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Second event theory

The Second Event theory is a theory in radiation biology which has been published by Chris Busby in the LLRC site. This is the idea that a manmade fission product or an anthropogenic form of a natural radioisotope (TENORM) is more able to exert a baneful effect upon cells than a radioisotope if it is able to engage in several radioactive decays in quick succession rather than a single radioactive decay. For instance 241Am and 239Pu decay to a long lived radioisotope (237Np and 235U) so on a human timescale it is only able to emit a single alpha particle while an atom of 218Po is able to emit a series of alpha and beta particles in quick succession. This theory is related to the self-repair processes which are responsible for the fact that fractionation of a dose reduces its ability to cause death. The "The Second Event theory" states that the self repair processes of the DNA in cells is defeated by the fact that a second radioactive decay is possible within a short time of the decay of strontium-90 or tellurium-132.

The decay of tin-132 and its decay products (daughters)
Element Isotope decay mode half life (minutes)
Sn 132 β 40 seconds
Sb 132 β 2.8
Te 132 β 3.2 days
I 132 β 2.3
Xe 132 - stable

It is noteworthy that in the decay chain of radium-226/radon-222 a large number of shortlived radioisotopes exist which could subject a cell to repeated radioactive events. This is because the daughters of radon often become attached to smoke and dust particles and hence are able to lodge in the lungs.[7]

The decay of radon-222 and its decay products (daughters)
Element Isotope decay mode half life (minutes)
Rn 222 α 3 days
Po 218 α 3.1
Pb 214 β 27
Bi 214 β 20
Po 214 α 0.164 seconds


Reactions to the theory by other scientists

Busby's views are often seen as controversial. The NRPB published a counterblast against the second event theory in which they suggest that it is a theory which is unlikely to be correct.[1] [8]. Busby in an open letter to the editor published a rebutal of this paper which can be read on line.[2], this in turn resulted in the NRPB writing a letter of their own to the journal in which they rebut the rebutal letter (Again this can be read on line).[3]

In addition the CERRIE committee concluded in their Scientific Briefing on the CERRIE Report that the second event theory was not supported by the available scientific evidence. For example, the evidence substantially contradicted the SET. The Report found a lack of biological plausibility for the basic preconditions of the SET; a lack of supporting evidence in the proponents’ reviews of the SET; weakness in the few studies cited in support of the SET; and no supporting evidence from experimental studies in an independent review of commissioned by the Committee.

The LLRC have stated that the CERRIE committee were unduely affected by "legalistic threats from Departmental lawyers right at the end of its two-and-a-half year deliberations" and then engauged in self-censorship of their findings.

Timing of DNA repair

According to Goodhead (UNSCEAR) as quoted in the book Radiochemistry and Nuclear Chemistry (G. Choppin et al.) a gamma ray passing through the cell nucleus is likely to cause about 70 ionizations which result in 1 DNA single strand break. While an alpha particle passing through a cell nucleus is able to cause about 23000 ionizations, which cause 200 single strand breaks and 35 double strand breaks. The single strand breaks can be repaired in about ten minutes while the double strand breaks require hours to be repaired. Hence if Goodhead is correct then it is less reasonable for the low LET radiation (beta/gamma) to be affected by the second event theory than the high LET radiation resulting from the decay of radon daughters (or some other alpha emitter).

Chris Busby disagrees with the views of Goodhead, he claims that DNA repair requires 8 to 15 hours and that during this time the cell is very susceptible to further radiation damage. Chris does not on the LLRC comment on the difference between single and double strand breaks within the second where he is discussing the second event theory.

Alpha emitters

Due to the low LET of a beta particle or gamma photon it is unlikely that the majority of the energy due to both radioactive decays of a fission product (mainly beta/gamma) will be deposited in the same cell. It has already been shown that the damage caused by alpha particles is more able to cause dire damage to DNA such as double strand breaks, this has been seen in some radiobiology experiments. The published work of Chris Busby includes an assertion that a hot particle of 239Pu is able to subject the biologcal tissues to a series of alpha particles. He suggests that this is one of the reasons why hot particles are able to cause health effects.

Preexposure to radiation with regards to acute health effects and other protective effects of irradiation

Some stuides have suggested that preexposure to radiation exerts a protective effect upon cells. Azzam, E.I., Radiation Research, 1994, 138(1), S28-S31. In mice it has been shown that a 200 mGy X-ray dose protects mice against both further X-ray exposure and ozone gas.[4] Furthermore it has been shown in a rodent study that low level (1 mGy hr-1) gamma irradiation prevents the development of cancer (induced by chemical means of methylcholanthrene).[5]

It has been shown that preexposure to radiation (50 to 100 mGy) results in four hours time in a small reduction of the ability of a 8 Gy dose to damage DNA in intact cells due to a shift in the cell cycle[6]

While it is clear that a large single exposure to plutonium dioxide powder is able to cause a fatal lung cancer in monkeys (and thus it is likely that PuO2 powder is carcinogenic in humans),[7] some studies have shown that moderate internal exposure to plutonium results in a reduction of the risk of getting cancer,[8]. Other studied have suggested that a small dose of radiation may be good for you.[9] However one explanation for this effect is the fact that the majority of radiation workers are subject to greater number of health checks than the general population, and thus as a result any sign of disease is more likely to be seen at an early (curable) stage. Also see the "healthy worker hypothesis". In plants radiation hormesis has been observed[10] However the existence of radiation hormesis in humans has been questioned, it is reasonable to state that for late effects (such as cancer) that the scientific community has not come to an agreement regarding this matter.[9] But in one recent case it was claimed (In Journal of American Physicians and Surgeons) that the persons living in a apartment block in Taiwan which was constructed using concrete which contained rebar contaminated with cobalt-60 experience a better state of health than the average person.[11]

Heavy metal poisoning as a model

It is known that many toxic metals can induce oxidative stress in tissue which may result in free radical induced damage. Also it is known that prior exposure to a small dose of cadmium can mitigate the effects of a second larger dose, this suggests that the first lower dose of the poison stimulates the DNA repair processes in the exposed tissue.[12][13][14] and[15]


  1. ^ A. A. Edwards and R. Cox, International Journal of Radiation Biology, 2000, 76, 119-125
  2. ^ [1]
  3. ^ [2]
  4. ^ Y Miyachi, The British Journal of Radiology, 2000, 73, 298-304.
  5. ^ Sakai, Kazuo; Iwasaki, Toshiyasu; Hoshi, Yuko; Nomura, Takaharu; Oda, Takeshi; Fujita, Kazuko; Yamada, Takeshi; Tanooka, Hiroshi, International Congress Series (2002), 1236 (Radiation and Homeostasis), 487-490.
  6. ^ Cramers P; Atanasova P; Vrolijk H; Darroudi F; van Zeeland AA; Huiskamp R; Mullenders LH; Kleinjans JC [3]
  7. ^ Hahn, F.F. ; Brooks, A.L. ; Mewhinney, J.A., Radiation Research, 1987, 112(2), 391-397
  8. ^ Kendall GM et al. Mortality and occupational exposure to radiation; First analysis of the National Registry for Radiation Workers. Brit Med Jour 1992; 304: 220
  9. ^ [4]
  10. ^ Atkinson, G.F., 1898. Report upon some preliminary experiments with Roentgen rays in plants. Science, 7: 7.
  11. ^ [5],[6]
  12. ^ Wahba, Z. Z., L. Hernandez, H. J. Issaq and M. P. Waalkes. 1990. Involvement of sulfhydryl metabolism in tolerance to cadmium in testicular cells. Toxicol. Appl. Pharmacol. 104:157-166.
  13. ^ Waalkes, M. P. and A. Perantoni. 1986. Isolation of a novel metal-binding protein from rat testes: characterization and distinction from metallothionein. J. Biol. Chem. 261:13079-13103.
  14. ^ Waalkes, M. P., S. Rehm, C. W. Riggs et al. 1988. Cadmium carcinogenesis in male Wistar (Crl:(WI)BR) rats: dose-response analysis of tumor induction in the prostate and testes, and at the injection site. Cancer Res. 48:4656-4663.
  15. ^ Rugstad, H. E. and T. Norseth. 1975. Cadmium resistance and content of cadmium-binding protein in cultured human cells. Nature 257:136-137.
This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Second_event_theory". A list of authors is available in Wikipedia.
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