Re: LNT, regs and lives

["Bjorn Cedervall" <bcradsafers@hotmail.com>]

Sometimes there seems like people in different subtopics of the radiation 
sciences are not really communicating because they refer to different 
endpoints. A fully metastatic, killing tumor is probably often the result of 
many (say 4 to 8) types of alterations on the DNA level (which may include 
chromosomal rearrangements and larger deletions). If you are old enough when 
obtaining these distinguished events in the same cell - you are likely to 
die from some other cause (CHD, infections, and so on). In practice you will 
then have a threshold - although the single events are probably quite random 
and may destroy any little strip of DNA. There are specific tumors where one 
hit is enough - like in the retinoblastoma case. This "hit" can for instance 
mean deletion, point mutation, or non-disjunction of chromosomes. With this 
in mind - certain kinds of tumors may in practice exhibit threshold like 
characteristics - but each case must be analyzed with respect to species, 
normal life span etc.

Then - when it comes to the individual induction of breaks (each one of 
which may be part of the tumor initiation-promotion-progression steps (this 
is a simplified description - some events may work in parallel also) - the 
only data I have seen have shown linear responses. Abramson-Zetterberg for 
instance showed in a paper quite recently (probably Mutation Research) a 
linear induction i micronuclei down to a level of 2.7 mGy/day (this is 
probably some kind of world record in terms of assay sensitivity).

I guess that there are few people in the field of DNA damage who don't 
believe that a DNA double-strand break for instance may be _one_ of the 
necessary (although not sufficient) events leading on to a tumor 
development. Now - if one such event results in genomic instability - which 
it very probably can - a mutation of the genes coding for say a microtubili 
protein (neeeded for correct spindle function during mitosis) or a repair 
enzyme may be enough - the subsequent probability for further mutational or 
chromosomal abnormal events increases and in that sense the original event 
has strongly contributed to the whole tumor development process. This 
remains to be analyzed in depth but it seems like a highly likely 
possibility.

Now - when it comes to decision makers - this possibility of such an event 
is often misunderstood - some people will ask for "no risks" without any 
deeper reflection or perspective. Sometimes a request for a "no risk" proof 
is also asked for as we have noted here earlier. This is the crazy part - 
that the wrong conclusions are drawn because of lack of perspective on 
trivial risks. Since a non-risk can't be proven strictly - I think it would 
be better to recognize that part of the discussion is a pseudo-character 
because we refer to different endpoints and therefore mean different things 
with "risk for causing cancer". In addition, the impossibility of proving 
non-risks at very low radiation doses makes part of the LNT debate 
meaningless are at least very complicated.

As I see it, it would be better if radiation protection institutions (like 
the ICRP - they like major revisions every 15-20 years I understand - why 
not skip one 20 years from now?) looked more at the constant "bombardment" 
(normal and abnormal physical, chemical, and biological) of DNA and analyzed 
"probability of causation" from all sources leading to DNA damage. From such 
a molecular biology approach _trivial risk levels_ (with which we shall not 
deal and/or worry about) could be recommended. Molecular biology has come up 
with several key findings/techniques during the last 10 years that may be 
valuable in the future radiation risk assessment. Rather than rushing to a 
standpoint ("threshold" as some general thought) that may only contribute to 
a negative image - it may be a good idea to look more at these new findings: 
Besides the phenomenon of genomic instability, there is the bystander 
effect, the discovery of "nicked" survival curves (initial alpha component 
(LQ model) that is higher than previously thought - in some cell lines), and 
also the potential in measuring repair/misrepair of DNA damage.

Side track: In the debate about radiation risks some people like to bring up 
the half-life of atoms like plutonium 239 and tell that it may kill far into 
the future. I say: A genetic mutation caused by a chemical (polyaromatic 
hydrocarbon for instance) may be inherited for many hundreds of generations 
and then finally contribute to a killing cancer 10,000 years from now 
(because it took that long before the damaged gene landed in a cell what had 
another critical mutation in it that came from the other parent or from some 
physical, chemical or biological event). Therefore, this time argument is 
not unique to radioactivity - the difference is in the distribution over 
time of the action of the DNA-damaging agent.

Back to trivial risks:
Suggested trivial risk levels can be used by national radiation protection 
authorities - hopefully they could identify a number of other trivial risks 
of the same magnitude that we don't regulate (molecules from a fast food 
restaurant could probably cause one of those necessary events mentioned 
above and contribute to killing someone far away, if I (voluntarily - well I 
may smoke also...) take an extra cookie with my coffee twice per month for 
30 years - that may hypothetically contribute to a catastrophic heart attack 
that kills me a few years earlier in life - it is a trivial risk (I hope) 
and I don't worry much about it).

BTW: Why don't the radiation protection regulators focus on Po-210, Pb-210 
etc in cigarette smoke?

These are my own ideas that may not necessarily coincide with those by 
others.

Bjorn Cedervall
bcradsafers@hotmail.com

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