Second event theory

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Second event theory is a pseudoscientific theory of health effects of ionizing radiation.[1][2] The main proponents of this theory are Christopher Busby, his environmental consultancy group Green Audit, and an anti-nuclear group called Low Level Radiation Campaign (which he set up and where he is the main scientific advisor). This theory is not accepted by the scientific community, because it is contradicted by experimental data.


The theory is based on the idea that when a cell struck with a particle of radiation is damaged by a second particle before it has the chance to repair, the risk of that cell becoming cancerous significantly increases. Basing on this hypothesis, it constructs a statistical model and postulates that "second event emitters", which means radionuclides that have a short-lived daughter isotope, such as strontium-90, are significantly more carcinogenic when ingested than other radionuclides.

Busby postulates that the second event theory explains a cancer cluster near the Sellafield site in the UK, and that it demonstrates that "man-made" radioactivity is more dangerous than natural radioactivity. The foremost problem with this proposition is that there is actually no such cluster, and Busby's claim is a result of systematic data dredging and various mistakes.[3][4]


The second event theory and supporting evidence were investigated by the Committee Examining Radiation Risks of Internal Emitters (CERRIE) in the United Kingdom.[5] The committee found many serious problems with the theory and rejected it, which led Busby and his follower Michael Meacher to write a separate counter-consensus report.[6]

Calculations indicated that irradiation with internal strontium-90 would result in only 1.3 times more double events than irradiation with external gamma rays, while Busby claimed the factor is 30. Furthermore, it would indicate that cancer risk from external gamma radiation is seriously overestimated. Busby tried to wiggle out of this by first reducing his estimate to 15, and then trying to accuse his critics of a simplification which he also used. Finally, he completely changed his argument and said that single hits in sensitive phases of cellular division are important. However, this eliminates any special role for double events and would yield a dose-response relationship equivalent to the commonly accepted linear no-threshold model.[7]

Furthermore, there is a lot of data on carcinogenicity available for both strontium-90 and strontium-89, which have the same chemical properties, but the latter is a single emitter. There is very little difference in carcinogenicity between those isotopes. This is a direct experimental falsification of the theory.[8]