ThorCon plan to have production reactors built (in Indonesia) within 10 years
Transatomic Power move ever closer to their waste-burning reactor which can run entirely off nuclear waste
Southern Company Services, a subsidiary of Southern Company, is developing the MCFR in partnership with Bill Gates' TerraPower, Electric Power Research Institute, Vanderbilt University, and ORNL
China pursues two kinds of MSR. The TMSR is a pure thorium MSR design like the LFTR, and a pebble fueled (TRISO), molten salt cooled design. TerraPower will also prototype their reactors in China.
"If the Nuclear Energy Agency (NEA) has accurately estimated the planet's economically accessible uranium resources, reactors could run more than 200 years at current rates of consumption."
-- "How long will the world's uranium supplies last?", Scientific American, 2009, by Steve Fetter
"There is an estimated forty trillion tonnes of uranium in the earth's crust."
-- Till & Chang, 2011
Surely both of these quotations can't be right. Because the energy we can get from uranium is 10 million times what we can get from fossil fuel. It's estimated there is about 57 zettajoule (ZJ) of fossil fuel on earth. Or 1.36 million MTOE = 1.36 trillion tonnes of oil equivalent (TOE). In energy terms: there is about 1.3 billion times more fission energy available in the earth's crust than fossil fuel energy.
Fetter only considered the current fuel cycle. Only 3.5% of fuel is used in the water-moderated reactor cycle, leaving 96.5% of the potential untapped. On the way to making the fuel, most of the uranium was left out - as depleted uranium (DU). Over 8 times more uranium becomes DU than fuel. Uranium-238 to plutonium-239 breeder reactors can use all uranium found in both spent fuel and DU.
Include thorium breeder reactors and there's thousands of times more available fuel. A lot of the thorium has already been mined and is just sitting around in tailing heaps waiting for us to do something useful with it. There's about 3.5 times more thorium in the earth's crust than uranium. About 140 trillion tonnes of it.
There's more uranium than Fetter wrote about.
We will find more uranium deposits by just looking for them. I've been told to expect peak oil for at least 35 years now. Every year we find more oil. We will also find a lot more uranium. For example the IAEA "identified resources" saw uranium increase 0.7m tonnes in just 4 years - from 4.7m tonnes (2005) to 5.4m tonnes (2009).
There are vast uranium deposits in the world's oceans : 4500 million tonnes of it - about 800 times more than Fetter accounted for. We already have technology to extract this (at about $600 per kg).
There's more uranium in lower quality ore deposits: Charles Till and Yoon Il Chang discuss uranium resources in pages 91 to 95 of 'Plentiful Energy' (pdf book)
Ref: Plentiful Energy - The story of the integral fast reactor, 2011, by , pages: 91 to 95.
Nuclear power is stuck in the past by rules and red tape. I don’t just mean nuclear regulations. Another reason technologies can’t advance is that anti-proliferators all but outlaw them.
Regulators obsessing over infinitesimally small radiation emissions which they claim are carcinogenic. When US built its nuclear fleet the AEC ran nuclear power with a dual mandate: to ensure safe nuclear plants were economically built. In respose to coal-industry lobbying, in 1974, the NRC took over regulation with a mission to "maximize safety". Even today, US regulators court radiophobes like Ian Fairlie. Tying up the nuclear industry in knots and spreading radiophobia seems to have been the NRC's main job. Since their formation, only 4 new nuclear plants have been licensed in USA.
The killer: Labour time. Nuclear power workers are relatively well-paid but spend an awful lot of time doing non-productive work. Bernard Cohen has a nice graph in his book. Here's a modified version of that chart. Notice a steep increase in labour costs from 1981 to 1983. Costs doubled.
Materials. NPP materials are specified to meet only the highest standards. Like military-grade materials, only squared; gold-plated materials, platinum-plated. New components must be custom-made, or made with very short production runs which can't take advantage of economies of scale.
The “cradle to grave” fuel cycle imposed on all Western countries by anti-proliferator rules. Companies like AREVA and Westinghouse make nuclear fuel and help ensure it can’t be diverted for A- or dirty bomb use. It’s a nice earner for them - cartel-wise. “Cradle to grave” means the responsible people are always in control of the fuel material, even after use. Another cosy agreement the mainstream nuclear industry made with government to cripple nuclear power by forcing everyone into the straight-jackets of cradle-to-grave, and conventional PWR uranium oxide pellet fuel.
Slowing advanced nuclear power down to a snail pace with rules and regulations over what materials can be used to make a reactor. The best materials can’t be used in molten salt reactors because they would take 15, or more, years to test and certify with the US regulatory agency. Nuke startups like Terrestrial Energy and ThorCon are reduced to inferior, but nuke-certified, stainless steel instead, if they want to see their designs in action before they die.
Lithium-7 is a good example. Li-7 is ideal for making molten salt reactors, MSR. These are, almost, a prerequisite for thorium reactors. Yet lithium is naturally a mixture of two isotopes: Li-7 and Li-6, in a ratio 12:1. Putting natural lithium in a reactor would result in the Li-6 making masses of tritium. It would waste a lot of neutrons too. No way would a regulator allow that. The isotopes must be separated. US Dept of Defence are not keen on you doing that. The old isotopic separation method used mercury. They won't allow you to do that today. You must develop a new isotopic separation technology, but if you tell anyone, the spooks will "have to kill you". Lithium-6 is considered a nuclear bomb proliferation risk because it can be used to make tritium (which is, officially, a H-bomb proliferation risk).
Likewise the Integral Fast Reactor was killed on very dubious anti-proliferation grounds. The myth that plutonium made in it was a bomb proliferation risk. IFR fuel recycling relied on a special development called pyroprocessing which IFR researcher(s) [e.g. Roger Blomquist] claim is only one seventh the cost of traditional, PUREX fuel recycling. Despite this massive cost advantage, we’ve seen no commercial development of pyroprocessing in over 20 years since it was prototyped in the EBR-II reactor.
Some of the above are just illustrative examples. Others are main causes. For the most part, private investors don't want to know. It's too expensive. We have regulated it out of existence, with many regulations based on myth and fear.
This is a, sort of, re-blog of Mohan Doss' submission to the U.S. Nuclear Regulatory Commission, NRC, on radiation protection standards (link is above). Don't let that put you off reading it. It is a well-written summary of what we currently know about the harms of radiation and actual causes of cancer.
by Mohan Doss
I am responding to comments received from many members of the public who have raised major concerns regarding the recent petitions to discontinue the use of the linear no-threshold (LNT) model for establishing radiation safety regulations, and the proposed higher radiation dose limits for the public. These concerns are based on a misunderstanding that exists regarding cancer and radiation effects in our society.
1. Misunderstanding of the Primary Reason for Cancers
It is generally accepted that the primary reason for cancer is the transformation of a normal cell into a cancer cell through mutations. In fact, this transformation is generally referred to as carcinogenesis. A recent publication noted that almost everyone has cancer cells in their bodies (Greaves, 2014). However, everyone does not have cancer, as the lifetime probability of developing or dying from cancer are ~43% and ~23%
respectively in the USA, for example (ACS, 2014). In an autopsy study, the presence of cancer cells was determined as a function of age (Imaida et al., 1997) (Figure 1). Whereas the percentage of patients having cancer cells was found to be relatively unchanged from age ~50 to age ~80, cancer mortality rates is known to increase by more than an order of magnitude between these ages (WHO, 2011) (Figure 2), indicating something other than cancerous mutations is the primary cause of clinical cancers. If cancerous mutations are not the primary cause of cancers, what is?
One hint is given by the observation that when the
immune system is suppressed, e.g. in organ
transplant or HIV patients, cancer risk increases by
a factor of 3 to 4 (Oliveira Cobucci et al., 2012)
(Figure 3). This is a huge increase, and indicates
suppression of the immune system may be the
primary cause of the cancers. Many characteristics
of cancers are consistent with this point of view
that cancers are caused by the suppression of the
immune system. For example, (A) As we age, our
immune system response reduces significantly
(Levin, 2012) (Figure 4), and indeed cancer risk
increases drastically with age (Figure 2).
(B) Increased rate of breastfeeding which boosts the immune system, and (C) earlier childcare attendance which subjects children to increased rate of infections and stimulation of the immune system, reduce the risk of childhood leukemias (Rudant et al., 2015) (Figures 5 & 6).
(D) Vigorous exercise, which causes increased DNA damage (Fogarty et al., 2011) (Figure 7) and boosts the immune system response (Simpson et al., 2012) (Figure 8), reduces the risk of cancers (Orsini et al., 2008) (Figure 9), consistent with the immune suppression model of cancer and contrary to the mutation model of cancer.
(E) In young growing age, when cells are dividing at the highest rates, they
would be most susceptible to mutations, and so the accumulation of
mutations would occur at the highest rates, as has been observed in an
animal study, for example (DeGregori, 2013) (Figure 10). Based on this, the
mutation model of cancer would suggest that cancer rates would reach a
high level at a young age. The immune system response, on the other
hand, is at the highest level at young age (Levin, 2012) (Figure 4), leading
to the prediction that cancer rates would be at the lowest levels at young
age, using the immune suppression model of cancer. The very low cancer
rates observed in young age is therefore not consistent with the mutation
model of cancer but is consistent with the immune suppression model of
cancer.
Summarizing, though mutations are necessary for causing cancers, they
are not the primary cause of cancers, and suppression of the immune
system is a key factor that causes cancers.
2. Misunderstanding of the effect of low-dose radiation on cancer
Since radiation causes mutations, using the widely accepted
mutation model of cancer, it is generally believed that even the
smallest amount of radiation can increase mutations and so can
increase the risk of cancer. This is the basis of the LNT model.
However, we have seen that there are naturally occurring
mutations including cancerous ones in almost everyone (Greaves,
2014). When there is a low level of radiation exposure, the
damage caused by it would stimulate the defenses in the body,
and these increased defenses would reduce the amount of
mutations that would have occurred naturally (Feinendegen et
al., 2013), resulting in less mutations overall. This has been
observed in animal studies, e.g. (Osipov et al., 2013) (Figure 11).
Thus, there is no justification for the LNT model even using the
mutation model of cancer, since a small amount of radiation does
not increase but decreases the overall mutations. The major error
in formulating the LNT model was that the defensive responses of
the body and their effect on the naturally occurring mutations
were completely ignored.
Another effect of low-dose radiation is that it stimulates the
immune system (Yang et al., 2014) (Figure 12). As noted earlier,
the boosted immune system would reduce cancers. This cancer
preventive effect of low-dose radiation, known as radiation
hormesis, was proposed in 1980 (Luckey, 1980) as a method of
reducing cancers.
The above arguments suggest that low levels of radiation would
reduce, rather than increase cancers as predicted by the LNT
model. Which of these opposing predictions is correct? The
scientific way of deciding between competing hypotheses is to
perform experiments and compare the results with predictions
from the hypotheses. However, since the LNT model was adopted
without any evidence for its validity in the 1950s, it caused fear of
the smallest amount of radiation, and so blocked prospective
human studies of the cancer preventive effect of low levels of radiation. Though such prospective studies
could not be conducted, there is indeed considerable amount of data from studies of population groups that
have been exposed incidentally or accidentally to radiation. There have also been some clinical trials using
low-dose radiation for the treatment of cancers. I will discuss some of these data now.
3. Studies of populations exposed to low levels of radiation
On several occasions in the past, populations have been incidentally or accidentally exposed to low levels of
radiation over prolonged periods of time. The graph below shows data on cancer rates in some of these
population groups, with radiation dose on the X-axis and estimated normalized cancer mortality rates (100
being the estimated cancer mortality rate for the un-irradiated control group) on the Y-axis. It is clear from
examining the green data points that cancer rates have reduced following exposure to low-dose radiation. The
red dashed line shows the effect of low-dose radiation on normalized cancer mortality rates, as predicted by
the LNT model, using the radiation cancer mortality risk factors recommended by BEIR VII Report (NRC, 2006).
It is clear the LNT model is not consistent with the data. The grey band indicates the range of normalized
cancer rates that would be observed in the absence of radiation, using the example of cancer rates in Japan
during the period 1960-1994 (FPCR, 2013) (black dots on the graph), a period during which cancer rates were
relatively stable. The blue line shows normalized age-adjusted cancer mortality rates during the period
1960-2007 in the USA (Remington and Brownson, 2011).
4. Harm from LNT model-based regulations
LNT model based regulations, by requiring reduction of radiation dose from 50 mSv (a dose someone might
receive but for the regulations) to 1 mSv (annual dose limit for the public), claim to reduce cancer rates from A
to B (Figure 13). In view of the year-to-year variation in cancer rates (grey band), this cannot be considered to
be any reduction in cancer rates, since both A and B are within the grey band, the range of variation of cancer
rates over the years. In reality, considering cancer outcomes observed in populations incidentally or
accidentally exposed to low-dose radiation (green data points), these regulations have likely increased cancer
rates by taking them from C to B and also prevented studies that could have reduced cancers to the level D
(~30% reduction) (Figure 13). Cancer mortality rates in USA have remained stubbornly high at level E, there
being only ~7% reduction in cancer mortality rates in 2007 in comparison to the rates in 1960 (Figure 13), with
little progress in ~50 years (Remington and Brownson, 2011), in spite of tremendous investments and efforts
in the war on cancer. This graph makes it clear the regulations have harmed the public by preventing the study
and use of radiation hormesis for reducing cancers.
Let us now examine some additional data on the effect of radiation on cancers.
5. Atomic Bomb Survivor Data
It is widely recognized that the most important data for determining the health effects of radiation are the data from the
atomic bomb survivors. For example, (Hall and Brenner, 2008) claimed that these are the gold standard data for
estimating the health effects of low-dose radiation. The BEIR VII Report from National Academy of Sciences stated (on p.
141) that these are the single most important source of data for evaluating risks of low-dose radiation. A
re these data consistent with the LNT model?
The atomic bomb survivor data, after the latest update (Ozasa et al., 2012),
no longer support the LNT model, because the dose-response data are not
linear any longer, and have a significant curvature (see Figure 14). Ozasa et
al. state: The curvature over the 0-2 Gy range has become stronger over
time, going from 0.20 for the period 19501985 to 0.81 for 19502003, and
has become significant with longer observationâ€. This significant curvature,
resulting from reduction of cancers when the radiation dose increases from
~0.25 Gy to ~0.5 Gy, cannot be explained by the LNT model. There is a
possible explanation for the curvature using the radiation hormesis model,
as explained in the publications (Doss, 2012, Doss, 2013). This idea, that
the atomic bomb survivor data no longer support the LNT model, is being
accepted implicitly by more and more scientists. For example, in the
recently published debate in Medical Physics journal (Doss et al., 2014), the
proponent of the LNT model did not use the atomic bomb survivor data to
justify low-dose radiation cancer risk in his opening statement whereas in
the 2009 debate in Radiology on the subject (Little et al., 2009), these data
played a prominent role, as he stated "Most of the information on radiation-induced cancer risk comes from (a) the
Japanese atomic bomb survivors (b) .....". Ian Fairlie, in his Comments to NRC http://www.ianfairlie.org/wp-content/uploads/2015/08/US-NRC-Consultation-4-1.pdf,
did not refer to the latest atomic bomb survivor data to justify
his concerns regarding low-dose radiation, after having referred to the atomic bomb survivor study as a major study in
2011 http://www.ianfairlie.org/news/are-radiation-risks-overrated/. In a recent article on the subject (Brenner, 2014),
the author used older atomic bomb survivor data (Preston et al., 2007) to justify cancer concerns from low-dose
radiation, ignoring the latest data (Ozasa et al., 2012). When he was challenged in a Letter to the Editor (Doss, 2014) for
this omission and other errors in his publication, he had no rebuttal to the arguments. Thus, the change in the status of
the atomic bomb survivor data is being recognized implicitly by authors of publications that have supported the LNT
model, though they have not acknowledged it explicitly.
6. 15-Country Study of Radiation Workers
Another dataset that has been used to claim increased cancers from low-dose
radiation are the 15-country study of radiation workers (Cardis et al., 2005).
When the data for all the countries are combined, the analysis showed
statistically significant increased risk of cancers among the radiation workers
who had been exposed to an average of 20 mSv radiation dose (See Figure 2). As
seen in the figure, the Canadian data show a much higher excess risk of cancer
when compared to other countries data. The authors stated in the publication
that if the Canadian data were excluded, the overall data would no longer show
a significant excess relative risk of cancers. Canadian Nuclear Safety Commission
(CNSC) investigated the discrepancy and found major problems with the data. As
a result, CNSC withdrew the Canadian data from use (CNSC, 2011). A revised
analysis indicates the Canadian worker risk estimates would be substantially
reduced (Zablotska et al., 2014). Hence, the conclusion of the 15-country study
would be that cancer risk is not increased following low-dose radiation
exposures.
7. Studies of Cancers following Childhood CT scans
Two recently published studies, (Pearce et al., 2012) and (Mathews et al., 2013), have claimed increased cancers
following childhood CT scans. These articles received high publicity in popular media, and have been cited in many
publications to claim that cancers are caused by low level radiation exposure to children. Both of these studies have
been discussed by several authors pointing out the major flaws in them, e.g. (Cohen, 2013), (Walsh, 2013), (Boice,
2013), (Walsh, 2014), (Socol, 2015), (Harvey, 2015). One of the main flaws is the likelihood of reverse causation, because
the authors did not take into consideration the reason why the CT scans were performed. When the reasons for the CT
scans were taken into consideration, two studies (Journy, 2015), (Krille et al., 2015) have shown no significant increased
risk of cancers following pediatric CT scans. The Mathews and Pearce studies are examples of faultily designed studies
that demonstrate increased cancer risk from low-dose radiation.
8. INWORKS study of leukemias and solid cancers in nuclear industry workers in France, UK, and USA
INWORKS study wanted to answer the question: Does increased radiation exposure over an extended period of time
increase the risk of leukemias and solid cancers?, by studying leukemias (Leuraud et al., 2015) and solid cancers
(Richardson et al., 2015) as a function of occupational radiation dose in nuclear industry workers during the period 1944
to 2004 in France, USA, and UK. If the occupational radiation dose were the most important part of radiation dose that
the workers received, and other radiation doses they received during the study period (1944-2004) were relatively
unchanged, then their study design would indeed be reasonable for answering the question they posed. However, as is
well known, medical radiation dose increased considerably during this time period (NCRP, 2009), and occupational
radiation dose in nuclear industry reduced drastically in the same period (Thierry-Chef et al., 2015). Therefore, during
the later period of the study, the medical radiation doses the workers received, assuming they underwent similar
amounts of diagnostic examinations as the average members of the public, would be significant in relation to their
occupational doses. Not including the medical radiation dose into consideration is therefore a major error in the design
of these studies. In addition there were other major flaws, rendering the conclusion of the studies not trustworthy
(Doss, 2015b, Doss, 2015a).
9. Claims of increased thyroid cancers in Fukushima children
A recent publication (Tsuda et al., 2015) has claimed increase in the rates of thyroid cancers in Fukushima area children
by a factor of about 30 in the years following the Fukushima nuclear reactor accidents in 2011, in comparison to the
observed thyroid cancer rates in Japan. As described in the detailed analysis (Boisvert, 2015), the reported results are
likely due to increased screening for thyroid cancers in the Fukushima children. It should be noted that the thyroid dose
to children were low in the Fukushima children, as indicated in Table 6 of (UNSCEAR, 2013) (maximum of ~80 mGy). In
another study, children who were subjected to median dose of ~1 Gy to thyroid from diagnostic administration of I-131
did not exhibit increased thyroid cancer risk (Hahn et al., 2001).
10. Claim of increased leukemias in children exposed to higher background radiation levels
A recent study (Kendall et al., 2013) has claimed that there were increased leukemias in children exposed to
higher background radiation levels. Breastfeeding and childcare attendance are known to be important factors
that affect childhood leukemias (Amitay and Keinan-Boker, 2015, Rudant et al., 2015). These were not
considered as confounding factors in the (Kendall et al., 2013) study. Since relative risk per mSv was 1.07 (with
95% CI: 1.01-1.13) small changes in these confounding factors could make the excess risk not significant.
Hence, we should await better studies which take into account the major confounding factors before
considering the excess risk estimation from this cohort.
11. Note on publications claiming that low-dose radiation inceases cancer risk
The above described situation, that publications report increased cancer risk from low-dose radiation because
of faulty data or analysis, is very common. Such publications receive high publicity in popular media, spreading
the fear of low-dose radiation among the public. When corrections or criticisms are published showing the
conclusions of such publications are no longer valid, these are not even mentioned in popular media, as they
are not sensational. The misinformation therefore persists among the public.
As seen in the above examples, publications claiming that low-dose radiation increases cancer risk do not
have a reliable record, with faults being identified sometime after they are published, negating their
conclusions. I would suggest popular media and the public do not pay attention to such publications for
several years to see if they withstand scrutiny by the scientific community.
13. Evidence for no increase in cancers following low-dose radiation exposures
Several studies have shown the existence of a large threshold dose, below which increased cancers do not
occur following radiation exposure. The data from some of these studies are shown below.
14. Repeated low-dose radiation treatments improved survival of cancer patients, performing as well or better than chemotherapies
Several clinical trials involving cancer patients showed that low-dose radiation treatments (TBI=Total Body
Irradiation, HBI=Half-Body Irradiation) resulted in patient survival as good or better than chemotherapies
(COP, CHOP) (Chaffey et al., 1976, Pollycove, 2007), and such treatments, used to supplement standard
radiation therapy, resulted in better patient survival (Sakamoto, 2004). (Figures 21-23)
15. Concerns regarding low-dose radiation exposures to genetically susceptible individuals
Concerns have been expressed about the potential harm from low-dose radiation exposure to genetically
susceptible individuals, e.g. (Brenner, 2015). In this presentation, Brenner quoted a study of meningiomas in
patients treated for tinea capitis which showed that genetically susceptible people had increased risk of
developing radiation-induced meningiomas (Flint-Richter and Sadetzki, 2007). However, this study involved
high doses of radiation, and its conclusion cannot be extrapolated to low doses.
16. Concerns regarding higher sensitivity of children to radiation
Concerns have been expressed about childrens higher radiosensitivity with
reference to the increased use of pediatric CT scans (Brenner et al., 2001). One
of the reasons quoted is the increased lifetime cancer risk per unit dose among
atomic bomb survivors who were exposed at younger ages (Figure 24 shows
newer data on these risks). However, the excess cancers were observed in the
survivors exposed to high radiation doses only, and only be using LNT
extrapolation can these risks be transferred to low doses. Such an extrapolation
does not have any justification since the LNT model does not have any valid
supportive evidence, as seen above.
Another reason generally quoted for the increased radiosensitivity of children is that they have more dividing
cells and so are more susceptible to radiation-induced mutations. This reasoning ignores the defensive
response to low-dose radiation exposure which would reduce the overall accumulated mutations
(Feinendegen et al., 2013, Osipov et al., 2013), and so would reduce the cancer risk using the mutation model
of cancer. Using the immune suppression model of cancer, since children have the highest immune system
response (Levin, 2012), and low-dose radiation boosts the immune system (Yang et al., 2014), children would
face reduced risk of cancer following low-dose radiation exposures. Thus, the concerns expressed regarding
higher sensitivity of children to low-dose radiation are not justified.
16. Opposing views on cancer risk from low-dose radiation
The evidence quoted in the pages above presents a coherent view of the health effects of low-dose radiation,
that it reduces cancer risk. There is no ambiguity in this conclusion. Though many publications have claimed
that low-dose radiation increases cancer risk, I have discussed several such publications and have shown why
their conclusions should be rejected because of updates to the data, identification of major flaws in them, etc.
Many scientists and advisory bodies have however reached an opposite conclusion, that low-dose radiation
increases cancer risk, after analyzing scientific literature. One of the reasons for this difference is that these
scientists and advisory bodies have failed to take into consideration published data such as shown above
without providing any reasons. For example, the BEIR VII Report (NRC, 2006) and the BEIR VIII scoping meeting
failed to consider the data discussed above. Similarly, scientists opposing the NRC petitions, e.g. Ian Fairlie,
have also failed to consider these data but have utilized already discredited data to justify low-dose radiation
cancer concerns. Since the conclusions from such incomplete analyses are more sensational, they receive
more publicity in popular media, perpetuating the misconception among the public that low-dose radiation
increases cancer risk.
17. Conclusion
In summary, we have seen that exposure to low-dose radiation in many different ways, including relatively
high cumulative doses when received over an extended period of time, has resulted in no increased cancer
risk or reduced cancer risk, completely contradicting the LNT model. Though there are many publications that
have claimed support for the LNT model, they have major flaws in them raising major doubts about their
conclusions. The most important data for estimating health effects of radiation, the atomic bomb survivor
data, no longer support the LNT model with the recent update to the data, and the data are more compatible
with radiation hormesis model. Thus, there is no longer any justification for the continued use of the LNT
model. In view of the observed cancer preventive effect of low-dose radiation, there should be no concerns
among the public regarding low levels of radiation exposures. A massive education program needs to be
initiated to educate the public about the health effects of low-dose radiation and allay their concerns about
the proposals in the NRC petitions.
Disclaimer: These comments are the personal professional opinions of the author and do not necessarily represent those of his employer.
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