Skip to main content
Log in

Biologische Wirkung und Tumorrisiko diagnostischer Röntgenstrahlen

Der „Krieg der Modelle“

Biological effect and tumor risk of diagnostic x-rays

The “war of the theories”

  • Leitthema
  • Published:
Der Radiologe Aims and scope Submit manuscript

Zusammenfassung

Seit der Einführung ionisierender Strahlen als ein Mittel zur Behandlung und Diagnose beim Menschen haben Wissenschaftler versucht, ihre Nebenwirkungen und potenziellen Risiken für die Gesundheit einzuschätzen. Es gibt nun ausreichende Evidenz für das grundsätzliche Vorliegen einer direkten Beziehung zwischen höheren Dosen und Nebenwirkungsrisiken. Die meisten Unsicherheiten liegen auf dem Gebiet der Niedrigdosisforschung v. a. im Hinblick auf das Risiko der Induktion von Krebs. Niedrigdosiseffekte sind üblicherweise von Bedeutung in der diagnostischen Medizin, während Hochdosisbestrahlungseffekte typischerweise nach strahlentherapeutischen Behandlungen oder nuklearen Unfällen beobachtet werden. Der derzeitige Stand der „Krieg der Theorien“ kann folgendermaßen zusammengefasst werden: die eine Partei von Wissenschaftlern und Vertretern der Gesundheitsbehörden bevorzugt die Hypothese, dass es keine Grenzdosis („linear no threshold hypothesis [LNT] of radiation“) gibt, welche als sicher betrachtet werden kann. Die Kritiker dieser Hypothese schlagen jedoch vor, dass die Risiken unterhalb von 50 mSv nicht messbar oder überhaupt von klinischer Signifikanz sind und außerdem nicht durch eine lineare Dosis-Wirkungs-Beziehung beschrieben werden können. Das Ziel dieses Artikels ist es, die wichtigsten nicht geklärten Fragen auf diesem Gebiet zusammen zu fassen. Argumente werden präsentiert, warum die Gültigkeit des LNT-Modells im Niedrigdosisbereich als zumindest inkonsistent und fragwürdig betrachtet werden sollte.

Abstract

Since the introduction of ionizing radiation as a treatment and diagnostic tool in humans, scientists have been trying to estimate its side effects and potential health risks. There is now ample evidence for the principal existence of a direct relationship between higher doses and the risks of side effects. Most of the uncertainties lie in the field of low-dose effects especially with respect to the risk of cancer induction. Low-dose effects are usually of relevance in diagnostic medicine while high-dose radiation effects are typically observed after radiotherapeutic treatment for cancer or after nuclear accidents. The current state of the “war of theories” may be summarized as follows: one group of scientists and health regulatory officials favors the hypothesis that there is no threshold dose, i.e. the linear-no-threshold hypothesis (LNT) of radiation which can be regarded as safe. On the contrary, the critics of this hypothesis suggest that the risks of doses below 50 mSv are not measurable or even of clinical relevance and are not adequately described by a linear dose-response relationship. The aim of this article is to summarize the major unresolved issues in this field. Arguments are presented why the validity of the LNT model in the low-dose range should be regarded as at least inconsistent and is thus questionable.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Institutional subscriptions

Abb. 1
Abb. 2

Literatur

  1. Alwan A et al (2011) Global status report on noncommunicable diseases 2010. World Health Organization, Geneva

  2. Allwright SPA, Colgan PA, McAulay IR, Mullins E (1983) Natural background radiation and cancer mortality in the Republic of Ireland. Int J Epidemiol 12:414–418

    Article  PubMed  CAS  Google Scholar 

  3. Antiseri D (1991) How to distinguish science from non science. Med Secoli 3:153–174

    PubMed  CAS  Google Scholar 

  4. Barnett GC, West CM, Dunning AM et al (2009) Normal tissue reactions to radiotherapy: towards tailoring treatment dose by genotype. Nat Rev Cancer 9:134–142

    Article  PubMed  CAS  Google Scholar 

  5. Bonner WM, Redon CE, Dickey JS et al (2008) GammaH2AX and cancer. Nat Rev Cancer 8:957–967

    Article  PubMed  CAS  Google Scholar 

  6. Burkart W, Jung T, Frasch G (1999) Damage pattern as a function of radiation quality and other factors. C R Acad Sci III 322:89–101

    Article  PubMed  CAS  Google Scholar 

  7. Clingen PH, Wu JY, Miller J et al (2008) Histone H2AX phosphorylation as a molecular pharmacological marker for DNA interstrand crosslink cancer chemotherapy. Biochem Pharmacol 76:19–27

    Article  PubMed  CAS  Google Scholar 

  8. Costes SV, Chiolo I, Pluth JM et al (2010) Spatiotemporal characterization of ionizing radiation induced DNA damage foci and their relation to chromatin organization. Mutat Res 704:78–87

    Article  PubMed  CAS  Google Scholar 

  9. Court Brown WM, Doll R et al (1960) Geographical variation in leukaemia mortality in relation to background radiation and other factors. Br Med J 1:1753–1759

    Article  Google Scholar 

  10. European Commission. Radiation Protection 125 (2001) Low dose ionizing radiation and cancer risk. Office for Official Publications of the EC, Luxembourg

  11. Fazel R, Krumholz HM, Wang Y et al (2009) Exposure to low-dose ionizing radiation from medical imaging procedures. N Engl J Med 361:849–857

    Article  PubMed  CAS  Google Scholar 

  12. Frieben A (1902) Demonstration eines Cancroides des rechten Handrückens, das sich nach langdauernder Einwirkung von Roentgenstrahlen entwickelt hat. Fortschr Rontgenstr 6:106–111

    Google Scholar 

  13. Hall EJ (1994) Radiobiology for the radiologist. Lippincott, Philadelphia

  14. Hanahan D, Weinberg RA (2011) Hallmarks of cancer: the next generation. Cell 144:646–674

    Article  PubMed  CAS  Google Scholar 

  15. Health Physics Society (1996) Radiation risk in perspective: position statement of the Health Physics Society (adopted January 1996). Health Physics Society directory and handbook, 1998–1999. Health Physics Society, McLean, pp 238–244

  16. Huang L, Snyder AR, Morgan WF (2003) Radiation-induced genomic instability and its implications for radiation carcinogenesis. Oncogene 22:5848–5854

    Article  PubMed  CAS  Google Scholar 

  17. Hussain SP, Hofseth LJ, Harris CC (2003) Radical causes of cancer. Nat Rev Cancer 3:276–285

    Article  PubMed  CAS  Google Scholar 

  18. ICRP Publication 103 (2007) The 2007 Recommendations of the International Commission on Radiological Protection. Ann ICRP 37

  19. Joiner MC, Marples B, Lambin P et al (2001) Low-dose hypersensitivity: current status and possible mechanisms. Int J Radiat Oncol Biol Phys 49:379–389

    Article  PubMed  CAS  Google Scholar 

  20. Kathren RL (1996) Pathway to a paradigm: the linear non-threshold dose-response model in historical context. The American Academy of Health Physics 1995 Radiology Centennial Hartman Oration. Health Phys 70:621–635

    Article  PubMed  CAS  Google Scholar 

  21. Morgan WF (2003) Non-targeted and delayed effects of exposure to ionizing radiation. I. Radiation induced genomic instability and bystander effects in vitro. Radiat Res 159:567–580

    Article  PubMed  CAS  Google Scholar 

  22. Mullenders L, Atkinson M, Paretzke H et al (2009) Assessing cancer risks of low-dose radiation. Nat Rev Cancer 9:596–604

    Article  PubMed  CAS  Google Scholar 

  23. Neumaier T, Swenson J, Pham C et al (2012) Evidence for formation of DNA repair centers and dose response nonlinearity in human cells. Proc Natl Acad Sci U S A 109:443–448

    Article  PubMed  Google Scholar 

  24. Okada M, Okabe A, Uchihori Y et al (2007) Single extreme low dose/low dose rate irradiation causes alteration in lifespan and genome instability in primary human cells. Br J Cancer 96:1707–1710

    Article  PubMed  CAS  Google Scholar 

  25. Platkiewicz J, Brette R (2010) A threshold equation for action potential initiation. PLoS Comput Biol 6:e1000850

    Article  PubMed  Google Scholar 

  26. Prise KM, O’Sullivan JM (2009) Radiation-induced bystander signalling in cancer therapy. Nat Rev Cancer 9:351–360

    Article  PubMed  CAS  Google Scholar 

  27. Richardson S, Monfort C, Green M et al (1995) Spatial variation of natural radiation and childhood leukaemia incidence in Great Britain. Stat Med 14:2487–2501

    Article  PubMed  CAS  Google Scholar 

  28. Rogakou EP, Pilch DR, Orr AH et al (1998) DNA double-stranded breaks induce histone H2AX phosphorylation on serine 139. J Biol Chem 273:5858–5868

    Article  PubMed  CAS  Google Scholar 

  29. Savitsky K, Bar-Shira A, Gilad S et al (1995) A single ataxia telangiectasia gene with a product similar to PI-3 kinase. Science 268:1749–1753

    Article  PubMed  CAS  Google Scholar 

  30. Selzer E, Hebar A (2012) Basic principles of molecular effects of irradiation. Wien Med Wochenschr 162:47–54

    Article  PubMed  Google Scholar 

  31. Smith RW, Wang J, Bucking CP et al (2007) Evidence for a protective response by the gill proteome of rainbow trout exposed to X-ray induced bystander signals. Proteomics 7:4171–4180

    Article  PubMed  CAS  Google Scholar 

  32. Stelling J, Sauer U, Szallasi Z et al (2004) Robustness of cellular functions. Cell 118:675–685

    Article  PubMed  CAS  Google Scholar 

  33. Taubes G (1995) Epidemiology faces its limits. Science 269:164–169

    Article  PubMed  CAS  Google Scholar 

  34. Tubiana M (2008) The linear no-threshold relationship and advances in our understanding of carcinogenesis. Int J Low Radiat 5:173–204

    Article  CAS  Google Scholar 

  35. Tubiana M, Feinendegen LE, Yang C, Kaminski JM (2009) The linear no-threshold relationship is inconsistent with radiation biologic and experimental data. Radiology 251:13–22

    Article  PubMed  Google Scholar 

  36. Wakeford R, Tawn EJ (2010) The meaning of low dose and low dose-rate. J Radiol Prot 30:1–3

    Article  PubMed  Google Scholar 

  37. West C, Rosenstein BS, Alsner J et al (2010) Establishment of a radiogenomics consortium. Int J Radiat Oncol Biol Phys 76:1295–1296

    Article  PubMed  Google Scholar 

Download references

Interessenkonflikt

Der korrespondierende Autor gibt für sich und seine Koautoren an, dass kein Interessenkonflikt besteht.

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to E. Selzer.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Selzer, E., Hebar, A. Biologische Wirkung und Tumorrisiko diagnostischer Röntgenstrahlen. Radiologe 52, 892–897 (2012). https://doi.org/10.1007/s00117-012-2336-x

Download citation

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1007/s00117-012-2336-x

Schlüsselwörter

Keywords

Navigation