Letter to the Editor – Brain Tumours: Rise in Glioblastoma Multiforme Incidence

Authors’ Comment on “Brain Tumours: Rise in Glioblastoma Multiforme Incidence in England 1995–2015 Suggests an Adverse Environmental or Lifestyle Factor”, Alasdair Philips, Denis L. Henshaw, Graham Lamburn, and Michael J. O’Carroll

Journal of Environmental and Public Health

Letter to the Editor (3 pages), Article ID 2170208, Volume 2018 (2018)

Published 25 June 2018

Abstract

Full-Text PDF

Full-Text HTML

Full-Text ePUB

Full-Text XML

Linked References

Citations to this Article

How to Cite this Article

Supplementary Materials

Views 573

Citations 1

ePub 0

PDF 21

Journal of Environmental and Public Health

Volume 2018, Article ID 7910754, 10 pages

https://doi.org/10.1155/2018/7910754

Research Article

Brain Tumours: Rise in Glioblastoma Multiforme Incidence in England 1995–2015 Suggests an Adverse Environmental or Lifestyle Factor

Alasdair Philips

,1,2 Denis L. Henshaw,1,3 Graham Lamburn,2 and Michael J. O’Carroll4

1Children with Cancer UK, 51 Great Ormond Street, London, WC1N 3JQ, UK

2Powerwatch, Cambridgeshire, UK

3Professor Emeritus, University of Bristol, UK

4Professor Emeritus, Vice–Chancellor’s Office, University of Sunderland, UK

Correspondence should be addressed to Alasdair Philips; alasdair.philips@childrenwithcancer.org.uk

Received 19 December 2017; Revised 14 March 2018; Accepted 21 March 2018; Published 24 June 2018

Academic Editor: Evelyn O. Talbott

Copyright © 2018 Alasdair Philips et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Objective. To investigate detailed trends in malignant brain tumour incidence over a recent time period. Methods. UK Office of National Statistics (ONS) data covering 81,135 ICD10 C71 brain tumours diagnosed in England (1995–2015) were used to calculate incidence rates (ASR) per 100k person–years, age–standardised to the European Standard Population (ESP–2013). Results. We report a sustained and highly statistically significant ASR rise in glioblastoma multiforme (GBM) across all ages. The ASR for GBM more than doubled from 2.4 to 5.0, with annual case numbers rising from 983 to 2531. Overall, this rise is mostly hidden in the overall data by a reduced incidence of lower-grade tumours. Conclusions. The rise is of importance for clinical resources and brain tumour aetiology. The rise cannot be fully accounted for by promotion of lower–grade tumours, random chance or improvement in diagnostic techniques as it affects specific areas of the brain and only one type of brain tumour. Despite the large variation in case numbers by age, the percentage rise is similar across the age groups, which suggests widespread environmental or lifestyle factors may be responsible. This article reports incidence data trends and does not provide additional evidence for the role of any particular risk factor.

1. Introduction

The causes of brain tumours in adults remain largely unknown [1]. In 2011, the World Health Organisation (WHO) prioritised the monitoring of detailed brain tumour incidence trends through population–based cancer registries [2]. This article reports recent changes in malignant brain tumour incidence in England that include age, sex, morphology and tumour location.

2. Materials and Methods

2.1. Data

The International Classification of Diseases for Oncology (ICD–O) is a dual classification, with coding systems for both topography and morphology [3]. The relevant topology codes are listed in Table 1, along with the number of tumours diagnosed in 1995 and 2015.

Table 1: ONS WHO ICD10 brain tumour data for England.

There are 102 different ICD–O–3.1 morphology codes used in the data set, though many have few cases. The morphology code describes the cell type and its biological activity / tumour behaviour.

WHO last updated their classifications in 2016, but their changes have minimal impact on our analysis of the data [4, 5]. Malignant brain neoplasms without histology are recorded as ICD–10 D43 (D43.0 & D43.2 supratentorial).

We used anonymised individual–level national cancer registration case data from the UK Office of National Statistics (ONS) for all 81,135 ICD10–C71 category primary malignant brain tumours diagnosed in England for the years from 1995 to 2015, plus 8,008 ICD10–D43 supratentorial malignant tumours without histology/morphology data from 1998–2015. The initial data is supplied by the National Cancer Registration Service (NCRS). The ONS then apply further validation checks and the UK Department of Health use the ONS data to inform policy making. The ONS state their cancer data are generally within 2% of the correct values [6]. Until about 2005, some cases in the oldest age–groups will not have been recorded in the cancer registries. Since 2005 this error is likely to be small.

Glioblastoma Multiforme (GBM), the most common and most malignant primary tumour of the brain, is associated with one of the worst five–year survival rates among all human cancers, with an average survival from diagnosis of only about 1 year. This ensures that few cases will be unrecorded in the ONS database and we show that their number of GBM tumours is similar to NHS hospital inpatient numbers. The data include the year of diagnosis, age at diagnosis, sex of patient, primary site and morphology code. National population estimates of age and gender by calendar year were also obtained from ONS data [7] and age–specific incidence rates per 100,000 person–years and for a wide variety of tumour types were calculated in 5-year age group bins for males and females separately.

Some published incidence analyses have used different criteria as to which glioma and astrocytoma should be considered malignant. WHO considers Grades I to IV as biologically malignant even if they have not been graded histologically malignant. We have taken the WHO/IARC morphology behaviour codes /3, /6 and /9 as being histologically malignant which means that Grade I and II tumours are classed as low–grade malignancies.

We are not aware of any specific bias in the ONS data. There is a slight data–lag in cancer registry data, which are regularly checked and updated if necessary, but are generally stable after 3 to 5 years. Our ONS data extract is dated July 2017.

Brodbelt et al. (2015) [8] reported an analysis of treatment and survival for 10,743 GBM cases in England over the period 2007–2011, which had an overall median survival of only 6.1 months, rising to 14.9 months with maximal treatment. Brodbelt et.al.’s GBM case total from English hospital data is only 0.5% higher that our ONS GBM total of 10,687 cases for the same time period; this suggests that a very complete UK cancer diagnosis and registration system is now in place. In contrast, Ostrom et al. (2015) [9] reporting on USA SEER brain tumour data provide a scatter–plot that shows a median complete registration and histological confirmation level of only about 65%, with the best examples returning less than 75% full completion in 2012.

2.2. Confounding

We had a large number of categories and sub–categories in the data. It was necessary to combine some of these to increase the resolving power. We ran analyses separately for each site (C71.0 to C71.9), for each main type of tumour, and for tumour grade (I to IV). It was immediately obvious that the most significant change was in the incidence of GBM in frontal and temporal lobes. The obvious potential confounders would be the C71.8 (overlapping) and C71.9 (unspecified) categories due to better imaging techniques and we discuss this later.

2.3. Standardisation

Incidence rates rise dramatically with age and standardisation is necessary as population age profiles are changing with time. We calculated age–standardised incidence rates (ASR) per 100k person–years to the current recommended European Standard Population (ESP–2013), as it best represents the reality of the case burden on society [10]. Adjusting European cancer incidence to the World Standard Population is not helpful as the age-spectra are so different.

Table 2 lists the morphology codes with the highest case numbers, totalling 80354 tumours. Included in our analyses are an additional 781 cases in 78 other categories,

each with fewer than 100 cases over the 21 years. A full listing of all the cases in the data set is provided in the Supplementary File [S1].

Table 2: ICD-O-3 morphology codes with more than 100 cases between 1995-2015 inclusive. (A full listing of all the morphology codes and cases is present in the Supplementary file).

We needed to group data to improve resolution and reduce random data noise. We examined infant and child neoplasms separately, but did not find any statistically significant time–trends. Three age-groups seemed reasonable. We chose a child, teenage and young-adult group (0-29), a main middle-age group (30-54) and an older age group (over 55 years of age). These reasonably split the population into three roughly equal (20, 18 and 16 million) groups of people. The case totals in the three groups were about 9.5k, 19.5k and 52k respectively. We tested moving the cut-point boundaries by 5 years in both directions and it made little difference to the overall results.

2.4. Analysis

The cases were analysed by morphology, topology, sex, age, age–specific and age–standardised incidence. The Annual Average Percentage Change (AAPC) and corresponding 95% CI and p–values were calculated using Stata SE12.1 (StataCorp). A linear model on the log of the age–standardised rates, which tests for a constant rate of change (), best fitted the data. See Supplementary File sections S2 and S3.

2.5. Background

In a major 2013 review article, Hiroko Ohgaki and Paul Kleihues [11] wrote “Glioblastoma is the most frequent and malignant brain tumor. The vast majority of glioblastomas (~90%) develop rapidly de novo in elderly patients, without clinical or histologic evidence of a less malignant precursor lesion (primary glioblastomas). Secondary glioblastomas progress from low-grade diffuse astrocytoma or anaplastic astrocytoma. They manifest in younger patients, have a lesser degree of necrosis, are preferentially located in the frontal lobe, and carry a significantly better prognosis.”

Overall primary malignant brain tumour ASRs are only rising slowly and are often considered fairly static. Figure 1 shows the age–standardised trends from 1971 to 2015. From the 1970s to about 2000 there was a fairly steady rise in recorded overall incidence, however since then the rise has slowed, though clinicians have been reporting a rise in high-grade, aggressive tumours.

Figure 1: Age–standardised overall trends from 1971 to 2015 using data in ONS MB1 series, including a smaller number of supratentorial neoplasms without histology or morphology data coded D43.0 & D43.2. The data table for this figure is in the SI file as [S4].

Overall adult survival for all malignant brain tumours after diagnosis during 2006–2010 was about 35% for one year and 15% for five years, falling to about 3% for aggressive grades–III and IV tumours. ONS data show age-standardised death rates from malignant brain tumours (C71) have increased by 7% between 2001 and 2015, showing that improvements in treatment alone are inadequate and that there is a need to find ways of preventing brain cancer [12].

3. Results

Comparing new case numbers in 2015 with 1995 shows an extra 1548 aggressive GBM tumour cases annually. Figure 2 and Table 3 show that up to about 2004 the

overall rise in GBM incidence (Annual Average Percentage Change (AAPC) 5.2%, 95% CI 3.7–6.6, p < 0·00003) could be mostly compensated for by the fall in incidence of all lower grade astrocytoma and “glioma, malignant, NOS, ICD10–93803”. This leaves a fairly steady rise in the GBM ASR from 2004 to 2015 (AAPC 2.2%, 95% CI 1.4–3.0, p < 0.0001).

Table 3: ICD10-C71 and (D43.0 + D43.2) cases and age-standardised (ESP-2013) incidence rates.

Figure 2: Age–standardised incidence rates for all C71 glioma cases diagnosed between 1995 and 2015 analysed by type and year (Data in Table 3). Grouping details: (1) = 94403–94433 (2) = 93843, 94003–94303 (3) = 93803 (4) = 93813, 93823, 93903–93943, 94503–94733.

Ohgaki and Kleihues [11] reported that most secondary GBMs are found in younger middle-age people and most primary GBMs are in over 60s. We tested our (30–54) and (>54) age group data, splitting the total GBM into de novo and promoted tumours. We estimated the maximum possible number of promoted tumours using the change in the grades II and III diffuse and anaplastic astrocytomas. The results are shown in Figures 3(a) and 3(b). These are discussed later.

Figure 3: Age–standardised rates for two age groups. The possible split between de novo and secondary promoted GBMs is based on incidence change of Grades II and III diffuse and anaplastic astrocytoma.

We found a large decrease of ASR over time for Grade–II diffuse astrocytoma, a slight rise in ASR for WHO Grade–III anaplastic astrocytoma (94013; 2832 cases). There was little change in rates of anaplastic oligodendroglioma (94513; 1339 cases), anaplastic ependymoma (93923; 313 cases) Grade–II oligodendroglioma (94503; 2671cases), embryonal, or ependymal tumours.

Figure 4 shows the relative increase in age-specific GBM incidence between the averaged periods (1995–1999) and (2011–2015) for 5–year age–groups. This 1.5-fold change is remarkably similar across the age–groups, suggesting a universal factor.

Figure 4: Relative change in GBM age–specific incidence rates (ASpR) averaged over two five-year periods 1995-1999 and 2011-2015 in 5-year age bands and gender.

Figure 5 shows ASR GBM rates for frontal lobe, temporal lobe, unspecified & overlapping (C71.8 & C71.9) and ‘all other brain regions’. Most of the rise is in the frontal and temporal lobes, and most of the cases are in people over 55 years of age, with a highly statistically significant overall AAPC of 7.6% (see Table 4). There was an extra rise in frontal and temporal GBM incidence between 2006 and 2008, which coincided with a slight reduction in the GBM ASR in overlapping and unspecified regions and may be due to improved imaging.

Table 4: Age standardised incidence rates to ESP-2013 (/100k people).

Figure 5: Frontal and temporal lobe GBM age–standardised incidence rates by tumour site and year (data table in the SI as [S6]).

4. Discussion

Using sufficiently high–quality data, we present a clearer picture of the changing pattern in incidence of brain tumour types than any previously published. We report a sustained and highly statistically significant ASR rise in GBM across all ages and throughout the 21 years (1995–2015), which is of importance both for clinical resources and brain tumour aetiology.

Dobes et al. (2011) [13] reported a significant increase in malignant tumour incidence from 2000 to 2008 in the ≥65–year age group. In a second article they noted an increasing incidence of GBM (APC, 3.0; 95% CI, 0.5–5.6) in patients in the same age group, especially in temporal and frontal lobes [14]. De Vocht et al. (2011) [15] reported a rise in temporal lobe tumour incidence in ONS data, but dismissed its significance. In a 2016 paper he claimed no increase in GBM incidence, but later published a major correction to the paper that shows an increase [16].

Zada et al. (2012) [17] using USA SEER data for 1992–2006 reported a rising trend in frontal and temporal lobe tumours, the majority of which were GBM, with a decreased incidence of tumours across all other anatomical sub–sites. Ho et al. (2014) [18] reported a 2.2–fold increase in glioblastoma incidence in the Netherlands over the period 1989–2010 (APC 3.1, p<0.001).

There were no material classification changes over the analysis period that might explain our findings [19], though multidisciplinary team working was strengthened (2005 onwards) and better imaging has resulted in improved diagnosis along with a more complete registration of brain tumours in the elderly. We analysed our data in 5-year age group categories to look for evidence of improved diagnosis; the data do suggest diagnosis and registration have improved in people aged over 70. However, at earlier ages the incidence rate of ‘all’ glioma (and all C71) registrations have remained almost constant, whereas the rates for lower–grade tumours fell until about 2006 and have since remained fairly static as the rate for GBM has risen steadily.

Most GBM cases seem to originate without any known genetic predisposition. GBMs from promoted lower–grade gliomas usually have different molecular genetic markers from de novo GBMs [20]. The 2016 revision of the WHO classification of CNS tumours [3, 4] highlights the need for recording molecular genetic markers and divides glioblastomas into two main groups. The IDH–wildtype mostly corresponds to clinically defined primary or de novo glioblastoma and accounts for about 90% of cases. The remaining 10% are IDH–mutant cases, which usually arise in younger patients and mostly correspond to secondary or promoted lower–grade diffuse glioma [11, 21]. Figures 3(a) and 3(b) support the conclusion of Ohgaki and Kleihues [11] that promoted (secondary) tumours mainly occur in younger people and that de novo GBMs dominate in the over-54 age group. It is important that this pattern is monitored using modern genetic techniques.

GBM tumours are almost always fatal and are not likely to have been undiagnosed in the time-frame of our data. It is possible that some elderly cases were not fully classified, but then they should have been recorded as ICD10–D43. However, as D43 rates have remained very constant over this time period (see Figure 1), this is unlikely to have been a significant confounder.

4.1. Possible Causal Factors

We cite examples of some possible causal factors that have been discussed in the literature that could contribute changes in GBM incidence. In an important 2014 “state of science” review of glioma epidemiology, Ostrom et al. [22] list and discuss a number of potential factors that have been associated with glioma incidence, some of which we list below.

Ionising radiation, especially from X-rays used in CT scans, has the most supportive evidence as a causal factor. Due to the easy availability of CT imaging and relative

lack and higher cost of MRI imaging in UK NHS hospitals, CT scans are often used, especially for initial investigations. Their use over the period 1995-2013 is shown in the Supplementary File S6. Given the time-frame of the trend that we have identified, we suggest that CT imaging X-ray exposures should be further investigated for both the promotion and initiation of the rising incidence of GBM tumours that we have identified.

Preston et al. (2007) [23] concluded that radiation–associated cancer persists throughout life regardless of age at exposure and that glioma incidence shows a statistically significant dose response. Our oldest age group also experienced atmospheric atomic bomb testing fallout and some association with ingested and inhaled radionuclides should not be dismissed as a possible factor. England was in one of the highest exposed regions for atmospheric testing fallout as determined by the United Nations Scientific Committee on the Effects of Atomic Radiation, UNSCEAR 2000 Report [24]. Further information is given in Supplementary File S7. If only some of the population were susceptible and received a significant dose, any resulting extra cancers would show up in the ONS data.

The European Study of Cohorts for Air Pollution Effects by Andersen et al. (2017) [25] found suggestive evidence of an association between traffic-related air pollution and malignant brain tumours.

There is increasing evidence literature that many cancers including glioma have a metabolic driver due to mitochondrial dysfunction resulting in downstream genetic changes in the nucleus [26–28].

The International Agency for Research on Cancer (IARC) judged both power–frequency ELF (2002) [29] and radio–frequency RF (2011) [30] electromagnetic fields as Group 2B ‘possible human carcinogens’. Villeneuve et al. (2002) [31] concluded that occupational (ELF) magnetic field exposure increases the risk of GBM with an OR = 5.36 (95% CI: 1.2 – 24.8). Hardell and Carlberg (2015) [32] have reported an increase in high–grade glioma associated with mobile phone use. The multi-country Interphone study [33] collected data from 2000 to 2003 and included few people over 55 years of age and would have been unable to resolve any association involving older–aged people. Volkow et al. (2011) [34] found that, in healthy participants and compared with no exposure, a 50-minute cell phone exposure produced a statistically significant increase in brain glucose metabolism in the orbitofrontal cortex and temporal pole regions closest to the handset.

5. Conclusions

(1)We show a linear, large and highly statistically significant increase in primary GBM tumours over 21 years from 1995–2015, especially in frontal and temporal lobes of the brain. This has aetiological and resource implications.(2)Although most of the cases are in the group over 54 years of age, the age–standardised AAPC rise is strongly statistically significant in all our three main analysis age groups.(3)The rise in age–standardised incidence cannot be fully accounted for by improved diagnosis, as it affects specific areas of the brain and just one type of brain tumour that is generally fatal. We suggest that widespread environmental or lifestyle factors may be responsible, although these results do not provide additional evidence for the role of any particular risk factor.(4)Our results highlight an urgent need for funding more research into the initiation and promotion of GBM tumours. This should include the use of CT imaging for diagnosis and also modern lifestyle factors that may affect tumour metabolism.

Data Availability

The data were obtained from the UK Office for National Statistics (ONS), who are the legal owners of the data. Some data are publicly available in the ONS annual MB1 data series, which are freely downloadable from the ONS website, but this article uses the latest updated data, plus ICD–O–3 morphology codes, extracted under personal researcher contract from the ONS database in July 2017. ONS Data Guardian approval was required for the supply, control and use of the data. A nominal charge is made by the ONS for such data extraction. We are not permitted to supply the raw ONS extracted data to anyone else. Other researchers can obtain the latest data directly from the ONS in a similar manner. The authors provide some extra tables and figures in the Supplementary File downloadable from the journal website.

Conflicts of Interest

Alasdair Philips: Independent Engineer and Scientist. (a) Trustee of Children with Cancer UK (unpaid); (b) On a voluntary unpaid basis, has run Powerwatch for 25 years (a small UK NGO providing free information on possible health associations with EMF/RF exposure); (c) Technical Director and shareholder of EMFields Solutions Ltd., who design and sell EMF/RF measuring instruments and protective shielding items; (d) Shareholder of Sensory Perspective Ltd.; (e) Occasional voluntary advisor to the Radiation Research Trust (Registered Charity). Denis L. Henshaw: (a) Scientific Director of Children with Cancer UK (honorarium basis); (b) Shareholder of Track Analysis Systems Ltd., a company offering radon measurement services; (c) Voluntary scientific advisor for Electrosensitivity UK (Registered Charity). Michael J. O’Carroll: (a) Chairman of Rural England against Overhead Line Transmission group; (b) Occasional advisor to the Radiation Research Trust. Graham Lamburn: (a) Acts as voluntary unpaid ‘Technical Manager’ for Powerwatch.

Authors’ Contributions

Alasdair Philips and Graham Lamburn conceived the study and first–drafted most of the manuscript with significant input from Denis L. Henshaw and Michael J. O’Carroll. Graham Lamburn organised the data obtained from the UK ONS and wrote the database analysis scripts. All authors had full access to the results of all analyses and have provided strategic input over several years of following the ONS brain tumour data. All authors have approved the final manuscript. Alasdair Philips is the guarantor for the ONS data.

Funding

This research received no funding from any external agency or body. The ONS data extracts were paid for personally by Alasdair Philips. Administration costs were paid for personally by the authors.

Acknowledgments

We are very grateful to Professor Geoffrey Pilkington and Professor Annie Sasco for their invaluable comments on early drafts of this paper. We thank the ONS for providing the data and Michael Carlberg, MSc for advice regarding statistical analysis.

Supplementary Materials

S1. Table of data morphology coding and the case numbers used in the study. S2. GBM case numbers and age-specific incidence rate data used in the study. S3. Sample STATA data and DO script. S4. Data table for Figure 1. S5. Data table for

Figure 5. S6. CT and MRI use in the UK NHS. S7. Some notes on atomic bomb testing and other nuclear fallout in England. (Supplementary Materials)

References

M. L. Bondy, M. E. Scheurer, B. Malmer et al., “Brain tumor epidemiology: Consensus from the Brain Tumor Epidemiology Consortium,” Cancer, vol. 113, no. 7, pp. 1953–1968, 2008. View at Publisher · View at Google Scholar · View at Scopus

E. Van Deventer, E. Van Rongen, and R. Saunders, “WHO research agenda for radiofrequency fields,” Bioelectromagnetics, vol. 32, no. 5, pp. 417–421, 2011. View at Publisher · View at Google Scholar · View at Scopus

“IARC – International Classification of Diseases of Oncology – ICD-O-3,” http://codes.iarc.fr/abouticdo.php.

D. N. Louis, A. Perry, G. Reifenberger et al., “The 2016 World Health Organization Classification of Tumors of the Central Nervous System: a summary,” Acta Neuropathologica, vol. 131, no. 6, pp. 803–820, 2016. View at Publisher · View at Google Scholar

D. N. Louis, H. Ohgaki, O. D. Wiestler et al., “WHO Classification of Tumours of the Central Nervous System. 4th (rev),” in IARC, ISBN–10 9283244923, 2016. View at Google Scholar

UK Office for National Statistics, “Cancer Statistics: Registrations Series MB1,” 2017, https://www.ons.gov.uk/peoplepopulationandcommunity/healthandsocialcare/conditionsanddiseases/bulletins/cancerregistrationstatisticsengland/2015#data-quality.

UK Office for National Statistics, “Population Estimates for UK, England and Wales, Scotland and Northern Ireland,” 2017, https://www.ons.gov.uk/peoplepopulationandcommunity/populationandmigration/populationestimates.

A. Brodbelt, D. Greenberg, T. Winters, M. Williams, S. Vernon, and V. P. Collins, “Glioblastoma in England: 2007–2011,” European Journal of Cancer, vol. 51, no. 4, pp. 533–542, 2015. View at Publisher · View at Google Scholar · View at Scopus

Q. T. Ostrom, H. Gittleman, J. Fulop et al., “CBTRUS statistical report: primary brain and central nervous system tumors diagnosed in the united states in 2008-2012,” Neuro-Oncology, vol. 17, Supplement 4, pp. iv1–iv62, 2015. View at Publisher · View at Google Scholar · View at Scopus

European Union, “European Standard Population,” http://ec.europa.eu/eurostat/en/web/products-manuals-and-guidelines/-/KS-RA-13-028.

H. Ohgaki and P. Kleihues, “The definition of primary and secondary glioblastoma,” Clinical Cancer Research, vol. 19, no. 4, pp. 764–772, 2013. View at Publisher · View at Google Scholar · View at Scopus

UK Office for National Statistics, “<1971–1994 8290769_tcm77–395904.xls>,” downloaded from the ONS, 26th September, and for 1995–2013 data, Table 13 in https://www.ons.gov.uk/file?uri=/peoplepopulationandcommunity/healthandsocialcare/conditionsanddiseases/datasets/cancerregistrationstatisticscancerregistrationstatisticsengland/2015/cancerregistrations2015final22.05.2017.xls downloaded from the ONS, 10th July 2017.

M. Dobes, V. G. Khurana, and B. Shadbolt, “Increasing incidence of glioblastoma multiforme and meningioma, and decreasing incidence of Schwannoma (2000–2008): findings of a multicenter Australian study,” Surgical Neurology International, vol. 2, no. 176, pp. 1–7, 2011. View at Publisher · View at Google Scholar

M. Dobes, B. Shadbolt, V. G. Khurana et al., “A multicenter study of primary brain tumor incidence in Australia (2000-2008),” Neuro-Oncology, vol. 13, no. 7, pp. 783–790, 2011. View at Publisher · View at Google Scholar · View at Scopus

F. De Vocht, “Inferring the 1985–2014 impact of mobile phone use on selected brain cancer subtypes using Bayesian structural time series and synthetic controls,” Environment International, vol. 97, pp. 100–107, 2016. View at Publisher · View at Google Scholar · View at Scopus

F. De Vocht, “Corrigendum to “Inferring the 1985–2014 impact of mobile phone use on selected brain cancer subtypes using Bayesian structural time series and synthetic controls. [Environ. Int. (2016), 97, 100-107],” Environment International, vol. 101, pp. 201-202, 2017, http://www.sciencedirect.com/science/article/pii/S0160412017301241. View at Publisher · View at Google Scholar

G. Zada, A. E. Bond, Y.-P. Wang, S. L. Giannotta, and D. Deapen, “Incidence trends in the anatomic location of primary malignant brain tumors in the United States: 1992–2006,” World Neurosurgery, vol. 77, no. 3-4, pp. 518–524, 2012. View at Publisher · View at Google Scholar · View at Scopus

V. K. Y. Ho, J. C. Reijneveld, R. H. Enting et al., “Changing incidence and improved survival of gliomas,” European Journal of Cancer, vol. 50, no. 13, pp. 2309–2318, 2014. View at Publisher · View at Google Scholar

Clinical Coding toolbox, “UK Health and Social Care Information Centre,” 2015, https://web.archive.org/web/20160723115526/http://systems.hscic.gov.uk:80/data/clinicalcoding/codingadvice/toolbox.

G. P. Dunn, M. L. Rinne, and J. Wykosky, “Emerging insights into the molecular and cellular basis of glioblastoma,” Genes & Development, vol. 26, pp. 756–784, 2012. View at Publisher · View at Google Scholar

H. Ohgaki and P. Kleihues, “Genetic alterations and signaling pathways in the evolution of gliomas,” Cancer Science, vol. 100, no. 12, pp. 2235–2241, 2009. View at Publisher · View at Google Scholar · View at Scopus

Q. T. Ostrom, L. Bauchet, F. G. Davis et al., “The epidemiology of glioma in adults: A state of the science review,” Neuro-Oncology, vol. 16, no. 7, pp. 896–913, 2014. View at Publisher · View at Google Scholar · View at Scopus

D. L. Preston, E. Ron, S. Tokuoka et al., “Solid cancer incidence in atomic bomb survivors:1958–1998,” Radiation Research, vol. 168, no. 1, pp. 1–64, 2007. View at Publisher · View at Google Scholar

United Nations Scientific Committee on the Effects of Atomic Radiation, UNSCEAR 2000 Report to the General Assembly, United Nations, New York, NY, USA, 2000.

Z. J. Andersen, M. Pedersen, G. Weinmayr et al., “Long-term exposure to ambient air pollution and incidence of brain tumor: the European Study of Cohorts for Air Pollution Effects (ESCAPE),” Neuro-Oncology, vol. 20, no. 3, pp. 420–432, 2017. View at Publisher · View at Google Scholar

T. N. Seyfried, “Cancer as a mitochondrial metabolic disease,” Frontiers in Cell and Developmental Biology, vol. 3, 43 pages, 2015. View at Publisher · View at Google Scholar

M. G. Abdelwahab, K. E. Fenton, M. C. Preul et al., “The ketogenic diet is an effective adjuvant to radiation therapy for the treatment of malignant glioma,” PLoS ONE, vol. 7, no. 5, Article ID e36197, 2012. View at Publisher · View at Google Scholar · View at Scopus

T. N. Seyfried, R. E. Flores, A. M. Poff, and D. P. D’Agostino, “Cancer as a metabolic disease: implications for novel therapeutics,” Carcinogenesis, vol. 35, no. 3, pp. 515–527, 2014. View at Publisher · View at Google Scholar · View at Scopus

IARC, Monographs on the Evaluation of Carcinogenic Risks to Humans, Non–Ionizing Radiation, Part 1: Static and Extremely Low–Frequency (ELF) Electric and Magnetic Fields, vol. 80, 2002.

IARC, Monographs on the Evaluation of Carcinogenic Risks to Humans, NonIonizing Radiation, Part 2:

Agnew, K. C. Johnson et al., “Brain cancer and occupational exposure to magnetic fields among men: Results from a Canadian population-based case-control study,” International Journal of Epidemiology, vol. 31, no. 1, pp. 210–217, 2002. View at Publisher · View at Google Scholar · View at Scopus

L. Hardell and M. Carlberg, “Mobile phone and cordless phone use and the risk for glioma—analysis of pooled case-control studies in Sweden, 1997–2003 and 2007–2009,” Pathophysiology, vol. 22, no. 1, pp. 1–13, 2015. View at Publisher · View at Google Scholar · View at Scopus

C. Wild, IARC Report to the Union for International Cancer Control (UICC) on the Interphone Study, WHO, IARC, Lyon, France, 03 October 2011.

N. D. Volkow, D. Tomasi, G.-J. Wang et al., “Effects of cell phone radiofrequency signal exposure on brain glucose metabolism,” The Journal of the American Medical Association, vol. 305, no. 8, pp. 808–813, 2011. View at Publisher · View at Google Scholar · View at Scopus

Letter to the Editor

What Can You Do? Inform yourself.

More than five decades of research by the world’s renowned and dedicated scientists and medics provide clear evidence of damage inflicted upon biological systems by electromagnetic fields. Do your own research using keywords.

The medical profession, schools, the media and other organisations are forced to follow government guidelines which claim ‘no harm’ in spite of the evidence. SAR ratings are a ploy to protect vested interests and have no clinical value. Consider the alarming rise in cancer and brain tumours which goes unquestioned with an apparent unwillingness to examine the wider causes. Why? Simply follow the money! For what reason is Cancer UK in denial over EMF pollution that cause cancer!

As the technology becomes more addictive, the public can be easily controlled, particularly through social media; for the young this level of control and compliance is becoming the norm. Things can be made safer only if the public demand it and resist the constant pressure to incorporate technology into every aspect of their lives. Do we need to stop and re-evaluate our relationship with this life threatening technology? The first step to improving your health and well- being is reducing your exposure to radiation. Try turning your mobile/ devices off to see how your life improves. Replace Wi-Fi and cordless phones with Ethernet cable and non- wireless routers. Withdraw your consent to SMART meters (link below). This is a democratic legal right and yes, one can refuse to have these meters installed.

Screening offers some protection, but be sceptical about EMF protection devices claiming to neutralise electromagnetic fields or harmonise the body. Also beware of scams using nonsensical pseudo-science in literature in order to trick sufferers of EMF pollution or other health issues into purchasing useless gadgets. In one third of cases the perceived short-term benefits are likely due to the well known placebo effect – or power of the mind.

More information. www.bemri.org Bio Electromagnetic Research Initiative –

stopsmartmeters.org.uk/ – powerwatch.org.uk/

Is Electromagnetic pollution making you ill?

More than five decades of research have linked electromagnetic pollution [EMP] to many health conditions. Microwaves, [RF] penetrate our body damaging cells and DNA. Electromagnetic frequencies [EMF’s] deplete immune systems and can bring about cancer, brain tumours and childhood leukaemia. More and more people experience sleeping difficulties, headaches, chronic fatigue, and other allergies. Additional symptoms include muscular complaints aches/weakness, irritability, nose bleeds, nausea, dizziness, flu like symptoms, tinnitus type noise, depression, sensitivity to chemical products, blurred vision, burning, itchy or tingly red skin, short-term memory loss, heart attacks, strokes, autoimmune diseases, and inability to concentrate. Behavioural problems in children are increasing and this technology is now recognised as an addiction.

Electromagnetic pollution continues rising above levels quite unimaginable, even twenty years ago. They follow a pattern linked to ever increasing cases of cancers, brain tumours, autism, childhood leukaemia and Alzheimer’s. The sudden rise among children aged below 15 years who suffer brain tumours is alarming news. The young have thinner sculls and tumours may take a while to grow.

Electromagnetic pollution affects all biological systems. Insects and some bird species numbers are declining and caused by a range of pollutants, electro and chemical. During experiments at Silwood Park Campus of Imperial Collage London, bees leaving a hive became disorientated after a DECT base station was placed about 1 metre from the hive and switched on for 5 minutes and when switched off, the bees returned to normal activity soon after. In Germany, a research team subjected bees to these signals over a longer period, found the hive abandoned and the bees never returned.

Electromagnetic Pollution within the Home [EMP]

Communities protest over the growing number of mobile base station antennas mounted close to residential properties and schools, but are seemingly unaware that a Wi-Fi router or cordless phone within their own home emit a high degree of radiation, most often far greater than those entering from external communication masts.

Wi-Fi also called Wireless LAN [wLan] Wi-Fi acts like a mobile phone mast pulsing microwaves 24/7 and not simply power levels from one device, but the cumulative radiation emitted from all units in the home, classroom or workplace. It includes transmissions from nearby cell phone masts, TETRA, Wi-Fi and radiation penetrating the building from neighbour’s devices.

IPAD’s, tablets, Wii and Xbox emits a high degree of radiation, is often placed on the lap dangerously close to the body. Babies and young children mostly at risk from any form of pollution, especially electro-pollution! Children have little choice, adults make it. The choice of wireless over Ethernet suggests everyone is affected.

Schools ban Wi-Fi The French Government and other countries have banned mobile phones in some schools and public buildings. Russia consistently set better safety standards over many years and are most concerned about EMF pollution. Some UK schools have outlawed phones, and prudently should now prohibit WI-FI.

Digital Enhanced Cordless Phone. [DECT] These produce powerful microwave radiation from their base units, 24/7, even when not being used. DECT signals can travel into adjacent buildings and gardens and often physically detected by those sensitive to this damaging radiation. Even if one is unable to feel it, our body is cumulatively responding to this radiation the same as one can have cancerous cells or other defects in the body without being immediately aware.

Wireless baby monitors. Digital Enhanced Cordless Telecommunications is the standard used for many baby monitors and can emit radio frequency fields of 6 volts/per metre. [Twice as strong as found 100 metres away from a mobile phone mast] For comparison, the maximum recommended 2002 Salzburg indoor level for GSM is just 0.02 volts per metre. Baby monitors are not safe when placed 1 metre from the child as some suppliers claim. Digital technology, due to its ‘pulsed’ nature becomes more harmful at lower levels of power than the older analogue technology.

Energy-saving CFL bulbs & fluorescent tubes. The EU ban on incandescent lamps may leave hundreds of thousands of vulnerable sick and disabled people in the UK unable to safely use electric light in their homes. Light sensitivity can arise from a range of health conditions, including the genetic disorder Xeroderma Pigmentosum (XP), the auto-immune disease lupus, forms of eczema and dermatitis, photosensitivity, ME, electro-sensitivity and many more. Some common symptoms are severe stinging, burning and itching of the skin, along with red rash. CFLs each contain mercury and when broken present a health hazard. Vast numbers will be dumped on landfill sites risking contamination of future water supplies.

Multiple Chemical Sensitivity is on the increase and some victims are also electrosensitive. [All biological systems are electro–chemical]. Sufferers may experience excruciating pain and sleep deprivation and unable to escape to a safe haven or have to endure family and friends failing to understand their condition and often believe the GP’s regular diagnosis, “It’s all in the mind’ who perhaps decide to pass the patient on to a psychiatrist. Neither receives training along these lines of investigation and drugs are the last thing sufferers need. Suicides are on the increase for these reasons.

Wireless Smart Meters. The plan is to replace electric and gas meters in all homes and business in the UK with smart meters under pretext they save energy and money. Costs in the USA and Australia increased after meters were installed, and people soon reported having headaches, insomnia, nausea, and dizziness, glaucoma, and heart palpitations.

As with other EMF sources, transmissions from wireless smart meters operating 24/7 can cause serious health issues. Apparently, the UK role out is estimated to cost over £12 billion and the consumer, as always, picks up the tab. Smart Meters are not compulsory [2018] and those already fitted will need replacing probably around 2020. Smart Meters also invade our privacy and are easily switched off remotely by the utility, hacked, [as with computers] or via other wirelessly linked devices. A route ripe for terrorists and hackers with little way to protect ourselves.

Courtesy of BEMRI – New-Awareness-1

Recently we found out the news via Ann Marie Carey that Mark Steele had been contacted by Bemri, Bio Electromagnetic experts with 60 + years of experience in EMF research. Their kind offer to come to Gateshead for free, and measure RFs coming from the street lights, to test for any possible anomalies that could be 5G was rejected by Mark. Im sure I was not the only one shocked by this news.
Having been previously involved in getting Mark some interviews with a couple of well respected alternative media news sites Windows on the World Mark Alexander Scott and BCfm Politics Show with Tony Gosling, I was gutted to hear that Mark had not only declined their offer to meet up, but had accused them of not knowing anything about 5G.
Living about 10 mins from Gateshead myself, I offered to meet one of the guys from Bemri, and take him to the places where Mark got his EMF readings in the 700Mhz range. Bemri used specialist sensitive equipment, including a log par directional meter and many other measuring devices. The RF readings were similar to Marks, but it was noted that there were huge mobile masts in each of the locations, which would have affected the readings. Also did Mark film his videos of EMF readings with a smart phone? Again this would interfere with the readings. He refuses to answer that question when I asked but he did call me ‘desperate’ for assuming so. Bemri obtained many readings, some with a smart phone switched on close to the meter. And yes, with the smart phone on, readings were in the 700Mhz range, similar to Marks.

During the visit to Gateshead, there were no anomalies picked up by the EMF equipment and a conclusion was made that no 5G signals were picked up, only 4G. The lamp posts were acknowledged to be emitting these RFs.
Annie and myself were very grateful to Bemri for taking the time to test the lights in Gateshead, and Stockport was found to have similar results from their antenna’d LED lamp posts too.
I have spoken to Mark Steele after Bemri’s visit and listened to his response. He still believes these people do not know what 5G is, and questions their expertise.
I, on the other hand question Marks choices he has made, in the fight to stop 5G. At no point during his interviews, did Mark choose to mention Annie’s FB group or her campaign resources. She had asked him to and he said he would, but he didn’t. Why would you do that to a fellow campaigner? It makes no sense. I would have thought that was a golden opportunity to let audiences of the shows know how they could get active on the street, handing out leaflets, making people aware of the 5G issue etc. Instead Mark used the platform to ask people to join his political party. A party that has 3 years to try getting to parliament to stop 5G, when 5G has a proposed roll out date of 2020. I joined this party a while back, but received no email newsletters.
I’ve stated facts here about the Gateshead 5G lamps visit by Bemri, and I’ve given only a small fraction of my opinion on Mark Steele. People will make up their own minds on him.

http://www.bemri.org/