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Portada del sitio > Estudios Científicos > Rápidas respuestas de varios científicos internacionales al último estudio (...)

Rápidas respuestas de varios científicos internacionales al último estudio danés sobre móviles y cáncer

Lunes 24 de octubre de 2011 · 3263 lecturas

El estudio original y las respuestas pueden descargarse AQUÍ

Mobile phone radiation could be detected by the human brain.

Denis L Henshaw, Emeritus Professor of Human Radiation Effects

School of Chemistry University of Bristol Cantocks Close, Bristol, BS8 1TS

Re: Use of mobile phones and risk of brain tumours: update of Danish cohort study. Frei, et al. 343:doi:10.1136/bmj.d6387

In their introduction, Frei et al. [1] state: "So far, the mechanism of potential non-thermal interaction between radio frequency electromagnetic fields (EMFs) and living systems is unknown." This statement does not concur with scientific knowledge.

Mobile phones typically have three types of EMF emissions associated with them: in the GSM system a 900 MHz radio frequency, a 217 Hz pulsing signal and an extremely low frequency magnetic field (ELF MF) associated with the battery [2]. The ELF component has so far been ignored in all epidemiological studies of mobile phone exposure and cancer. During phone use, this ELF component exposures the whole brain to MFs ranging from a few to tens of micro-tesla, above the intensity of power frequency ELF-MFs that have been repeatedly associated with increased risk of brain tumours in adults [3,4].

Animals across a wide range of species detect small changes in the Earth’s magnetic field, which is exploited for navigation. Homing pigeons and newts are estimated to have a limiting magnetic detection sensitivity of 0.01 micro-tesla and magnetic compass sensitivity below 0.2 degrees [5]. Two types of magneto-receptor are widely discussed [6, 7], one based on structures of magnetite particles, the other on a chemical compass exploiting the radical pair mechanism, RPM in which low intensity MFs alter the quantum spin state of the unpaired electrons in a free radical pair. Both mechanisms are relevant to the interaction of mobile phone EMFs in humans.

Thus, the human brain contains magnetite particles [8], some up to 600 nm in size, capable at body temperature of transducing both low intensity ELF MFs and microwave EMFs [9, 10].

The RPM forms part of basic spin chemistry [11] in which low intensity MFs can increase the lifetime of free radical pairs by singlet- to-triplet, S-T, interconversion of their quantum spin states. The increased lifetime of free radicals allows increased availability to cause biological damage, for example to DNA. The energy levels involved are some ten million times below thermal energy, the action being of the nature of a quantum mechanical switch.

There is compelling evidence that the avian magnetic compass utilises the RPM acting in the eye on cryptochromes protein molecules [12], best known for their function in controlling circadian rhythms. The magnetic compass can be disrupted by radio frequency fields. In the American cockroach disruption was seen by 1.2 MHz fields at 0.018 micro-telsa [13], well below current ICNIRP public exposure guidelines [14]. There is evidence that human cryptochromes are magneto-sensitive [15] and that ELF MFs disrupt circadian rhythms in man [16].

IARC has recently classifieds radio frequency EMFs as a 2B possible carcinogen, based on the main body of case-control epidemiology and accumulated exposure to mobile phone radiation and increased risk of brain tumours in heavy users [17]. Research into the possible health effects of mobile phones should now concentrate on designing epidemiological studies with more relevant exposure metrics and at investigating further the mechanistic pathways by which exposure may increase the risk of brain tumours and other adverse health outcomes. Meanwhile, precaution against undue exposure is warranted and should be encouraged.


1. Frei P, Poulsen AH, Olsen JH, Schuz J. 2011 Use of mobile phones and risk of brain tumours:update of Danish cohort study. BMJ 2011;343:d6387 doi: 10.1136/bmj.d6387

2. Tuor M, Ebert S, Schuderer J, Kuster N. Assessment of ELF Exposure from GSM Handsets and Development of an Optimized RF/ELF Exposure Setup for Studies of Human Volunteers. Foundation for Research on Information Technologies in Society, Report: BAG Reg. No. 2.23.02.-18/02.001778, Zurich, January 2005.

3. O’Carroll MJ, Henshaw DL. 2008. Aggregating epidemiological evidence: comparing two seminal EMF reviews. Risk Anal 28:225-234.

4. Kheifets L, Monroe J, Vergara X, Mezei G, Afifi AA. 2008. Occupational electromagnetic fields and leukaemia and brain cancer: An update to two meta-analyses. JOEM 50:677-688.

5. Gould JL. 2010 Animal Navigation: Longitude at Last. Curr Biol 21;R226 DOI: 10.1016/j.cub.2011.01.063

6. Lohmann KJ. 2010. Magnetic-field perception. Nature 464:1140-1142.

7. Phillips JB, Muheim R, Jorge PE. 2110. A behavioral perspective on the biophysics of the light-dependent magnetic compass: a link between directional and spatial perception? J Exp Biol 213, 3247-3255. doi:10.1242/jeb.020792.

8. Kirschvink JL, Kobayashi-Kirschvink A, Woodford BJ. 1992. Magnetite biomineralization in the human brain. PNAS USA 89:7683-7687.

9. Vanderstraeten J, Gillis P. 2010. Theoretical Evaluation of Magnetoreception of Power-Frequency Fields. Bioelectromagnetics 31:371- 379.

10. Kirschvink JL. 1996. Microwave Absorption by Magnetite: A Possible Mechanism for Coupling Nonthermal Levels of Radiation to Biological Systems. Bioelectromagnetics 17:187-194.

11. Brocklehurst R, McLauchlan KA 1996. Free radical mechanism for the effects of environmental electromagnetic fields on biological systems. Int J Radiat Biol. 69:3-34.

12. Ritz T, Wiltschko R, Hore PJ, Rodgers CT, Stapput K, Thalau P, Timmel CR, Wiltschko W. 2009. Magnetic compass of birds is based on a molecule with optimal directional sensitivity. Biophys J. 96, 3451-3457. (doi:10. 1016/j.bpj.2008.11.072)

13. V?cha M, P??ov? T,and Mark?ta Kv??alov? M. 2009. Radio frequency magnetic fields disrupt magnetoreception in American cockroach. J Exp Biol. 212;3473-3477.

14. ICNIRP Guidelines 1998: International Commission on Non-Ionizing Radiation Protection: Guidelines for limiting exposure to time-varying electric, magnetic and electromagnetic field (up to 300 GHz). Health Phys 74(4):494-522.

15. Foley LE, Gegear1 RJ, Reppert SM. 2011. Human cryptochrome exhibits light-dependent magnetosensitivity. Nature Comm. DOI: 10.1038/ncomms1364

16. Henshaw DL, Reiter RJ. 2005. Do magnetic fields cause increased risk of childhood leukaemia via melatonin disruption? Bioelectromagnetics Suppl 7:S86-S97.

17. WHO IARC Monograph Working Group, Carcinogenicity of radiofrequency electromagnetic fields. Lancet Oncol. 2011 Jul;12(7):624-6.

Competing interests: None declared
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Published 23 October 2011
Updated study contains poor science and should be disregarded

Alasdair M Philips, Engineer and scientist
Graham Lamburn

Powerwatch (UK NGO)

This update has failed to control for a number of flaws and omissions that severely detracted from the quality of data in the previous paper, published in 2006 [1].

The first flaw in the paper is the ability to correctly identify the mobile phone subscribers between 1987 and 1995. 620,602 early subscribers were validated in their original data set. 200,507 were corporate users whose names were unknown and were excluded, leaving 420,095 ’early users’. This update has excluded another 61,692 of the ’early users’ resulting in a participation rate of only 58% of identified early subscribers. All of the remaining 42% will be placed in the "non-user" category (the majority of which, by the author’s own admissions, will be likely to be the heaviest user group in the data set).

Even for the remaining 58% of identified subscribers, no information was collected pertaining to actual mobile phone usage, using "number of subscription years" as a surrogate. Not only does the paper contain no data on mobile phone subscribers since 1995, it has absolutely no information about actual exposure - despite frequently using the term ’exposure’ in the paper. In the 2011 update on the carcinogenicity of radiofrequency electromagnetic fields, the 30 scientist IARC monograph panel were quite critical of the failings in the original paper: "In this study, reliance on subscription to a mobile phone provider, as a surrogate for mobile phone use, could have resulted in considerable misclassification in exposure assessment." [2]

An even more damaging limitation is the exposure classification in the "non-subscriber" part of the cohort, which has been analysed as if it is a group of individuals with no mobile phone exposure. On top of containing the 42% from the originally identified dataset, the proportion of the Danish population that held a mobile phone subscription increased from 10% to 95% between 1995 and 2004. This not only means that a significant majority of the non-subscriber category will be mobile phone users, but many of whom will have used their phone for over 10 years, despite being classified in the study as "non-users". The magnitute of this confounder makes meaningful comparisons in the data impossible.

Finally, the authors made no effort to control for any other forms of RF exposure. The primary author (Frei) has previously demonstrated that about only about 30% of adult microwave exposure now comes from their mobile phone handset use [3], with approximately 30% from cordless phones, 30% base stations and 10% other sources. These other exposures could be highly relevant, as Lennart Hardell has repeatedly shown increases in brain tumours associated with extensive cordless phone use [4], a technology that has been in widespread use since 1995.

It is unclear how this latest paper makes any novel contributions to the existing literature on mobile phones and brain tumours, as it contains significantly worse flaws than either the INTERPHONE group’s research or the papers published by Lennart Hardell. The magnitude of the limitations in this research make meaningful analyses and conclusions virtually impossible.

It is also unclear how this study is meant to help doctors and other health professionals make better decisions that will improve outcomes for patients as stated in BMJ’s publication mission statement [5].

Alasdair Philips and Graham Lamburn

1. Schuz J, et al. (2006) Cellular telephone use and cancer risk: update of a nationwide Danish cohort. JNCI 2006. 98:1707-13.

2. WHO IARC Monograph Working Group, Carcinogenicity of radiofrequency electromagnetic fields. Lancet Oncol. 2011 Jul;12(7):624-6.

3. Frei P, et al, (2010) Classification of personal exposure to radio frequency electromagnetic fields (RF-EMF) for epidemiological research: Evaluation of different exposure assessment methods., Environ Int 2010 Oct;36(7):714-20

4. Hardell L, Carlberg M, Hansson Mild K. (2011) 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 May;38(5):1465-74. doi: 10.3892/ijo.2011.947. Epub 2011 Feb 17.

5. BMJ website. What does the BMJ publish?

Competing interests: We are both involved in running Powerwatch, a small UK NGO active in the field of EMF exposure and health since 1987. We currently advise a precautionary approach to mobile phone use, especially by children.
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Published 22 October 2011
Danish cohort study: Questions regarding selection, exposure, and tumour incidence

Vini G. Khurana, Neurosurgeon & Associate Professor

Australian National University Medical School

In this era, the value of long-term, large cohort studies examining any association between mobile phone use and primary brain tumour incidence cannot be overstated. While the importance of the study by Frei et al. [Ref. 1] is widely recognised, the authors’ responses to the following questions regarding participant selection, exposure and tumour incidence would be appreciated:

1. SELECTION: To which subpopulation do the study’s results actually apply? It is plausible that mobile phone-using subpopulations such as (i) corporate users (which might diversely include business executives, government officials, telecommunication industry field workers, real estate agents, media staff, lawyers and doctors whose subscriptions happen to be on corporate accounts), (ii) children and adolescents, and (iii) people with a family history of (i.e., genetic predisposition to) cancer might be at a higher risk of developing a brain tumour following near- field exposure to mobile phone electromagnetic radiation over a long-term (e.g., 10-20 years). However, as indicated in Figure 1 of their study [Ref. 1], all of these perhaps more tumour-predisposed subpopulations (in total accounting for 206 174 or nearly 30% of the initial 723 421 eligible records) were excluded from participation and/or statistical analysis. The recording and analysis of data from these important subgroups could surely have been expected to enhance our knowledge.

2. EXPOSURE: If actual phone records could not be obtained, why was the amount of mobile phone usage in this large cohort not estimated or extrapolated by some means? This omission is particularly important given that the 13-nation INTERPHONE study [Ref. 2] found a significantly increased risk of glioma among the highest decile (> 1640 hours) of cumulative time that mobile phones were recalled as being used, a finding that supported a preceding meta-analysis of brain tumour risk in long-term (>= 10-year) mobile phone users [Ref. 3].

3. INCIDENCE: Does the greater than 10-fold increase in the number of brain tumours among long-term subscribers over the additional 5 years of follow-up between the authors’ present and previous publications reflect an actual increase in yearly tumour incidence within the cohort? The most recent primary brain tumour incidence rates in Western populations are reported to range from 11 [Ref. 4] to 19 [Ref. 5] primary brain tumours per 100,000 person-years. In their previous publication [Ref. 6] with follow-up to 2002, the authors reported 28 cases of brain tumours in long- term subscribers. In their present publication [Ref. 1] with follow-up to 2007, they report 316 cases. What was the yearly incidence of primary brain tumours in this cohort over the duration of follow-up?


[Ref. 1:] Frei P, Poulsen AH, Johansen C, et al. Use of mobile phones and risk of brain tumours: update of Danish cohort study. BMJ 2011;343.

[Ref. 2:] INTERPHONE Study Group. Brain tumour risk in relation to mobile telephone use: results of the INTERPHONE international case-control study. Int J Epidemiol 2010;39:675-94.

[Ref. 3:] Khurana VG, Teo C, Kundi M, et al. Cell phones and brain tumors: a review including the long-term epidemiologic data. Surg Neurol 2009;72:205-14; discussion 14-15.

[Ref. 4:] Dobes M, Shadbolt B, Khurana VG, et al. A multicenter study of primary brain tumor incidence in Australia (2000-2008). Neuro Oncol 2011;13:783- 790.

[Ref. 5:] CBTRUS Statistical Report. Primary brain and central nervous system tumors diagnosed in the United States in 2004-2007. Central Brain Tumor Registry of the United States. http://cbtrus.org/reports/reports.html (downloaded 22 October 2011).

[Ref 6:]. Schuz J, Jacobsen R, Olsen JH, et al. Cellular telephone use and cancer risk: update of a nationwide Danish cohort. J Natl Cancer Inst 2006;98:1707-13.

Competing interests: None declared
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Published 22 October 2011

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