Wednesday October 14 2009
Sir, I would like to respond to Dr Nolan's letter on safety issues with mobile phone masts, published in The Kerryman of October 7.
Dr Nolan is wrong when he says that non-ionising radiation cannot affect living things if it is too weak to generate significant heat. The most obvious examples are the effects of visible light, which is of course non-ionising. Were it not for its effects on chlorophyll, plants would not be able to photosynthesise and, were it not for its effects on our visual pigments, we would not be able to see.
From: Denis Henshaw
There is another irony in what Dr Nolan failed to understand and what Andrew tells us.
For something like 50 years it was axiomatic that DNA strand breaks and cancer induced by ionising radiation was (and only could be) a result of the ionising particle (alpha, beta or gamma ray) actually cutting the DNA at the point the break is seen.
Then suddenly these assumptions ended with the discovery of The Bystander Effect in which cells that had never been hit by ionising radiation, but were in the vicinity of those that were, or were cultured in culture medium which had previously had cells in them that were irradiated, had DNA strand breaks induced in them. This occurs by a cell signaling effect from hit cells. In fact, we now know that the link between radon exposure in the home and lung cancer is NOT primarily an effect of DIRECT alpha-particle hits to cells, rather is an effect in ‘Bystander cells’ – on those not hit !.
The problem is that the term ‘strand break’ is itself misleading. Here is an extract from some of my notes on this:
Magnetic Fields and DNA strand breaks
Historically, it was argued that unlike ionizing radiation, the low quantum energy of MFs was insufficient to cause DNA strand breaks and therefore could not cause cancer. The term ‘strand break’ is potentially misleading to the general reader. Lea (1946) used the term structural change to describe breakages in chromosomes, which appeared to be caused by an ionising particle passing through or in the immediate vicinity of the chromosome at the point where the breakage occurred. Lea acknowledged that such changes were actually due to radiation given to the cell at a stage prior to metaphase. However, adoption of the term breakage implied that the DNA had been broken, chopped or cut by the passage of radiation at that specific location on the chromosome. Almost 50 years later Nagaswa & Little (1992) demonstrated that genetic chromosomal damage may be induced by low doses of a-radiation in cell nuclei not actually traversed by an a-particle. The phenomenon was termed the bystander effect. It has since been demonstrated for high and low-LET radiation, certain chemicals and heavy metals (Little 2006, Xiao et al. 2004) and forms a central concept in modern radiobiology. The important conceptual conclusion is that chromosomal aberrations reflecting DNA strand breaks represent replication failures in the DNA template. Such failures are associated with coding information and not necessarily quantum energy at the level associated with ionising radiation. The myriad of responses involving genetic damage seen following exposures to MFs are consistent with such loss of coding information.
Lea DE. 1946. Actions of radiations on living cells. Cambridge University Press.
Nagasawa H and Little JB, 1992. Induction of sister chromatid exchanges by extremely low doses of a-particles. Cancer Research, 52, 6394-6396
Xiao Y, de Feyter E, van Outen CH, Stap J, Hoebe R, Havenith S, van Noorden CJF, Aten JA. 2004. Induction and detection of bystander effects after combined treatment of cells with 5-bromo-2’-deoxyurine, Hoechst 33 258 and ultraviolet A light. International Journal of Radiation Biology 80:105-114.
Little JB. 2006. Cellular radiation effects and the bystander response. Mutation Research 597:113-118.
Thanks again to Andrew
Professor Denis L Henshaw
H H Wills Physics Laboratory
University of Bristol
Bristol BS8 1TL, UK
Tel: +44 (0) 1179 260353
Fax: +44 (0) 1179 251723
Informant: Martin Weatherall