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      Comments on the US National Toxicology Program technical reports on toxicology and carcinogenesis study in rats exposed to whole-body radiofrequency radiation at 900 MHz and in mice exposed to whole-body radiofrequency radiation at 1,900 MHz

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          Abstract

          During the use of handheld mobile and cordless phones, the brain is the main target of radiofrequency (RF) radiation. An increased risk of developing glioma and acoustic neuroma has been found in human epidemiological studies. Primarily based on these findings, the International Agency for Research on Cancer (IARC) at the World Health Organization (WHO) classified in May, 2011 RF radiation at the frequency range of 30 kHz-300 GHz as a ‘possible’ human carcinogen, Group 2B. A carcinogenic potential for RF radiation in animal studies was already published in 1982. This has been confirmed over the years, more recently in the Ramazzini Institute rat study. An increased incidence of glioma in the brain and malignant schwannoma in the heart was found in the US National Toxicology Program (NTP) study on rats and mice. The NTP final report is to be published; however, the extended reports are published on the internet for evaluation and are reviewed herein in more detail in relation to human epidemiological studies. Thus, the main aim of this study was to compare earlier human epidemiological studies with NTP findings, including a short review of animal studies. We conclude that there is clear evidence that RF radiation is a human carcinogen, causing glioma and vestibular schwannoma (acoustic neuroma). There is some evidence of an increased risk of developing thyroid cancer, and clear evidence that RF radiation is a multi-site carcinogen. Based on the Preamble to the IARC Monographs, RF radiation should be classified as carcinogenic to humans, Group 1.

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          Population-based studies on incidence, survival rates, and genetic alterations in astrocytic and oligodendroglial gliomas.

          Published data on prognostic and predictive factors in patients with gliomas are largely based on clinical trials and hospital-based studies. This review summarizes data on incidence rates, survival, and genetic alterations from population-based studies of astrocytic and oligodendrogliomas that were carried out in the Canton of Zurich, Switzerland (approximately 1.16 million inhabitants). A total of 987 cases were diagnosed between 1980 and 1994 and patients were followed up at least until 1999. While survival rates for pilocytic astrocytomas were excellent (96% at 10 years), the prognosis of diffusely infiltrating gliomas was poorer, with median survival times (MST) of 5.6 years for low-grade astrocytoma WHO grade II, 1.6 years for anaplastic astrocytoma grade III, and 0.4 years for glioblastoma. For oligodendrogliomas the MSTwas 11.6 years for grade II and 3.5 years for grade III. TP53 mutations were most frequent in gemistocytic astrocytomas (88%), followed by fibrillary astrocytomas (53%) and oligoastrocytomas (44%), but infrequent (13%) in oligodendrogliomas. LOH 1p/19q typically occurred in tumors without TP53 mutations and were most frequent in oligodendrogliomas (69%), followed by oligoastrocytomas (45%), but were rare in fibrillary astrocytomas (7%) and absent in gemistocytic astrocytomas. Glioblastomas were most frequent (3.55 cases per 100,000 persons per year) adjusted to the European Standard Population, amounting to 69% of total incident cases. Observed survival rates were 42.4% at 6 months, 17.7% at one year, and 3.3% at 2 years. For all age groups, survival was inversely correlated with age, ranging from an MST of 8.8 months ( 80 years). In glioblastomas, LOH 10q was the most frequent genetic alteration (69%), followed by EGFR amplification (34%), TP53 mutations (31%), p16INK4a deletion (31%), and PTEN mutations (24%). LOH 10q occurred in association with any of the other genetic alterations, and was the only alteration associated with shorter survival of glioblastoma patients. Primary (de novo) glioblastomas prevailed (95%), while secondary glioblastomas that progressed from low-grade or anaplastic gliomas were rare (5%). Secondary glioblastomas were characterized by frequent LOH 10q (63%) and TP53 mutations (65%). Of the TP53 mutations in secondary glioblastomas, 57% were in hot-spot codons 248 and 273, while in primary glioblastomas, mutations were more evenly distributed. G:C-->A:T mutations at CpG sites were more frequent in secondary than primary glioblastomas, suggesting that the acquisition of TP53 mutations in these glioblastoma subtypes may occur through different mechanisms.
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            Carcinogenicity of radiofrequency electromagnetic fields.

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              Brain tumour risk in relation to mobile telephone use: results of the INTERPHONE international case-control study.

              The rapid increase in mobile telephone use has generated concern about possible health risks related to radiofrequency electromagnetic fields from this technology. An interview-based case-control study with 2708 glioma and 2409 meningioma cases and matched controls was conducted in 13 countries using a common protocol. A reduced odds ratio (OR) related to ever having been a regular mobile phone user was seen for glioma [OR 0.81; 95% confidence interval (CI) 0.70-0.94] and meningioma (OR 0.79; 95% CI 0.68-0.91), possibly reflecting participation bias or other methodological limitations. No elevated OR was observed > or =10 years after first phone use (glioma: OR 0.98; 95% CI 0.76-1.26; meningioma: OR 0.83; 95% CI 0.61-1.14). ORs were or =1640 h, the OR was 1.40 (95% CI 1.03-1.89) for glioma, and 1.15 (95% CI 0.81-1.62) for meningioma; but there are implausible values of reported use in this group. ORs for glioma tended to be greater in the temporal lobe than in other lobes of the brain, but the CIs around the lobe-specific estimates were wide. ORs for glioma tended to be greater in subjects who reported usual phone use on the same side of the head as their tumour than on the opposite side. Overall, no increase in risk of glioma or meningioma was observed with use of mobile phones. There were suggestions of an increased risk of glioma at the highest exposure levels, but biases and error prevent a causal interpretation. The possible effects of long-term heavy use of mobile phones require further investigation.
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                Author and article information

                Journal
                Int J Oncol
                Int. J. Oncol
                IJO
                International Journal of Oncology
                D.A. Spandidos
                1019-6439
                1791-2423
                January 2019
                24 October 2018
                24 October 2018
                : 54
                : 1
                : 111-127
                Affiliations
                [1 ]Department of Oncology, University Hospital, SE-701 85 Örebro
                [2 ]The Environment and Cancer Research Foundation, SE 702 17 Örebro, Sweden
                Author notes
                Correspondence to: Dr Lennart Hardell, Present address: The Environment and Cancer Research Foundation, Studievägen 35, SE 702 17 Örebro, Sweden, E-mail: lennart_hardell@ 123456hotmail.com
                Article
                ijo-54-01-0111
                10.3892/ijo.2018.4606
                6254861
                30365129
                b24d33f8-b94b-4fea-aa70-0643c3395a2d
                Copyright: © Hardell et al.

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

                History
                : 06 July 2018
                : 03 October 2018
                Categories
                Articles

                national toxicology program study,carcinogenesis,radiofrequency radiation,glioma,acoustic neuroma,cancer

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