Monday, July 2, 2012

Somatic or Genetic Effects?


A somatic effect is roughly defined as a visible change in bodily characteristics or processes. A tumor would be indicative of a somatic change, as would be changes in white blood cell counts.

A genetic effect is defined by a mutation in DNA or a mutation in the progeny of an irradiated cell.

The concept of "permissible dose" was and continues to be based on somatic changes, not genetic ones. 

Some background:


 Studies on chromosomal changes conducted as early as 1928 found genetic changes in the absence of somatic alterations. However, scientists disagreed upon the significance of those findings for somatic, or bodily changes, for decades. 
 In 1925 a “tolerance dose” for radium was proposed as a guide for workplace exposure although the author of the proposed dose argued there was no safe level of exposure (Calabrese). In 1928 a national committee, the U.S. Advisory Committee on X-Ray and Radium Protection (NCRPM) made up of physicians and scientists formed and offered suggestive guidelines for safe handling of radiation; however, this committee had no official standing or statutory authority (Walker, 7). An International Committee on Radiation Protection, the ICRP, was also established in 1928, issuing its first publication that year on radiation safety.The ICRP recommended a tolerance dose for workers based on 1/100 of the dose of radium believed to be needed to produce visible reddening of the skin. The US NCRPM did not issue recommendations for tolerance doses for radium in their radiation exposure standards until 1934; once proposed the standards were significantly higher (ten times) than those proposed in 1925. The new standards presumed that an equilibrium state existed between somatic injury and repair. Proposed, but not enforceable, new guidelines by these committees did not halt the continued use of radium in homeopathic medicine.
 In 1947 the NCRPM, acting in response to AEC pressure, introduced the idea of maximum “permissible dose” for occupational exposure; although, the author of this concept, G. Failla of Columbia University, recognized that if genetic hazards served as the basis for setting the tolerance dose, than only zero exposure could serve. Fallia therefore rejected genetic hazards as the basis for setting the permissible dose, favoring instead a formulation that emphasized somatic (i.e., bodily), non-genetic detection (Calabrese). There was considerable push back to Fallia’s formulation of permissible dose from geneticists on the committee concerned about the long term effect of exposure on human chromosomes, especially across generations. However, proving genetic changes in human genes before explication of DNA in 1953 was challenging. Permissible dose therefore was understood as accepting some level of genetic injury (Calabrese).
Recent laboratory research studies on the effects of radiation explain how genetic changes produce somatic changes across time. The “bystander effect” and “delayed effect” describe the phenomena whereby cells not directly targeted by the radiation can exhibit damage and produce damaged progeny over time. Furthermore, the research on alpha particles demonstrates conclusively that transversal of a single alpha particle can break DNA bonds. Thus, todays sophisticated technologies for viewing DNA alterations are better able to link DNA mutations to subsequent somatic changes, such as tumor development. 




               Edward J. Calabrese The Road to Linearity: Why Linearity at Low Doses Became the Basis for Carcinogen Risk Assessment. Archives in Toxicology 83, 203-225 (2009), p 204.

           Bo Lindell§, H John Dunster*, and Jack Valentin† INTERNATIONAL COMMISSION ON RADIOLOGICAL PROTECTION: HISTORY, POLICIES, PROCEDUREShttp://www.icrp.org/docs/Histpol.pdf

            J. Samuel Walker Permissible Dose. Berkeley: University of California Press, 2000.

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