Friday, March 16, 2012

Estimating Dose and the History of Radiation Research


The recently declassified Nuclear Regulatory Transcripts (page 143 and 183-187) discuss the projected thyroid dose for 1 year old California children from Fukushima Fallout http://pbadupws.nrc.gov/docs/ML1205/ML12052A109.pdf

The method used to project the dose to the thyroid from radioactive iodine was developed by Harold Knapp. 

His method was controversial because it demonstrated amplified harm from doses that other scientists at the time considered "safe."

Knapp was part of a community of scientists and other professionals who braved the consternation of their colleagues and the disapproval of their institutions.

By calling into question establishment "truths," scientists, physicians, journalists and academics such as Harold Knapp, Jay Gould, John Goffman, Helen Caldicott, Harvey Wasserman, Alice Stewart, Robert Alavarez, Philip Fradkin, and many others have risked their professional careers.


Here is some background on efforts to measure the thyroid dose to children:

Kirsch, S. (2004). Harold Knapp and the Geography of Normal Controversy: Radioiodine in the Historical Environment. Osiris, 19: 167-181

[excerpted] In 1962, after high levels of the isotope Iodine-131 were detected in Utah milk supplies, Dr. Harold Knapp, a mathematician working for the AEC's Division of Biology and Medicine, developed a new model for estimating, first, the relation between a single deposition of radioactive fallout on pasturage and the levels of Iodine-131 in fresh milk and, second, the total dose to human thyroids resulting from daily intake of the contaminated milk.  

The implications of Knapp's findings were enormous. They suggested that short-living radioiodine, rather than long-living nuclides such as radiostrontium, posed the greatest hazard from nuclear test fallout and that children raised in Nevada and Utah during the 1950s had been exposed to internal radiation doses far in excess of recommended guidelines. 

This paper explores the explicit historical revisionism of Knapp's study, his refusal, contra normal AEC practices of knowledge production and spatial representation, to distance himself from the people and places downwind from the Nevada Test Site, and the reactions his work provoked among his AEC colleagues.

Majia here: Another finding that has called into question establishment truth about the damaging effects from low-level radiation is the bystander effect. This effect suggests that very low levels of exposure to radiation can have unpredictable and damaging effects to cells not directly hit by radiation. Below find an excerpt from a research article that elucidates the bystander effect:

Dietrich Averbeck, a, Towards a New Paradigm for Evaluating the Effects of Exposure to Ionizing Radiation Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis Volume 687, Issues 1-2, 1 May 2010 pages 7-12

[excerpted] 1.1. Bystander effects

The finding that low-dose radiation exposures of single cells can also affect unirradiated neighbouring cells has been termed the bystander effect. The group of J.B. Little at Harvard University in Boston (USA) was one of the first to report genetic alterations such as sister-chromatid exchanges (SCEs) and mutations induced by ionizing radiation in the neighbours of cells that had received direct radiation insults [5]

For example, the neighbours of cells that were directly traversed by alpha particles showed increased frequency of point mutations of the spontaneous type (i.e. quasi-absence of deletions) likely reflecting damage from oxidative metabolism. It is a striking feature of bystander effects that they rely either on direct intercellular communication by intercellular gap junctions or indirect mediators such as long lived free radicals and cytokines released into the surrounding medium of irradiated cells [5], [6] and [7].

Obviously, such non-targeted effects change the actual radiation target size and give rise to non-linear responses in cell populations and tissues. Moreover, they put very much into question the overall validity of the LNT hypothesis [8], [9] and [10].

Bystander effects occur at low doses where not every cell in the population has been hit by irradiation. In this situation, irradiated mammalian cells clearly influence the response of unirradiated bystander cells. However, it cannot be excluded that similar intercellular communication may also occur among irradiated cells when every cell in the cell population received at least one radiation hit.

Low-dose-induced bystander effects are known to increase cell killing and produce SCEs, micronuclei, point mutations and clastogenic effects [11] E.I. Azzam, S.M. de Toledo and J.B. Little, Expression of CONNEXIN43 is highly sensitive to ionizing radiation and other environmental stresses, Cancer Res. 63 (2003), pp. 7128–7135. View Record in ScopusCited By in Scopus (63)[11], [12] and [13]. Also some factors such as TGFbeta can be induced as well as reactive oxygen species (ROS), i.e. superoxide anion and hydrogen superoxide, that can be inhibited by SOD and catalase, respectively [11]. |

In fact, irradiated mammalian cells were shown to generate and transmit signals to the unirradiated neighbours involving reactive oxygen species [12], nitric oxide species [14], [15], [16] and [17] and cytokines [16] and [18].

Earlier work on bystander responses after alpha-particle irradiation [19] showed that repair deficient cells showed a more pronounced bystander effect mediated by cell–cell gap junctions. However, using medium transfer experiments DNA repair defects did not seem to play a role [6].
 
Majia here: A critique of hormesis--the idea that low levels of ionizing radiation always promote cellular repair--can be found here:

Kitchin KT, Drane JW. A critique of the use of hormesis in risk assessment. Hum Exp Toxicol. 2005 May;24(5):249-53.
http://is.gd/bOuIlx

Abstract There are severe problems and limitations with the use of hormesis as the principal dose-response default assumption in risk assessment. These problems and limitations include: (a) unknown prevalence of hormetic dose-response curves; (b) random chance occurrence of hormesis and the shortage of data on the repeatability of hormesis; (c) unknown degree of generalizability of hormesis; (d) there are dose-response curves that are not hormetic, therefore hormesis cannot be universally generalized; (e) problems of post hoc rather than a priori hypothesis testing; (f) a possible large problem of ‘false positive’ hormetic data sets which have not been extensively replicated; (g) the ‘mechanism of hormesis’ is not understood at a rigorous scientific level; (h) in some cases hormesis may merely be the overall sum of many different mechanisms and many different dose-response curves – some beneficial and some toxic. For all of these reasons, hormesis should not now be used as the principal dose-response default assumption in risk assessment. At this point, it appears that hormesis is a long way away from common scientific acceptance and wide utility in biomedicine and use as the principal default assumption in a risk assessment process charged with ensuring public health protection.

Majia here: Some important background research and commentary on the effects of low-levels of ionizing radiation can be found here:

What Is Factually Wrong with This Belief: "Harm from Low-Dose Radiation Is Just Hypothetical --- Not Proven" By John W. Gofman, M.D., Ph.D. Fall 1995 http://www.ratical.com/radiation/CNR/NoSafeThreshP.html

HELEN CALDICOTT Unsafe at Any Dose Op-Ed Contributor Published: April 30, 2011http://www.nytimes.com/2011/05/01/opinion/01caldicott.html?_r=1&nl=todaysheadlines&emc=tha212

Majia here:Background on how the Permissible Dose Was Created

Permissible Dose: A History of Radiation Protection in the 20th Century by J. Samuel Walker published in 2000 by University of California Press.

[paraphrasing with direct quotes indicated] Regarding limits to radiation doses to the population: The International Commission on Radiological Protection (ICRP) 1953 “recommendation on the issue were arbitrary and tentative” although they represented the first formal efforts to establish radiation protection (p. 12)

The United States Atomic Energy Commission, established by the Atomic Energy Act of 1946, sponsored experiments between 1945 and 1947 where 18 patients “received injections of plutonium as a part of efforts to calibrate body burdens… The researchers did not expect that the patients would receive any therapeutic benefits from the plutonium they received and made a deliberate effort to prevent them from learning about their unwitting participation in the experiments” (p. 16).

In 1946 and between 1950 and 1953, the AEC working with the National Institutes of Health and the Quaker Oats Company funded research carried out by MIT scientists “that fed radioactive iron or calcium to students at the Walter E. Fernald School, an institution for mentally retarded children in Massachusetts…as in the case of the plutonium injections, the experiments were not designed or expected to provide any health benefits to the subjects. Although the school asked parents of the children to sign a consent form, the information it offered was neither completely frank about the purpose or the possible risks of the tests. Indeed, it misleadingly suggested that the experiments could improve the children’s condition” (p. 17)

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