The Cancer Risk from Low Level Radiation

Part of the Medical Radiology book series (MEDRAD)


We present a wide variety of experimental data indicating that linear no-threshold theory (LNT) greatly exaggerates the cancer risk from low level radiation. LNT is based on cancer initiating hits on DNA molecules, but many other factors affect the progression from DNA damage to a fatal tumor, such as availability of DNA repair enzymes, immune response, and cell suicide. Data are presented to show that these are generally stimulated by low level radiation (LLR) and suppressed by high doses that serve as calibrations for LNT. Since the great majority of cancers are caused by natural chemical processes, the protection against these provided by LLR may make LLR beneficial rather than harmful. Genes turned on and turned off by LLR are often different from those affected by high doses. Direct studies of cancer risk vs dose are reviewed: animal experiments generally indicate that LNT exaggerates the risk of low level radiation, and the same is true of most data on humans except possibly where dose rates are very high. Data show that the time delay between receipt of dose and cancer death increases with decreasing dose, which means that, with low level radiation, death from natural causes will often occur first. This implies an effective threshold. Responses to this type of information by various official and prestigious groups charged with estimating cancer risks from radiation are reviewed.


Cancer Risk Chromosome Aberration Priming Dose Challenge Dose Radon Exposure 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.



The author acknowledges a great debt to Myron Pollycove, Jerry Cuttler, and James Muckerheide for help in pointing out references involved in this paper.


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© Springer-Verlag Berlin Heidelberg  2011

Authors and Affiliations

  1. 1.Department of PhysicsUniversity of PittsburghPittsburghUSA

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