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
    • "In low grade gliomas, although mobile phone use has been associated with increased risk, when focusing on survival, a survival benefit was reported in low grade glioma patients with mobile phone use. The authors hypothesis was that tumor volume was larger in exposed than in unexposed patients, which would permit an earlier diagnosis and surgicalintervention[30]. In 2010 Hardell et al reported an increased risk for glioma for both short and long term mobile phone users. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Mobile phone use has been discussed over the last few decades with increased risk for intracranial tumors. The majority of studies have been conducted on gliomas and meningiomas. Although some case-control studies have found a positive association between the use of mobile phones and the risk of tumors, other studies have reported no significant association. A possible long-term mobile phone use may lead to increased risk however, the evidences are not yet conclusive and further studies are needed. In the present study we reviewed the current evidence for the association between mobile phone use and risk for intracranial tumors.
    Full-text · Article · Dec 2015 · Journal of Negative Results in BioMedicine
  • Source
    • "Although it is agreed that tumorigenesis is linked to physical stress and environmental alterations, the nature or existence of carcinogenic effects related to EMF exposure have remained unclear12345. To date, most epidemiological studies have not demonstrated an increased risk of brain tumor development with overall mobile phone usage6789. However, some positive associations have been reported, such as a relationship between an increased risk of acoustic neuroma and long-term mobile phone use[10,11]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Background: The increase in mobile phone use has generated concerns about possible risks to human health, especially the development of brain tumors. Whether tumor patients should continue to use mobile telephones has remained unclear because of a paucity of information. Herein, we investigated whether electromagnetic fields from mobile phones could alter the biological features of human tumor cells and act as a tumor-promoting agent. Methods: Human glioblastoma cell lines, U251-MG and U87-MG, were exposed to 1950-MHz time division-synchronous code division multiple access (TD-SCDMA) at a specific absorption rate (maximum SAR = 5.0 W/kg) for 12, 24, and 48 h. Cell morphologies and ultra-structures were observed by microscopy and the rates of apoptosis and cell cycle progression were monitored by flow cytometry. Additionally, cell growth was determined using the CKK-8 assay, and the expression levels of tumor and apoptosis-related genes and proteins were analyzed by real-time PCR and western blotting, respectively. Tumor formation and invasiveness were measured using a tumorigenicity assay in vivo and migration assays in vitro. Results: No significant differences in either biological features or tumor formation ability were observed between unexposed and exposed glioblastoma cells. Our data showed that exposure to 1950-MHz TD-SCDMA electromagnetic fields for up to 48 h did not act as a cytotoxic or tumor-promoting agent to affect the proliferation or gene expression profile of glioblastoma cells. Conclusions: Our findings implied that exposing brain tumor cells in vitro for up to 48 h to 1950-MHz continuous TD-SCDMA electromagnetic fields did not elicit a general cell stress response.
    Full-text · Article · Aug 2015 · BMC Public Health
  • 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.
    Full-text · Article · Mar 2014 · Journal of Neuroinflammation
Show more