Wednesday, April 18, 2012

Research Demonstrating Significant Effects at Low Dose Rates of Exposure to Ionizing Radiation

The linear, no-threshold model for radiation exposure holds that there is no dose of exposure to ionizing radiation that poses no risk.

However, an assumption of the linear no-threshold model is that low-level exposure poses fewer risks than higher levels of exposure because the exposure increments are essentially homogenized so that more of them produce more risks.

The model is important because it is used in risk-assessments of exposure to ionizing radiation.

However, J.M.Gould and B.A.Goldman found that low-levels of exposure to Chernobyl radiation produced effects that could not be predicted by this model. They documented an inverse effects model in Deadly Deceit: Low-Level Radiation High Level Cover-Up, Four Wall Eight Windows, New York, 1991.

Below find another study that documents an inverse dose-rate effect.

This type of research does not in any way call into question the horrific effects of acute radiation exposure.

Rather, this research documents that relatively low levels of exposure to radiation can have significant effects that are not predicted by the dominant risk model.

The significance of this research is that our risk models are wrong and we are consequently under-stating health risks from exposure to low levels of ionizing radiation.

Here is a study that examines how low levels of exposure effect human cells.
Krokosz, A., Koziczak, R., Gonciarz, M., Szweda-Lewandowska, Z. (2006). Study of the Effect of Dose-Rate on Radiation-Induced Damage to Human Erythocytes. Radiation Physics and Chemistry 75.1, 95-10

Human erythrocytes suspended in an isotonic Na-phosphate buffer, pH 7.4 (hematocrit of 2%) were irradiated with ╬│-rays at three dose-rates of 66.7, 36.7, 25 Gy min−1 in order to investigate the influence of the dose-rate on radiation-induced membrane damage, hemoglobin oxidation and loss of reduced glutathione.

The obtained results showed that such processes as erythrocyte hemolysis, lipid and protein destruction depend on the radiation dose-rate. The parameter values describing these processes showed an inverse dose-rate effect.

Excerpt from Conclusion:
"Our results indicate that the processes of lipid and protein destruction show an inverse dose-rate effect not only in isolated systems, as it was observed earlier . . . but also in the cells. The inverse dose-rate effect was also observed during hemoglobin oxidation, which is the main intracellular erythrocyte target for radiation. The interphase death of the cell connected with damage to membrane proteins and lipids indicates the inverse dose-rate effect" (p. 104)

Majia here: Another study found here postulates that the bystander effect is responsible for the detrimental effects of low-levels of radon gas on human health.

However, I acknowledge that it is an oversimplification to assert all doses, of all forms of radiation, cause cancer or other health effects.

Yet another study, below, suggests that the bystander effect can both promote repair and inhibit repair of low levels of exposure to ionizing radiation.
Bobby R. Scott,1* Dale M. Walker,1 Yohannes Tesfaigzi,1 Helmut Sch├Âllnberger,2 and Vernon Walker. Mechanistic Basis for Nonlinear Dose-Response Relationships for Low-Dose Radiation-Induced Stochastic Effects. Nonlinearity Biol Toxicol Med. 2003 January; 1(1): 93–122.

Here is an excerpt from the article describing some of the DNA repair mechanisms. What is interesting is that the bystander effect is postulated as both promoting the adaptive response and inhibiting it in this study:

[excerpt] Numerous repair processes are now known and include nucleotide excision repair, base excision repair, transcription-coupled repair, mismatch repair, and nonhomologous end joining (Friedberg et al. 1995; Scicchitano and Mellon 1997; Hanawalt 2001). The indicated repair processes operate at the individual cell level and provide for individual cell resilience to vulnerable states. A complex cell signaling network regulates the individual-resilience system. The failure of this system can lead to repair errors, which in turn can lead to problematic lethal and nonlethal mutations (forms of genomic instability).

Majia here: The relationship between dose and DNA damage is extraordinarily complicated because the body routinely repairs DNA damage. The factors that promote repair, and inhibit it, can range from the type of radiation to the age and health of the radiated individual.

The linear, no-threshold model acknowledges that no level of exposure is every safe, but over-simplifies expected effects by homogenizing the doses.

Unfortunately, the variables mediating effects, ranging from the type of radiation to the characteristics of the radiated bodies, are simply not understood well.

We do know from the mortality statistics collected on Chernobyl and now on Fukushima that the very young, the very old, and the immune compromised are the most likely to suffer the adverse health effects from even very low levels of exposure.

None of the research that I've seen when scanning the data bases (Science Direct in particular) that addresses the protective, repair aspects of the bystander effect address variable such as age or condition of health.

Furthermore, none of the research touting the protective aspects of the bystander effect address the cumulative damage that occurs to bodies as a result of radiation exposure over time, and the effects of cumulative damage on repair mechanisms and efficacy.

This research is really in its infancy. Unfortunately, Fukushima now presents an opportunity for studying in real world conditions the hell radiation can wreck upon human health. Let us hope that the researchers do not manipulate the data and findings, as have been common practices in past studies.

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