Friday, May 11, 2012

On Internal Emitters

Majia here: I have been considering taking my family to the southern hemisphere for summer vacation to escape the radiation. However, I realize now that strategy is not going to be effective. 

Why? As I see it, the main problem in the US is not from our exposure to external gamma radiation from Fukushima. Rather, the problem is the bio-accumulation of radiation fallout in our food chain.

At the May 4 conference on Fukushima held in New York City Dr. Junro FUSE, Internist and head of Kosugi Medical Clinic near Tokyo, Japan (in Japanese with English interpretation) asserted:

“The European Commission [Committee] on Radiation Risk has stated that they believe the risk from internal exposure is between 200 and 600 times greater than the risk from external exposure.” Footage of the NYC Press Conference May 4th 2012 Cinema Forum Fukushima (hat tip Enenews

MAJIA HERE: There are relatively few studies on the risks from internal exposure, as compared to external exposure. In 2004, a committee was set up to look at the available research on the subject.  

Findings were published in a report:

Committee Examining Radiation Risks of Internal Emitters (CERRIE) Report of the Committee Examining Radiation Risks of Internal Emitters (CERRIE) National Radiological Protection Board; Chilton, UK: 2004. Available:

Page 29 Conclusions
To the extent that ionising radiations from both internal emitters and external sources generate similar physical and chemical interactions in living matter, there are no fundamental differences between the two sources of radiation that suggest that their effects cannot be combined for radiological protection purposes. However, short-range charged particle emissions, both electron (eg low energy beta particles) and alpha particles, are important contributors to internal but not external radiation exposures. The potential heterogeneity of energy deposition in tissues resulting from these internal emitters contrasts with the relatively uniform irradiation of tissues from most external sources and defines the central difference between these two sources of radiation exposure. The Committee agreed that a methodology for combining radiation effects from both types of source should, in principle, be achievable. However, the Committee was more divided on the adequacy of methods used to take account of such heterogeneity, and these matters have been a central issue addressed by the Committee….

The chemical properties of an element determine its distribution and retention in body tissues and cells and hence determine the extent to which it may be located in a way that short-range emissions may have an accentuated effect (ie in terms of damage caused to cellular targets for the induction of cancer and genetic effects). Biokinetic and dosimetric models are used to determine this relationship between the distribution of radionuclides and target cells. In some cases, simple models suffice because the element and its radioisotopes are known to be uniformly distributed in body tissues and the pattern of energy deposition is similar to that resulting from external irradiation. In other cases, complex models are required to account for heterogeneous energy distribution within tissues, requiring knowledge of the location of the radionuclide at different times after intake and the location of target cells. Data available for model development are of variable quality – in some cases, particularly for some of the more important radionuclides, good information is available, including human data, but in other cases reliance is placed on sparse animal data. In many cases, there is little information on variability between individuals and within human populations. The Committee concluded that in general the combination of biokinetic and dosimetric models gave rise to estimates of central values with widely variable uncertainty ranges. The Committee was more divided on the likely span of uncertainties for specific radionuclides and situations of exposure, but there was agreement that in some cases uncertainties could extend over at least an order of magnitude.

68 The location of radionuclides within tissues is particularly important for alpha particles that typically have a range of a few tens of μm (traversing a few cells). It is also important for low energy electrons, such as the beta particle emissions from tritium with a range of <10 μm, and Auger electrons. For these radionuclides, sub-cellular location can be important, as location within the cell nucleus can increase carcinogenic potential while within cytoplasm it can decrease risk. On the basis of substantial experimental data, it is recognised that these radiation types can cause greater damage per unit energy deposition, because of the density of their ionisations in small tissue volumes, than sparsely ionising radiations such as gamma rays and X-rays, and higher energy electrons. The understanding of these differences, termed relative biological effectiveness (RBE), in terms of three-dimensional track structure, and consequent interactions with DNA and other molecules, is a key goal of microdosimetry. The Committee was generally in agreement that this field of research is not yet far enough advanced for microdosimetric techniques to present viable alternatives to current risk-related radiation dosimetry. However, there was agreement that advances in microdosimetry were likely to provide insights into the reliability of dose estimates and may ultimately provide complementary approaches. The desirability of further research was emphasized

MAJIA HERE: Essentially, the committee found that there were heterogeneities across internal and external exposure because of the special risks posed by ingestion of alpha particles. The current risk model, the ICRP method, fails to adequately account for this heterogeneity; however, the committee concluded that the risk model has heuristic value (especially given the lack of alternatives) in real-world radiological risk assessment.

Another review of the ICRP model comes to the same conclusion.

Harrison, J., & Day, P. (2008). Radiation doses and risks from internal emitters. Journal of Radiological Protection, 28, 137-159.
Harrison and Day explain here the limitations of the ICRP methodology for risk estimates, wr and effective dose:

“Risk estimates for radiation-induced cancers are largely derived from studies of the effects of external radiation, the principal source of information being long-term studies of those who survived the immediate effects of were the atomic weapons’ explosions at Hiroshima and Nagasaki, in 1945 (the so-called A-bomb survivors). Thus, the risk of developing or dying from each observed type of cancer has been related to the estimated external radiation dose received at the time of the explosion, and for a short time thereafter from gamma radiation from environmentally deposited radionuclides. Doses from inhaled or ingested radionuclides were not assessed…. (p. 145)

 “A central concern of CERRIE (2004) was whether the risk factors derived from studies of the A-bomb survivors can be applied generally. These risk factors, which applied to short, homogeneous, high external doses of gamma radiation at a high dose rate, are applied in all situations, including those at the opposite extreme in all respects: namely heterogeneous, low dose exposure to charged particles at low dose rates over protracted periods. Although CERRIE concluded that these risks factors were the best available, the Committee expressed considerable reservations and considered that the application of these factors constituted an important source of uncertainty in dose and risk estimates.” (146)

MAJIA HERE: The backstory on CERRIE is interesting. 

I found this account in the European Committee on Radiation Risk’s 2010 Recommendations of the ECRR The Health Effects of Exposure to Low Doses of Ionizing Radiation Regulators' Edition (

“The Committee on Radiation Risk from Internal Emitters CERRIE was set up by the UK Environment Minister Michael Meacher in 2001 along just these lines. Its remit was to discuss the evidence for the failure of the ICRP model for internal emitters and present both evidence which supported and opposed such a belief. In the event, this process failed when the Minister was removed in 2003 before the final report was published and a new Environment Minister, Elliot Morley, was appointed by Tony Blair. Morley shut down the Committee before it could carry out the key research which had been agreed to decide the issue and legal threats were used to prevent the oppositional report being included (see endnote Morley 2010). The minority oppositional report (which was excluded by the legal treats) was separately published in 2004 (CERRIE 2004b). (page 14

MAJIA HERE: The European Committee on Radiation Risk (ECRR) expressed concerns about the decision of the ICRP committee to omit CERRIE’s concerns about the uncertainty and heterogeneity of internal effects from its 2007 report:

“But ICRP did nothing to change any of the dose coefficients for isotopes that caused such exposures or to apply such empirical and pragmatic procedures. and the embarrassing paragraph above was quietly dropped from the final ICRP 2007 report.
This brief review of the 2007 ICRP report demonstrates that there has essentially been no change in the model from that which was published in 1990, and that new evidence and arguments which scientifically falsify that model have been totally ignored. The ICRP continues to support the same risk factors for exposures to ionizing radiation and its model is still the basis for limits to releases to the environment. The ICRP 2007 model does not discuss the evidence: it is selective and partial and clearly does not conform to the philosophical requirements of science outlined in this chapter. As the Lesvos Declaration in the appendix demands, it must now be abandoned (page 16

MAJIA HERE: The ECRR report claims that the 2007 ICRP report fails to update its models of internal exposure appropriately and therefore is no different from the 1990 ICRP report. The ECRR report claims its model’s superiority in calculating epidemiological effects of internal emitters. Here is an excerpt illustrating comparing ICRP estimates with ECRP estimates:

“Table 10.5 UNSCEAR 1993 calculations of fallout average committed effective doses in person Sv to world populations. Doses were calculated using ICRP models and would be much larger using the ECRR model where internal doses carry various weightings….” (page 116)

Cancer risk total 29,000,000  [UNSCEAR 1993 Table 11] (page 116)

“Table 10.6 (from UNSCEAR 1993) shows committed effective doses to northern temperate latitudes (40-50 deg. N) from each of the main isotopes involved. For comparison the table also shows the total doses calculated using the proposed model of ECRR, which recognises excess risk from internal emitters. Use of the ECRR adjustment for internal risk using the ratios of external to internal isotopes given in Table 10.6 would increase the cancer yield from the 1990 ICRP value given above to more than 60,000,000 persons. The greater part of this yield would be in the 50 years following the exposure, and these cancer increases predicted are, of course, only too visible” (page 117

MAJIA HERE: In this excerpt Chris Busby explains the basic difference beween the ICRP and ECRR models:

“The radiation risk model of the European Committee on Radiation Risk is described in ECRR2010. It differs from the model currently employed by radiation protection agencies which are based on the recommendations of the International Commission on Radiological Protection ICRP. The latter (ICRP) model deals with radiation exposure from all sources in the same way, as if it were external to the body, and generally averages the dose to the body as if it were uniform across tissues more massive than 1 kilogram. The ICRP model then takes this dose and multiplies it by a risk factor for cancer linearly  based on the cancer yield at high acute doses of the Japanese survivor populations of Hiroshima and Nagasaki who have been studied since 1952. This method cannot apply to internal doses from radioactive substances, called radionuclides, which have been inhaled or ingested in food or water”
(Busby The health outcome of the Fukushima catastrophe Initial analysis from risk model of the European Committee on Radiation Risk ECRR

MAJIA HERE: Here is one Example of Why the ICRP and EPA Models for Radiation Risk Understate Risks Significantly 

EPA: Cancer Risk Coefficients for Environmental Exposure to Radionuclides
"For both internal and external exposure, a risk coefficient for a given radionuclide is based on the assumption that this is the only radionuclide present in the environmental medium. That is, doses due to decay chain members produced in the environment prior to the intake of, or external exposure to, the radionuclides are not considered”  (p. 3)

MAJIA HERE: Now let us look at some other evidence of the effects of internal radiation:

Paul Langley sites an interesting research study on the ”The Metabolism of the Fission Products, Hamilton 1942 on.

Langley writes: The individual and regular reports made by Hamilton to the Manhattan Project from 1942 are listed at the DOE Opennet online archive. The following is a post war paper dealing with what was learnt.
The Metabolism of the Fission Products and the Heaviest Elements
Jos. G. Hamilton, M.D. + Author Affiliations Division of Medical Physics (Berkeley), Divisions of Medicine and Radiology (San Francisco) University of California
This document is based on work performed under Contract No. W-7405-eng-48-A for the Manhattan Project and the Atomic Energy Commission.
It is a brief version of material to be published in the Plutonium Project Record of the Manhattan Project Technical Series. Presented at the Thirty-second Annual Meeting of the Radiological Society of North America, Chicago, Ill., Dec. 1–6, 1946.
Introduction and Methods During the early phases of the development of the Plutonium Project, it became apparent that one of the most serious problems to be encountered was the protection of personnel working in this field against the immense quantities of radiation and radioactive materials produced by the chain-reacting pile. The most important hazard that arises from the release of nuclear energy are radiations produced directly from fission and subsequently emitted by the resultant fission products and plutonium. The fission products can produce injury either as an external source of radiation or, if they gain entry into the body, by acting as an internal radioactive poison, quite analogous to radium poisoning. This latter consideration is a major concern, since the amounts required within the body to produce injurious effects are minute compared to the quantities necessary to induce damage by external beta and gamma irradiation.


A single dose of 3.8 millicuries (140 MBq, 4.1 μg of caesium-137) per kilogram was lethal in a study of dogs within three weeks
Redman, H. C.; McClellan, R. O.; Jones, R. K.; Boecker, B. B.; Chiffelle, T. L.; Pickrell, J. A.; Rypka, E. W. (1972). "Toxicity of 137-CsCl in the Beagle. Early Biological Effects". Radiation Research 50 (3): 629–648. doi:10.2307/3573559. JSTOR 3573559. PMID 5030090.

Possible associations between exposure to plutonium and mortality have been examined in studies of workers at the U.S. plutonium production and/or processing facilities (Hanford, Los Alamos, Rocky Flats), as well as facilities in Russia (e.g., Mayak) and the United Kingdom (e.g., Sellafield). The Mayak studies provide relatively strong evidence for an association between cancer mortality (bone, liver, lung) and exposure to plutonium….

Prof. Yuri Bandazhevsky found that children contaminated with cesium-137 producing 50 disintegrations per second (becquerels) per kilogram of body weight suffered irreversible heart damage  . (Starrr, S. 2012 Health Threat From Cesium 1-137. Japan Times Feb 16. Available:


Helen Caldicott reports: “Internal radiation, on the other hand, emanates from radioactive elements which enter the body by inhalation, ingestion, or skin absorption. Hazardous radionuclides such as iodine-131, caesium 137, and other isotopes currently being released in the sea and air around Fukushima bio-concentrate at each step of various food chains (for example into algae, crustaceans, small fish, bigger fish, then humans; or soil, grass, cow's meat and milk, then humans). [2] 

After they enter the body, these elements – called internal emitters – migrate to specific organs such as the thyroid, liver, bone, and brain, where they continuously irradiate small volumes of cells with high doses of alpha, beta and/or gamma radiation, and over many years, can induce uncontrolled cell replication – that is, cancer. Further, many of the nuclides remain radioactive in the environment for generations, and ultimately will cause increased incidences of cancer and genetic diseases over time.
“The grave effects of internal emitters are of the most profound concern at Fukushima. It is inaccurate and misleading to use the term "acceptable levels of external radiation" in assessing internal radiation exposures…”


  1. Yep, the 80,000 pound gorilla that they try to hide under bed. Internal is bad.

    One of the myriad lies of nuke. Pretending that mSv can say it all, without directly addressing internal or external.

  2. The ECRR is not the established radiation protection authority.

    Their methods point to finding a way to justify their conjecture of "no safe level of radiation", when that statement has not been proven.

  3. Even Low-Level Radioactivity Is Damaging, Scientists Conclude. Science Daily. November 13, 2012

    [Excerpted] The organisms studied included plants and animals, but had a large preponderance of human subjects. Each study examined one or more possible effects of radiation, such as DNA damage measured in the lab, prevalence of a disease such as Down's Syndrome, or the sex ratio produced in offspring. For each effect, a statistical algorithm was used to generate a single value, the effect size, which could be compared across all the studies.

    The scientists reported significant negative effects in a range of categories, including immunology, physiology, mutation and disease occurrence. The frequency of negative effects was beyond that of random chance.

    "There's been a sentiment in the community that because we don't see obvious effects in some of these places, or that what we see tends to be small and localized, that maybe there aren't any negative effects from low levels of radiation," said Mousseau. "But when you do the meta-analysis, you do see significant negative effects."

    "It also provides evidence that there is no threshold below which there are no effects of radiation," he added. "A theory that has been batted around a lot over the last couple of decades is the idea that is there a threshold of exposure below which there are no negative consequences. These data provide fairly strong evidence that there is no threshold -- radiation effects are measurable as far down as you can go, given the statistical power you have at hand."

    Mousseau hopes their results, which are consistent with the "linear-no-threshold" model for radiation effects, will better inform the debate about exposure risks. "

  4. I am currently an Environmental Attorney but interested in internal emitters (hot particles) because of my own experience. I worked in a nuclear power plant 25 years ago and was contaminated by a hot particle internally. in 1999 i was diagnosed with a large cancerous tumor at the point of exposure. It originated in my colon but had attached to the small intestine. My doctors are convinced the particle was the cause and hare noted that in my medical record,, but i do not believe cause and effect can be established. at least not to the level required to meet the "Daubert standard" for the admission of scientific evidence in American courts. Always interested in any insight

    1. Hi Brian
      Email me at for more discussion.