The Second Event theory

The Second Event theory
Summary
Links to other pages are at the bottom of this page

The Second Event theory proposes a radiobiological mechanism explaining how low doses of radiation from some man-made radionuclides and anthropogenic forms of natural radioactive substances are significantly more likely to cause genetic mutations leading to a range of diseases than radiation from natural sources.

It is a serious challenge to the present model of radiation risk at the kind of doses involved in environmental contamination from industrial processes.
Its predictions easily accommodate phenomena such as the Seascale leukaemia cluster, which the Committee on Medical Aspects of Radiation in the Environment fails to ascribe to known radioactive pollution.

It is now well established that living cells in vitro respond to sub-lethal radiation damage by proceeding into cell-cycle arrest which involves the setting up of an irreversible sequence of chromosomal DNA repair, followed by a forced replication.

This repair-replication cycle, which lasts for 8 - 15 hours, is known to contain a period which is exquisitely susceptible to radiation damage. In the last ten years the existence of such a critical period has been used to explain a number of anomalous low dose effects involving split or protracted doses. In addition, and in support of the existence of a critical phase, the very earliest reearch shows that dividing cells are much more susceptible to radiation than cells in G0 or quiescent phase.

Since 1945 there have existed on earth a number of novel beta emitters which have sequential decay pathways. Examples of such isotopes are the series

  • Strontium-90 - Yttrium-90
  • Tellurium-132 - Iodine-132

The Second Event theory argues that when such isotopes are incorporated and immobilised in body tissue their initial decay is capable of initiating cell cycle repair/replication sequences, during which the second decay damages the repair at some critical point. The repair sequence is irreversible, and sub-lethal damage sustained during the sequence will be passed on to one or both daughter cells and to their progeny.

At natural background levels of radiation (NBR) cells receive on average one hit per cell per year. Calculations using simple probability theory show that the chances of NBR intercepting the critical window in a replicating cell are very low, but that dose for dose, internal radiation from incorporated sequential emitters is thousands of times more likely to cause the two event hazard.


The following page summarises responses to the Theory and further developments,
with links to other pages.

If you are seeing this page full screen (i.e. without a navigation bar on the left) you can't see how the rest of the site is organised.
This Home page link takes you to the index page, which has links to all the topics we discuss on the site [only use it if this page is full screen]
Use the Wings of Death link to see what else we have to say on this topic.


Send email to:
. with questions or comments about this web site.

This page was last updated May 2001