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The incidence of brain cancer in Australia since the introduction of mobile phones    
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The incidence of brain cancer in Australia since the introduction of mobile phones
donderdag, 12 mei 2016 - Dossier: Algemeen

Cancer Epidemiol. 2016 May 4. pii: S1877-7821(16)30050-9. doi: 10.1016/j.canep.2016.04.010. (Epub ahead of print)

Has the incidence of brain cancer risen in Australia since the introduction of mobile phones 29 years ago?

Chapman S1, Azizi L2, Luo Q3, Sitas F4.

1School of Public Health, University of Sydney, Australia. Electronic address:
2School of Public Health, University of Sydney, Australia.
3School of Public Health, University of Sydney, Australia; Cancer Council NSW, Sydney, Australia.
4School of Public Health, University of Sydney, Australia; School of Public Health and Community Medicine, University of New South Wales, Australia.


Mobile phone use in Australia has increased rapidly since its introduction in 1987 with whole population usage being 94% by 2014. We explored the popularly hypothesised association between brain cancer incidence and mobile phone use.

Using national cancer registration data, we examined age and gender specific incidence rates of 19,858 male and 14,222 females diagnosed with brain cancer in Australia between 1982 and 2012, and mobile phone usage data from 1987 to 2012. We modelled expected age specific rates (20-39, 40-59, 60-69, 70-84 years), based on published reports of relative risks (RR) of 1.5 in ever-users of mobile phones, and RR of 2.5 in a proportion of 'heavy users' (19% of all users), assuming a 10-year lag period between use and incidence.

Age adjusted brain cancer incidence rates (20-84 years, per 100,000) have risen slightly in males (p<0.05) but were stable over 30 years in females (p>0.05) and are higher in males 8.7 (CI=8.1-9.3) than in females, 5.8 (CI=5.3-6.3). Assuming a causal RR of 1.5 and 10-year lag period, the expected incidence rate in males in 2012 would be 11.7 (11-12.4) and in females 7.7 (CI=7.2-8.3), both p<0.01; 1434 cases observed in 2012, vs. 1867 expected. Significant increases in brain cancer incidence were observed (in keeping with modelled rates) only in those aged ≥70 years (both sexes), but the increase in incidence in this age group began from 1982, before the introduction of mobile phones. Modelled expected incidence rates were higher in all age groups in comparison to what was observed. Assuming a causal RR of 2.5 among 'heavy users' gave 2038 expected cases in all age groups.

This is an ecological trends analysis, with no data on individual mobile phone use and outcome.

The observed stability of brain cancer incidence in Australia between 1982 and 2012 in all age groups except in those over 70 years compared to increasing modelled expected estimates, suggests that the observed increases in brain cancer incidence in the older age group are unlikely to be related to mobile phone use. Rather, we hypothesize that the observed increases in brain cancer incidence in Australia are related to the advent of improved diagnostic procedures when computed tomography and related imaging technologies were introduced in the early 1980s.

Copyright © 2016 Elsevier Ltd. All rights reserved.
Brain cancer; Cell phone; EMF; Incidence; Mobile phone; Radiofrequency radiation; Trends

With comments by Dariusz Leszczynski:

Professor Simon Chapman responds…
GALLERY Posted on May 10, 2016
Updated May 10, 2016 at 12:10 (see at the end of post)

Recent epidemiological study from Australia, on cell phones and brain cancer, made headline news: Chapman S, Azizi L, Luo Q, Sitas F. Has the incidence of brain cancer risen in Australia since the introduction of mobile phones 29 years ago? Cancer Epidemiology, 2016 May 4.

Reason for this global interest is simple, the authors claim to have proven that cell phones do not cause brain cancer and the issue should be put to rest. The study analyzed the 29 year history of cell phone use in Australia and compared it with the numbers of brain cancer reported to cancer registry.

However, I think the authors greatly overstated significance of their results leading to misinformation of the readers and the general public at large.

The title of the study is correct but it is also misleading. The 29 years since introduction of cell phones in Australia is a correct time-frame. However, the broad introduction of cell phones in Australia begun only after year 2000, after the saturation of the “market” reached 70 – 90% of the population, as shown in Figure 1 of the study.

The other problem is the latency period for brain cancer that Chapman and colleagues used for calculations – only 10 years (!). For brain cancer, a disease that we do not know how it is caused, we do not know what is the time-point when it begins and we do not know what is the period of time before it becomes symptomatic and can be diagnosed, it is not correct to use in calculations only 10-year latency period. It might be so short but, as well, it might be much longer. This is why predictive calculations made by Chapman et al for brain cancer trends with 10 years latency, should be extended to latencies of 20, 30, 40 or even 50 years. Also, the latency might be different for different causes of brain cancer.

In my opinion there are two major problems in this study. First, the misleading claim of 29 years of cell phone use in Australia should be replaced with at the most 15 years, when the phones become really common. Second, use of latency period of 10 years only gives false impression that we should expect that something should be already seen in cancer statistics. If we do not see rise then there is not problem. This is misleading too.

I asked Professor Simon Chapman, Professor Emeritus from the School of Public Health of the University of Sydney, about the two above issues and he, graciously, provided brief answers. With his permission, the questions and answers are copy/pasted below:

Leszczynski: You selected 10 years as the only lag period used in your calculations (page 3 of your manuscript)). How the curves would look like for 20, 30 40 or even 50 years of lag period. Since we do not exactly know what is really the lag period for the brain cancer, it would be more informative to consider several of the possibilities and not only a single, very short (10 years) lag period.

Chapman: We selected a 10 year lag for the reason explained in the paper. I won’t speculate about what the data would look like in 40 or 50 years, but we know that peak incidence of cancers do not appear suddenly out of nothing. The peak is preceded by a steady rise which can be slow at first and then increase. With brain cancer in Australia we are seeing no evidence of any steady rise, so it would be very surprising if suddenly there was any significant and sustained rise.

Leszczynski: Your claim of the 29 year period of usage of cell phones in Australia is correct but at the same time it is misleading. As it comes out from your figure 1, the 70% of saturation with cell phone accounts in Australia was reached only in year 2003. At that time, as I recall myself, the usage of cell phones was limited by the costs. Even though people owned cell phone they limited its usage. Therefore, the really avid use of cell phones, and exposing brains, began only after year 2003. This means that your Australian data should be referred as to analyzing only the last 10-13 years of use, and not 29 years. The first 16 years (from 1987) was the time of a very limited spread of cell phones and of a limited use because of prohibitively high costs, at least for private users.

Chapman: I’m afraid I don’t agree at all that “avid use” of mobile phones began only after 2003 in Australia. Figure 1 sourced from both the Australian government regulator & the mobile communication industry show that 70% of Australians were using mobiles by 2003, with about 1 in 4 using them by 1997.

From the answers of Professor Chapman, clearly appears that our opinions differ and that he does not accept my concerns. Likewise, I do not accept Professor Chapman’s explanations.

Also, the authors of the study did not provide any information on where from the funding was provided. It is important omission. The journal of Cancer Epidemiology should have asked and insisted on providing this. Transparency in the area on the border of business and science is important.

In my opinion the authors of the study overstated their findings and misled the non-scientific readers. No study is perfect and every study can be improved. However, providing unfounded conclusions, not supported by the evidence is wrong.

The conclusion of the Australian study: “…After nearly 30 years of mobile phone use in Australia among the millions of people, there is no evidence of any rise in any age group that could be plausibly attributed to mobile phones…” is completely false because it is not supported by the evidence.

and further comments

L. Lloyd Morgan’s Comments on Australian Study by Chapman et al
07.05.2016 by Camilla Category Electromagnetic Health Blog

An Australian study purporting to show no risk for brain tumors from cell phone use has been critiqued here by L. Lloyd Morgan of the Environmental Health Trust (Chapman et al, “Has the incidence of brain cancer risen in Australia since the introduction of mobile phones 29 years ago?”, Cancer Epidemiology).

Morgan states:
Chapman uses a classic technique of obfuscation. Instead of examining the annual percent incidence change per year of brain cancers located in the anatomical regions of the brain that absorb almost all of the radiation, and incidence among the brain cancers with the highest risk of brain cancer from cellphone use: glioblastoma multiforme (GBM) he switches the topic from annual percent change (APC) to a “what if” relative risk approach. SWITCH THE TOPIC, LOSE THE PICTURE

This “what if” approach has many false assumptions:

1. All regions of the brain are equally at risk. NOT TRUE.
a. Almost all the absorbed radiation is on the side of head where the cellphone is place to the ear and is in the frontal lobe, temporal lobe and cerebellum.
b. Zada et al’s analysis of California Cancer Registry APCs in these 3 regions are (from Table 3):
i. frontal lobe, APC=2.4%, p<0.001 (99.9% confidence);
ii. temporal lobe, APC=1.9%, p=0.026 (97% confidence), and;
iii. cerebellum, APC=11.9%, p<0.001 (99.9% confidence. Because there are two lobes (left and right) these APCs would be about double if we knew which side of the head the cellphone was held.

2. The entire population was cellphone users from 1987 to 2014. NOT TRUE.
a. Chapman paper’s Fig. 1, “Percentage of Australians with mobile phone accounts.
i. Seven year after first use, in 1993 only about 10% had cellphone accounts
1. No information is provided about the average hours of use
a. Did the authors ask ACMA if they had this data?
ii. Ten year after first use in 1996 about 20% had cellphone accounts (see 1.& a., above)
iii. It was not until 2001 (15 years after first use) that >50% had cellphone accounts (15 of the 29 years in Fig. 1).
iv. Fig. 1 shows data for every year but there was NO DATA for 10 of these 15 years (1978–1990, 1992–1997) but the missing data were “estimated by linear interpolation.”

3. All ages use cellphones equally. NOT TRUE.
4. Both genders use cellphones equally. NOT TRUE.

In addition the Summary answers: section contradicts itself. “Age adjusted brain cancer incidence rates (20–84 years, per 100,000) have risen slightly in males (p < 0.05) … .” This sentence is contradicted several sentences later, “Significant increases in brain cancer incidence were observed … only in those aged >=70 years … .”
The value of “slightly’ is not stated but it was a statistically significant increase.
The source of funding is not mentioned. Absence of funding information is a red flag.
Further comments expected and we will post as they become available.

Comments from Martin Pall, PhD
Thanks Lloyd Morgan for your comments. One question: from 2 iv it states that there are no data for 10 of those 15 years. Unless Chapman has invented some new way of doing statistics with no data, doesn’t that mean that the statistics are fictional?

Chapman claimed that it is not thought that EMFs can damage DNA, apparently substituting industry propaganda for thought. Yet that there is extensive data on EMF causation of large amounts of single strand breaks in cellular DNA via comet assays and causation of double strand breaks in cellular DNA, with each of these having been reviewed in several places. There are also many studies showing elevation of 8-OHdG in cellular DNA following EMF exposures. Each of these are produced by free radicals which can be produced as breakdown products of peroxynitrite, so there are not only extensive data on these but also plausible causal mechanisms on each of them.

Comments from Devra Davis, PhD
We expect no increase in all brain cancers YET
Several widely circulated opinion pieces assert that because there is no detectable increase in all brain cancers in Australia in the past three decades cell phones do not have any impact on the disease. There are three basic reasons why this conclusion is wrong.

First of all there are more than 200 different types of brain cancer most of which are understood to have a relatively long latency by all serious researchers on the topic. In fact, gliomas are the type of brain cancer tied with cell phone use and constitute about 30% of all brain cancers. These cell-phone related cancers are increased in Australia and in the U.S. in precisely those parts of the brain that absorb most of the microwave radiation emitted or received by phones.

Secondly, proportionally few Australians were heavy users of cell phones thirty years ago. In 1990 just 1 out of every 100 Australians owned a phone and calls were short and relatively costly. Only in the last few years have phones become ubiquitous, with the heaviest use occurring in relatively young users.

Finally, the lag between when an exposure takes place and evidence of a disease occurs depends on two factors: how many people were in fact exposed and how extensive their exposure has been. While cell phones have been around since the 1990s, they have only lately become essential components of modern life.

Consider what we know happened with tobacco smoking, according to the U.S. Centers for Disease Control. The rate of smoking reached close to 70% in U.S. males in the late 1950s, while the rate of lung cancer did not peak until the late-1990s. Thus, a lag of nearly 4 decades took place between an exposure that was shared by most of the population and increase in a related disease, as can be seen by this graph from the CDC.

Peak cigarette smoking occurred in the late 1950s, while peak lung cancer rates did not occur until the late 1990s—a lag of forty years for an exposure that once affected 70% of U.S. males. The link between the carcinogenic effects of tobacco and cancer did not come about from studying population trends, but by special study of high risk groups using case-control designs of selected cases and comparing their histories with those of persons who were otherwise similar but did not smoke. The fact that population-based trends in Australia do not yet show an increase in brain cancer dose not mean it will not be detectable in the future, perhaps soon.

In point of fact, several studies from Australia and the U.S. do find increased rates of gliomas—the same type of brain cancer established to be caused by cell phones in those who have been the heaviest users of cell phones for a decade or longer. A paper from noted neurosurgeons Vini Khurana and colleagues examined reports from centers in New South Wales (NSW) and the Australian Capital Territory (ACT), with a combined population of >7 million and reported that from 2000–2008 there was an annual increase of 2.5 % each year, with an even greater increase occurring in the last three years of the study, that is after 2006.

Another study by Zada and colleagues also found significant increases in tumors reported to be increased with regular cell phone use—gliomas. Industry modeling studies have established that three parts of the brain absorb radiation from cell phones—the cerebellum and the frontal and temporal lobes. Paralleling this result, the California Cancer Registry which covers 36 million people also reported significantly increased risks of gliomas in precisely those regions of the brain that absorb the greatest amounts of radiation. Recent studies from China as well as those from the U.S. Director of the National Institute of Drug Abuse, Nora Volkow, reporting in the Journal of the American Medical Association have also found increased metabolic activity in these same components of the brain after thirty minutes of exposure to cell phone radiation.

Only a generation ago, the hazards of ionising radiation were unrecognized. It was common to find X-ray machines freely available in shoe stores so that you could see how new shoes fit relative to the skeletal bones of your feet. Teens were treated for the disease of acne with radiation to their faces, and those treated with X-rays for ringworm, later incurred increased thyroid and other cancers. Pelvic X-rays of pregnant mothers were routine until the 1970s when leukemia risks were established in children who had been exposed prenatally decades earlier. Today those who worked as radiographers and radiologists years ago and now understood to have increased rates of a number of types of cancer. In every one of the preceding instances, the hazards were not recognized by population-based data, but by special studies that compared detailed information on exposures that took place in those with diseases in contrast to those without them.

The lack of an increase in all brain cancers in the general population of Australia or any other modern country is to be expected in light of what is known about this complex of more than 200 different diseases. Increases in glioma remain gravely worrisome as this is the tumor type that we expect to see grow if indeed cell phones and wireless radiation are playing an important role.

As public health experts who have documented the dangers of smoking, both active and passive, and tracked the growing experimental and epidemiological literature on the dangers of cell phone radiation to reproductive and brain health, we appreciate that the need for precaution must be exercised judiciously. In our considered judgment, based on more than 100 years of professional experience in this field, it is our concerted view that precaution is appropriate at this time to reduce and control exposures to cell phones and other wireless radiation devices, especially to infants, toddlers and young children.

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