Monday, September 3, 2012

Propaganda at Princeton?



I was looking for research on the immediate biological effects from an increase in exposure to ionizing radiation and I came across this source:

Open Source Radiation Safety Training Module 3: Biological Effects

Majia here: The amazing thing about this site is the outrageous and patently false claim that there is no direct evidence of radiation-induced genetic effects in humans, even at high doses. Here is what the site has to say. Notice that "Prenatal Radiation Exposure" is immediately under the assertion of no genetic effects:

[Excerpted] Genetic Effects (Open Source Radiation Safety Training: Biological Effects)

There is no direct evidence of radiation-induced genetic effects in humans, even at high doses. Various analyses indicate that the rate of genetic disorders produced in humans is expected to be extremely low, on the order of a few disorders per million live born per rem of parental exposure.

Prenatal Radiation Exposure

Rapidly proliferating and differentiating tissues are most sensitive to radiation damage. Consequently, radiation exposure can produce developmental problems, particularly in the developing brain, when an embryo/fetus is exposed prenatally.

The developmental conditions most commonly associated with prenatal radiation exposure include low birth weight, microcephaly, mental retardation, and other neurological problems. These effects are related to the developmental stage at which the exposure occurs. The threshold dose for developmental effects is approximately 10 rems.
[end excerpt]

MAJIA here: Am I misunderstanding what they are trying to argue? How can the claim be made that there are no genetic effects from exposure to radiation?

Maybe Princeton folks need to go study at Columbia or some other university that is studying the genetic effects of ionizing radiation, particularly in relation to the bystander effect, genomic instability, and genetic moscaicism:

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: COLUMBIA UNIVERSITY REPORTS:
“Radiation-induced bystander effect represents a paradigm shift in our understanding of the radiobiological effects of ionizing radiation in that extranuclear and extracellular effects may also contribute to the final biological consequences of exposure to low doses of radiation. There is evidence that targeted cytoplasmic irradiation results in mutation in the nucleus of the hit cells and that cells that are not directly hit by an alpha particle, whether nuclear or cytoplasm, but in the vicinity of one that does, contribute to the genotoxic response of the cell population” http://www.radiation-bystander.columbia.edu/

Also see discussion of the bystander effect and genomic instability at UNSCEAR:
Non-Targeted and Delayed Effects of Exposure to Ionizing Radiation 2006
http://www.unscear.org/docs/reports/2006/09-81160_Report_Annex_C_2006_Web.pdf

Some MORE studies perhaps:

Ionizing radiation-induced mutant frequencies increase transiently in male germ cells of older mice  Guogang Xua, C. Alex McMahanb, Kim Hildretha, Rebecca A. Garciaa, Damon C. Herberta, Christi A. Walter Mutation Research/Genetic Toxicology and Environmental Mutagenesis Available online 31 January 2012

 
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
 
Majia here: I'm really confused about why Princeton would produce open source materials that erroneously claim there is no direct evidence of radiation-induced genetic effects?

Geneticists have been studying the adverse effects of radiation on genetics for decades.


GENETICS and radiation










 

4 comments:

  1. "Cancer is now widely seen, in the medical community, as a genetic disease expressed at the cellular level, and both early and recent research have supported the idea that the origin of the disease is essentially environmental exposure to a mutagen."

    2010 ECRR recommendations
    http://www.inaco.co.jp/isaac/shiryo/pdf/ECRR_2010_recommendations_of_the_european_committee_on_radiation_risk.pdf

    Radiation causing genetic damage has been known since the 1920s. There are tens of thousands of papers demonstrating this.

    So much for Princeton. Einstein isn't there any more, and if he was still alive, he wouldn't be associated with that kind of scientific fraud.

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  2. I also wanted to say before I forgot, that in the ECRR report, Busby et al discuss the effects of uranium on DNA. It seems uranium binds to DNA, and if there is gamma radiation in the environment, there is a secondary photoelectric effect, in which photons are emitted from the uranium, knocking electrons in DNA molecules out of their orbits. Uranium is assigned a high weight of health damage, higher than plutonium, per becquerel. This has nothing to do with its radioactive properties, it has do with its high atomic number and its propensity for binding with DNA.

    This suggests that other nonradioactive heavy metals that also bind with DNA have the same property. Mercury binds with DNA. So vaccines that contain mercury should also exhibit this photoelectric effect. If there is a radiation event, such as a nuclear power plant blowing up, and a person eats food contaminated with gamma emitters, like cesium, and this person has been vaccinated with a mercury-containing vaccine, the mercury would focus this radiation on the DNA. This would explain the result I mentioned in my blog about how radiation potentiates the effects of mercury. It would also potentiate heritable genetic damage, causing diseases like autism in progeny.

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  3. I think the answer is simple, some universities, which happen to be, I am not joking, the largest donors to politicians, making Goldman sachs look like an also ran in the donation department....well many universities have simply become paid pimps to promote nuke. Easy to research on the web.

    Disgusting beyond belief, that sexy science that kills us.

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  4. Thank you both for your input.

    Bobby1: Thank you for the very education update on uranium!

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