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The bystander effect introduces an entirely new type of effect produced by ionizing radiation, namely a disruption of intracellular and intercellular communication pathways. The study of this phenomenon is in it infancy and may lead to a revolution in understanding radiation effects. Rosalie Bertell has provided a few insights into this fascinating avenue of research:
"In addition to these general affects on the whole organism, there are micro-biological effects and biomarkers of exposure which have been neglected by the ICRP because of their focus on cancer death and only one mechanism, namely, direct damage to the DNA molecule initiating a malignant growth. Professor Michael Vicker, University of Bremen, has documented the acute radiosensitivity of blood to micro-Gray doses of radiation, causing the arachidonic acid cascade (Vicker). Rather than trying to extrapolate the DNA damage hypothesis from the high dose exposures to radiation into theoretical happenings in the low dose range, researchers would do better to expand the mechanisms studied to include those which actually occur at the low dose and their sequelae.
With all of the sweeping changes which have occurred in biology and microbiology since the 1952 discovery of DNA by Watson and Crick, radiobiology has stayed focused on cancer and direct damage to DNA. Other branches of biology have expanded to consider the entire cell, systems influencing cellular behavior including functional levels and coupled feedback reactions of networks of inter- and intracellular responses regulating cell communication. Without a holistic view of biology and physiology, radiobiology has been consumed with detail and elaborate mathematical picture of the small world which was delimited by the very first administrative decisions of the nuclear bomb era.
In an organism, cells communicate with one another through the exchange of specific information, for example through a hormone, and the translation of this signal into intracellular messages. Paracrine (hormones secreted from tissues other than endocrine glands) and endocrine hormones are unable to pass through cell membranes. Therefore their information (the hormone) requires a cellular receptor on the outside surface of the cell, a transmembrane signaling that is connected to the receptor, called a “second messenger-generating enzyme”, and a correct interpretation of the second messenger system. Various second messengers are released into the cell after stimulation of a particular receptor enzyme system, and which systems may be activated depends on the genetically determined receptors possessed by the cell. This communication system between cells in complex systems, can be modified, for example by phosphorylating particular proteins, and two second messengers can interact through feedback and cross talk. Ionizing radiation causes many interferences and disruption in this delicately balanced intercellular communication system. In radiobiology, these problems are dismissed and assume to be either trivial or perfectly repaired. Ionizing radiation induces oxidative stress, something admitted by radiobiology but discussed only in terms of its thermal effects. This same oxidative stress induces measurable inflammation, including a massive cascade of fatty acids in various states of oxidation. These mediate inflammatory reactions in the blood and other tissues, such as blood vessel endothelium, and function as second messengers, even controlling such things as pain and chemiluminescence.
The perturbation of cellular communication, regulation and homeostasis by low doses has major consequences for human health and development. It is irrational, as the physicists are now doing, to count on the failure to observe high dose effects at low doses as “proof” that such doses are “safe”. DNA damage is a statistical phenomena, called stochastic by the physicists, while the inflammatory response is nonstochastic, or deterministic as it is now called. Unlike skin burns, these internal inflammatory responses occur at microGray doses. The ICRP assumes that deterministic effects do not occur below 500 mGy doses.
The ionizing radiation stimulations are “illicit” in the sense that there is no equivalent stimulation of the arachidonic pathway after non-radiological physiological stimulation, making it pathogenic in character, difficult for the body to regulate and return to homeostasis. This response activates the monocytes, which kill themselves by the oxidants they produce, often ending up as pus along with their digested cellular victims. They can endanger the host by killing other tissue, for example, transplants or infarcted heart tissue.
Activated monocytes are carcinogenic, provoking hitherto latent oncogenic systems and genomic errors to replicate. This may well be one of the mechanisms by which cancers were increased within the first ten years after the Chernobyl disaster. These cancers were dismissed by the IAEA as not radiation related because the ICRP required latency period of ten years had not been completed. These were radiation promoted or accelerated cancers, not radiation induced cancers. Again, we see ICRP recognizing only radiation induced cancers, whereas the victim will experience both mechanisms as due to the disaster" [1].
Bibliography
[1] Bertell R. Limitations of the ICRP Recommendations for Worker and Public Protection from Ionizing Radiation. For Presentation at the STOA Workshop: Survey and Evaluation of Criticism of Basic Safety Standards for the Protection of Workers and the Public against Ionizing Radiation. Brussels: European Parliament, February 5, 1998a. http://ccnr.org/radiation_standards.html
