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Evaluation of Mobile Phone and Cordless Phone Use and Glioma Risk Using the Bradford Hill Viewpoints from 1965 on Association or Causation
Region Örebro län. Department of Oncology, Örebro University Hospital, Örebro, Sweden.ORCID-id: 0000-0002-7816-0755
Region Örebro län. Department of Oncology, Örebro University Hospital, Örebro, Sweden.
2017 (engelsk)Inngår i: BioMed Research International, ISSN 2314-6133, E-ISSN 2314-6141, Vol. 2017, artikkel-id 9218486Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Objective. Bradford Hill's viewpoints from 1965 on association or causation were used on glioma risk and use of mobile or cordless phones. Methods. All nine viewpoints were evaluated based on epidemiology and laboratory studies. Results. Strength: meta-analysis of case-control studies gave odds ratio (OR) = 1.90, 95% confidence interval (CI) = 1.31-2.76 with highest cumulative exposure. Consistency: the risk increased with latency, meta-analysis gave in the 10+ years' latency group OR = 1.62, 95% CI = 1.20-2.19. Specificity: increased risk for glioma was in the temporal lobe. Using meningioma cases as comparison group still increased the risk. Temporality: highest risk was in the 20+ years' latency group, OR = 2.01, 95% CI =1.41-2.88, for wireless phones. Biological gradient: cumulative use of wireless phones increased the risk. Plausibility: animal studies showed an increased incidence of glioma and malignant schwannoma in rats exposed to radiofrequency (RF) radiation. There is increased production of reactive oxygen species (ROS) from RF radiation. Coherence: there is a change in the natural history of glioma and increasing incidence. Experiment: antioxidants reduced ROS production from RF radiation. Analogy: there is an increased risk in subjects exposed to extremely low-frequency electromagnetic fields. Conclusion. RF radiation should be regarded as a human carcinogen causing glioma.

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Hindawi Publishing Corporation, 2017. Vol. 2017, artikkel-id 9218486
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URN: urn:nbn:se:oru:diva-57327DOI: 10.1155/2017/9218486ISI: 000398798300001PubMedID: 28401165Scopus ID: 2-s2.0-85016467564OAI: oai:DiVA.org:oru-57327DiVA, id: diva2:1103644
Merknad

Funding agencies:

Cancer-och Allergifonden  

Cancerhjalpen  

Pandora-Foundation for Independent Research, Berlin, Germany  

Tilgjengelig fra: 2017-05-30 Laget: 2017-05-30 Sist oppdatert: 2018-07-31bibliografisk kontrollert

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