Excessive cesium-134 at Daiini. Evidence of criticality there April 2012 or after.

This table was recently released by Tepco. The first row shows radioactive cesium measurements made of fallout at Fukushima Daiichi on December 25, 2013. Note that the amount of cesium-134 is about 39% that of cesium-137. At 3/11 the ratio of Cs-134 to Cs-137 was around 100%. Cs-134 has a half-life of 2 years, and has now decayed to around 35-40% of Cs-137.

The second row shows radioactive cesium measurements made of fallout at Fukushima Daiini on December 26, 2013. The amount of Cs-134 is about 57% of Cs-137.

From Wikipedia,

Caesium-134 has a half-life of 2.0652 years. It is produced both directly (at a very small yield because 134Xe is stable) as a fission product and via neutron capture from nonradioactive Cs-133 (neutron capture cross section 29 barns), which is a common fission product. Caesium 134 is not produced via beta decay of other fission product nuclides of mass 134 since beta decay stops at stable 134Xe. It is also not produced by nuclear weapons because 133Cs is created by beta decay of original fission products only long after the nuclear explosion is over.

So cesium-134 is mainly an activation product, which means it needs neutrons flying around and interacting with nonradioactive cesium-133 to be produced in significant quantities.

I used a radioactive decay application to figure how far back in time Cs-134 would have to have been produced to get the current ratio of 57% of Cs-137. The Cs-134 would have been produced around April 1, 2012.

This means there has been a criticality at Daiini sometime after April 1, 2012. How long after this date is unknown.

Radiation plume from the Perry nuclear plant in Ohio.

Around 3PM today, my thyroid started to swell up again. I took some Lugol’s iodine for it. This has happened several times the past few weeks. There was a steam release and apparent criticality in late December (see Unit 3 steaming and the latest plume). Others have reported thyroid problems also. My thyroid even swelled up after eating some Mexican tomato sauce. This is the first time I have found apparent radioactive iodine in a Mexican food product since 2011.

And the graph from CRIIRAD shows radiation levels in Rhône river water in Avignon, France. The energy range of these gamma radionuclides includes naturally occurring NORM (Naturally Occurring Radioactive Materials) nuclides, and also iodine-131. CRIIRAD claims this spike and others like it are from NORM and NOT from Fukushima. But the spike on January 13 is interesting nonetheless. A crummy online translation:

Within minutes following with the first threshold exceeded alert, call personnel at CRIIRAD were remotely connected to the central management. The detailed examination of the data has to verify that the observed exceedances were most probably related to variations in the flow of the Rhone and its load of natural radioactive elements in the context of an intense rainfall episode.

So maybe iodine-131 is behind the spike or maybe not. (See Email exchange with Bruno Chareyron, head of CRIIRAD.)

Having said all this, the iodine behind the thyroid issue today was very likely NOT from Fukushima.

The reason is, after the snowstorm yesterday, a bitter cold front came through Maryland. Temperatures were down to 4 degrees this morning. This air originated from Siberia. (See the animation here.) This was an extremely cold pool of air, far from Fukushima. Cold air is dense and compressed, and does not mix with the relatively warm air off Japan. And, since the iodine-laden air would have had to make it to Siberia first, and then come all the way down to the east coast of the US, it would have taken a long time to do so. Iodine-131 has a half-life of 8 days. Whatever did get mixed in with the bitterly cold dome would have mostly decayed.

But where did the iodine come from? There was a leak at the Perry nuclear plant in Ohio on Monday, January 20. Radioactive tritium leaked into the groundwater outside the building where the leak occurred. (FirstEnergy, the owner of the plant, says the leak was fixed last night.) Maybe some of the tritium leaked into the air too, along with some iodine-131.

The graphs below show the wind direction and wind speed for yesterday and today in Baltimore. Around midnight last night, the winds started coming from the northwest, the direction that the Perry plant is located. They continued throughout today. I looked up the distance from Cleveland to Baltimore in air miles, it is slightly over 300 miles. If the wind was blowing a 20 miles an hour, the plume would have been here in 15 hours. At 3PM, when my thyroid was tweaking, it was 15 hours after the wind shifted.
Jan. 21:
Jan. 22:
Congressman Dennis Kucinich initiated congressional oversight over the Perry plant in 2007 after a shutdown of the plant.

In response to the emergency closure of FirstEnergy’s Perry Nuclear Power Plant, Congressman Dennis Kucinich (D-OH), Chairman of the Domestic Policy Subcommittee, sent a letter to the Nuclear Regulatory Commission (NRC) today requesting a briefing on the findings of its special inspection of the facility.

The NRC was notified in the early morning of Wednesday, Nov. 28 that the Perry Nuclear Power Plant had automatically shut down and that two water cooling pumps malfunctioned and portions of the backup systems failed. The NRC today announced that it would conduct a special inspection of the plant.

Kucinich’s letter to the NRC detailed the history of poor management at the plant and requested a briefing a soon as is “reasonably practicable.” The NRC has stated that their inspection would be finished in seven days, with a report to follow in 45 days.

“I think the people of Ohio have reason to be concerned about FirstEnergy’s record in operating its nuclear power plants. I intend to get answers, to press the NRC to protect the safety to Ohio residents, and to hold FirstEnergy accountable,” Kucinich said.

Kucinich’s Subcommittee, which is part of the Oversight and Government Reform Committee, has oversight authority over the NRC. Earlier this year, FirstEnergy tried to escape the final two years of a required independent assessment of its Davis-Besse plant. However, after Kucinich wrote a letter expressing his concerns, FirstEnergy withdrew its request to avoid assessment.

FirstEnergy is the same company that was responsible for a massive power blackout, which forced parts of eight states and part of Canada into darkness in the summer of 2003…

Dear Mr. Klein:

Yesterday, FirstEnergy’s Perry nuclear power station experienced an unscheduled automatic shutdown and the failure of multiple equipment systems. Today, the U.S. Nuclear Regulatory Commission (NRC) announced that it would conduct a special inspection at the Perry plant to determine the causes of the shutdown, as well as the equipment failures.

As you know, NRC has over the years uncovered a number of serious management problems at the Perry facility. Namely,

• On September 26, 2002, the NRC Office of Investigations concluded that FENOC’s application for access was falsified at Perry;

• On October 6, 2003, the NRC Office of Investigations concluded that overtime records were deliberately falsified at Perry so as to appear to comply with technical specifications; and

• On April 1, 2004, the NRC informed FirstEnergy that it found “creative timekeeping” at the Perry plant.

As you also know, FENOC has exhibited an inclination toward evading oversight. Thus, in March, 2007, I wrote to NRC out of concern that FENOC had requested to be relieved from independent oversight mandated by NRC after a near catastrophe at the Davis-Besse Nuclear facility in 2002. As you know, the mandated independent assessments followed NRC’s investigation into FirstEnergy’s efforts to deceive the government about safety violations at the Davis-Besse facility that resulted in a football-sized crater in the reactor vessel.

Only a slim steel liner stood in the way of radioactive release into the air, which would have jeopardized the safety of millions of residents of the state of Ohio.

The design of the reactor is similar to the GE-designed reactors at Fukushima.

With an elected official like Kucinich calling for a new review of nuclear power plants, especially the two Ohio plants owned by FirstEnergy, it’s no surprise that FirstEnergy has a different view. A FirstEnergy spokesman said that while there are similarities between The Fukushima nuclear power plant, now in serious trouble with four of its six reactors leaking radioactive materials, and its Perry plant in Lake County, there are differences, too. Todd Schneider told Dan Haggerty of WEWS news that both plants are boiling water nuclear reactors built by General Electric, with Perry being an evolution from the plants in Japan. Schneider also identified differences, saying the Perry plant has a larger containment unit and underground backup fuel tanks while the Fukushima reactors have above-ground backup fuel tanks, which rushing waters from the tsunami washed away.

The backup fuel tanks are underground rather than aboveground. Big deal. Sounds like a potential Fukushima to me.

This is just my opinion… a sensitive thyroid and a little bit of facts and logic.

Cesium-134 and iodine-131 in Australia?

This is in response to a post from Enenews user vital1. A rainstorm with radioactive rain occurred in Caloundra, Australia on January 6, 2014.

January 9, 2014 at 6:59 pm Log in to Reply
Took a rain swab off a car here on the 6th January 2013.

This swab was tested using a Theremino Geiger counter kit using a Russian SBT-10 pancake probe. Initial peak was around 5 uSv/hr 3,000 cpm. This is the hottest rain washout detected here so far.



The decay chart of the rain swab showed classic Radon-222 decay daughter decay.



January 10, 2014 at 12:26 am Log in to Reply
Here is the scintillator test chart preliminary assessment, of that rain swab. I used experimental MCA Theremino software for this test. It can get a bit noisy near background. This experimental software is pushing the limits of what can be detected with the equipment here. I have placed peak markers at the top of the chart for reference.

The rain swab Geiger counter and scintillator tests showed that the rain event on the 6th January was mainly Radon-222, and Radon-220 washout.


You can see some of the peaks for Radon-222 and Radon-220 decay daughters still present in the test chart. The main peaks are for Radon-220 daughters at, Pb-212 X-ray (77 kev), Lead Pb-212 (238 keV) and Tl-208 583 keV.

As you can see there is no Cesium present, but traces of Iodine I-129 40 keV?, Lead Pb-210 47keV, U-235 at 185 keV?, and Beryllium Be-7 477 keV. The peak between the Be-7 and 511 peak markers is probably a sum peak of the two.

Any further discussion, or corrections to this assessment are welcome?

Previous rain water tests can be found here.


This rain sample was measured at 5 μSv/hr. This is 50 times the normal background level for this location.

Since he said further discussion was welcome, I took the liberty of looking at this a little further.

He mentioned that radon-222 (and its daughters) were found. This isotope is part of the uranium-238 decay chain. Nuclear fuel at Fukushima is made up mostly of U-238. It is found naturally underground, though, also. That is what uranium miners dig up from the ground. Uranium-235, the ingredient in enriched uranium, which is present in nuclear fuel, and in small quantities naturally, was also mentioned.

But he also found radon-220 (thorium decay series), and also iodine-129. I-129 is being emitted by Fuku, but it is also being dumped by the La Hague plant, and is probably a small contributor to ordinary nuclear power plant emissions.

But there may be a couple definite Fukushima-related isotopes in this spectrum, cesium-134 and iodine-131. My additions to this graphic are in red. To see this, we need to know the energies (in kEv) of these isotopes, as well as the branching ratios of each peak in the spectrum. From Wikipedia:

In particle physics and nuclear physics, the branching fraction for a decay is the fraction of particles which decay by an individual decay mode with respect to the total number of particles which decay. (link)

Which just means the some energy peaks are larger (in probability) than others, because they decay with different probabilities for the different peaks, and we know how much larger the peaks should be by comparing the branching ratios of the peaks.

isotope   energy (kEv)   branching ratio
-------   ------------   ---------------
Cs-134       569.3            15.4
Cs-134       604.7            97.6
Cs-134       795.8            85.4
Cs-134       801.9             8.7
I-131         80.2             2.6
I-131        284.3             6.1
I-131        364.5            81.7
I-131        637.0             7.2

So the peak of Cs-134 at 604.7 is 14% higher than the 795.8 peak. And the peak of I-131 at 364.5 is over 11 times higher than the peak at 637.

The graphic shows that it is plausible that these isotopes are in the rain sample. And if so, they are certainly from Fukushima. But they fall short of the 95% confidence level (or whatever this level might be) that would indicate “scientific proof” that these isotopes are present, according to whatever definition of what this proof is.

But, the opposite of “scientific proof of the existence of A” is NOT “scientific proof of the non-existence of A”. The opposite is “scientific uncertainty of the existence of A.” Something to keep in mind.

Fukushima AIDS, part 3: Protracted radiation exposure, the immune system, and cancer.

Fukushima AIDS, part 1 was a general overview of the immune system, and dealt with how Fukushima is affecting and will affect it in the coming years. Fukushima AIDS, part 2: Chronic radiation sickness described radiation illness in its different stages. This post will deal with protracted exposure to radiation, that is, radiation that lasts a long time, rather than in one shot, and how this affects the immune system and increases the risk of cancer.


Washington’s blog (1) has a good entry on the effects of low-level radiation and protracted exposure. Fukushima has been emitting radionuclides into the air and sea for almost 3 years now. This is a fundamentally different situation from the atomic bombings of Hiroshima and Nagasaki. It is also different from Chernobyl, which burned for 11 days.

Japan Times reports:

Protracted exposure to low-level radiation is associated with a significant increase in the risk of leukemia, according to a long-term study published Thursday in a U.S. research journal.

The study released in the monthly Environmental Health Perspectives was based on a 20-year survey of around 110,000 workers who engaged in cleanup work related to the Chernobyl nuclear plant disaster in 1986.

Scientists from the University of California, San Francisco, the U.S. National Cancer Institute and the National Research Center for Radiation Medicine in Ukraine were among those who participated in the research…

Dr. Beyea challenges a concept adopted by American safety regulators about small doses of radiation. The prevailing theory is that the relationship between dose and effect is linear – that is, that if a big dose is bad for you, half that dose is half that bad, and a quarter of that dose is one-quarter as bad, and a millionth of that dose is one-millionth as bad, with no level being harmless.

The idea is known as the “linear no-threshold hypothesis,” and while most scientists say there is no way to measure its validity at the lower end, applying it constitutes a conservative approach to public safety.

Some radiation professionals disagree, arguing that there is no reason to protect against supposed effects that cannot be measured. But Dr. Beyea contends that small doses could actually be disproportionately worse.

Radiation experts have formed a consensus that if a given dose of radiation delivered over a short period poses a given hazard, that hazard will be smaller if the dose is spread out. To use an imprecise analogy, if swallowing an entire bottle of aspirin at one sitting could kill you, consuming it over a few days might merely make you sick.

In radiation studies, this is called a dose rate effectiveness factor. Generally, a spread-out dose is judged to be half as harmful as a dose given all at once.

The so-called “radiation protection” organizations subscribe to this myth, that spreading out the dose over time is less harmful.

According to BEIR VII, cancer risk after LDRMD (low dose rate, moderate dose) exposure is expected to be by a factor of 1.5, according to the ICRP by a factor of 2, smaller than among atomic bomb survivors. However, the best estimates of the cancer risk in 11 of the 12 LDRMD studies are larger than both expectations (tables 3 and 4)…

The ICRP and BEIR VII base their DDREFs mainly on radiobiological results including animal data, which, in their majority, suggest a characteristically low risk for low-dose-rate exposures. It remains an open question as to why this characteristic is apparently not reflected in the human epidemiological data. (2)

But Dr. Beyea retorts: Dr. Beyea, however, proposes that doses spread out over time might be more dangerous than doses given all at once. [Background] He suggests two reasons: first, some effects may result from genetic damage that manifests itself only after several generations of cells have been exposed, and, second, a “bystander effect,” in which a cell absorbs radiation and seems unhurt but communicates damage to a neighboring cell, which can lead to cancer.

One problem in the radiation field is that little of the data on hand addresses the problem of protracted exposure. Most of the health data used to estimate the health effects of radiation exposure comes from survivors of the Hiroshima and Nagasaki bombings of 1945. That was mostly a one-time exposure… (1)

For example, in a study of 400,000 nuclear workers, Cardis et al. (2005) reported excess cancer from protracted exposure at a rate per Gray higher than that found in studies of one-time exposures in atomic bomb (A-bomb) survivors. In a study of 175,000 radiation workers receiving protracted exposures in the United Kingdom, Muirhead et al. (2009) observed excess cancer at the same rate as found in A-bomb survivors. Krestinina et al. (2007) found excess cancer in 17,000 members of the civilian population who received protracted exposure from emissions from the Soviet weapons complex—also at a higher rate than found in the A-bomb cohort. In addition, Chernobyl thyroid exposures meet the protracted test because > 90% of the dose came from iodine-131, which has an 8-day half-life (Gavrilin et al. 2004). (3)

This dependence on duration of time in radiation exposure is called the Petkau Effect:

… the chronic irradiation dose protracted in time can produce a stronger effect than the same dose delivered upon short-term exposure at a high rate.

The Canadian scientist A. Petkau first detected this effect in 1972 on cell membranes… Thus, for the radiobiological effect to be evident upon long-term exposure to low-intensity radiation, a dose five thousand times lower than upon irradiation at a high dose rate was sufficient. The phenomenon of the inverse dose rate dependence of radiation effect upon irradiation of cells with low doses and of cell hypersensitivity upon irradiation with superlow doses, estimated by some criteria, was later called the Petkau effect. (4)


Brash and Cairns delve into internal mutagens, and ask why there is a time delay from the exposure to the carcinogen and the appearance of cancer. Cesium, strontium, and plutonium in our bodies are mutagens, mutators of DNA, like any other carcinogen.

Why does there have to be a long interval between a cell’s exposure to a mutagen and the expression of the resulting mutations, and why do only a minority of the cell’s descendants express these mutations?

It would have been tempting to postulate that the various methods for producing cancer in the cells of animals are not good models of human carcinogenesis, were it not for the fact that humans and animals show the same strange relationship between dose of carcinogen and time of appearance of their cancers. For example, although the incidence of lung cancer in smokers appears to be directly proportional to the number of cigarettes smoked per day (Zaridze and Peto, 1986), it is proportional to roughly the sixth power of the duration of smoking. Similarly, when rats are continuously exposed to dietary carcinogens, their incidence of cancer rises as the first or second power of the dose rate but as a much higher power of time (Druckrey, 1967; Peto et al, 1997). If the carcinogen had simply to mutate a set of N genes to create cancer, the frequency of cancer should rise as the Nth power of the dose, and time would not be a major factor. These numerous experiments suggest, therefore, that mutagenic carcinogens cause just one or two events and that these (similar to the initial event in in vitro carcinogenesis) are then followed by steps that accumulate solely with the passage of time, driven perhaps by cell division. (5)

The higher the power of time, the more important is the duration of exposure to the carcinogen. Protracted exposure to carcinogens is widely known, and illustrated by cigarette smoking and carcinogens in food. There is no controversy here. Why is there a controversy when the carcinogen is internal particles of cesium and plutonium?

Low-dose ionizing radiation enhances cell proliferation and division:

This study shows the human cellular responses and the mechanism of low-dose ionizing radiation in CCD 18 Lu cells, which are derived from normal human lung fibroblasts… These results suggest that 0.05 Gy of ionizing radiation enhances cell proliferation through the activation of ERK1/2 and p38 in normal human lung fibroblasts. (6)

Cell proliferation, which is part of the cancer process, itself may induce cancer:

Does cell proliferation modify the carcinogenesis process? The obvious answer is that there would not be a carcinogenesis process without cell proliferation and that cell proliferation is an essential component of the process. Two other questions would then need to be answered: Is cell proliferation carcinogenic per se? Should investigations on cell proliferation be included in routine tests on chemicals?…

The IARC Working Group of June 1991 recognized that cell proliferation is an important mechanistic aspect for both genotoxic and nongenotoxic carcinogens. Cell proliferation may act at each stage of the carcinogenesis process, altering the size of the pool of cells at risk for a next event. Cell proliferation was considered to be a potentially important factor, especially as a part of the process of converting DNA adducts to mutation, as a potential enhancing factor of the mutation frequency by increasing the number of DNA errors during replication, and for determining dose-response relationships for some carcinogens. (7)

So when cells proliferate by cell division, it is an important factor in the development of cancer. Radiation promotes this division. The time period between exposure and cancer is influenced by the rate of proliferation. Radiation also enhances the number of DNA errors in the daughter cell, that is, the cell which was created when the original cell divided into two… both directly and by the enhanced rate of replication itself.


Cairns (8) developed a mathematical model of DNA damage to stem cells:

It seems that the combination, in the stem cell, of immortal strands and the choice of death rather than error-prone repair makes epithelial stem cell systems resistant to short exposures to DNA-damaging agents, because the stem cell accumulates few if any errors, and any errors made by the daughters are destined to be discarded. This paper discusses these issues and shows that they lead to a model that explains the strange kinetics of mutagenesis and carcinogenesis in adult mammalian tissues…

(i) If left undisturbed, stem cells accumulate few mutations, first because they are defective in DNA repair and tend to die if they suffer DNA damage, and second because they conserve immortal strands and therefore do not accumulate replication errors.

(ii) Most of the mutant clones in epithelia arose because a stem cell died and was replaced by a mutant daughter. To produce a permanently mutant clone, two events therefore are necessary: the existing stem cell has to be killed, and the mutation must have occurred in the lineage of the daughter that takes its place.

The original stem cell has to die first for this process to take place. DNA damage from ionizing radiation or other carcinogens does this. They are defective in DNA repair mechanisms.

(iii) The immediate descendants of a stem cell are growing exponentially, and thus, unlike the stem cell, they cannot avoid accumulating spontaneous errors of replication. This rather than mutagenesis driven by DNA damage is postulated to be their main route for acquiring changes in sequence.

We have already seen that ionizing radiation increases both cell proliferation and replication errors.

(iv) During continuous exposure to a DNA-damaging agent, no daughter cell can complete the steps needed to convert it into an immutable stem cell. Thus the probability that any given epithelial clone is mutant will be proportional to (a) the probability that at some point its stem cell was killed, and this will be proportional to the dose rate of the DNA-damaging agent and the duration of exposure, and (b) the probability that the replacing daughter has acquired a replication error, and this will be proportional simply to the time or the number of daughter cell divisions that have occurred since the stem cell was killed.

Part (a), the probability of the stem cell being killed, is proportion to the dose of radiation only. We shall see below that the immune system has a hand in this also. Part (b), is proportional to time.

… the incidence of cancer in experimental animals continuously exposed to carcinogens commonly increases as the first power of dose and a higher power of time. This is true for a wide variety of carcinogens and for many different tissues… The best studied example of human carcinogenesis is smoking-induced lung cancer, and here too the frequency of cancer is roughly proportional to the first or possibly second power of dose rate D (cigarettes per day) and to the sixth power of the duration of smoking… Fig. 2 shows the observed cumulative incidence of lung cancer in smokers in relation to duration of smoking (age  21) on the assumption that smokers
start smoking when they are 17 and that on average 4 years elapse between the creation of a cell with the requisite changes and the emergence of a detectable cancer.

The main curve on the graph would be a straight line if cancer rates were proportional to dose only. But the duration is to the sixth power. As time goes on, cancer rates skyrocket with continued smoking, which cannot be explained merely by the number of cigarettes smoked.

Cancer models that only take into account radiation doses do not work. They grossly underestimate cancer rates. Both dose and duration of radiation exposure must be taken into account.

As Fukushima goes on emitting radioactive poison into the air and ocean, the duration of protracted exposure becomes more and more important relative to dose rate, and cancer rates will skyrocket. This will happen at a much higher rate than at Hiroshima or Chernobyl.


The immune system plays a role both in protecting the body from cancer, and in promoting cancer in it.

Cellular transformation and tumor development result from an accumulation of mutational and epigenetic changes that alter normal cell growth and survival pathways. For the last 100 years, there has been a vigorous debate as to whether the unmanipulated immune system can detect and eliminate such altered host derived cells despite the fact that cancer cells frequently express either abnormal proteins or abnormal levels of normal cellular proteins that function as tumor antigens. In this review, we discuss the current state of this argument and point out some of the recent key experiments demonstrating that immunity not only protects the host from cancer development (i.e., provides a cancer immunosurveillance function) but also can promote tumor growth, sometimes by generating more aggressive tumors. The terminology “cancer immunoediting” has been used to describe this dual host protective and tumor promoting action of immunity, and herein we summarize the ever-increasing experimental and clinical data that support the validity of this concept. (9)

Elimination is the hallmark of the original concept in cancer immune surveillance for the successful eradication of developing tumour cells, working in concert with the
intrinsic tumour suppressor mechanisms of the non-immunogenic surveillance process. The process of elimination includes innate and adaptive immune responses to tumour cells…

The TA-specific T lymphocytes are recruited to the primary tumour site, and directly attack and kill tumour cells with the production of cytotoxic IFN-γ (interferon-gamma). (10)

The immune system attacks tumor cells with the cytokine IFN-γ. This is a Th1-associated cytokine (see Part 1). It is associated with autoimmunity rather than allergy. IFN-γ is given to people who have a genetic defect in producing this important immune system cytokine. It has side effects:

More common:
Aching muscles
fever and chills
general feeling of discomfort or illness
nausea or vomiting
skin rash
unusual tiredness

Less common:
Back pain
joint pain
loss of appetite
weight loss

Black, tarry stools
blood in urine or stools
cough or hoarseness
loss of balance control
lower back or side pain
mask-like face
painful or difficult urination
pinpoint red spots on skin
shuffling walk
stiffness of arms or legs
trembling and shaking of hands and fingers
trouble in speaking or swallowing
trouble in thinking or concentrating
trouble in walking
unusual bleeding or bruising

These side effects pretty much make up “Fuku flu”. The body is eliminating tumors from itself.

The next step in cancer immunoediting proceeds to the equilibrium phase in which a continuous sculpting of tumour cells produces cells resistant to immune effector cells. This process leads to the immune selection of tumour cells with reduced immunogenicity. These cells are more capable of surviving in an immunocompetent host, which explains the apparent paradox of tumour formation in immunologically intact individuals… Since the equilibrium phase involves the continuous elimination of tumour cells and the production of resistant tumour variants by immune selection pressure, it is likely that equilibrium is the longest of the three processes in cancer immunoediting and may occur over a period of many years. In this process, lymphocytes and IFN-γ play a critical role in exerting immune selection pressure on tumour cells. During this period of Darwinian selection, many tumour variants from the original are killed but new variants emerge carrying different mutations that increase resistance to immune attack. (10)

So here in the equilibrium phase, tumor cells are continuously being destroyed. Also, stem cells are being destroyed, and we know from above that this is necessary for mutated daughter cells to proliferate. If the stem cells are killed, but not all the mutant daughter cells, the exponential rise in tumor cells will occur.

Also natural selection provides that tumors now arise that are resistant to the immune system’s cytokine attacks, and they start sticking around.

In the final escape phase, the tumors express anti-inflammatory factors which are resistant to immune surveillance. A variety of tumour-derived soluble factors contribute to the emergence of complex local and regional immunosuppressive networks, including vascular endothelial growth factor (VEGF), IL-10, TGF-β, prostaglandin E2 (10)

Now the individual “has cancer”. There is nothing to stop its progression.

Many drugs and treatments for cancer have been proposed or are being developed based on the immunosurveillance model. Personally, I think it is a matter of finding the right balance of Th1, Th2, Th17, and Treg. Autoimmune-dominant people (like myself) have their bodies constantly being cleared of tumors, but the Darwinian selection of anti-inflammatory expressing tumors is speeded up also. Allergy-dominant individuals may wish to boost Th1 through probiotics or herbs.

But if Fukushima keeps going on for years and years, it’s going to finish everyone. People will die from cancer, autoimmune-related diseases, or from genetic defects passed on to future generations. Do not think, that there is X amount of radiation at Fuku, and that is not enough. That does not take into account protracted exposure. At some point it becomes an ELE.


(1) What Is The ACTUAL Risk for Pacific Coast Residents from Fukushima Radiation?

(2) Is cancer risk of radiation workers larger than expected?

(3) DNA Damage after Continuous Irradiation: Findings in Mice Compared with Human Epidemiologic Data

(4) Radiation Biophysics (Ionizing Radiations)

(5) The mysterious steps in carcinogenesis

(6) Low-dose of Ionizing Radiation Enhances Cell Proliferation Via Transient ERK1/2 and p38 Activation in Normal Human Lung Fibroblasts

(7) Cell Proliferation and Carcinogenesis: A Brief History and Current View Based on an IARC Workshop Report

(8) Somatic stem cells and the kinetics of mutagenesis and carcinogenesis

(9) Cancer immunosurveillance and immunoediting: the roles of immunity in suppressing tumor development and shaping tumor immunogenicity.

(10) Cancer immunoediting from immune surveillance to immune escape

(11) Interferon gamma-1b Side Effects

Unit 3 steaming and the latest plume.

Tepco has reported steam rising from Unit 3 at Fukushima Daiichi, in the period Dec. 19-27. Radiation has spiked in Hirono town, which is near the Fukushima plant, on the ocean. Majia has reported activity on the webcam, though a small portion of it is related to Unit 3. Another small earthquake has also occurred in the area.

It is likely that a radiation plume is on the way.

But it is not the Armageddon which has been pushed by turnerradionetwork.com:

Persons residing on the west coast of North America should IMMEDIATELY begin preparing for another possible onslaught of dangerous atmospheric radiation from the Fukushima nuclear disaster site in Japan. The Tokyo Electric Power Company (TEPCO) says radioactive steam has suddenly begun emanating from previously exploded nuclear reactor building #3 at the Fukuishima disaster site in Japan. TEPCO says they do not know why this is happening and cannot go into the building to see what’s happening due to damage and lethal radiation levels in that building. Experts say this could be the beginning of a “spent fuel pool criticality (meltdown)” involving up to 89 TONS of nuclear fuel burning up into the atmosphere and heading to North America.

This network was founded by Hal Turner, a white supremacist. The website denies that it now has any connection to Turner, but I think skepticism is called for.

On July 28, 2009 in the case of United States v. Turner in Chicago, Turner pleaded not guilty to threatening to kill three federal appellate judges there and then sought his release from custody, saying he had been an informant for the FBI… His lawyer said the defense would use “Turner’s background as an FBI informant” and argue that he was “trained by the FBI” as “an agent provocateur” to incite people.” (link)

I would think that the website has some spook thing involved with it. It is not a place to get valid information from.

It is not just Unit 3 that has problems. There is a large amount of strontium accumulating in a well near Unit 2. And there have been emissions at the common spent fuel pool (CSFP), and also at an area south of Unit 4. The CSFP is extremely concerning, due to the immense amount of radioactivity in the spent fuel rods stored there.

This is not the first time that Tepco has announced steam rising from Unit 3. According to Fukushima Diary, steam was reported by them on September 7 – September 20, and July 18 – August 7. Both of these steam events were associated with iodine-131 releases. This is the most major risk. Iodine prophylaxis may be needed. I use a couple drops of Lugol’s iodine… the potassium iodide pills typically contain huge amounts of iodide. I don’t want to take the pills, because my TSH level is elevated.

The prior events had much webcam activity going on… not so much this time. There may or may not be a criticality. This is probably not a humongous iodine release, but all these nickel-and-dime iodine events can build up into hypothyroidism or thyroid cancer.