Professor Simon Chapman responds…

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.

Update: read also comment, submitted by Prof. Chapman in response to my blog post, available below.


21 thoughts on “Professor Simon Chapman responds…

  1. Pingback: NTP-Studie: Verfälschungen der Daten – Eiertänze um Risiken der Mobilfunkstrahlung | PRAVDA TV – Lebe die Rebellion – Andreas Große

  2. Pingback: NTP-Studie: Verfälschungen der Daten – Eiertänze um Risiken der Mobilfunkstrahlung | Der Honigmann sagt...

  3. Every study costs money. The time of the scientists is money. How did they get the time to di such a study? Who is funding them? It is ludicrous to state that the study “costs nothing”.
    If that is the case then why not rerun the numbers (since it costs nothing) but just look at glioma and stratify it into various age ranges.
    I dare Chapman to do such a thing.
    If he can do this then he will prove his worth in gold.

    Then he can prove he is right and we can rest easy.

  4. In reply to Ms. Nilsson, if she believes that because 18 years ago, when Mr. Chapman wrote a paper and book with funding from the AMTA, there is a conflict of interest, I encourage her to state so on Mr. Chapman’s lay article about the study, as well as write to the journal in question. I take the claim on the other hand as trivial poppycock, and wonder if Mr. Leszczynski might express his opinion on the matter.

    Ms. Nilsson also suggests that there are problems with Sweden’s cancer registry, citing Hardell & Carlberg (2015). However, to dismiss the registry with only their analysis of several brain tumors is rather premature. I’m not aware of further analysis as to the integrity of the registry done by others (perhaps someone else is aware)? Furthermore, the same pattern of no increase of brain tumors has been seen in multiple registries in multiple countries, including others in the Nordic region, and now as Chapman reports, in Australia. One can’t simply wave that away.

    Finally, Ms. Nilsson’s conclusions with comments about dead bodies (echoing Devra Davis) and an anecdote about a child are emotive and wholly unscientific.

  5. The results of Chapman’s study are neither surprising nor misleading – but, entirely consistent with other high quality studies examining the question. It is in full accord with the view held by the World Health Organization, with national regulatory bodies – and with the conclusions of numerous expert review panels. Of course this type of study has limitations – but none as serious as the crude exposure surrogates used in case-control studies which come to a different conclusion!

    Check out the links:

  6. What a great discussion. unfortunately no one here, including prof. Leszczynski and prof. Chapman could answer a question which is quite complicated and far from its definitive answer.
    Perhaps no one at ICNIRP and WHO, this is the very bad news.

    What I’m writing here is my sadness for 20 years and over of publications worldwide, without a clear and definitive statement about this controversial issue, at the end.

    Anyway, thanks Dariusz for continuing to post interesting news on that matter, leaving the opportunity to people to publish their idea here.
    I recognized your effort.


  7. With the advent of the smart phone, mobile phone exposure profile today is radically different than it was just 5 years ago. Smart phones are ‘always on’, with multiple RF sources (cell, wifi, bluetooth) and the devices have continual data connections rather than occasional cell-tower interactions. Remember when Nokias used to last 2 weeks on a single charge? Further, the flip-phone crowd used to wear their devices on belt clips that provided distance between the body and the device. The number of high-dose devices has also increased exponentially. If you’ve been on a commuter train lately you’ll see that everyone looking at their phone for the entire journey. Have you measured EMF rates on commuter trains? I have and they’re staggering.
    And finally we have the recent massive build-out of the cell phone infrastructure with much higher density of 4G towers to provide adequate bandwidth demanded by users.
    I don’t know what the RF ratings of the old-style feature phones was but the latest smartphones (iphones et al) are right at the legal limits of exposure (when used in unrealistic scenarios, like 10mm from the body) *and* generate that level of exposure for much longer durations.

  8. Simon – I am very disappointed with your very simplistic analysis, just taking all brain tumours bundled in one heap – and also specifically using this to dismiss an association with brain cancer. In most countries that is either static or rising very slowly. However, there are underlying trends that are concerning.

    Back in 2011 the World Health Organisation (WHO) research agenda prioritised the monitoring of detailed brain tumour incidence trends through well-established population-based cancer registries [1].

    Australian data presented by Dobes, et al, (2011)[2,3] showed an overall rising trend in agressive glioblastoma multiforme (GBM) in frontal and temporal lobes and a decrease in lower grade tumours and also tumours in other sites in the brain. You actually cite my Ref [3] Dobes paper but omit mentioning the main point (in the title!) which was the rise in age-standardised GBM. Why?

    Zada, et al, (2012)[4] 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 very poor prognosis. They also reported a decreased incidence of tumours across all other anatomical sub-sites. Ho, et al, (2014)[5] also reported an increase in GBM in the Danish data. UK data shows a similar rising trend in agressive GBM tumors with poor prognosis.

    In the interests of good epidemiology, I ask that you go back to the data and just look at the trends in GBM over the same time period. I, and others, await the results with interest.

    Alasdair Philips

    1/. van Deventer E, van Rongen E, Saunders R, WHO research agenda for radiofrequency fields. Bioelectromagnetics 2011, v32(5):417-421. Pub online Mar 14, 2011
    2/. Dobes M, Shadbolt B, Khurana VG, A multicenter study of primary brain tumor incidence in Australia (2000–2008). Neuro-Oncology 2011, 13(7):783–790 doi:10.1093/neuonc/nor052
    3/. Dobes M, Khurana VG, Shadbolt B, et al. Increasing incidence of glioblastoma multiforme and meningioma, and decreasing incidence of Schwannoma (2000-2008): Findings of a multicenter Australian study. Surg Neurol Int 2011, 2:176.
    4/. Zada G, Bond A E, Wang Y-P, et al, Incidence Trends in the Anatomic Location of Primary Malignant Brain Tumors in the United States: 1992–2006, World Neurosurg. 2012, 77, 3/4:518-524
    5/. Ho VKY, Reijneveld JC, Enting RH, et al, Changing incidence and improved survival of gliomas, European Journal of Cancer 2014, 50:2309–2318

  9. Pingback: Recent epidemiological study from Australia, on cell phones and brain cancer… | Smart Meter News

  10. Re claims that the author, professor Chapman had no conflict of interests, the history has learned that such a statement might not be true and should be controlled independently particularly when it comes to issues where huge economic interests are involved. Let me remind of the claim from professor Anders Ahlbom of “no conflict of interests” repeated over many years, while at the same time his brother was a vice president EU affairs for TeliaSonera in Brussels and also about the involvement on the board of his brothers own consulting firm. According to this article professor Chapman has previously received funding for an article and a book from AMTA, the mobile phone industry lobby organisation.
    Another critique of the study and the claims from it (Express wrote: “Its safe”) is the reliability of the cancer registries on brain tumours, which I suppose is not controlled in depth in this article. As Dr Lennart Hardell and myself has pointed out, at least Sweden has problems with underreported brain tumour incidence. The reasons are more image diagnostic and fewer pathological investigations. It is sad and very irresposible from the part of those who claim no risk from mobile phones with reference to cancer registries, since the reality indicates something quite different. It also means that the risk deniers suggest we as a society need a huge amount of human dead bodies as proof before warning and precautionary measures are to be taken. Indeed not moral at all. Last week I spoke to a nurse whose son died 2 years ago from aggressive brain tumour. She asked : Why does so many young persons get brain tumours now?

  11. Pasi, no… but it could be done using smart phones and suitable apps.

  12. Is someone in Australia (like Arpansa) making RF Exposure measurements (phone + network + wifi) from the user’s point of view in real-time? As in most of the world the limits of 2.0w/kg and 1.6w/kg seem to be clearly exceeded…

  13. I apparently stepped on Professor Chapman’s “toes” and badly, causing outbursts on twitter… If I read the tweets properly, I was being called “turkey”… What it means in Australia? Should I be afraid of the Thanksgiving?

    Chapman’s tweets are here: @SimonChapman6

    My tweets are here: @blogBRHP

    There is also someone calling itself Fake Simon Chapman (@SimonChapmanAO ) who joined the conversation on twitter…

    Lots of fun…

  14. With some forty years of epidemiology experience under my belt, it continues to baffle me as to why emphasis on ecological correlations as evidence of ‘presence or absence’ of risk garners such attention. ‘Ecological fallacy’ is a decades-old reality that renders broad, longitudinal statistical correlations, where meaningful control for selection, misclassification, confounding and underlying biology are near impossible, to having context value but not as determinative evidence — either way — regarding causation. The plotting of trends tells us what society is doing, and that is important. But the tool is non-determinative with respect to safety or danger.

  15. Professor Chapman, will you kindly make this controversial paper available in full so that we may critique it properly. I do not possess credit cards to pay USD31.50 for the privilege. I am a professional scientific editor of statistical and econometric manuscripts, and I want to take a proper look at your methods. I have access to JSTOR, but it is not available there. You are making very big claims without allowing the public to see your full argument.

  16. Professor Chapman,

    You argue about the wrong issue. Funding source was not provided and this is a mistake but this does not, automatically, invalidate the results of the study.

    However, the misleading statements on length of the use of cell phones by the majority of Australians and singled out only a 10 year latency period for brain cancer, these invalidate final conclusion of your study.

    Conclusions of your study are not fully supported by the presented scientific evidence. The extreme conclusions of your article should be toned down, to fit the data presented.

    This is the problem.

  17. Professor Chapman,
    No competing interests is not equal disclosure of funding sources… If no money was needed then it should have been stated. Period.

  18. This comment was submitted as from ‘Anonymous’ but, as appears from the twitter, the author of the comment is Professor Chapman…

    Unless you missed our competing interest statement at the end of the paper (nothing to declare) you cannot be serious in saying that you feel the journal should ensure that “all pertinent information is there”. The journal has a mandatory disclosure question on submission. We declared we had no competing interests. Obviously if we had received any funding for the study we would have disclosed it.
    So what are you suggesting? That authors make their declaration, and then journal editors should make it again? Something like “The authors declared no competing interests. We are telling you too.”? Your statement ” I was not pointing out where from your funding might be coming.” is quite disingenuous. Of course you were (and possibly still) are trying to imply that we have received funding from cell phone interests and that by making our declaration of no competing interests, we are lying. This is just disgraceful.

  19. Professor Chapman, I feel offended by your statement: “…Your lame attempt to smear us here is really quite pathetic. …”. My comment on funding was very general and directed rather towards the journal for not making sure that all pertinent information is there. I was not pointing out where from your funding might be coming. Just insisting the funding source should have been provided. If it was as you stated that journal asked and you provided info, then this info should have been included in the manuscript, to avoid misunderstandings. I honestly wonder why this funding info was not included.

    I stand by my comments, as you stand by yours. Clearly, we live on different planets, as you suggested…

  20. You should have asked me about study funding. Because of course the journal did ask. I told them and I would have told you that study required no funding. The data we used are publicly available. Your lame attempt to smear us here is really quite pathetic. If you do not regard a daily exposure of approx 25% of the entire population of a country for 19 years as significant, we are living in a different planet. The 10 year latency period, as our paper explain,was taken from the paper of Hardell we wrote (“To illustrate the purported effect of mobile phones on brain cancer incidence, we assumed a 10-year lag period between exposure to mobile phones, and estimated expected rates per age group over 20 years (RE) assuming prevalence/use to be spread evenly across all age groups (due to lack of age specific usage data) (P), by multiplying the pre-mobile phone baseline rate in 1982-1987 (R1982-7) by a (conservative) relative risk (RR) of 1.5, the RR found for ‘ever-users’ of mobile phones, estimated by Hardell et al [15], used by Little et al [8]) using the formula for each age group: RE= (R1982-7*Pmob*RRmob)+( R1982-7*(1-Pmob)), and then obtaining the all-age rate by summation of the age specific groups. Using a recent paper [9] we also modelled brain cancer incidence using a RR of 2.5, among heavy users (>896h cumulative use), and assumed that 19% of the Australian population falls in this top category, based on data from the INTERPHONE study [Hardell L, Carlberg M, Hansson Mild K. Pooled analysis of case-control studies on malignant brain tumours and the use of mobile and cordless phones including living and deceased subjects. Int J Oncol 2011;38(5):1465-74. doi: 10.3892/ijo.2011.947. Epub 2011 Feb 17]

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