Mobile phone use and risk of glioma in adults: a UK case-control study

The University of Manchester, Manchester, England, United Kingdom
BMJ (online) (Impact Factor: 17.45). 05/2006; 332(7546):883-7. DOI: 10.1136/bmj.38720.687975.55
Source: PubMed


To investigate the risk of glioma in adults in relation to mobile phone use.
Population based case-control study with collection of personal interview data.
Five areas of the United Kingdom.
966 people aged 18 to 69 years diagnosed with a glioma from 1 December 2000 to 29 February 2004 and 1716 controls randomly selected from general practitioner lists.
Odds ratios for risk of glioma in relation to mobile phone use.
The overall odds ratio for regular phone use was 0.94 (95% confidence interval 0.78 to 1.13). There was no relation for risk of glioma and time since first use, lifetime years of use, and cumulative number of calls and hours of use. A significant excess risk for reported phone use ipsilateral to the tumour (1.24, 1.02 to 1.52) was paralleled by a significant reduction in risk (0.75, 0.61 to 0.93) for contralateral use.
Use of a mobile phone, either in the short or medium term, is not associated with an increased risk of glioma. This is consistent with most but not all published studies. The complementary positive and negative risks associated with ipsilateral and contralateral use of the phone in relation to the side of the tumour might be due to recall bias.

Download full-text


Available from: Martie van Tongeren,
  • Source
    • "The application of electromagnetic fields (EMFs) is ubiquitous in modern society [1]. Several epidemiological and experimental studies have shown that EMF exposure may have detrimental effects on cognitive function [2,3] and may increase the risk of neurological diseases, such as gliomas [4,5] and Alzheimer’s disease [6,7]. EMF exposure has also been demonstrated to induce strong glial reactivity in different brain regions [8-10]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Insufficient clearance by microglial cells, prevalent in several neurological conditions and diseases, is intricately intertwined with MFG-E8 expression and inflammatory responses. Electromagnetic field (EMF) exposure can elicit the pro-inflammatory activation and may also trigger an alteration of the clearance function in microglial cells. Curcumin has important roles in the anti-inflammatory and phagocytic process. Here, we evaluated the ability of curcumin to ameliorate the phagocytic ability of EMF-exposed microglial cells (N9 cells) and documented relative pathways. N9 cells were pretreated with or without recombinant murine MFG-E8 (rmMFG-E8), curcumin and an antibody of toll-like receptor 4 (anti-TLR4), and subsequently treated with EMF or a sham exposure. Their phagocytic ability was evaluated using phosphatidylserine-containing fluorescent bioparticles. The pro-inflammatory activation of microglia was assessed via CD11b immunoreactivity and the production of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), interleukin-1beta (IL-1beta) and nitric oxide (NO) via the enzyme-linked immunosorbent assay or the Griess test. We evaluated the ability of curcumin to ameliorate the phagocytic ability of EMF-exposed N9 cells, including checking the expression of MFG-E8, alphavbeta3 integrin, TLR4, nuclear factor-kappaB (NF-kappaB) and signal transducer and activator of transcription 3 (STAT3) using Western blotting. EMF exposure dramatically enhanced the expression of CD11b and depressed the phagocytic ability of N9 cells. rmMFG-E8 could clearly ameliorate the phagocytic ability of N9 cells after EMF exposure. We also found that EMF exposure significantly increased the secretion of pro-inflammatory cytokines (TNF-alpha, IL-6 and IL-1beta) and the production of NO; however, these increases were efficiently chilled by the addition of curcumin to the culture medium. This reduction led to the amelioration of the phagocytic ability of EMF-exposed N9 cells. Western blot analysis revealed that curcumin and naloxone restored the expression of MFG-E8 but had no effect on TLR4 and cytosolic STAT3. Moreover, curcumin significantly reduced the expression of NF-kappaB p65 in nuclei and phospho-STAT3 (p-STAT3) in cytosols and nuclei. This study indicates that curcumin ameliorates the depressed MFG-E8 expression and the attenuated phagocytic ability of EMF-exposed N9 cells, which is attributable to the inhibition of the pro-inflammatory response through the NF-kappaB and STAT3 pathways.
    Journal of Neuroinflammation 03/2014; 11(1):49. DOI:10.1186/1742-2094-11-49 · 5.41 Impact Factor
    • "Interphone results have been published at the local level by a number of participating teams: Denmark [Christensen et al., 2004, 2005], France [Hours et al., 2007], Germany [Schüz et al., 2006; Schlehofer et al., 2007], Japan [Takebayashi et al., 2006, 2008], Norway [Klaeboe et al., 2007], Sweden [Lönn et al., 2004, 2005], and UK [Hepworth et al., 2006]. There are also pooled analyses of studies from five Northern European countries (Denmark, 80 Lagorio and R€ o€ osli Bioelectromagnetics Finland, Norway, Sweden, and UK) [Schoemaker et al., 2005; Lahkola et al., 2007, 2008], and pooled analyses of studies from all 13 participating countries [Interphone Study Group, 2010, 2011]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: A meta-analysis of studies on intracranial tumors and mobile phone use published by the end of 2012 was performed to evaluate the overall consistency of findings, assess the sensitivity of results to changes in the dataset, and try to detect the sources of between-study heterogeneity. Twenty-nine papers met our inclusion criteria. These papers reported on 47 eligible studies (17 on glioma, 15 on meningioma, 15 on acoustic neuroma), consisting of either primary investigations or pooled analyses. Five combinations of non-overlapping studies per outcome were identified. The combined relative risks (cRRs) in long-term mobile phone users (≥10 years) ranged between 0.98 (0.75-1.28) and 1.11 (0.86-1.44) for meningioma, with little heterogeneity across studies. High heterogeneity was detected across estimates of glioma and acoustic neuroma risk in long term users, with cRRs ranging between 1.19 (95% CI 0.86-1.64) and 1.40 (0.96-2.04), and from 1.14 (0.65-1.99) to 1.33 (0.65-2.73), respectively. A meta-regression of primary studies showed that the methodological differences embedded in the variable "study-group" explained most of the overall heterogeneity in results. Summary risk estimates based on heterogeneous findings should not be over-interpreted. Overall, the results of our study detract from the hypothesis that mobile phone use affects the occurrence of intracranial tumors. However, reproducibility (or lack of) is just one clue in the critical appraisal of epidemiological evidence. Based on other considerations, such as the limited knowledge currently available on risk beyond 15 years from first exposure, or following mobile phone use started in childhood, the pursuance of epidemiological surveillance is warranted. Bioelectromagnetics. © 2013 Wiley Periodicals, Inc.
    Bioelectromagnetics 02/2014; 35(2). DOI:10.1002/bem.21829 · 1.71 Impact Factor
  • Source
    • "2183 ACKNOWLEDGEMENTS We are grateful to all the patients and individuals for their participation and we also thank the clinicians and other hospital staff, cancer registries and study staff in respective centres who contributed to the blood sample and data collection. For the UK GWA study, we acknowledge the participation of the clinicians and other hospital staff, cancer registries, study staff and funders who contributed to the blood sample and data collection for this study as listed in Hepworth et al (2006). MD Anderson acknowledges the work on the USA GWA study of Phyllis Adatto, Fabian Morice, "
    [Show abstract] [Hide abstract]
    ABSTRACT: Background: Most of the heritable risk of glioma is presently unaccounted for by mutations in known genes. In addition to rare inactivating germline mutations in TP53 causing glioma in the context of the Li-Fraumeni syndrome, polymorphic variation in TP53 may also contribute to the risk of developing glioma. Methods: To comprehensively evaluate the impact of variation in TP53 on risk, we analysed 23 tagSNPs and imputed 2377 unobserved genotypes in four series totaling 4147 glioma cases and 7435 controls. Results: The strongest validated association signal was shown by the imputed single-nucleotide polymorphism (SNP) rs78378222 (P=6.86 × 10(-24), minor allele frequency ~0.013). Confirmatory genotyping confirmed the high quality of the imputation. The association between rs78378222 and risk was seen for both glioblastoma multiforme (GBM) and non-GBM tumours. We comprehensively examined the relationship between rs78378222 and overall survival in two of the case series totaling 1699 individuals. Despite employing statistical tests sensitive to the detection of differences in early survival, no association was shown. Conclusion: Our data provided strong validation of rs78378222 as a risk factor for glioma but do not support the tenet that the polymorphism being a clinically useful prognostic marker. Acquired TP53 inactivation is a common feature of glioma. As rs78378222 changes the polyadenylation signal of TP53 leading to impaired 3'-end processing of TP53 mRNA, the SNP has strong plausibility for being directly functional contributing to the aetiological basis of glioma.
    British Journal of Cancer 04/2013; 108(10). DOI:10.1038/bjc.2013.155 · 4.84 Impact Factor
Show more