On November 1, 2018 the National Institutes of Environmental Health Sciences National Toxicology Program released their final reports on their $25 M study on cell phone radiation.

Read the NIH  Press release 11/1/2018: High Exposure to Radio Frequency Radiation Associated With Cancer in Male Rats. 

The National Toxicology Program (NTP) concluded there is clear evidence that male rats exposed to high levels of radio frequency radiation (RFR) like that used in 2G and 3G cell phones developed cancerous heart tumors, according to final reports released today. There was also some evidence of tumors in the brain and adrenal gland of exposed male rats. For female rats, and male and female mice, the evidence was equivocal as to whether cancers observed were associated with exposure to RFR. The final reports represent the consensus of NTP and a panel of external scientific experts who reviewed the studies in March after draft reports were issued in February.

“The exposures used in the studies cannot be compared directly to the exposure that humans experience when using a cell phone,” said John Bucher, Ph.D., NTP senior scientist. “In our studies, rats and mice received radio frequency radiation across their whole bodies. By contrast, people are mostly exposed in specific local tissues close to where they hold the phone. In addition, the exposure levels and durations in our studies were greater than what people experience.”

The lowest exposure level used in the studies was equal to the maximum local tissue exposure currently allowed for cell phone users. This power level rarely occurs with typical cell phone use. The highest exposure level in the studies was four times higher than the maximum power level permitted.

“We believe that the link between radio frequency radiation and tumors in male rats is real, and the external experts agreed,” said Bucher.

The $30 million NTP studies took more than 10 years to complete and are the most comprehensive assessment, to date, of health effects in animals exposed to RFR with modulations used in 2G and 3G cell phones. 2G and 3G networks were standard when the studies were designed and are still used for phone calls and texting.

“A major strength of our studies is that we were able to control exactly how much radio frequency radiation the animals received — something that’s not possible when studying human cell phone use, which has often relied on questionnaires,” said Michael Wyde, Ph.D., lead toxicologist on the studies.

He also noted the unexpected finding of longer lifespans among the exposed male rats. “This may be explained by an observed decrease in chronic kidney problems that are often the cause of death in older rats,” Wyde said.

The animals were housed in chambers specifically designed and built for these studies. Exposure to RFR began in the womb for rats and at 5 to 6 weeks old for mice, and continued for up to two years, or most of their natural lifetime. The RFR exposure was intermittent, 10 minutes on and 10 minutes off, totaling about nine hours each day. RFR levels ranged from 1.5-6 watts per kilogram in rats, and 2.5-10 watts per kilogram in mice.

These studies did not investigate the types of RFR used for Wi-Fi or 5G networks.

5G is an emerging technology that hasn’t really been defined yet. From what we currently understand, it likely differs dramatically from what we studied,” said Wyde.

For future studies, NTP is building smaller RFR exposure chambers that will make it easier to evaluate newer telecommunications technologies in weeks or months, rather than years. These studies will focus on developing measurable physical indicators, or biomarkers, of potential effects from RFR. These may include changes in metrics like DNA damage in exposed tissues, which can be detected much sooner than cancer.

The U.S. Food and Drug Administration nominated cell phone RFR for study by NTP because of widespread public use of cell phones and limited knowledge about potential health effects from long-term exposure. NTP will provide the results of these studies to FDA and the Federal Communications Commission, who will review the information as they continue to monitor new research on the potential effects of RFR.

NTP uses four categories to summarize the evidence that a substance may cause cancer:

  • Clear evidence (highest)
  • Some evidence
  • Equivocal evidence
  • No evidence (lowest)

Then the FDA issued a statement stating they did not accept the findings.https://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm624809.htm
Given that 5G Technology has had NO long term studies undertaken before it is rolled out, I think it is up to the public to make these govt agencies and others, cease this roll out before it affects us and independent studies are studied in the long term.

Alasdair Philips is one of the UK,s leading voices on Electro-Magnetic fields  and RF, he has run Powerwatch which has been researching the links between electromagnetic fields (EMFs) and health risks for about 30 years, and is completely independent of government and industry. https://www.powerwatch.org.uk/docs/aboutus.asp

He is also a member of SSITA, Safe Schools Information Technology Alliance which addresses the concerns of Wi-Fi in schools.https://ssita.org.uk/about-us/

He is a member of BEMRI

The Bio-Electromagnetic Research Initiative (BEMRI) has been formed to create a research portal, for the scientific community and interested members of the lay public, which helps to rapidly disseminate international research findings, best practice measures and scientific hypotheses on matters related to electromagnetic (EM) phenomena.http://www.bemri.org/

He is also an advisor to Radiation Research Trust and was once the news letter editor for Electronics and Computing for peace. He has also been involved in investigations into the misuse of electromagnetic weapons by the military.

Alasdair Philips is a scientist who has been involved in research in this area for the past 50 years.

He also is involved in two companies that supply equipment to test EMR and RF and protective shielding items.

Here is Alasdair Philips being interviewed by Dr Mercola on YT.https://www.youtube.com/watch?v=NYV8YWESt_Y

In June 2018, he had a study published in the peer reviewed Journal of Environmental and Public Health, in which he studied the rise of brain tumours between 1995 to 2015 and concluded that one possible factor is the widespread use of cell phones.https://microwavenews.com/news-center/gbms-rising-uk

Alasdair Philips has chaired and presented at international conferences on these topics.

EMFields was established to provide high quality measurement equipment and screening products to protect people from the ever-increasing levels of Electromagnetic radiation, or electrosmog, in our environment designed by Alasdair  Philips. https://emfields-solutions.com/aboutus.asp

Alasdair Philips is also one of the 230 scientists and doctors who have signed a moratorium to stop the 5G roll out.

And yet when reports came out from Mark Steele in Gateshead that the lamposts were emitting 5G, Mark was contacted by Alasdair Philips.

This is part of an email that was sent to me when I asked this organisation their views on the  lamposts emitting 5G.

I have been in contact with Mark Steele and also offered to visit Gateshead with a range of more professional test equipment than he used. He used a very basic “broad band” [isotropic] meter that would pick up any signal within 50MHz – 3.5GHz coming from all directions. He would need equipment that includes a Log Per [Directional] antenna and indeed covers a wider range of frequencies. Did you see the video clip of waving his meter pointing towards a street light he claimed was producing 4,000 millivolts,  but  afraid not possible coming from the small transmitter where he was pointing his meter. [Not suitable meter for the particular task]

Along with another member of our group, have phoned him several times to offer my services freely if he could arrange for me to carry out a  free survey for members of the public of whom he has contact who are suffering heath issues that is suggested are coming from these lamp post transmitters that he claims are 5G.   Mark may be correct about 5G, but until proper measurements are carried out I cannot make comment. We would like to take measurements at Gateshead,  though  must ensure we have with  contact someone like Mark and  most importantly independent folk who suffer the effects of ELF pollution living in close proximity to  these transmitters.

We find it very strange he has not taken us up on our offer. I told him it could help him with his very worthy campaign and we certainly need more people like Mark to bring about  awareness.




Steele had become hostile to Alasdair during this communication process and had told Alasdair that he, “did not know what he was talking about” when it was pointed out that Steele’s  equipment was insufficient.

Given the fact that Alasdair Philips designed such equipment and  that he was one of the UK,s most prominent anti EMF proponents, that accusation was staggering to me.https://emfields-solutions.com/aboutus.asp

I then arranged for a member of the public to meet with the research group. They tested the lamposts that were shown in his videos and here is that report.

Report on Gateshead Lampposts to investigate alleged 5G signals

In May 2018 Bemri visited Gateshead at locations where it had been suggested 5G transmitters’ were mounted on lamp posts and were operating and producing around 4,000 m/V. [4 mV/m] These were said to be found at locations such as the shopping arcade [by bus stop] at Whickham from video recordings by a certain third party. The instrument used by the third party was an isotropic RF meter that records signals received from all directions not simply the direction the meter is pointing.

We used professional Gigahertz RF test meters and spectrum analyzer and the strongest signal recorded at this location was 1.4V/m emitted from an array of mobile phone transmitters located a few hundred yards down the opposite side of the Main Rd from the shopping arcade. After testing around a five mile radius from Whickham readings ranged from 0.25 V/m to 6.5 V/m.

It could be seen from the video recordings of the said third party RF meter readings consistently ranged around a 4V/m mark wherever any measurements were taken, even from the inside of a car travelling along a main carriageway, which is really not possible unless perhaps a Smart phone was nearby or used to video the RF meter readings. Trying to monitor signals from the inside of a car [especially moving vehicles] is a rather pointless exercise.

A Smart phone easily produces readings around levels shown in these video recordings, even when it’s not in transmission mode. All RF meters monitor frequencies from sources with the highest power density, not lower, or accumulation of other signals.

We could not find 5G signals coming from street lighting at any location we surveyed.

Bemri is an independent self funded research group strongly apposed to 5G and other electromagnetic pollution, of which long proven causes harm to all biological systems.


Now, after hearing supporters of Steele claim that Alasdair Philips was no expert and that he was a charlatan, I decided to provide the evidence to prove that this was not the case.

The charlatan is Mark Steele, a man who is getting main stream media coverage, claiming that these lamposts were 5G, when experts in this field have shown them  not to be.

A man who is supposedly fighting this issue with his answer being a new political party.

A man who calls anyone who mentions these facts, a 5G denier.

Despite the fact that I am running a 5G mass action campaign that has shared leaflets to people to campaign in over 160 areas around the UK, and despite the fact that I have this website updated on many aspects of the dangers of 5G, I am also called a 5G denier.

So an expert with 50 years experience, peer reviewed  studies on the link between mobile phones and EMF, respected as one of the UK,s leading spokesmen against the dangers of EMF and RF, who has even built equipment to test it, is named a charlatan whilst Steele, who is self proclaimed weapons expert who has worked on secret nuclear programmes, makes himself the expert on 5G whilst ignoring the facts.

The facts being, Gateshead lamposts were NOT transmitting 5G in the first place.

Controlled Opposition, with a political party for you to join.

This is article number two in a series about 5G. We have no choice but to cover this because our friends and family in the Sacramento area are suffering from symptoms now, according to their firsthand accounts of nausea, headaches, and chest pains, from Natomas to downtown Sacramento.

If we’re going to understand Verizon’s 4-city rollout of 5G and the 23 city AT&T deployment, we have to understand what frequency WiFi currently operates at, and the consequences we’ve already been suffering from that.

One correction must be issued to the last article: most 4G, WiFi these days operates at a frequency of 2.45 GHz, or at maximum 5 GHz.

Verizon’s 5G, just installed in Sacramento, Houston, Indianapolis, and Los Angeles operates at between 28 GHz and 39 GHz. The headline of this article said 35 GHz in particular because that’s in the middle of their spectrum, and studies have shown 35 GHz frequencies seem to cause immune system problems in rats.

Full Article: https://www.wakingtimes.com/2018/10/25/study-normal-2-45-ghz-wi-fi-damages-fertility-what-is-verizons-35-ghz-5g-doing/?fbclid=IwAR2RPNju3Xg_jgbwg8PliMBClL19vLGfGvX-UjMdLlRyzlkCwiQ1S5_Ags0

(Washington, DC) – Researchers with the renowned Ramazzini Institute (RI) in Italy announced that a large-scale lifetime study of lab animals exposed to environmental levels of cell tower radiation developed cancer. A $25 million study of much higher levels of cell phone radiofrequency (RF) radiation, from the US National Toxicology Program (NTP), has also reported finding the same unusual cancer called Schwannoma of the heart in male rats treated at the highest dose. In addition, the RI study of cell tower radiation also found increases in malignant brain (glial) tumors in female rats and precancerous conditions including Schwann cells hyperplasia in both male and female rats.

The study findings are making headline news. Read the Corriere Di Bologna article “Cellulari, a study by Ramazzini: “They cause very rare tumours.

“Our findings of cancerous tumours in rats exposed to environmental levels of RF are consistent with and reinforce the results of the US NTP studies on cell phone radiation, as both reported increases in the same types of tumours of the brain and heart in Sprague-Dawley rats. Together, these studies provide sufficient evidence to call for the International Agency for Research on Cancer (IARC) to re-evaluate and re-classify their conclusions regarding the carcinogenic potential of RFR in humans,” said Fiorella Belpoggi Ph.D., study author and RI Director of Research.

The Ramazzini study exposed 2448 Sprague-Dawley rats from prenatal life until their natural death to “environmental” cell tower radiation for 19 hours per day (1.8 GHz GSM radiofrequency radiation (RFR) of 5, 25 and 50 V/m). RI exposures mimicked base station emissions like those from cell tower antennas, and exposure levels were far less than those used in the NTP studies of cell phone radiation.

Full Article; https://www.collective-evolution.com/2018/08/17/worlds-largest-animal-study-on-cell-tower-radiation-confirms-cancer-link/


Evidence is UNDENIABLE: Smart meters cause massive changes to the heart

Wednesday, July 25, 2018 by 

An expert in smart meter microwave transmission power has published new research showing that, contrary to the official government narrative, the radiation emitted from smart meters directly interferes with normal heart function.

To come to this conclusion, Warren Woodward connected himself to an EKG monitor while lying near an Elster smart meter, which was connected to a high-frequency analyzer that measures microwave frequencies.

As it alternated between normal readings of 00.1 and 00.2, a monitor display showed that Woodward’s heart patterns were normal and symmetrical. But during times when it spiked to 139.3 – this being the time when the smart meter initiated data transmissions – Woodward’s EKG pattern changed dramatically in response.

In other words, when the smart meter was not sending high amounts of power, Woodward’s EKG readings were normal and natural. But when it kicked into higher output mode, the changes were “massive.”

Brief periods of alteration to normal heart rhythm aren’t much to worry about. But when these irregularities are ongoing, the heart can end up working too hard, resulting in fatigued cardiac function.

Dr. Gilberto Leon, a holistic medicine doctor from Chandler, Arizona, warns about this. He says that changes to the heart caused by smart meters are anything but symptomless or “silent,” and that major damage can take place without people even realizing it.

The constant bombardment of microwave radiation from smart meters represents “an unnatural sequence of events that we’re not programmed to respond to,” he says. Long-term exposure to smart meters, he says, can be extremely damaging to normal myocardial function.

Many of the smart meters attached to people’s homes are much stronger than the one that Woodward tested

Keep in mind that the Elster smart meter that Woodward tested only transmits at about one-quarter of a watt. Other brands like Landis and Gyr Focus, for instance, transmit closer to one watt – or nearly three times the output of the Elster brand.

This suggests that these other smart meters are perhaps even more damaging to heart function than the Elster – with potentially far worse health consequences, especially in people with pre-existing health conditions.

Woodward is also a generally healthy man who has no pre-existing heart conditions. The symptoms he suffered, in other words, were entirely the result of exposure to the Elster smart meter.

Many smart meters charge more than the electricity actually used

Another study out of the Amsterdam University of Applied Sciences has identified some other serious problems with smart meters – mainly that many of them overcharge customers.

More than half of the smart meters tested as part of an experiment were found to be riddled with computational and energy use errors. In some cases, false readings clocked in as high as 582 percent beyond actual usage. Right behind this were meters that had false readings of 581, 566, and 475 percent higher than the amount of energy that was actually used.

In theory, such figures could lead to some customers being charged as much as six times more than they should be for electricity usage – meaning big bucks for the utility companies pushing these things.

There are also concerns about smart meter safety, as there have been reports of the devices suddenly exploding and catching on fire. When smart meters are improperly installed, they can cause what’s known as “arcing,” which can lead to their spontaneous combustion accompanied by an electrical fire.

This is why groups like the American Academy of Environmental Medicine are calling on a total recall of all smart meters until their true effects have been properly studied. The public needs to know the risks before smart meters become so ubiquitous that turning back is no longer and option.

To learn more about the dangers of smart meters, visit SmartMeters.news.

Sources for this article include:






“United States Patent 6,017,302 Loos January 25, 2000
Subliminal acoustic manipulation of nervous systems

AbstractIn human subjects, sensory resonances can be excited by subliminal atmospheric acoustic pulses that are tuned to the resonance frequency. The 1/2 Hz sensory resonance affects the autonomic nervous system and may cause relaxation, drowsiness, or sexual excitement, depending on the precise acoustic frequency near 1/2 Hz used. The effects of the 2.5 Hz resonance include slowing of certain cortical processes, sleepiness, and disorientation. For these effects to occur, the acoustic intensity must lie in a certain deeply subliminal range. Suitable apparatus consists of a portable battery-powered source of weak subaudio acoustic radiation. The method and apparatus can be used by the general public as an aid to relaxation, sleep, or sexual arousal, and clinically for the control and perhaps treatment of insomnia, tremors, epileptic seizures, and anxiety disorders. There is further application as a nonlethal weapon that can be used in law enforcement standoff situations, for causing drowsiness and disorientation in targeted subjects. It is then preferable to use venting acoustic monopoles in the form of a device that inhales and exhales air with subaudio frequency.

Inventors: Loos; Hendricus G. (Laguna Beach, CA)Family ID:25505170Appl. No.:08/961,907Filed:October 31, 1997…


The central nervous system can be manipulated via sensory pathways. Of interest here is a resonance method wherein periodic sensory stimulation evokes a physiological response that peaks at certain stimulus frequencies. This occurs for instance when rocking a baby, which typically provides relaxation at frequencies near 1/2 Hz. The peaking of the physiological response versus frequency suggests that one is dealing here with a resonance mechanism, wherein the periodic sensory signals evoke an excitation of oscillatory modes in certain neural circuits. The sensory pathway involved in the rocking example is the vestibular nerve. However, a similar relaxing response at much the same frequencies can be obtained by gently stroking a child’s hair, or by administering weak heat pulses to the skin, as discussed in U.S. Pat. No. 5,800,481, Sep. 1, 1998. These three types of stimulation involve different sensory modalities, but the similarity in responses and effective frequencies suggests that the resonant neural circuitry is the same. Apparently, the resonance can be excited either via vestibular pathways or via cutaneous sensory pathways that carry tactile or temperature information.

Near 2.5 Hz another sensory resonance has been found that can be excited by weak heat pulses induced in the skin, as discussed in U.S. Pat. No. 5,800,481, Sep. 1, 1998. This sensory resonance brings on a slowing of certain cortical functions, as indicated by a pronounced increase in the time needed to silently count backward from 100 to 70 with the eyes closed. The effect is sharply dependent on frequency, as shown by a response peak a mere 0.13 Hz wide. The thermally excited 2.5 Hz resonance was found to also cause sleepiness, and after long exposure, dizziness and disorientation.

Other, more obscure types of stimulation in the form of weak magnetic fields or weak external electric fields can also cause the excitation of sensory resonances, as


Experiments have shown that atmospheric acoustic stimulation of deeply subliminal intensity can excite in a human subject the sensory resonances near 1/2 Hz and 2.5 Hz. The 1/2 Hz resonance is characterized by ptosis of the eyelids, relaxation, drowsiness, a tonic smile, tenseness, or sexual excitement, depending on the precise acoustic frequency near 1/2 Hz that is used. The observable effects of the 2.5 Hz resonance include a slowing of certain cortical functions, sleepiness, and, after long exposure, dizziness and disorientation. The finding that these sensory resonances can be excited by atmospheric acoustic signals of deeply subliminal intensity opens the way to an apparatus and method for acoustic manipulation of a subject’s nervous system, wherein weak acoustic pulses are induced in the atmosphere at the subject’s ears, and the pulse frequency is tuned to the resonance frequency of the selected sensory resonance. The method can be used by the general public for control of insomnia and anxiety, and for facilitation of relaxation and sexual arousal. Clinical use of the method includes the control and perhaps a treatment of anxiety disorders, tremors, and seizures. A suitable embodiment for these applications is a small portable battery-powered subaudio acoustic radiator which can be tuned to the resonance frequency of the selected sensory resonance.

There is an embodiment suitable for law enforcement operations in which a subject’s nervous system is manipulated from a considerable distance, as in a standoff situation. Subliminal subaudio acoustic pulses at the subject’s location may then be induced by acoustic waves radiating from a venting acoustic monopole, or by a pulsed air jet, especially when aimed at the subject or at another material surface, where the jet velocity fluctuations are wholly or partly converted into static pressure fluctuations.

The described physiological effects occur only if the intensity of the acoustic stimulation falls in a certain range, called the effective intensity window. This window has been measured in exploratory fashion for the 2.5 Hz resonance.” 



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


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


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.


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.


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.


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)


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