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Most recent update: Saturday, 24 May 2014 This post continues here: https://miningawareness.wordpress.com/2014/05/26/radioactive-reindeer-nuclear-guinea-pigs-part-x-of-a-series/ It is a continuation of: https://miningawareness.wordpress.com/2014/04/10/radioactive-reindeer-chernobyl-guinea-pigs-part-viii-of-a-series/
Previous posts should be read before drawing conclusions, as to the content. The following post is related: https://miningawareness.wordpress.com/2014/03/14/alzheimers-disease-and-ionizing-radiation/
Alpha radiation tracks (Hi LET) in typical star pattern in lymph node..plutonium, Los Alamos Sci, no 23, 1995
(High-LET), Alpha particles from plutonium:
The image … is an autoradiograph of a tracheobronchial lymph node from a former worker at the Laboratory. It shows alpha tracks radiating in a typical star pattern from tiny alpha-active clumps of matierial. Chemical analyses of the radioisotopes in this individual’s lungs and lymph nodes indicated that those clumps most likely consisted of an aggregate of plutonium particles.” (pp. 234-235, James McInroy, “True Measure of Exposure“, Los Alamos Science, No. 23, 1995 (Emphasis our own).

As we pointed out toward the end of Part VIII, one thing which appears, conspicuously, mostly lacking, is research on plutonium and the brain, or the brain and other (internal) radionuclides – excepting those used as tracers, such as Technetium. Reading a US military document, on the topic, leads to the conclusion that this is because the primary concern was if troops could function during a nuclear war long enough to win a battle. The governments didn’t give a damn about what happened to anyone afterwards, including the “Atomic veterans”, who have shockingly had, and sometimes still are having, trouble getting their benefits in the US, UK, Australia, and France. There are, for instance, now lists of the right cancers, and if you have the wrong cancer, you are excluded, whereas ionizing radiation can cause any cancer! The governments-nuclear industry haven’t given a damn about the impact on the people, either, with the exception of President Kennedy who, subsequent to Jackie’s miscarriage, pushed for a stop to above ground nuclear testing. While the US and Russia stopped above ground testing, though underground tests still leaked, France, China and others continued to do them for longer. If above ground testing continued, there would probably be no life left on earth. And, so, that poor Kennedy baby who died, gave life to us all, like a sacrificial lamb.  However, if the nuclear industry is not stopped promptly, and if past accidents and the waste are not dealt with seriously and sensibly, life on earth is still doomed. The impacts of the nuclear industry are cumulative – something which they want us to forget, by speaking only of short or shorter-lived radionuclides. Even these are damaging, especially when they are routinely emitted from nuclear power plants, as is accepted practice.

Despite the apparent paucity of research, available to the public, we know that plutonium and other radionuclides can get around the blood-brain barrier and enter the brain, because we know that iron does, and we know of plutonium’s behavioral similarities to iron. And, we can deduce that researchers at the US Dept. of Energy and its predecessors, and in the UK, either knew or suspected an impact on the brain, because they appear to have been very anxious to get hold of the brains of dead plutonium workers, as discussed in the previous post.

Recall that Jensen et. al. (2012) pointed out the importance of “Understanding how a synthetic element like plutonium subverts existing biological metal-acquisition pathways to enter cells and where the pathways of plutonium and essential metals, such as iron, converge or diverge.” Since plutonium has only existed on earth, in biologically significant amounts, since it was first manufactured in 1941, living beings “have no natural mechanism for specifically recognizing plutonium.” Plutonium is radiologically (as well as a chemically) toxic and is, in their words, “strongly retained” by the body, so its uptake, due to environmental contamination “can pose significant health risks.” (Mark P. Jensen, et., al., 2012, “An iron-dependent and transferrin-mediated cellular uptake pathway for plutonium,” Nat Chem Biol.; 7(8): 560–565, NIH library: http://www.ncbi.nlm.nih.gov/pmc/ )

According to Jensen et. al. (2012) (and others), plutonium shares some important similarities with biologically important transition metals, especially iron. “Plutonium is highly redox active with four oxidation states (III, IV, V, and VI) potentially relevant to living organisms, although Pu(IV) has long been considered the most important under physiological conditions.” Pu (IV) is strongly hydrolyzed at physiological pH, and if there are no steric constraints, “Pu4+ tends to form complexes that are about as stable as those of trivalent first row transition metals, notably Fe3+“. The chemical similarities between Iron (Fe) and Plutonium (Pu) “are particularly important to the metal transport protein serum transferrin (Tf). Transferrin functions to strongly bind and carry two Fe3+ ions into cells, but it also binds Pu4+ strongly…” They “found that mammalian cells could acquire Pu through the common Fe uptake pathway of receptor-mediated endocytosis of metallo-transferrins. However, to be taken into the cell by receptor-mediated endocytosis, Pu needed help from Fe.” Plutonium associates in vivo with transferrin and ferritin. (The entire paper is available here: Mark P. Jensen, et. al., 2012, “An iron-dependent and transferrin-mediated cellular uptake pathway for plutonium,” Nat Chem Biol. ; 7(8): 560–565, NIH library: http://www.ncbi.nlm.nih.gov/pmc/ So, plutonium cannot get into the cell by itself, but it can ride into the cell, on transferrin, along with an iron ion. However, it can only fit adequately in one of the two slots available on the transferrin. Atkinson, et. al. 2005, have presented “evidence for a more general pathway for the irradiation of target cells, mediated through the sequestration of heavy-metal radionuclides by the intracellular iron-storage protein ferritin… Since both transferrin and ferritin are capable of sequestering a multitude of other metals, including radioactive heavy metals “, they have postulated “that ferritin may be a significant reservoir for radionuclide deposition…” (Atkinson (2005) et. al., “Intracellular sequestration of 223Ra by the iron-storage protein ferritin,” Radiat Res. 2005 Aug;164(2):230-3 See: http://www.ncbi.nlm.nih.gov/pubmed/16038594

Furthermore, according to Raven, et. al., 2013, the hippocampus is heavily damaged in Alzheimer’s Disease, whereas the thalamus, is resistant to Alzheimer’s Disease damage. They found that, compared with healthy controls, those with Alzheimer’s Disease had increased ferritin iron in the hippocampus, but not in the thalamus. They conclude that hippocampus damage “occurs in conjunction with ferritin iron accumulation“. (Raven EP, et. al., 2013, “Increased iron levels and decreased tissue integrity in hippocampus of Alzheimer’s disease detected in vivo with magnetic resonance imaging,” J Alzheimers Dis. 2013;37(1):127-36, http://www.ncbi.nlm.nih.gov/pubmed/23792695 ) Plutonium can only attach to transferrin, in conjunction with iron. It is found associated with the iron-storage protein ferritin. Thus, plutonium could be in the brain, along with the iron, irradiating it.

Wistar rat

One of the rare papers which discusses plutonium and the brain was written 58 years ago. It compares recovery from impacts of external irradiation with x-rays and internal irradiation from injected plutonium.  (Plutonium is a more damaging, internal, alpha emitter, as seen in the photo at the very top): “Effects of Total Body X-Irradiation and Plutonium Injection on the Cholinesterase of Erythrocytes and Brain1″, by Jean C. Sabine2, American Journal of Physiology, 31 October 1956,Vol. 187, no. 275-279.(With The Technical Assistance of Helen M. Miller and Dorothy J. Nickolai, From the Health Division, Los Alamos Scientific Laboratory, University of California, Los Alamos, New Mexico, Work done under the auspices of the U.S. Atomic Energy Commission. 2 Present address: University of California School of X-rays were delivered from two 25o-kvp machines Medicine, San Francisco 22, Calif.)

Sabine (1956) appears to have found plutonium’s role as a neurotoxin. To understand the findings, we must first know the following:
Acetylcholinesterase (AChE), also known as RBC cholinesterase, and erythrocyte cholinesterase is found in the blood on red blood cell membranes, in neuromuscular junctions, and in neural synapses. In the mammalian brain the majority of AChE occurs as a tetrameric G4 form (See:  http://en.wikipedia.org/wiki/Cholinesterase).  “A cholinesterase inhibitor (or ‘anticholinesterase’) suppresses the action of the enzyme. Because of its essential function, chemicals that interfere with the action of cholinesterase are potent neurotoxins, causing excessive salivation and eye-watering in low doses, followed by muscle spasms and ultimately death… The so-called nerve gases and many substances used in insecticides have been shown to act by combining with a residue of serine in the active site of acetylcholinesterase, inhibiting the enzyme completely. The enzyme acetylcholinesterase breaks down the neurotransmitter acetylcholine, which is released at nerve and muscle junctions, in order to allow the muscle or organ to relax. The result of acetylcholinesterase inhibition is that acetylcholine builds up and continues to act so that any nerve impulses are continually transmitted and muscle contractions do not stop.“. (Emphasis added, http://en.wikipedia.org/wiki/Cholinesterase)

And, importantly, “Damage to the cholinergic (acetylcholine-producing) system in the brain has been shown to be plausibly associated with the memory deficits associated with Alzheimer’s disease.http://en.wikipedia.org/wiki/Acetylcholine

The Sabine (1956) article appears rather incomplete in its discussion about plutonium and the brain, choosing instead to focus primarily on the relationship between external irradiation with x-rays and red blood cell formation. The abstract is probably as, or more, useful than the full article. For both the x-ray irradiated and plutonium injected mice, the cholinesterase activity initially increased, only to later fall sharply to levels far below normal. However, whereas the x-ray irradiated mice recovered, there was no recovery of the plutonium injected mice in the 63 days which they were observed. See the abstract here: http://ajplegacy.physiology.org/content/187/2/275 This study also found “that moderate to very small doses of x-rays deliver some kind of insult to the erythrocyte system,…” (p. 278)

Considering the ongoing inhibition of cholinesterase activity in the plutonium injected mice, it is interesting that the plutonium used was Pu (VI), “Plutonium as Pu+6 in 0.5% citrate was injected intraperitoneally” (p. 276), whereas according to Jensen et. al. (2012), it is Pu (IV) which is the most important in the body: “Plutonium is highly redox active with four oxidation states (III, IV, V, and VI) potentially relevant to living organisms, although Pu(IV) has long been considered the most important under physiological conditions.“(Intraperitoneal injection is the injection of a substance into the peritoneum, i.e. lining of the body cavity. http://en.wikipedia.org/wiki/Intraperitoneal_injection Don’t you feel warm and fuzzy now! )

Monday, 5 May 2014

After looking at this we wondered, again, if the falls by one of the victims of the US human plutonium experiments, and by a contaminated plutonium worker at Sellafield, UK, were purely coincidental? Or were they somehow related to this inhibition of acetylcholinesterase? Stair falls are apparently frequent, but neither of these were of an age likely to bounce up and down stairs.
AChe inhibitors pic
Acetylcholinesterase inhibition. Image by Sbolmer via wikimedia

Inhibition of Acetylcholinesterase, as happened for weeks after the mice were irradiated with x-rays and longer term (over 63 days) for the mice injected with plutonium, leads to accumulation of Acetylcholine, thus impeding nerve transmission. Irreversible inhibitors of Acetylcholinesterase can cause muscle paralysis, convulsions, bronchial constriction, and death by asphyxiation. Some are used as insecticides and nerve gases for chemical warfare (e.g., Sarin). Reversible inhibitors, which occupy the esteratic site for short periods of time (seconds to minutes), are used to treat some diseases of the central nervous system. Mir-132 microRNA is an Acetylcholinesterase inhibitor, occurring naturally in the body. It may counter brain inflammation, by allowing Acetylcholine to build up and act as an anti-inflammatory. http://en.wikipedia.org/wiki/Acetylcholinesterase This last point appears to suggest that the impact of plutonium and x-rays on acetylcholinesterase levels could be a natural reaction to radiation-induced inflammation. For those interested in reading on this last topic there is: “MicroRNA-132 potentiates cholinergic anti-inflammatory signaling by targeting acetylcholinesterase“, Shaked I. et. al., Immunity, 2009 Dec 18, 31(6): 965-7 http://www.ncbi.nlm.nih.gov/pubmed/20005135 (Link to full article dead, so we based our understanding on the wikipedia article, hoping that the author of the wikipedia article read it). See also: http://en.wikipedia.org/wiki/Cholinergic_neuron

According to wikipedia: “Acetylcholinesterase inhibitors: Occur naturally as venoms and poisons; Are used as weapons in the form of nerve agents; Are used as insecticides; Are used medicinally… Compounds which function as quasi-irreversible inhibitors of cholinesterase are those most likely to have use as chemical weapons or pesticides.Acetylcholinesterase inhibitors can be reversible, irreversible or quasi-irreversible. http://en.wikipedia.org/wiki/Acetylcholinesterase_inhibitor Reversible inhibitors, which act for seconds to minutes are used to treat central nervous system diseases. http://en.wikipedia.org/wiki/Acetylcholinesterase

Not too surprisingly, some doubt the safety and efficacy of acetylcholine inhibitors, as medication. In “Efficacy and safety of cognitive enhancers for patients with mild cognitive impairment: a systematic review and meta-analysis” by Andrea C. Tricco PhD, et. al., 2013, CMAJ November 5, 2013 vol. 185 no. 16, the authors note that “…cholinesterase inhibitors…are used to treat dementia, but their effectiveness for mild cognitive impairment is unclear.” The authors reviewed previous research and found that these drugs “did not improve cognition or function among patients with mild cognitive impairment and were associated with a greater risk of gastrointestinal harms“. Their findings did “not support the use” of them for “mild cognitive impairment.http://www.ncbi.nlm.nih.gov/pubmed/24043661 According to wikipedia, side effects of acetylcholinesterase inhibitors, include:
mild – usually goes away: Diarrhea, Headache, Insomnia, Nausea, Vomiting; potentially serious: Abdominal pain … Dizziness, Slow heartbeat, … Weaknesshttp://en.wikipedia.org/wiki/Acetylcholinesterase_inhibitor See also: http://en.wikipedia.org/wiki/SLUDGE_syndromel

Pietro Longhi 027
Syncope, fainting or passing out: http://en.wikipedia.org/wiki/Syncope_(medicine)
Bradycardia is low resting heartbeat which “sometimes results in fatigue, weakness, dizziness, and at very low rates fainting.http://en.wikipedia.org/wiki/Bradycardia

Gill SS, et. al. (2009) in “Syncope and its consequences in patients with dementia receiving cholinesterase inhibitors: a population-based cohort study“, Arch Intern Med, 2009 May 11, 169(9):867-73, remark that “Cholinesterase inhibitors are commonly prescribed to treat dementia, but their adverse effect profile has received little attention. These drugs can provoke symptomatic bradycardia and syncope, which may lead to permanent pacemaker insertion. Drug-induced syncope may also precipitate fall-related injuries, including hip fracture. In a population-based cohort study, we investigated the relationship between cholinesterase inhibitor use and syncope-related outcomes using health care databases from Ontario, Canada, with accrual from April 1, 2002, to March 31, 2004. We identified 19 803 community-dwelling older adults with dementia who were prescribed cholinesterase inhibitors and 61 499 controls who were not.” They found that “Hospital visits for syncope were more frequent in people receiving cholinesterase inhibitors than in controls… Other syncope-related events were also more common among people receiving cholinesterase inhibitors compared with controls: hospital visits for bradycardia…, permanent pacemaker insertion…, and hip fracture… Results were consistent in additional analyses in which subjects were either matched on their baseline comorbidity status or matched using propensity scores.” They conclude that “Use of cholinesterase inhibitors is associated with increased rates of syncope, bradycardia, pacemaker insertion, and hip fracture in older adults with dementia. The risk of these previously underrecognized serious adverse events must be weighed carefully against the drugs’ generally modest benefits.http://www.ncbi.nlm.nih.gov/pubmed/19433698 (May be read online for free; emphasis added)

This gets us back to the stair incidents:
Stairway baluster in Hanoi, Vietnam
An investigative journalist, Eileen Welsome, set out to discover the identities of those injected with plutonium, in the US plutonium experiments of the 1940s. She wrote a book called “The Plutonium Files“, published in 1999. Speaking of victim HP-3, believed to be Eda Schultz Charlton, Welsome says that “On July 25, 1946, eight months after she had been injected with plutonium, Eda fell down her basement stairs. She told doctors she didn’t recall striking her head or losing consciousness, but afterward she became dizzy and vomited. Blood trickled from her right ear and her spinal fluid was bloody. X-rays revealed no evidence of an old or new fracture. Eda was hospitalized for two weeks and complained frequently of a severe headache and upset stomach“. For the rest of her life, she “suffered from severe attacks of vertigo, nausea, blurred vision, and unsteady gait.” Furthermore, she eventually developed blood cells of rare shapes and sizes, which could be indicative of anemia (Welsome, 1999). An association between plutonium and anemia is well-known.

We must also mention William Purcell, a 48 year old hemophiliac, injected with plutonium on Oct 23, 1945, as HP-2, and who died Aug 4, 1948, two and a half years later of “Brain disease” (Los Alamos Sci, p. 208; Welsome, 1999). He didn’t fall down the stairs, to our knowledge, he simply died of “brain disease“, at age 50. According to Welsome (1999) he “was a cheerful, red-haired Irishman” and “was well known and well liked by the staff.“. They did not even get the three control samples of his blood prior to the injection. (Welsome, 1999, emphasis added)

A plutonium worker from Sellafield who did also fall down the stairs, according to the Redfern Inquiry, was Edward McMullen:
Edward McMullen died on 13 April 1973, aged 48. He was survived by his wife, Catherine, who has since died, and two daughters,… After service in the Royal Navy, Mr McMullen was employed as a process worker by the United Kingdom Atomic Energy Authority (UKAEA) at Sellafield from 1949 until 1953 and from 1956 until his death. He was exposed to plutonium on three occasions in 1960 and 1961 and was later permanently excluded from plutonium work. In mid-March 1973, Mr McMullen fell down the stairs at home, sustaining a serious head injury.” (“The Redfern Inquiry into human tissue analysis in UK nuclear facilities, Volume 1: Report, Ordered by the House of Commons to be printed, 16 November 2010“; emphasis added) Entire document is here: https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/229155/0571_i.pdf

Wednesday, 7 May 2014

In her research for the book “The Plutonium Files” (1999), Welsome ran across a victim of the uranium injection experiments, while looking for the victims of plutonium injection. Mary Jeanne Connell was injected with uranium, in 1946, at the age of 24 years old at Strong Memorial Hospital-University of Rochester. There was nothing at all wrong with her. Doctors simply wanted to know why she didn’t gain weight – whereas, it seems that thinness runs in her family. It seems that the saying “No woman can be too thin or too rich”, had not yet become vogue in Rochester, New York, at the time. Or, more likely, it was a flimsy excuse to inject a healthy victim with uranium. As we have stated elsewhere, the researchers wanted to know the impact of radionuclides on healthy workers in the nuclear industry and so making sick people into guinea pigs was of limited use. By quoting Ms. Connell, Eileen Welsome answers the question, which many have been wondering: What did it feel like to be injected with a radionuclide? Did it burn like would be suspected? One morning Connell awoke to find herself strapped down, surrounding by a large group of doctors. She remarked that one doctor was “trying to open a small vial of orange-colored liquid” and that “Everyone in the room appeared to be afraid of the mixture. There was no cork, no cap, no way to open the sealed bottle. Finally someone smashed the vial against of the edge of a table and a small amount of the orangey stuff trickled onto the floor.” She “couldn’t believe her eyes: The material had burned a hole in the floor. ‘I never forgot that,’ she said. One of the doctors then injected the mixture into her veins. As the radioactive material flooded through her body, she said, ‘I felt like I was laying on hot coals. I almost passed out.’ Later she was woozy and sick to her stomach.” (Welsome, 1999, emphasis our own) That says it all.

We found a full copy of the paper “MicroRNA-132 Potentiates Cholinergic Anti-Inflammatory Signaling by Targeting Acetylcholinesterase” by Iftach Shaked, et. al. Immunity 31, 965–973, December 18, 2009 , mentioned earlier. The authors, following Pollak et al., 2005, and Pavlov et al., 2009, state that Acetylcholesterase (AChE) “inhibition restricts inflammation in both the peripheral and the central nervous system (CNS)“. Thus, they had “predicted that microRNAs targeting AChE can attenuate inflammation“. (p.966) Their “findings demonstrate that AChE-targeting miR-132 can attenuate inflammation by reducing AChE amounts, thus enhancing the brain’s ability to govern inflammation via cholinergic signaling“. They “found that excessive inflammation upregulates miR-132“(p. 968). They further note that Acetylcholesterase “is a stress-induced gene” and that their “findings suggest that the poststress surge in these processes can be terminated by miR-132-mediated downregulation of AChE,“(Acetylcholesterase)(p. 969). (“Downregulation is the process by which a cell decreases the quantity of a cellular component, such as RNA or protein, in response to an external variable. An increase of a cellular component is called upregulation“. http://en.wikipedia.org/wiki/Downregulation_and_upregulation )

And, so probably the Acetylcholinesterase increased, as part of a stress response, when the mice (Sabine, 1956) were initially exposed to x-rays and injected with plutonium, only to subsequently decrease, due to downregulation. Since the advent of x-rays, it has been known that ionizing radiation is associated with burns and inflammation. Inflammation is part of the innate immune system, also known as non-specific immune system, which is the first line of immune defense. It is a generic and non-specific reaction, in contrast to the adaptive immune system, found only in vertebrates. Unlike the adaptive immune system, “it does not confer long-lasting or protective immunity to the host.” Rather, the “Innate immune systems provide immediate defense against infection, and are found in all classes of plant and animal life. They include both humoral immunity components and cell-mediated immunity components. The innate immune system is an evolutionarily older defense strategy, and is the dominant immune system found in plants, fungi, insects, and primitive multicellular organisms.http://en.wikipedia.org/wiki/Innate_immune_system

The neural circuit that regulates the immune response to injury and invasion is called the inflammatory reflex. Its sensory, afferent arc, activated by cytokines, causes inflammaiton. But, too much inflammation for too long can be damaging to the body and so it also has “a motor, or efferent arc, which transmits action potentials in the vagus nerve to suppress cytokine production. Increased signaling in the efferent arc inhibits inflammation and prevents organ damage…http://en.wikipedia.org/wiki/Inflammatory_reflex This requires the acetylcholine, which acetylcholinesterase destroys. Thus the need for inhibition-decline of acetylcholinesterase: “The molecular basis of cytokine-inhibiting signals requires the neurotransmitter acetylcholine, and the Alpha-7 nicotinic receptor receptor expressed on cytokine-producing cells. The release of acetylcholine in spleen suppresses the production of TNF and other cytokines which cause damaging inflammation. Signaling in the efferent arc of the inflammatory reflex, termed the ‘Cholinergic anti-inflammatory pathway,’ provides a regulatory check on the innate immune system response to invasion and injury. The action potentials arising in the vagus nerve are transmitted to spleen, where a subset of specialized T cells is activated to secrete acetylcholine. The net effect if the reflex is to prevent the damage caused by excessive cytokine production.http://en.wikipedia.org/wiki/Inflammatory_reflex (Emphasis added)

Saturday, 10 May 2014

Historically, researchers from the US Atomic Energy Commission (AEC), ancestor to the US Nuclear Regulatory Commission (NRC), understood the dangers of plutonium. One such researcher is cited in this 1974 comment from “Proceedings of Public Hearings: Plutonium and the other Transuranic Elements, vol. 3, additional Material Received, USEPA, (ca 1974):
US EPA Comment 1974 on Pu
Pages are missing in the original document. However, this comment is interesting. It was written now 40 years ago:
1974 US EPA Comment on Pu p. 2

What does the US Nuclear Regulatory say now about “Plutonium in the Body” Well, first they start with a patent lie, “Most people will never come into contact with plutonium.” This is a lie because since the dropping of the first plutonium based nuclear bombs, Trinity, then Nagasaki (Hiroshima was uranium based), and all the above ground nuclear weapons tests, the whole entire world is exposed to the dangerous alpha emitter plutonium…the only plutonium that would have gone away is Plutonium 241, which would now be dangerous alpha emitter Americium 241 – the rest of the plutoniums have half lives ranging from 87.7 years (plutonium 238) to 24,110 years (plutonium 239). So, in less than 70 years they’ve gone nowhere! Plutonium is even found in sardines. As such, one study found that frequent eaters of sardines had more elevated levels of plutonium in their bones (because most people eat bones and liver of sardines). Warning: if you eat sardines do not eat its bones or internal organs; if you can even find sardines, as they have declined or disappeared in the Pacific – whether this is normal cycles or Fukushima (or Hanford) cannot be known for certain. Some sardines are too tiny to remove the bones. See: https://miningawareness.wordpress.com/2014/02/27/plutonium-in-fish-and-seafood/ Notice what it says about bottom feeders, which could help explain why the Chernobyl catfish are so highly radioactive. For those of us who have known since at least the 1960s that it was dangerous to eat tuna because of the mercury, it came as a huge shock to recently learn that the tiny sardine, so low on the food chain that it should be the safest food, is contaminated with plutonium, and most certainly strontium and other radioactive nasties. Why aren’t those people telling everyone not to eat sardines because of BPA in the cans, warning us of the real problem? Plutonium!

This year supposedly small, safe amounts of Americium and Plutonium got lose into the air at the WIPP facility in New Mexico. Considering that it is cumulative both in the environment and in the body, with a half-life in the body of decades and in the environment of hundreds and even thousands of years, the amount which escaped is not ok, especially as that area has been subjected to nuclear weapons testings, experiments, etc. (Also, there was the Church Rock uranium mining disaster, though it didn’t involve plutonium).

Now, they have decided that WIPP may have been an chemical reaction-explosion caused by a nitrate salt. Would that have been plutonium nitrate perhaps? Maybe americium nitrate? Was the flash of green light seen during the accident caused by plutonium nitrate or perhaps plutonium fluoride? There is plutonium fluoride at WIPP from Rocky Flats, which arrived early on. Notice that inhaled plutonium nitrate, due to its solubility, moves out of the lungs, into the body itself, more quickly than plutonium oxide. (NRC below). Upon ingestion plutonium nitrate is more readily absorbed by the body. (See: http://www.crios.be/ionizing_radiation/internal/actinides/biological_characteristics.htm) This is not surprising, since it is more soluable. It would also move more readily throughout the environment.

This is what the US Nuclear Regulatory Commissions says currently:
Plutonium in the Body
Most people will never come into contact with plutonium. But for scientists and engineers that have worked with it, it is important to know about the potential health effects. The most common form of plutonium is plutonium oxide—a compound of plutonium bonded with oxygen. In this form, plutonium does not easily dissolve. Plutonium oxide’s impact on human health depends on how it enters the body. If someone eats or drinks it, a large percentage will be eliminated rapidly as waste. If plutonium oxide is inhaled, some of it remains in the lungs. Between 20 and 60 percent can remain, depending upon the size of the particles and other factors. The rest is eliminated from the body within several days. Of the plutonium remaining in the lungs, about half will be removed each year. Some is excreted, some lodges in the lymph nodes, and a very small amount migrates, settling in other organs but mainly in bones. If plutonium oxide gets into an open wound, it may move directly into bones and other organs, mainly the liver.

The next most common form is plutonium nitrate—a compound of plutonium, oxygen and nitrogen. This chemical dissolves somewhat more readily than the oxide. Plutonium nitrate behaves much like plutonium oxide in the body but moves out of the lungs more rapidly.

Research shows plutonium can be chemically toxic and contribute to tumor development. But the most common form of plutonium has more radiological than chemical toxicity.” http://www.nrc. gov/reading-rm/doc-collections/fact-sheets/plutonium.html (Emphasis Added)

In January, an article was produced about the effects of plutonium nitrate, but strangely upon the lungs – where the impact is less than plutonium oxide. And, they don’t let up on the poor beagles, which they compare to lung samples from one human: “Carcinogenic and inflammatory effects of plutonium-nitrate retention in an exposed nuclear worker and beagle dogs“, by CE Nielsen, et. al., Int J Radiat Biol, 2014 Jan;90(1):60-70.
Having first noted that “Previous studies have shown an unexpected retention of soluble plutonium in the beagles and human case studied here.” Their conclusions relate to “the inflammatory responses following prolonged plutonium exposure“. All radioactive roads appear to lead to inflammation – even WIPP! As we will see, it also leads to Alzheimer’s again.

Monday, 12 May 2014

Plutonium can do this to the lungs
End-stage interstitial lung disease (honeycomb lung)
End-stage pulmonary fibrosis of unknown origin, taken from an autopsy in the 1980s. http://en.wikipedia.org/wiki/Interstitial_lung_disease

Before looking at their abstract, let’s look quickly at some terminology. Nielsen et. al. (2014) found that the plutonium “exposed human showed interstitial fibrosis in peripheral regions of the lung“:
Pulmonary fibrosis is the formation or development of excess fibrous connective tissue (fibrosis) in the lungs. It is also described as ‘scarring of the lung’…
Symptoms of pulmonary fibrosis are mainly:
Shortness of breath, particularly with exertion
Chronic dry, hacking coughing
Fatigue and weakness
Chest discomfort
Loss of appetite and rapid weight loss
http://en.wikipedia.org/wiki/Pulmonary_fibrosis

How many takers for pulmonary fibrosis?

Nielsen (2014) et. al. concluded that their “data suggests that FASLG, BCL2, CASP3 and apoptosis play a role in the inflammatory responses following prolonged plutonium exposure.” They found that “In both the beagles and human there were statistically significant modifications in the expression of Fas ligand (FASLG), B-cell lymphoma 2 (BCL2), and Caspase 3 (CASP3)“.

Fas ligands, play a role in killing off cancer cells:
Fas ligand (FasL or CD95L) is a type-II transmembrane protein that belongs to the tumor necrosis factor (TNF) family. Its binding with its receptor induces apoptosis. Fas ligand/receptor interactions play an important role in the regulation of the immune system and the progression of cancer… Fas forms the death-inducing signaling complex (DISC) upon ligand binding.
http://en.wikipedia.org/wiki/Fas_ligand (see: http://www.ncbi.nlm.nih.gov/gene/356)

An oncogene is a gene that has the potential to cause cancerhttp://en.wikipedia.org/wiki/Oncogene An Oak Ridge trained biochemist has happily spoken of poor fruit flies having oncogenes!

More potential bad impacts of plutonium nitrate:
Bcl-2 (B-cell lymphoma 2), encoded in humans by the BCL2 gene, is the founding member of the Bcl-2 family of regulator proteins that regulate cell death (apoptosis), by either inducing (pro-apoptotic) it or inhibiting it (anti-apoptotic). Bci-2 is specifically considered as an important anti-apoptotic protein and is thus classified as an oncogene.
Bcl-2 derives its name from B-cell lymphoma 2, as it is the second member of a range of proteins initially described in chromosomal translocations involving chromosomes 14 and 18 in follicular lymphomas… The two isoforms of Bcl-2, Isoform 1, also known as 1G5M, and Isoform 2, also known as 1G5O/1GJH, exhibit similar fold. However, results in the ability of these isoforms to bind to the BAD and BAK proteins, as well as in the structural topology and electrostatic potential of the binding groove, suggest differences in antiapoptotic activity for the two isoforms. …it has clinical significance in lymphoma. Damage to the Bcl-2 gene has been identified as a cause of a number of cancers, including melanoma, breast, prostate, chronic lymphocytic leukemia, and lung cancer, and a possible cause of schizophrenia and autoimmunity. It is also a cause of resistance to cancer treatments.
” (Emphasis added) http://en.wikipedia.org/wiki/Bcl-2 (references and more at link)

Would you like those diseases?! That’s the cost of the nuclear industry, and when governments and companies are allowed to improperly dispose of the existing nuclear waste. If the pro-nuclear people (or anyone undecided) still have functional brains then this alone should be sufficient for them to become anti-nuclear now.

Oh, oh! Alzheimer’s again!
The CASP3 protein is a member of the cysteine-aspartic acid protease (caspase) family. Sequential activation of caspases plays a central role in the execution-phase of cell apoptosis… It is the predominant caspase involved in the cleavage of amyloid-beta 4A precursor protein, which is associated with neuronal death in Alzheimer’s disease. Alternative splicing of this gene results in two transcript variants that encode the same protein.http://en.wikipedia.org/wiki/Caspase_3 ( references and more at link)

Caspase-3 triggers early synaptic dysfunction in a mouse model of Alzheimer’s disease”, by D’Amelio M, Cavallucci V, Middei S, Marchetti C, Pacioni S, Ferri A, Diamantini A, De Zio D, Carrara P, Battistini L, Moreno S, Bacci A, Ammassari-Teule M, Marie H, Cecconi F., Nat Neurosci. 2011 Jan;14(1):69-76.
Abstract
Synaptic loss is the best pathological correlate of the cognitive decline in Alzheimer’s disease; however, the molecular mechanisms underlying synaptic failure are unknown. We found a non-apoptotic baseline caspase-3 activity in hippocampal dendritic spines and an enhancement of this activity at the onset of memory decline in the Tg2576-APPswe mouse model of Alzheimer’s disease. In spines, caspase-3 activated calcineurin, which in turn triggered dephosphorylation and removal of the GluR1 subunit of AMPA-type receptor from postsynaptic sites. These molecular modifications led to alterations of glutamatergic synaptic transmission and plasticity and correlated with spine degeneration and a deficit in hippocampal-dependent memory. Notably, pharmacological inhibition of caspase-3 activity in Tg2576 mice rescued the observed Alzheimer-like phenotypes. Our results identify a previously unknown caspase-3-dependent mechanism that drives synaptic failure and contributes to cognitive dysfunction in Alzheimer’s disease. These findings indicate that caspase-3 is a potential target for pharmacological therapy during early disease stages.
http://www.ncbi.nlm.nih.gov/pubmed/21151119 (Emphasis added)

Radiation is Bad for you!
We can’t even start to count the ways!

And, here is the Nielsen, et. al. (2014) abstract on plutonium nitrate, inflammation and the lungs!
Carcinogenic and inflammatory effects of plutonium-nitrate retention in an exposed nuclear worker and beagle dogs.
Int J Radiat Biol. 2014 Jan;90(1):60-70.
Nielsen CE1, Wang X, Robinson RJ, Brooks AL, Lovaglio J, Patton KM, McComish SL, Tolmachev SY, Morgan WF. 1Biological Sciences Division, Pacific Northwest National Laboratory , Richland , WA.
PURPOSE:
Plutonium-nitrate has a moderately rapid translocation rate from the lung to blood stream. Previous studies have shown an unexpected retention of soluble plutonium in the beagles and human case studied here. The inflammatory responses that may be associated with long-term exposure to ionizing radiation were characterized. These pathways include tissue injury, apoptosis, and gene expression modifications. Other protein modifications related to carcinogenesis and inflammation and the various factors that may play a role in orchestrating complex interactions which influence tissue integrity following irradiation were investigated.
MATERIALS AND METHODS:
We have examined numerous lung samples from a plutonium-exposed worker, a human control, and a variety of plutonium-exposed beagle dogs using immunohistochemistry and quantitative Reverse Transcriptase-Polymerase Chain Reaction (RT-PCR).
RESULTS:
The exposed human showed interstitial fibrosis in peripheral regions of the lung, but no pulmonary tumors. Beagles with similar doses were diagnosed with tumors in bronchiolo-alveolar, peripheral and sub-pleural alveolar regions of the lung. The terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay showed an elevation of apoptosis in tracheal mucosa, tumor cells, and nuclear debris in the alveoli and lymph nodes of the beagles but not in the human case. In both the beagles and human there were statistically significant modifications in the expression of Fas ligand (FASLG), B-cell lymphoma 2 (BCL2), and Caspase 3 (CASP3).
CONCLUSIONS:
The data suggests that FASLG, BCL2, CASP3 and apoptosis play a role in the inflammatory responses following prolonged plutonium exposure. Utilizing these unique tissues revealed which pathways are triggered following the internal deposition and long-term retention of plutonium-nitrate in a human and a large animal model.
http://www.ncbi.nlm.nih.gov/pubmed/24279338

Thursday, 15 May 2014

We have already discussed the Mayak facility, where not only workers, but people living nearby, were exposed to plutonium and other radionuclides, both routinely and due to an accident: https://miningawareness.wordpress.com/2014/04/29/russia-radioactive-teeth-poisoning-their-own/ https://miningawareness.wordpress.com/2014/02/22/radioactive-reindeer-chernobyl-guinea-pigs-part-vi-of-a-series/

The workers at the Mayak nuclear facility in Russia are considered “the only adequate human data for evaluating cancer risks from exposure to plutonium.” This is, in part, because the Soviet Union was a few years behind in discovering the impacts of inhaled and ingested plutonium, but not that far behind. So, in reality, this cohort data is probably flawed. Initially baffled because those falling ill were not exposed to high level gamma radiation, the Russians learned the dangers of plutonium very quickly due to sick plutonium workers, rather than animal experiments. They quickly learned to give Gulag prisoners the most dangerous jobs and to rotate hired workers out before they got too sick, based on their blood work. Kate Brown in her book “Plutopia” (2013), Ch. 23, “The Walking Wounded”, tells the story of these people who were excluded from the medical data at Mayak. According to her research, those who have been consistently monitored comprise less than 10% of workers – the main paid staff who remained in town. The worst work was done by Gulag prisoners and soldiers were also exposed. In a 2012 article she refers to a population study of 1,059 people compared to a cohort of 17,740 mentioned in the study on Mayak below. It is possible that additional information was declassified leading to the 17,740 cohort. Nonetheless, if the workers were “hired”, as stated below, it appears to mean that the study below excludes prisoners and soldiers.

According to an article by Kate Brown (2012) “GE had a secret contract with the Washington State Department of Labor and Industries to redact evidence of radiation accidents for reasons of national security… Because of the secret agreement to redact information related to radiation poisoning, there is no way of knowing for sure how many workers fell ill or died on the job at Hanford.” (Kate Brown, 2012, “In the House that Plutonium Built: The history of plutonium, radiation and the communities that learned to love their bombhttp://history.msu.edu/files/2012/03/The-House-that-Plutonium-Built.docx ) This, along with exposure of temporary workers, would very obviously make Hanford data flawed. It appears that Japan is not the only country that has used migrant labour at its nuclear plants. While Japan has reached new lows, with the treatment of workers at Fukushima, it has always had seasonal nuclear worker migration. This practice of migrating lower level workers reportedly occurs in the US today, as discussed by Laramée (2012) http://www.radiationtruth.org/2012/10/nuclear-nomads-glow-boys-atomic-gypsies-gamma-sponges-liquidators-jumpers-and-bio-robots-the-disposable-migrant-workers-of-the-nuclear-energy-industry/ J. Samuel Walker (2012) in “Permissible Dose: A History of Radiation Protection in the 20th Century“, U. Cal-NRC, informs us that by the early 1970s there was an increase in temporary nuclear workers, with about a third having been employed for less than three months. They were used to reduce exposure of permanent staff. These workers were often poorly informed of the dangers and the workers were hired repeatedly and received high doses each time. “… the exposure of growing numbers of individuals increased the risks of genetic consequences for the entire population“. (Walker, 2012, p. 104) Recall that since the 1920s it has been known that genetic impacts of ionizing radiation can be inherited. Sometimes the mutations are recessive and sometimes do not appear for several generations.

This is an abstract, but the full text is available and in the public domain in the US, as a US government work. The Walker book above was paid for by the US NRC (i.e. US taxpayers) and yet must be purchased for a small fortune!
Lung, liver and bone cancer mortality in Mayak workers“, by Sokolnikov ME, Gilbert ES, Preston DL, Ron E, Shilnikova NS, Khokhryakov VV, Vasilenko EK, Koshurnikova NA, Int J Cancer. 2008 Aug 15;123(4):905-11.
Abstract
Workers at the Mayak nuclear facility in the Russian Federation offer the only adequate human data for evaluating cancer risks from exposure to plutonium. Risks of mortality from cancers of the lung, liver and bone, the organs receiving the largest doses from plutonium, were evaluated in a cohort of 17,740 workers initially hired 1948-1972 using, for the first time, recently improved individual organ dose estimates. Excess relative risk (ERR) models were used to evaluate risks as functions of internal (plutonium) dose, external (primarily gamma) dose, gender, attained age and smoking. By December 31, 2003, 681 lung cancer deaths, 75 liver cancer deaths and 30 bone cancer deaths had occurred. Of these 786 deaths, 239 (30%) were attributed to plutonium exposure. Significant plutonium dose-response relationships (p < 0.001) were observed for all 3 endpoints, with lung and liver cancer risks reasonably described by linear functions. At attained age 60, the ERRs per Gy for lung cancer were 7.1 for males and 15 for females; the averaged-attained age ERRs for liver cancer were 2.6 and 29 for males and females, respectively; those for bone cancer were 0.76 and 3.4. This study is the first to present and compare dose-response analyses for cancers of all 3 organs. The unique Mayak cohort with its high exposures and well characterized doses has allowed quantification of the plutonium dose-response for lung, liver and bone cancer risks based on direct human data. These results will play an important role in plutonium risk assessment.

†This article is a US Government work and, as such, is in the public domain in the United States of America. http://www.ncbi.nlm.nih.gov/pubmed/18528867 (Emphasis added)

In the original article Sokolnikov, et. al. (2008) further note that:
Nevertheless, some cancers indicated as the cause of death, especially liver cancers, could represent metastasis from primary cancers of other organs. This misclassification could lead to underestimation of the ERR” [Excess relative risk]. “Analyses in this paper were based on improved plutonium and external organ dose estimates. Nevertheless, estimating internal organ doses from plutonium and their pattern over time is subject to many uncertainties including imprecision in urine measurements, uncertainties in when plutonium exposure occurred and the form of the plutonium, uncertainties in the biokinetic models and parameter values used to estimate deposition and clearance in organs of the body, and the fact that models can only approximate the behavior of plutonium in a given individual. Current estimates use different models for smokers and nonsmokers, but could not take account of detailed smoking histories, and smoking data were not available for all workers. The Mayak data provide the first direct estimates of cancer risks from plutonium. It is expected that future plutonium risk assessments will make strong use of these data along with data from other sources including data on persons exposed to other alpha-emitter” Sokolnikov, M. E., Gilbert, E. S., Preston, D. L., Ron, E., Shilnikova, N. S., Khokhryakov, V. V., Vasilenko, E. K. and Koshurnikova, N. A. (2008), “Lung, liver and bone cancer mortality in Mayak workers”. Int. J. Cancer, 123: 905–911. doi: 10.1002/ijc.23581 †This article is a US Government work and, as such, is in the public domain in the United States of America. http://www.ncbi.nlm.nih.gov/pubmed/18528867

Saturday, 17 May 2014

Relative risk is the ratio of the risk of a particular health effect in an exposed group to that in a comparable unexposed group. A relative risk of one implies that exposure has no effect on risk.http://www.rerf.jp/glossary_e/riskrela.htm. This is because if the risk is the same it cancels itself out and becomes one.

What is ERR discussed in the Sokolnikov et. al.’s 2008 study?
Excess relative risk is expressed as relative risk (RR) minus one, or that portion of the RR accounted for by the particular risk factor under study (A-bomb radiation, in this instance).http://www.rerf.jp/glossary_e/eriskrela.htm In other words, the extra risk caused by radiation.

Writing ERR = RR – 1 may leave some or even many perplexed. Again one has to return to very basic math. The exposed group is actually an “experimental” group (aka “nuclear guinea pigs”!) and the unexposed group what is called the “control” group. We will call the exposed or experimental group Re and the unexposed or control group Rc. ERR = Re-Rc/Rc, which is the same as ERR = Re/Rc – Rc/Rc which is the same as ERR = Re/Rc – 1. Hopefully everyone recalls that Rc/Rc cancels itself out and becomes 1. In the case of the study they found that 786 Mayak workers exposed to radiation had died by Dec 21, 2003. Of the 786 workers, 239 or one third (30%) died as a result of Plutonium exposure. They furthermore found that by age 60, the Excess Relative Risk (ERRs) per Gy for lung cancer were 7.1 for males and 15 for females; and the ERRs for liver cancer were 2.6 and 29 for males and females, respectively; those for bone cancer were 0.76 and 3.4 . So by the age of 60, the extra risk for lung cancer per Gy was 710% higher for males and 1500% higher for females than the normal population. For liver cancer the extra risk for these workers was 260% for men and 2900% for women above the normal risk. Similarly, for bone cancer the extra risk for these workers was 76% above the normal risk for men and 340% above the normal risk for women. Note that in each case of liver, bone and lung cancer, women had a substantially higher ERR than men. Presumably all of these ERRs are per Gy or Gray of exposure. But, as usual there is a hitch because we are dealing here with extra dangerous alpha emitter (plutonium) and Gy is for gamma emitters and x-rays.

Recall: “When alpha particle emitting isotopes are ingested, they are far more dangerous than their half-life or decay rate would suggest, due to the high relative biological effectiveness of alpha radiation to cause biological damage, after alpha-emitting radioisotopes enter living cells.
….
It is estimated that chromosome damage from alpha particles is anywhere from 10 to 1000 times greater than that caused by an equivalent amount of gamma or beta radiation, with the average being set at 20 times.
http://en.wikipedia.org/wiki/Alpha_particle

It is difficult to see how 20 is an average of between 10 and 1,000. It certainly isn’t the mean or arithmetic average. It appears unlikely that it would be the median with half above and half below. Perhaps it is the modal average or most frequently occurring? Even that appears strange. How likely and how accurate is an average of 20 in a range from 10 to 1,000? What does “average being set at 20” mean? Also, the type of chromosomal damage is different, as we have seen already, but may repeat soon, because it is of critical importance.

Not surprisingly, it has been suggested that 20 is an arbitrary weighting factor established by the ICRP (We will return to this point), which is apparently based on their arbitrary definition of accepted risk of disease and death and used to establish safe radiation doses. Who are they to determine how many live and how many die?

Perhaps for those working in radiation fields and exposed routinely to gamma one might come up with a comparative factor for alpha, but not for the general population.

Rather, it is common sense that you cannot compare transient gamma to alpha radiation, such as plutonium and americium, which will stay in the body for decades and probably a lifetime. How can anyone possibly compare the two? One is external and less damaging and one is internal. If the nuclear madness is not stopped, eventually people, plants and animals will be totally contaminated (equilibrium state) inside and out and only then can the two – high LET internal alpha and low LET external gamma- be compared and by then it is too late.

Monday, 19 May 2014

SI Radiation dose units
SI Radiation Dose Units by Doug Sim, Creative Commons via Wikimedia

The Japanese RERF focuses on external radiation during the atomic bombings of Japan. So the following statement may be appropriate for external gamma radiation but not for alpha radiation: “For instance, the relative risk of leukemia is the largest among various late effects; RR is about 5 or 6 per Gy.http://www.rerf.jp/glossary_e/riskrela.htm

What is the Gy Gray unit? And, why is it not always appropriate?
The Gray measures the absorbed energy of radiation, but the biological effects vary by the type and energy of the radiation and the organism and tissues involved. This is expressed by the Sievert, which has the same dimensions as the Gray, but is a measure of the potential for damage to human tissue. It is related to the Gray by weighting factors…

For X-rays and Gamma rays the Gray is numerically the same value when expressed as the Sievert (Sv), but for Alpha particles one Gray is equivalent to twenty Sieverts because of the radiation weighting factor that is applied. To avoid any risk of confusion between the absorbed dose (by matter) and the equivalent dose (by biological tissues), one must use the corresponding special units;…” http://en.wikipedia.org/wiki/Gray_(unit)#Biological_risk

We really want to know first of all HOW 20 is an average of 10 to 1000 times greater risk for alpha!? http://en.wikipedia.org/wiki/Alpha_particle Furthermore, how can anyone possibly compare high energy, High LET, internal exposures with half lives of decades to a Low LET exposure that might last less than a second? Not only are we speaking of decades, but there are 10 years in a decade and 365 days in a year and 24 hours in a day and 60 minutes in an hour and 60 seconds in a minute. An X-ray lasts for about a millisecond (1/1,000 of a second). For those who survived the atomic bombings of Hiroshima-Nagasaki the gamma exposure was brief but intense, and the illnesses continued on and continue to this day, even though gamma exposure stopped because it is external.

The online atomic bomb museum has an image of an alpha particle similar to the one on the top of this post, though with lower magnification. It is presumably plutonium: “The black star in the middle shows the tracks of alpha rays emitted by a particle of plutonium 239 in the lung tissue of an ape. These rays do not travel very far, but once in the body, they can penetrate more than 10,000 cells within their range. This set of alpha tracks (magnified 500 times) occurred over a 48-hour period. The plutonium particle that emitted them has a half-life of 24,400 years.” (Emphasis added; image at link) http://atomicbombmuseum.org/3_health.shtml Note that plutonium would have had the most impacts further out from ground zero at Nagasaki where black rain fell into the water reservoir, and where there is less monitoring of victims.

Given all of the above, the weighting factor of 20 to convert Gray (Gy) to Sieverts (Sv) appears patent hogwash. It cannot even start to account for the risk involved in internal long-lived alpha emitters like plutonium and americium. The weighting factor of risk would have to be so high that the tolerance of ingested alpha emitters must simply be none. No one should be allowed to ingest alpha emitters! The exposure is constant!

Thursday, 22 May 2014

The whole issue of radiation protection continues to be hotly debated from different sides (among those able to enter the debate). The ICRP rules are recommendations only. This makes the debate even broader. The US EPA has not updated its rules for how much nuclear power plants and reprocessing plants can leak since the 1970s and is taking feedback for June 4th. You can be sure that the pro-nuclear lobby is prepared. The anti-nuclear lobby appears unprepared. The big thing at stake is if the rules will be more or less protective. The only water protection is through the US NRC and it is voluntary, it seems. So, any protection is better than none for water emissions. Talk about Fukushima dumping radiation into the ocean – US nuclear plants can apparently dump all they please into the rivers and oceans. The rivers feed into the oceans so it is all the same. The ICRP rules have changed again and again and must be obtained through a library or purchased. The language is also often unfathomable for even those, like ourselves, who are expert at reading bureaucratic nonsense. The EPA asks if people want the old 1990s ICRP rules or the rules from the 2000s, among other things. First one must figure out how protective the 1970s rules are or are not for emissions of radionuclides into air and then make sure that emissions are decreased and not increased. While expressing risks in sieverts seems appropriate to us for external radiation, given that radiation detectors are in sieverts (although US ones apparently are in rems or mrems, which is another complication), expressing internal risks of alpha particles appears problematic. Some prefer a direct concept of actual cancer (or other disease) risk, such as 1 in 1,000 chance of getting cancer. But, that conclusion will depend on the studies used. It seems to us that it should not be an either or but a both – express the exposure in sieverts and also tell people the risk of getting cancer or another illness. Another either or which has been expressed by the US EPA is either chance of getting cancer or other illness (morbidity) or chance of dying (mortality), whereas both matter. If you have to pick and choose, the risk of radiation induced illness (morbidity) is most important for both the individual and society. Such illnesses put a high financial and social burden upon society. The nuclear industry is putting a huge financial and social burden upon society, from many angles, and it is difficult to understand how it continues to perpetuate itself. It appears to do so through legal bribery (campaign donations) and most likely illegal bribery.

The ICRP draft edition, which is available for free, made the following observation about “effective dose” being introduced to describe random, i.e. stochastic effects:
(39) The quantity effective dose has been introduced in order to limit the risk of stochastic effects. It has been intended that the risk of stochastic effects at exposures corresponding to the dose limits should be equal, regardless of the manner of irradiation – whether the body is uniformly or heterogeneously irradiated from external radiation or from intakes of radionuclides. This has been accomplished by first weighting the absorbed dose according to the biological effectiveness of the different radiation qualities with a radiation weighting factor wR. The summation of the radiation weighted doses to the various tissues and organs of the human body, modified by tissue weighting factors, wT, then gives the effective dose. The tissue weighting factors account for the varying radiation sensitivity of tissues to the induction of stochastic effects.http://www.icrp.org/docs/2005_recs_CONSULTATION_Draft1a.pdf

David Kocher, an expert in radiation risks from Oak Ridge, made the following comment about the above paragraph:
Paragraph (39). I think that these discussions overstate the degree of correspondence between effective dose and risk of stochastic health effects. Yes, there is some correspondence, but it is only approximate. There are several issues here including that (1) radiation weighting factors are based on the Commission’s definition of detriment, rather than risk itself, (2) tissue weighting factors are rough approximations, as appropriately acknowledged by the Commission, and (3) effective dose often corresponds poorly to risk in cases of intakes of long-lived alpha emitters which are tenaciously retained in the body (use of committed effective dose is the culprit here). A minor issue is that effective dose takes into account risks of hereditary effects as well as cancers, and these two kinds of risk are not experienced in the same individuals. Thus, I think that the Commission needs to be more careful not to overstate the correspondence between effective dose and risk of stochastic effects.” (emphasis added) http://www.icrp.org/consultation_viewitem.asp?guid=%7BE00BBF55-477E-4FE9-BB71-DC4E97656CEA%7D (David C. Kocher, SENES Oak Ridge, Inc., Commenting as an individual, Document 2005 ICRP Recommendation) Elsewhere David Kocher has come up with a bizarre idea that individuals may choose to be exposed where they know the risks and undue pressure is not exerted upon them. From this last we see that he is not anti-nuclear, but rather trying to state the flaws as he understands them.

Thus we need to take very seriously his concern that “effective dose often corresponds poorly to risk in cases of intakes of long-lived alpha emitters which are tenaciously retained in the body” His mention of hereditary-genetic risks reminds us that the most recent ICRP standards reduce genetic protections. And, they only count impacts on two generations, whereas many decades ago concerns were expressed, because experiments showed that genetic damage could be recessive and not show up for many generations. Killing off current generations is bad enough but how can we justify making those future generations ill due to the selfish stupidity of so many leaders and of the nuclear lobby? And, why do we need to wade through these ICRP rules when we know that nuclear is dangerous and it is simply game playing where the nuclear lobby tries to get out from under responsibility.

Medical insurance companies need to take a stand against nuclear, for ultimately it costs them a fortune. They finally did so against the tobacco lobby. The Nuclear Industry is THE reason for the cancer epidemic (along with smoking). It is clearly THE major cause of cancer and many other illnesses and yet researchers search endlessly for other explanations. What is the point of making us all guinea pigs and why are they getting by with it?

Saturday, 24 May 2014

Comparing Apples and Oranges

Another critic of the ICRP standards is an expert in radiology at Columbia University (D.J. Brenner). Most of his interest seems to be in the area of medical radiology. Beware, however: He is not necessarily concerned with giving the patient more protection, but sometimes less. We will probably return to him, as his points, both good and bad, are still sometimes relevant to nuclear standards. Medical and Nuclear Industry Standards are mixed in the ICRP.

This raises a larger and more fundamental question and that is the mixing of standards for external radiation and internal radiation, of mixing very short-lived exposures in a medical context for some presumed personal benefit vs. standards for the nuclear industry where the fairly debatable alleged benefits are “social” benefits of electricity and financial benefits for corporate stock-holders (along with money for government officials who have been legally or illegally bribed). The “social benefits” of electricity (or profit) may not even be for you; they may not even be for your country; but the risk IS still yours. And, the exposure from the nuclear industry is for a much longer period (days, months, years, decades) and sometimes permanent (for the individual, a lifetime; for the environment, 100s to 1,000s of years). We leave aside here the fact that due to newer technologies the use of ionizing radiation for most diagnosis is largely unneeded today and the use may be related to profit motives. And, for medical procedures you have CHOICE of exposure, at least if you are willing to challenge your doctor. There has been little to no choice with the nuclear industry. In the 1980s, the US Surgeon General, Everett Koop took the logical, yet virtually non-existent, step of sending out, by mail, health educational brochures to every household in the USA. There was one about AIDS and maybe one about the dangers of smoking. How many in the US or elsewhere have received information about their leaking nuclear power plants and the impact on health? How many in the US were notified by mail, by their government, of a request for feedback about the amount of radionuclides which the US FDA would allow in food? How many were notified by mail of the 120 day call for comment regarding how much the EPA will allow nuclear power plants to leak (deadline June 4, 2014)? The answer is clearly none. Virtually no one is or was aware of these topics, except the nuclear industry. Citizens in Tennessee actually requested a hearing with the US gov regarding the burning of German rad waste in Tennessee and their request was ignored. The US gov allowed the burning of the German waste to go forward in Tennessee.

In the very first mathematics class, if not before, we were taught that you cannot add apples and oranges (or blue sticks and red sticks), although they are both fruit, their nature/nutritional value is different. Thus, the whole system of “radiation protection” standards set forth by the ICRP (and others) is fundamentally flawed on its most basic levels. It is flawed because it tries to compare high-LET radiation, including neutrons and alpha particles to low-LET radiation of external x-rays used in medical diagnosis. It tries to compare internal radiation and external radiation and radiation exposure which lasts for less than a second to exposures lasting a life-time. Internal, short-lived radioactive tracers, although still dangerous, are generally not as dangerous as much of that which is emitted by the nuclear industry:
Diagnostic treatment involving technetium-99m will result in radiation exposure to technicians, patients, and passers-by. Typical quantities of technetium administered for immunoscintigraphy tests, such as SPECT tests, range from 400 to 1,100 MBq (11 to 30 mCi) (millicurie or mCi; and Mega-Becquerel or MBq) for adults.[64][65] These doses result in radiation exposures to the patient around 10 mSv (1000 mrem), the equivalent of about 500 chest X-ray exposures.[66] This level of radiation exposure carries a 1 in 1000 lifetime risk of developing a solid cancer or leukemia in the patient.[67] The risk is higher in younger patients, and lower in older ones.[68] Unlike a chest x-ray, the radiation source is inside the patient and will be carried around for a few days, exposing others to second-hand radiation. A spouse who stays constantly by the side of the patient through this time might receive one thousandth of patient’s radiation dose this way.Note that this 1 in 1000 lifetime risk of a solid cancer or leukemia is the risk of a planned, one time, limited exposure. Technetium-99 m is a low-LET gammer emitter with a half-life of only 6.0058 hours (93.7% of it decays to 99Tc in 24 hours). The biological half-life is one day, though Technetium-99 has a half-life of 211,000 years and is a problematic byproduct of the nuclear industry. http://en.wikipedia.org/wiki/Technetium-99m Plutonium is a higher energy, High LET emitter, which stays in your body for a lifetime. It has no medical benefits.

Like apples and oranges are both fruit, High LET alpha particles, and Low LET x-rays, gamma rays and beta particles; internal and external; medical and nuclear power – all are ionizing radiation but the impacts differ. The distribution of costs-risks vs. who benefits also differs.

THIS POST IS ONGOING AND SHOULD BE UPDATED FOR Monday 26 May 2014 UTC-GMT (barring unforeseen circumstances) or a part X will be opened in a new post. IF YOU ARE INTERESTED IN THIS GENERAL TOPIC OF RADIATION, RADIONUCLIDES, AND DISEASE, PLEASE COME BACK SOON. This is basically a learning, exploration, review series. There will be sometimes technical, sometimes not so technical things.

Due to the fierce urgency of educating the public about the dangers of nuclear power, before the nuclear lobby and its minions destroy humanity and the earth, we are currently unable to handle comments. Unlike the Queen we are short-staffed. So, we apologize not only for any errors found by our readers in the past or present, but we also apologize in advance for future errors. We try our best, but are mortals, unlike the nuclear lobby who think they are radiation-proof immortals. We are very behind in posting, so do not know when or if we will re-open comments. We seem to fall farther behind each day. When we say nuclear power, we include the dangers of mining and waste, as well. With no nuclear power there will be no new mining and no new waste. Then, in an intelligent, educated way, everyone must take care of the waste properly. It is NOT by denying the dangers and diluting and dumping the radioactive waste, that the problem is solved!