidelines based on As Low As Reasonably Achievable (ALARA)
principle. Political opposition to nuclear energy facilities and all other
nuclear-related issues resulted from this [421]. Despite a vast amount
of published literature to the contrary, there are signi icant political
and vested interests that oppose radiation hormesis today [422]. Not
all government of icials supported the LNT, George Kistiakowsky, a
former nuclear scientist who participated in the Manhattan Project
and served as President Eisenhower's science advisor, thought that the
usage of the LNT was completely arbitrary [422]. A Scientist at the
White House, published in 1976, quotes Kistiakowsky's 1960 journal
entry on learning about the LNT from the Federal Radiation Council: “…
a linear relation between dose and effect … I still believe is entirely
unnecessary for the de inition of the current radiation guidelines, since
they are pulled out of thin air without any knowledge on which to base
them” [422].
The ICRP's Abel Gonzalez made an effort to adopt a moderate

political stance on the LNT. Gonzalez claims that the LNT approach
produces phantom, hypothetical, unveri ied and undetected igures.
But he believes that the LNT approach is sensible for radiation
protection [423].
102 Page
THE SOLID EVIDENCE OF LNT INAPPLICABILITY
Gonzalez states that:

“While prudent for radiological protection, the LNT model is
not universally accepted as biological truth, and its in luence
and inappropriate use, to attribute health effects to low-dose
exposure situations is often ignored. Speculative, unproven,
undetectable, and “phantom” numbers are obtained by
multiplying the nominal risk coef icients by an estimate of the
collective dose received by a huge number of individuals,
theoretically incurring very tiny doses that are hypothesized
from radioactive substances released into the environment”
[423].
NCRP-136 wrote:
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 decrease. However today, neither ICRP nor NCRP
promulgates radiation dose regulations that take into account
the bene its of low-dose radiation but continues to remain
“prudent.” [423]
8.2. LNT is not based on solid data

Muller's tenacity to maintain LNT
The discovery by Muller that X-rays caused sex-linked recessive
mortality in Drosophila melanogaster in 1927 is the origin of LNT
[424]. This "data-poor/discussion-rich" paper probably avoided the
standard peer review process deftly [370]. He then presented
pertinent information. Without experimental data, apparent linearity
at extremely high doses was extrapolated by Muller to lower doses.
Muller proposed the proportionality rule, which is LNT. World War II
(WWII) then started in 1939. Under the auspices of its Manhattan
Project, the United States of America (USA) started making the A-
bomb. Radiation effects on living organisms were investigated
intensively. In Drosophila melanogaster fruit lies testing for recessive
lethality, Muller discovered a threshold for positive excess risk [425]. In
1945, the US attacked Hiroshima and Nagasaki with atomic bombs. In
1946, Muller won the Nobel Prize in physics for his study of radiation.
Although he knew of thresholds to damage from radiation, he declared
in his Nobel Prize lecture that there was “no escape from the conclusion
that there is no threshold dose” [426].
Page 103
8.3. The enforcement of LNT for radiation dose limits

Oil industries felt uneasy about nuclear energy and took over
the National Academy of Sciences
The discovery of atomic energy showed great promises of
signi icantly large energy supply through ission process. The fossil
industries, including oil, might have felt competition in the energy
market. The Rockefeller Foundation (RF), founded in 1913, decided to
fund a sizable project to assess ionising radiation in 1954. The
programme was organised by RF at the request of the American National
Academy of Sciences (NAS), which was overseen by NAS President Bronk
of Rockefeller University, who is also a trustee of RF[113].
On June 12, 1956, Genetics Panel (GP) recommended LNT

without any serious discussion [113], [425], [427]. The 500 mGy/y
upper limit dosage for nuclear workers, in effect since 1934, was
abolished. The next day, the front page of the New York Times reported
that radiation is dangerous. Other media did the same. Soon, a number
of eminent biologists requested supporting material for LNT from GP.
However, GP declined to do so [113], [428].
In conclusion, the LNT has been enforced for deciding the dose
limits. In view of the above, ICRP dose limits need to be re-evaluated in
order to remove the public concerns and fear of radiation.
104 Page
Impact of Dose vs
Dose rate of radiation
9
Health consequences from radiation exposure are mostly
dependent on the intensity of the radiation (dose/unit area/unit time).
When the same dose is administered over a long period of time
(fractionated dose) or quickly (acute dose), the effects are different.
This means that, even though the integrated dose is the same, the
behaviour of human tissues to the dose rate varies; a greater dose rate
for a brief period might have a signi icant in luence on the tissue as
opposed to a low dose rate over a longer period.
Schematic representation of molecular and cellular mechanisms

operating at low- and high-dose radiation exposures. B, Time schedule
of pathways involved in radiation-induced adaptive response. HSR
indicates heat shock response.
Page 105
However, usually always, we are referring about dose rather than

dose rate, which have a greater impact on the health of tissues exposed
to radiation. Given the foregoing, it is necessary to assess the dose
requirements in light of the importance of the intensity of dose as a
factor in radiation protection [429], [430].
The LNT model, which was previously described, makes the
implicit assumption that an organism's capacity to repair ionising
radiation-induced damage (including genomic integrity and cellular
viability) is largely dependent on radiation dose and that mostly repair
is impossible. As already mentioned, the LNT concept is the subject of
active debate. This debate was triggered during the past decades
following the accumulation of biological indings that contradict the
aforementioned hypothesis, showing that damage repair ability
actually does depend not only on the radiation dose but also on the
dose rate. For instance, as was mentioned in Section 6.2, Caspari and
Stern's (1948) [370] research indings showed that the mutation rate
in fruit lies is dose rate dependent. These observations, together with
Spencer and Stern's (1948) [371] indings, showed that the mutation
rate of fruit lies was affected by both a threshold and dose rate effect.
For fruit lies, Muller had used an acute dosage of 1000 to 4000 R to get
results more quickly. The results were later shown to be dose rate
dependent by Curt Stern (1948-1949), who discovered doses <50 R or
roughly 500 mGy did not affect the mutation rate when delivered
continuously over a 21-day period [370], [372]. In fact, the dose rate for
one batch of lies was 13,000 time less than the high acute doses
employed by Muller and 80 times less than his highest dose.
The LNT model, which assumes that carcinogenic hazards are

proportional to radiation exposure for all radiation doses without
taking dose rates into account, is the basis of today's radiation safety
laws. Growing evidence suggests that the current, excessively strict
radiation protection regulations are not the most effective means of
safeguarding the general public's health. Therefore, there are already
enough factors for policymakers to think about.
106 Page
IMPACT OF DOSE V/S DOSE RATE OF RADIATION
Although a lot of information has been gained regarding the

biological effects of low-dose radiation, there are many important
issues that require further research by scientists. Certainly, caution
should be exercised when changing the current practices. However,
bearing in mind the social, economic, and ethical aspects of the current
LNT-based regulations, and taking into account their extremely high
cost (both economic and human cost) for society, there is little doubt
that the ionised radiation–related regulation should be reconsidered.
The exposure limits should be raised and the regulatory burden be
lightened [431].
It is necessary to re-evaluate the extrapolation of biological

effects, seen at high doses and high dose rates to the low doses and low
dose rates of ionising radiation, common in radiological protection
situations. Since Rontgen's discovery of X-rays in 1895, the scienti ic
data on this topic has been continuously examined. In particular, since
1958, UNSCEAR has released a number of publications that ICRP has
utilised in their attempts to safeguard personnel, patients, and the
general public from the harmful effects of ionising radiation, while
unreasonably restricting its bene icial applications [432].
Page 107
108 Page
Closure
10
In this book, we have endeavoured to bring out the historical
evidences of health effects of ionising radiation through a large
literature review without any personal bias. Since the discovery of X-
ray, efforts have been made to study the use of radiation in various
applications including medicine. Major breakthrough in the ield of
radioactivity and radiation occurred with Enrico Fermi demonstrating
existence of radioactive elements produced by neutron irradiation,
which further led to discovery of ission. With the irst self-sustaining
nuclear ission chain reaction demonstrated at Chicago Pile-1 in 1942,
the immediate application was the development of atomic bomb and
nuclear power reactors. The USA tested the two atom bombs at the two
Japanese cities in 1945, which led to large scale devastation and shock
not only to the Japanese people but also to the entire world.
Following the horrendous nuclear bombings at the two cities,

nuclear radiation phobia developed in common people without
understanding what was the cause of “death”, what was the extent of
“radiation release”, effects of “radiation on health”, etc. The prime
reason is that “there was no radiation measuring devices at the time of
bomb explosions”. Many scientists in USA and Japan worked almost 60
years to create dosimetry systems for estimating doses. Only
simulation tests and computations could reveal the doses which
Japanese people might have encountered some hypothetical or derived
relation for risk due to atomic radiation in form of death and cancer.
The doses received ranged from lethal (for those living nearer to the
epicentre) to in initesimal for those living away or shielded by
buildings or terrains in Hiroshima and Nagasaki cities. Further
investigation into the impact of the atomic bombs on Japan showed
that the energy of A-bombs is made up of roughly 35% thermal energy
(heat and light), 50% blast energy (pressure shock waves), and only
15% radioactive radiation (5 % prompt and 10 % residual, which
consists of minor induced radioactivity and major fallout). The
majority of the immediate deaths, were therefore, could have been
Page 109
caused by heat and blast energy, which the general population, even
today, is least aware of and think that the deaths were only due to
radiation. The threat of cancer has persisted in the public
consciousness even today. Data from the Life Span Study (LSS) of
survivors of the Japanese atomic bomb reveal a threshold dosage range
of 100 to 200 mSv below which no detectable risk of cancer has been
observed. In reality, compared to normal Japanese population,
"average life span" was enhanced and "average death rate" was
decreased for such low-dose radiation for those people who were
exposed. Furthermore, even 62 years later, offspring of those who were
exposed to the atomic bombs dropped on Hiroshima and Nagasaki
show no signs of having negative health impacts. In addition,
thousands of military and servicemen who participated in nuclear
weapon tests in the UK, Australia, USA, and USSR have been the subject
of numerous research on the health implications of low dosage
radiation exposure. No signi icant effects were reported on the
mortality or subsequent risk of cancer and other fatal diseases of these
personnel.
Apart from atomic weapons, the nuclear energy was used for
commercial electricity production in atomic power reactors. Many
countries including USA, Canada, USSR, UK, France, Germany, Japan,
South Korea and other European countries constructed several atomic
power reactors during 1970 to 1980, which is termed as golden era of
n-power until the irst nuclear accident at TMI-2 occurred in 1979. The
accident led to signi icant melting of uranium fuel and release of
radioactive gases. However, due to robust construction of nuclear
reactors with several layers of safety protection against radioactivity
release, only 0.01% of ission products escaped to environment (only
10 Ci was released in 16 hrs. and ~ 70 Ci of Iodine was released in next
30 days). Out of fear of radioactivity, Governor of Pennsylvania ordered
evacuation of people. Several studies con irmed that no signi icant rise
in rate of cancer in and around the area was observed since the accident
occurred. The other nuclear accident, more severe than the TMI-2, was
the Chernobyl reactor core melt down and damage of structural
materials and release of large amount of radioactive gases to the
environment. In fact, the Chernobyl accident was much more severe
than the Japanese atomic bombings. Subsequent to the accident, the
110 Page
CLOSURE
then Soviet administration over-reacted, forcibly evacuating large

number of people without warning, and causing panic and social
dislocation. This caused more deaths than due to the accident. Dose
received by people in Chernobyl region showed that liquidators
received a maximum dose of 100 mSv. There is no evidence of them
having cancer. Abundant wildlife populations in the Chernobyl
Exclusion Zone have made it a magni icent nature preserve. The recent
accident at Fukushima nuclear power plants also caused large panic in
Government and public. Even at a release dose of meagre 1 mSv, public
evacuation was ordered causing more stress and deaths of these
people as compared to civilians who lived there. The hazard of the
evacuation outweighed any potential risk of radiation exposure,
especially for the elderly. Instead of protecting human health, the
evacuation actually created more risk in form of death than radiation
could make. The mortality risk of nursing home residents who left after
the Fukushima accident was 2.7 times higher than it was for those who
stayed back, proving that the stress of leaving is signi icantly more
dangerous than radiation. Similarly in Chernobyl accident, several
hundred women in Greece went for abortion due to fear of radiation.
In general, the public is exposed to very low levels of radiation, (a

few mSv) with the exception of a small number of individuals who were
speci ically exposed to high levels of radiation during atomic bomb
explosions, as shown by data from survivors of atomic bombs.
Similarly, the accidents in civil nuclear power reactors showed that the
public received very low levels of radiation due to multiple layers of
protection in atomic power reactors. Therefore, we focused more on
evidences trials and the consequences of low-dose radiation on human
health. In this regard, we took evidences of low-dose radiation
occurrences in roughly 10,000 residents living in homes made of
recycled steel contaminated with Co-60 in Taipei city, capital of
Taiwan. The study revealed that the exposed residents experienced
comparatively less cancer deaths than the general Taiwanese
population. Similar case studies were reported from Karunagapally-
Kerala, Goiania-Brazil and many more. In fact, several hundreds of
manuscripts are available in open literature (even though we have
referred to around 400 manuscripts here) supporting the positive
Page 111
health bene its of low-dose radiation or radiation hormesis for cure of

several in lammation diseases including infectious ones such as gas
gangrene, pneumonia, bronchitis, tuberculosis, diphtheria, dermatitis,
HIV/AIDS, etc. and non-infectious ones such as cancer, Alzheimer's
disease, vascular disease, heart disease, Type 2 diabetes, painful
degenerative disorders such as spondylitis, arthritis, asthma,
ibromyalgia, multiple sclerosis, psoriasis, ulcers, etc. Besides, there
are strong evidences that low dose radiation increases life span of
exposed individuals.
A large number of studies were conducted by Chinese

researchers supporting the above results, particularly the effects of
low-dose radiation on tumour cell growth, diabetes, stochastic effects,
etc. The health effects of low-dose radiation in cohorts of physicians
and technical personnel working in their related ield show that the
overall mortality rate and cancer mortality rates have been
substantially reduced of these personnel as compared to those who
were not exposed.
Having said so much for the bene icial effects of radiation on

human health, cure of life threatening diseases, enhancement of life
span, there is a big question “Why do people fear radiation?”
The answer is: When people think about nuclear, they don't think
about electricity, medicine, or food self-life enhancement, or cure of
diseases including cancer, increase in life span due to direct or indirect
applications of radiation - they think about nuclear warheads,
Hiroshima and Nagasaki, Chernobyl, Fukushima, and inally, cancer. It
may be emphasised that “The public paradigm that “nuclear radiation
is a carcinogen” is a more political, scienti ic misinterpretation and
“cherry-picking” than actual science”. In particular, governments used
fear of radiation as an effective weapon during the Cold War. Ultimately,
it resulted in collateral damage to public morale about radiation.
Regulatory bodies promoted the concept of Linear No Threshold
theory (LNT), which meant no matter how small the radiation dose is, it
has the potential to induce cancer. The history of LNT goes to discovery
of X-ray-induced mutations by the German Scientist, Muller, which
suggest that cosmic/terrestrial radiation-induced mutations provide
the principal mechanism of the driving force for evolution. For this
112 Page
CLOSURE
concept to be general, a LNT dose relationship was assumed by Muller

with genetic damage proportional to the energy absorbed. Muller
extended the linear dose response to ionising radiation-induced
mutations supporting the evolutionary hypothesis. In his 1946 Nobel
Prize lecture, Muller tried to impress his personal bias and announced
to the world that there was no escape from the conclusion that
radiation harms linearly down to zero doses, regardless of dose rate. It
may be noted that Muller had conducted experiments in fruit lies at
very high doses (1000 R to 4000 R) to get quickly the signi icant
mutations. However, the subsequent studies by others showed that for
doses <50 R or about 500 mGy did not increase the mutation rate when
given continuously over a 21-day period. In fact, the results were dose
rate dependent. In the process, Muller ignored and withheld data that
showed he was wrong. In fact, more recent studies in fruit lies have
shown that X-ray and γ-ray doses (as low as 200 mGy) to eggs
signi icantly increased adult ly longevity, whether given as an acute or
chronic dose.
The LNT approach was eventually expanded to include chemical

carcinogen risk assessment and is now utilised by regulatory and
public health organisations all over the world. The general consensus
was that if ionising radiation can cause mutagenesis in fruit lies, it can
also cause cancer in people. Muller and other prominent members of
the radiation genetics community were ardent supporters of the LNT
model for genomic alterations and the development of cancer, despite
the fact that many others did not continue to maintain major support
for it.
The LNT model was suggested by the U.S. NAS BEAR I

Committee's Genetics Panel, and it was quickly adopted by all
governments and regulatory organisations throughout the world,
except France. The NAS Genetics Panel did not check thoroughly the
human genetic risk to radiation exposures. Others who supported the
LNT theory based their arguments on the assumption and incorrect
information of delayed cancer deaths among Hiroshima and Nagasaki
blast survivors. Based on linear extrapolation and statistics, the line
was stretched from 1 to "zero" grey (100 to 0 rad) without any
statistical cancer data of atomic bomb survivors, who had an
Page 113
immediate exposure in the high dosage range from 1 to 10 Gy (100 to

1000 rad).
What does the LNT model ignore? Low doses of radiation have
proven to improve the health of the subjects with hundreds of proofs
given in this manuscript. Radiation at large doses can be deadly,
however it is false to say that radiation at any dose is harmful. The LNT
model is based on this concept and recommends that zero dose is the
best estimate for a dose threshold for cancer mortality. In this process,
the LNT model neglects the negative risk values of low-dose radiation
based on atomic bomb survivor data, which indicated the errors in the
model.
Despite the vast amount of published scienti ic material that
demonstrates thresholds and the positive effects of low-dose ionising
radiation, today, every regulatory agency in the world, with the
exception of France, bases its regulations on the LNT as a conservative
major without specifying the degree of conservatism. Because of the
assumption and recommendation that zero dose is the threshold and
any dose above zero has a proportional risk of cancer, fear developed in
public mind. Thus, radiation phobia has been successfully implanted in
the public consciousness by the LNT. Today, the LNT has broad
implications for nuclear and diagnostic medicine, radiography, nuclear
power, "dirty" weapons, nuclear waste management, food irradiation,
and home radon.
On June 12, 1956, the NAS Biological Effects of Atomic Radiation

(BEAR) committee's Genetics Panel (GP) approved LNT. The 500
mGy/y upper limit dosage for nuclear workers, in effect since 1934,
was abolished. The next day, the front page of the New York Times,
reported that radiation is dangerous. Other media did the same. This
choice was presented, and appropriately so, as being motivated by
ideology and not on facts.
Today the societal cost of radiophobia and fear mongering is

exorbitant, and those that continue to promote it stand the most to
gain. The cost of implementing such stringent radiation dose limits
increase the cost signi icantly especially in nuclear power plants,
which the public has to bear for the cost of electricity. Similar things
114 Page
CLOSURE
hold good for all radiation devices. LNT does not increase the safety of
plants or people's health; rather, it results in the loss of tens of
thousands of lives each year across the globe because of preventing
public from bene its of such low dose radiation. Sticking to ALARA
principles add fear, cost and dif iculty to implement.
The LNT model, which assumes that carcinogenic hazards are

proportional to radiation exposure for all radiation doses without taking
dose rates into account, is the basis of today's radiation safety laws.
Growing evidence suggests that the current, excessively strict radiation
protection regulations are not the most effective means of safeguarding
the general public's health. Therefore, there are already enough factors
for policymakers to think about. Re-evaluating the ICRP dosage standards
is necessary in order to allay public radiation fears as well as concerns
among policymakers related to nuclear power plants. While numerous
studies show that low dosage radiation has bene icial impacts on people's
lives and health (increase in life span, cure of several diseases, reduction
in cancer cases, etc.). To maximise the curative effects of low-dose
radiation, more focussed research must be done to assess the threshold
doses against various diseases.
Page 115
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Page 161
162 Page
Index
A Cancer mortality 8, 13, 26, 37,
adaptive response 37, 42, 43, 38, 61, 65, 66,
52, 53, 70, 86, 90, 101 67, 68, 95, 108, 109
allergic and atopic eczema 44 carbuncles 49
amyotrophia 44 cardiovascular 13, 30, 51,
arthritis 39, 45, 46, 107 70, 86
As High As Relatively Safe cardiovascular disease 30,
(AHARS) 96 51, 86
As Low As Reasonably carpal tunnel syndrome 43
Achievable (ALARA) 96 chemotherapy 55, 56, 70
Asthma 43, 44 Chernobyl 19, 20, 21, 22, 23,
atomic bomb survivors 5, 6, 25, 26, 27, 28, 29,
11, 78, 87, 109 30, 71, 84, 88,
average lifetime 8 106, 107, 108
Chicago Pile 3, 5, 105
B cholera 47
Becquerel 1, 2 chromatin modifications 35
Becquerel rays 2 chronic inflammation 43
black rain 10 chronic polyarthritis 46
blue zones 41 Clostridium perfringens 48
bronchitis 47, 107 Cologne and Preston 9
bursitis 44 computed tomography 60
constipation 44
C Curie 2, 39
Calcifying tendonitis 45 cyto-skeletal organisation 35
Cancer 7, 8, 10, 11, 12, 13, 18, Czech beads 39
20, 21, 24, 25, 26, 27,
28, 29, 30, 34, 35, 36, D
37, 38, 39, 40, 43, 44, degenerative diseases 44
51, 52, 53, 54, 55, 59, Diabetes 51, 56, 58
60, 61, 65, 66, 67, 68, digestive diseases 38
69, 70, 71, 73, 76, 78, diphtheria 47, 107
80, 83, 84, 85, 86, 87, disorientation 44
89, 91, 95, 96, 97, 99, Dmitri Mendeleev 1
105, 106, 107, 108, DNA repair 35, 69, 85, 88
109, 110 double strand breaks (DSB) 88
Page 163
Drosophila files 73 HIV/AIDS 47, 50, 107

drowsiness 44 Hormesis 42, 85, 86, 87
dyslipidaemia 30, 57 hyperglycaemia 56, 57, 59
hyperlipidaemia 56, 57
E hypertension 30, 44
Excess Relative Risk (ERR) 35
I
F inflammation 43, 45, 46, 47,
fear 18, 19, 23, 24, 28, 48, 49, 50, 51,
31, 71, 95, 97, 100, 56, 57, 58, 59, 107
106, 108, 110 influenza 48
Fermi 2, 3, 105 International Atomic
fibromyalgia 43, 107 Energy Agency 30, 36
fibrosis 59 ionising radiation 1, 8, 9, 33,
fluoroscopy 65, 67, 68 40, 41, 43, 44,
Frederick Soddy 2 46, 69, 73, 74,
Frisch 2 76, 77, 79, 80,
frontal sinusitis 49 81, 85, 88, 96,
Fukushima 22, 23, 24, 25, 97, 99, 102, 103,
26, 30, 71, 89, 105, 108, 109
96, 107, 108 ischaemia 85
Furuncles 49
K
G Karunagappally 34
gas gangrene 47, 48, 107 Kerala 21, 34, 37, 107
Goiania 36, 107 kidney 51, 57
Gonarthrosis 45 klotho gene 40
H L
hearing loss 48 leukaemia 7, 24, 28, 35, 37,
heart disease 13, 43, 107 38, 50, 60, 61,
Heel spur syndrome 45 65, 87, 89, 91
hepatitis 37, 44 Life Span Study 7, 78, 106
High-Level Natural lifespan 8, 9, 10, 41, 42,
Radiation Areas (HLNRA) 34 47, 50, 51, 82,
Hiroshima 3, 5, 7, 8, 9, 10, 11, 86, 89, 107
19, 71, 78, 86, 87, lifestyle disorders 30
99, 106, 108, 109 Linear No Threshold
164 Page
INDEX
theory (LNT) 71, 108 nuclear warheads 3, 71, 108

liquidators 28, 106 nuclear weapon tests 11, 106
liver cancer 37, 38, 68
LNT theory 78, 85, 96, 109 O
Low Dose obesity 30
Radiation (LDR) 40 Obninsk 15
low dose, low dose Oppenheimer 5
rate (LDDR) 71 osteoarthritis 46
Low-Dose Radiation osteoporosis 44
Treatment (LD-RT) 45 otitis media 47, 48
low-linear energy outdoor air kerma 35, 37
transfer radiation (LET) 88 oxidative damage 57, 59
Luckey 40, 42
P
M Pennsylvania 18, 106
Mary Mycio 21 Periarthritis of
mastoiditis 47, 48 the shoulder 45
medical professionals 60, 61, 66 peripheral vascular
Muller 73, 74, 75, 76, 77, disease 43
80, 81, 82, 83, 86, plantar fasciitis 46
97, 99, 102, 108, 109 Plantar fasciitis 45
multiple sclerosis 43, 107 Plantar fibromatosis 45
mushroom cloud 10, 11 pneumonia 47, 49, 107
myeloma 12 pro-inflammatory
cytokines 46
N psoriasis 43, 107
Nagasaki 3, 5, 7, 8, 10, 11, psychological risks 31
71, 78, 99, 106, public evacuation 31, 107
108, 109
natural disaster 31 R
nausea 44 radiation 1, 2, 5, 6, 7, 8, 9, 10,
nephropathy 51, 57 11, 12, 15, 18, 19,
neuralgia 44 21, 22, 23, 24, 25,
Nevada test site 13 26, 27, 28, 29, 30,
Normal Level Natural 31, 33, 34, 35, 36,
Radiation Area (NLNRA) 37 37, 38, 39, 40, 41,
Nuclear Power Plant 15, 24 42, 43, 44, 45, 46,
Nuclear test 11 47, 48, 50, 51, 52,
Page 165
54, 55, 56, 57, 58, Standard Mortality
59, 60, 61, 62, 65, Ratios (SMR) 12
66, 67, 68, 69, 70, staphylococcus 47
71, 73, 74, 75, 76, steam explosion 16, 19
77, 78, 79, 80, 81, Strassmann 2
82, 83, 84, 85, 86, Sunao Tsuboi 9
88, 89, 90, 91, 92,
93, 95, 96, 97, 98, T
99, 100, 101, 102, Taipei City 33
103, 105, 106, 107, tennis/golfer's elbow 46
108, 109, 110 tenosynovitis 44
radioactive Thermal radiation 10
materials 1 Three-Mile Island 26
radiologic technologists 61, 62, threshold 7, 27, 69, 75,
65, 66 76, 79, 81, 82,
radiologists 61, 62, 65, 66 85, 89, 95, 97,
Ramsar 36, 37 99, 102, 106,
Reactive Oxygen 109, 110
Species (ROS) 88 thyroid 21, 24, 27, 28,
Relative Risk 13, 26, 37, 29, 30, 60
38, 77, 78 tissue necrosis 48
Retinitis Pigmentosa 45 TMI-2 17, 19, 106
RNA processing 35 tonsillitis 48
rotator cuff syndrome 46 Trans-generational effects 11
Russell 80, 83 Tsutomu Yamaguchi 8
Rutherford 2 tuberculosis 38, 47, 67, 107
type 2 diabetes 30, 43, 51, 57
S
scleroderma 43 U
Semipalatinsk 13 ulcerative colitis 43, 50
Shigeaki Mori 9 ulcerative dermatitis 47
sinus 49
skin erythema 48 W
solid tumours 13, 24, 35, whole-life dose 38
78, 91
Soviet Union 15, 24, 29 Y
spondylitis 44, 107 Yangjiang 37, 52, 59
166 Page
About the Authors
Dr. Arun Kumar Nayak is a graduate in Mechanical

Engineering from NIT Rourkela in 1987 and
postgraduate in Mechanical Engineering from NIT
Warangal, 1989. He joined the Reactor Design and
Development Group in BARC in 1990 after
completing one year orientation course in Nuclear
Engineering from the 33rd batch of BARC Training
School. He did his PhD in nuclear engineering from Tokyo Institute of
Technology, Japan in 2000 and worked as a Post-doc Fellow in
Interfaculty Reactor Institute, Technical University of Delft, The
Netherlands in year 2002-2003, and, in Nuclear Power Safety Division,
Royal Institute of Technology, Sweden in year 2003-2004. He also
worked in Institute of Nuclear Energy, Stuttgart University, Germany
under DST-DAAD project in year 2007-2009.
He has made seminal contributions to several domain areas of Indian
nuclear power programme. He played a key role in design of AHWR
with several innovative 'First-of-a-kind' passive-safety-systems.He
was consultant to IAEA for several years for resolving key design issues
of passive systems deployed in advanced reactors. He is internationally
known for managing core melt accidents in nuclear reactors. He
demonstrated the resilience of PHWRs against core melt accidents. He
was actively involved on development of an innovative Small Modular
Reactor (SMR) which is inherently safe, passive by design, factory built
and shipped to site for direct installation; and have the potential to
build the min vacated sites of coal based thermal power plants.
He has been actively involved with HBNI for teaching and guiding MTech
and PhD students. He is Associate Editor of ASME Journal of Nuclear
Engineering and Radiation Science, and Journal of Computational
Thermal Science. He is recipient of several awards which include Homi
Bhabha Science & Technology Awards, DAE SRC Outstanding
Investigator Award, DAE Scientific & Technical Excellence Award, DAE
Group Achievement Award, JSPS RONPAKU Fellowship, JSPS
Postdoctoral Fellowship, etc. He has written 4 books and published more
than 500 research papers in academic journals and conferences.
Page 167
AUTHORS
He has served BARC for more than 3 decades at different capacities. He

is at present, Head, Nuclear Controls& Planning Wing, Department of
Atomic Energy and Senior Professor, Homi Bhabha National Institute.
He is a Fellow of Indian National Academy of Engineering &
Maharashtra Academy of Science.
Ratan Kumar Sinha, is an Indian nuclear scientist

and mechanical engineer. He graduated in
Mechanical Engineering from Patna University in
1972, securing the first position in the University. He
joined the Reactor Engineering Division of BARC in
the year 1973 after completing one year training
course at BARC Training School. After serving in
various capacities in BARC, he headed the organisation as the Director
during May 2010 to April 2012. He served as Secretary, Department of
Atomic Energy and Chairman, Atomic Energy Commission of India
from May 2012 till his superannuation in October 2015. Subsequently,
he was conferred the position of DAE Homi Bhabha Chair Professor. He
has represented India in several important technical and policy-
making forums of the International Atomic Energy Agency (IAEA).
These include the Steering Committee of IAEA's International Project
on Innovative Nuclear Reactors and Fuel Cycles (INPRO), of which he
was the Chairman for four years from the year 2005 to 2008.
He is nationally and internationally recognised expert in the field of
nuclear reactor technology. During the four decades of his career, he
held several important positions related to design & development of
nuclear reactors which include the Advanced Heavy Water Reactor
(AHWR) and Compact High Temperature Reactor (CHTR), two of the
highly acknowledged technological innovations which are suitable for
large scale deployment of nuclear power, particularly in India. Major
thrust areas, in continuation to his research at BARC, include advanced
nuclear energy systems for thorium utilisation and accelerator
technology. He had given high priority to application of radiation
technology in the areas of healthcare management, agriculture, food
preservation and water purification. He had also strengthened
168 Page
outreach activities of DAE for spreading awareness about the peaceful
uses of atomic energy among the general public. Under his leadership,
DAE displayed its first ever tableau in the 66th Republic Day Parade
2015. He has coined the phrase jeä^ JeÀer mesJee ceW HejceeCeg (Atoms in Service of
the Nation) which has been imbibed as the motto of the Department of
Atomic Energy in January 2014.
He is a member of International Nuclear Energy Academy (INEA). He is
a Fellow of Indian National Academy of Engineering (INAE) and
Maharashtra Academy of Sciences. He has several awards and honours
to his credit including the first of the prestigious Homi Bhabha Science
and Technology Award (1992), VASVIK Award (2000), Indian Nuclear
Society (INS) Award (2001), the DAE Special Contributions Award
(2006), INAE Prof. S. N. Mitra Memorial Award (2006). He was
conferred the honorary Doctorate of Sciences (D. Sc.) degree by the
University of Mysore (2009), Ph. D. (h. c.) of Defence Institute of
Advanced Technology, Pune (2013) and honorary Doctorate of
Sciences (D. Sc.) by Amity University (2014). He is the recipient of
Distinguished Academician Award from IIT Patna (2013), the
Kurukshetra University Goyal Award (2015) and the South Indian
Education Society's National Eminence Award for Science and
Technology (2015).
Samyak Sanjay Munot is a postgraduate in Nuclear

Science and Technology from Amity Institute of
Nuclear Science and Technology, Amity University,
Noida. Following this, he pursued his doctorate in
Engineering Sciences from the prestigious Bhabha
Atomic Research Centre under the Homi Bhabha
National Institute, India.
He is a Board Member of Indian Youth Nuclear Society (IYNS) and
serves as voluntary IT Manager at IYNS.
He made contributions towards development of core catcher, a safety
system used during the severe accident in a nuclear reactor. He played a
seminal role in development of numerical models for Computational
Page 169
Fluid Dynamics and Experimental Simulations. He is a recipient of the
prestigious DAE Doctoral Fellowship (DDFS). He has written 1 book, 2
chapters and published more than 15 research papers in academic
journals and conferences.
His interests include educational and outreach activities in STEAM
education, awareness towards climate change and carbon free energy
security of India.
170 Page
Page 171
172 Page
About the Book
The growing carbon footprint calls for immediate deployment of clean and
green sources of energy to save the humankind against the devastating effects
of global warming. The limitations of solar and wind to meet the energy demand
of the world especially for the developing nations like India, necessitates large
scale deployment of nuclear energy to meet the energy demand for realising its
vision of an ambitious GDP growth rate. Apart from a low carbon energy source,
nuclear energy is vital for producing radioisotopes for the treatment of cancer,
healthcare, industry, agriculture, food security, etc.
The world got introduced to nuclear through the deployment of nuclear weapon
causing horrific repercussions. This backdrop has served as a great deterrent to
the well-deserved deployment and growth of nuclear power all over the world.
Time has now come to make a directed effort to address this perception about
the harmful effects of nuclear radiation on the basis of a large volume of scientif-
ic research findings on the subject of nuclear radiation on living beings.
To accelerate nuclear power growth, one of the biggest hurdles is the public fear
of nuclear power due to concerns of nuclear safety, radiation leak, radiation
causing cancer and finally death. Is this fear scientific or scientific misinterpreta-
tion and "cherry-picking" than actual science”?
This book gives a summary of the hundreds of studies that have been conducted
in the past to prove the health benefits of radiation to cure several diseases,
increase in lifespan and reduced cancer mortality. These conclusions were found
not only in survivors of Hiroshima and Nagasaki bombings, but also the civilians
and servicemen involved in nuclear tests, medical professionals, people living in
high background radiation fields, apart from experiences of the people exposed
to the radiation leaks from the three civilian major nuclear accidents.In spite of
hundreds of such proofs, the biggest question is “Why people are afraid of radia-
tion?” The book explains the root cause of fear of radiation and its history, and
how it became the part of the regulation.
This book is expected to be of immense help to scientists, engineers, and

students in all fields, as well as people in general, to overcome an irrational fear
of low-dose radiation. It's a must-read for people who work in the field of nuclear
safety, as well as for students and researchers in this broad field.

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THE UNREASONED

Arun Kumar Nayak

Ratan Kumar Sinha

Samyak Sanjay Munot

Copyright @ Department of Atomic Energy

All rights reserved. No part of this book may be reproduced or

Foreword by Anil Kakodkar ix

The Linear No Threshold (LNT) hypothesis, which is the basis of

This is a larger public policy matter. One needs opinion makers

The world is at crossroads today in terms of the risks of

While doing so, it becomes paramount to address the people’s

I wish all the readers an enjoyable journey through this book.

Additionally, today, nuclear radiation and isotopes find its

This book provides a summary of the several hundreds of studies

This book will definitely benefit the scientists, engineers and

Ajit Kumar Mohanty

The same has already happened with radiation, which people

Following the devastating nuclear bombings at the two cities,

In general, it can be emphasised that the public is exposed to low

There are several thousands of publications available in open

Having said so much on the beneficial effects of radiation on

The LNT approach was eventually expanded to include chemical

The LNT model was suggested by the U.S. National Academy of

In conclusion, despite the vast amount of published scientific

On June 12, 1956, the National Academy of Sciences (NAS)

1.1. Discovery of ionising radiation

He exposed potassium uranyl sulphate to sunlight for the

1.2. Discovery of fission and its consequences

At the University of Chicago, Fermi and his colleagues

Schematic of the Fission Reaction

2.1. The aftermath of Hiroshima and Nagasaki bombing

Retrospective radiation dose measurements were conducted

2.2. Further analysis of atom bomb radiation eﬀects in Japan

From the analysis [14] of the impacts of A-bomb survivors on

2.3. Evidence of longer lifespan of some people who were

Sunao Tsuboi, Chairman of the Japan Confederation of A-Bomb

2.4. A-bomb survivor's lifespan was statistically shortened

2.5. More analysis of atom bomb explosion

The mushroom clouds created during the bombing at Hiroshima

According to a report, the area west of the epicenter has a higher

2.6. Trans-generational eﬀects of radiation

“…models of the trans-generational eﬀects of radiation

2.7. Nuclear test participants exposure

were again con irmed [28], [29]. A cohort of Australians (n = 10983)

In the Semipalatinsk (Union of Soviet Socialist Republics)

3.1. Risk of nuclear power

When the USNRC was created in 1974, Prof. Rasmussen of MIT

Table 3 Early fatality due to various accidents [39]

Accident Type Total Nu mber for 1969 Approximate Individual Rise

The WASH-1400 results, which provided an individual's

The damaged core of the TMI-2

Gaseous release during TMI Accident

disaster), from midnight until 8:00 in the morning. The governor of

The public's fear of radiation increased despite multiple

A more serious catastrophe happened at one of Chernobyl's

The Chernobyl disaster dealt more blows to the ield of nuclear

Evacuation of the Public due to Chernobyl accident

Ukraine, the average eﬀective doses for the general population in