Month: August, 2011

Mobile Phones, Brain Tumours and the Interphone Study: Where Are We Now?

Anthony J. Swerdlow, Maria Feychting, Adele C Green, Leeka Kheifets, David A Savitz

1 July 2011

Mobile Phones, Brain Tumours and the Interphone Study:

Where Are We Now?

Anthony J. Swerdlow1, Maria Feychting2, Adele C Green3, Leeka Kheifets4,
David A Savitz5 (International Commission for Non-Ionizing Radiation
Protection Standing Committee on Epidemiology)
1 Section of Epidemiology, Institute of Cancer Research, Sutton, UK;
2 Karolinska Institutet, Institute of Environmental Medicine, Stockholm, Sweden;
3 Cancer and Population Studies Unit, Queensland Institute of Medical Research, Brisbane, Australia & School of Translational Medicine, University of Manchester, Manchester, UK;
4 Department of Epidemiology, University of California at Los Angeles, Los Angeles, USA;
5 Departments of Community Health and Obstetrics and Gynaecology, Brown University, Providence, USA.

Correspondence to: Anthony Swerdlow, Section of Epidemiology, Institute of Cancer Research, 15 Cotswold Road, Sutton, Surrey SM2 5NG, UK. (Telephone: +442087224012; fax: +44 2087224019; email: Running title: Mobile Phones and Brain Tumour Risk

Key words: Brain cancer, cancer and radiation, epidemiology.
Acknowledgements. We thank Sharon Squires for secretarial help. This report was
prepared under the auspices of the International Commission for Non-Ioniz2 Radiation Protection. The Institute of Cancer Research and Royal Marsden Hospital acknowledge funding to the NIHR Biomedical Research Centre. Adele Green is partly supported by a Fellowship from the Australian Medical Research Council (No. 89912).

Conflict of Interest Statement
Funding for research undertaken by MF and AJS has been provided by a number of sources, including the European Fifth Framework Program; the International Union against Cancer, which receives funds from the Mobile Manufacturers’ Forum and the
GSM Association; the Mobile Telecommunications Health and Research Programme; the Swedish Research Council; AFA Insurance; and VINNOVA (The Swedish Governmental Agency for Innovation Systems). VINNOVA received funds from TeliaSonera, EricssonAB, and Telenor. All funds from commercial sources were via firewalls. The authors certify that their freedom to design, conduct, interpret, and publish research was not compromised by any controlling sponsor. AJS holds shares in the telecoms companies Cable and Wireless Worldwide and Cable and Wireless Communications. AJS’ wife holds shares in the BT group, a global telecommunications services company. MF, ACG, and AJS are members of the International Commission on Non-Ionizing Radiation Protection, an independent body setting guidelines for non-ionizing radiation protection. MF and AJS serve as advisors to a number of public advisory and research steering groups concerning the potential health effects of exposure to non-ionizing radiation.

Abbreviations: CI = confidence interval; OR = odds ratio; RF = radiofrequency; SAR
= specific (energy) absorption rate


In the past 15 years, mobile phone use has evolved from an uncommon activity to onewith over 4.6 billion subscriptions worldwide. There is, however, public concern about the possibility that mobile phones might cause cancer, especially brain tumours.

To review the evidence on whether mobile phone use raises risk of the main types of brain tumour, glioma and meningioma, with a particular focus on the recent publication of the largest epidemiological study yet – the 13-country Interphone Study.

Methodological deficits limit the conclusions that can be drawn from Interphone, but its results, along with those from other epidemiological, biological and animal studies, and brain tumour incidence trends, suggest that within about 10-15 years after first
use of mobile phones there is unlikely to be a material increase in the risk of brain tumours in adults. Data for childhood tumours and for periods beyond 15 years are currently lacking.


Although there remains some uncertainty, the trend in the accumulating evidence is increasingly against the hypothesis that mobile phone use can cause brain tumours in adults.

In just 15 years the mobile phone has evolved from an uncommon, expensive, brickshaped object used in restricted areas of Western countries to a convenient and ubiquitous part of modern life, with more than 4.6 billion subscriptions worldwide (International Telecommunication Union 2010). The arrival of this mass technology has been accompanied by some public and media concern about the possibility that the radiofrequency (RF) fields emitted by the phones might cause cancer, especially brain tumours. Numerous committees have considered the evidence and recommended more research (IEGMP 2000; SCENIHR 2009). Since 1999, a series of epidemiological studies of mobile phone use and cancer have been published, mainly focused on brain tumour risks. Collectively, they have not provided evidence of a relationship, but they have had sufficient limitations to leave the question unresolved (Ahlbom et al. 2009). The Interphone study was launched in 2000, to provide a more powerful and
methodologically rigorous investigation of this issue by collecting data in 13 countries. Now, 10 years and €19M later, after much anticipation and a lengthy delay, the key results on brain tumours have been published (INTERPHONE Study Group 2010). What should be made of them, considered along with the rest of the literature? Do we now know whether mobile phones cause brain tumours? Or if not, how much closer are we to knowing?

The Interphone Study
The Interphone study was an international, coordinated interview case-control study, investigating the potential effect of mobile phone use on the risk of the two commonest types of brain tumour, glioma and meningioma (and, although not yet published, also acoustic neuromas and parotid gland tumours). It used a common core questionnaire and to some extent a common core protocol, but deviations and
additions were allowed: for instance, cases were population-based in most countries but hospital-based in Japan and France, and controls were pair matched at 9 centres but stratum matched in the other 7. These methodological inconsistencies add to the
difficulty of interpreting the overall results. Nevertheless, the multicentre structure
enabled a study of exceptional size: more than 5,000 patients with these relatively
uncommon tumours were interviewed in a five year period – a considerable feat.
The study questionnaire asked in detail about the type and pattern of use of each
mobile phone the respondent had used, and about other RF exposures and brain
tumour risk factors. The questionnaire was administered by an interviewer using a
computerised laptop data entry system (except in Finland), with practical advantages
but with the disadvantage that there were no original paper records available to check
the fidelity of data entry for apparently erroneous values. The questionnaire collected
information on hands-free phone use, which was excluded from analyses since head
exposure is then negligible. It is unknown, however, how well subjects can recall past
use of hands-free devices, and whether recall differed between cases and controls.
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The analyses employed post hoc matching of one control per case (two for Germany)
for the centres that had used a stratified control selection. Individually matched
analyses were then used for the analyses. This resulted in loss of data: 70 cases and
over 2000 interviewed controls were not included in the final analyses. Furthermore,
most of the national studies that contributed to Interphone covered a wider age-range
(as low as 18 and/or up to 69) than the Interphone analyses (30-59), so that a
considerable proportion of the national data (e.g., 58% for Sweden (Lonn et al.
2005)), were not included in the overall pooled analyses. The national publications
need to be considered, therefore, as additional semi-independent sources of evidence,
not simply as subsets of the overall Interphone analysis.
The Interphone publication (INTERPHONE Study Group 2010) compared 2708
glioma cases diagnosed at ages 30-59 yers during 2000-2004, with 2972 controls,
and 2409 meningioma cases with 2662 controls. Participation rates were 64% for
glioma cases, 78% for meningioma cases, and 53% for controls, with considerable
variation among study centres; proxies were used for 13% of glioma cases, 2% of
meningioma cases and 1% of controls. Sensitivity analyses did not suggest, however,
that the results were dependent on participation rates across centres or on inclusion of
Key findings were a significantly diminished risk of both glioma and meningioma in
regular users compared with people who were not users or were occasional users
(“non-users”); no trend in risk of either tumour type with cumulative hours of use but
an apparent raised risk of glioma, and to a lesser extent meningioma, in those in the
top decile of cumulative hours of use; and no relation of risk of either tumour type to

cumulative number of calls, years of use or years since first use. These results raise
several important issues:-
Reduced Risk of Brain Tumours in Mobile Phone Users
The Interphone Study, as well as some previous case-control studies (Inskip et al.
2001; Muscat et al. 2000) and the only large cohort study (Schuz et al. 2006),
identified a reduced risk of brain tumours among mobile phone users compared with
non-users. In the Interphone study as a whole, ever-regular use was associated with
an odds ratio of 0.79 (0.68-0.91) for meningioma, and 0.81 (0.70-0.94) for glioma.
The pattern was consistent across the Interphone study sites and statistically precise,
calling for explanation.
There is empirical evidence that the reduced risks were in part due to non-response
bias (Vrijheid et al. 2009). Cases and controls who initially declined to participate but
agreed to complete a short non-response questionnaire had lower frequencies of
regular mobile phone use than those who participated fully. The quantitative results
from this non-response questionnaire imply that selection bias would produce an odds
ratio of 0.87-0.92 if the null hypothesis were true. It seems unlikely that differential
response based on mobile phone use could explain the diminished risk entirely since
the reduction in risk was similar for study centres that did and did not reveal to
potential participants the study’s focus on mobile phone use.
Even if the same pattern of diminished response by non-users occurred for cases and
controls, which it did not, the overall greater non-participation among controls due to
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refusal would result in a downward bias in the odds ratio. Whereas only 11% of
glioma and meningioma cases refused to participate, 30% of controls did so.
Furthermore, the phone use of those who did not complete even the non-response
questionnaire (e.g. because of refusal or death) is unknown, adding further uncertainty
to the extent of the overall bias.
Other likely contributors to the diminished ORs in users are prodromal symptoms
such as headaches and impaired cognition, which may have prevented recent initiation
of mobile phone use among subjects with as yet undiagnosed brain tumours. Thus
some cases who would otherwise have become short term users may have remained
non-users, leading to artefactually reduced odds ratios for brain tumour in phone
users, especially short term users (and low cumulative users, since short term use will
tend to result in low cumulative use). It seems likely that this accounts for at least part
of the decreased risk in users because the strongest reduction in glioma risk was found
in the shortest term users. Other potential contributors to diminished ORs can be
hypothesised, but there is no evidence for them (see Supplemental Material, page 1).
The appropriate analytic approach and interpretation in the light of this presumably
non-causal reduction in risk is not obvious. One suggested response has been to alter
the referent group, by using low regular use rather than non-use plus occasional use as
the referent. This results in an upward shift in the odds ratios across the board, more
for glioma than meningioma, but no change in the magnitude of those odds ratios
relative to one another across the range of exposure (INTERPHONE Study Group
2010). However, whether this decreases or increases the bias is dependent on two
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factors –whether the diminished risk is due to non-response, and whether the biases
apply also to low level users as well as non-users. Neither of these factors is known,
but to the extent that the diminished risk is due to prodromal symptoms, changing the
referent group would produce upward bias. If short term users (or low cumulative
users) are used as the referent exposure group, the more pronounced risk reduction in
this group caused by prodromal symptoms would make relative risks for long term
users (or high cumulative users) biased upward.
Risks after prolonged and heavy mobile phone use
If exposure to RF fields through mobile phone use were tumourigenic, people using
mobile phones longest and those who were the heaviest users would be expected to
show the highest risks of brain tumours. Reliability of recall of amount of use a
decade ago is unknown, and the average amount of use is likely to have shifted over
time as phone use has escalated universally. Validation studies of recall of phone use
in the last six months, and up to approximately 5 years in the past, have found that
even in the short term, subjects on average underestimate the number of calls per
month but overestimate duration of calls, with moderate systematic error
(underestimation by light users, overestimation by heavy users) and a large amount of
random error (Vrijheid et al. 2006). Recall of number of calls was found to be better
than recall of their duration. Furthermore cases in Interphone more often than controls
gave implausibly high estimates of overall time spent on calls (e.g., 10 cases and no
controls reported average use of >12 hours/day). A validation study including both
cases and controls found that there was overestimation by cases in more distant time
periods that could cause positive bias in risk estimates (Vrijheid et al. 2009). It thus
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appears that recall of amount of use was appreciably erroneous and quite likely
different for cases than controls. It is possible that recall of year of first use, and
hence duration of use, may have been more reliable than recall of amount of use.
Notwithstanding the inherent unreliability of recalled amount of use, the only
cumulative mobile phone exposure measures available in Interphone were duration
and amount. Neither yielded material evidence of a positive association with brain
tumours. Specifically, for the longest-term users (10+years since first use), no
association was seen for glioma (OR 0.98 (95% CI 0.76–1.26)), or meningioma (OR
0.83 (95% CI 0.61–1.14)). Most ORs were <1.0 and no dose-response pattern was
seen. This is consistent with results from a cohort study based on subscriber lists
(Schuz et al. 2006) but in contrast with the raised risks for long-term use reported by
Hardell et al (Hardell et al. 2006a; Hardell et al 2006b). For heavy use measured by
estimated total number of calls, again there was no positive association with brain
tumours: ORs were <1.0 in all categories of numbers of calls, including those in the
top decile, for both glioma and meningioma. For heavy use assessed by cumulative
duration of calls, again there was no dose-response effect for either type of tumour.
For glioma, while the risk estimate for subjects in the highest decile of total call-time
(>1640 hours) was modestly raised at OR 1.40 (95% CI 1.03– 1.89), it was disjointed
from the risk in the next heaviest users, the second highest decile, which was one of
the lowest risk estimates: OR 0.71 (95% CI 0.53-0.96). Similarly for meningioma the
OR in the highest decile of total call-time OR was 1.15 (95% CI 0.81– 1.62), while in
the next heaviest decile of users it was 0.76 (95% CI 0.54-1.08). Furthermore, the top
‘decile’ category presented was not actually 10% of the control data – it is unknown
to what extent risk would have been raised in the true top decile, or to what extent the
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raised risk is a function of the cut-point chosen (about the 7th centile for menigioma,
and the 8th centile for glioma).
The only previously available risk estimates among comparably heavy users are from
case-control studies conducted by Hardell et al (2006a, 2006b) in Sweden, who
reported a markedly raised risk and positive dose-response gradient for “malignant
tumours” but not for meningioma. We have discussed elsewhere why the Hardell
results are problematic (Ahlbom et al. 2009). Assessment of the findings with respect
to cumulative call time in individual published component studies of Interphone,
whose participants variously covered a wider range of ages than Interphone,
confirmed the lack of dose-response effect with glioma (see Supplemental Material,
page 2). Furthermore, for number of calls, which validation studies suggest may be
better-reported than cumulative hours of exposure, there was no indication of raised
risk in the top decile or of dose-response.
Finally, participants who had been using mobile phones the longest (>10 years) and
had accumulated highest lifetime call hours (>1640 hours) might be expected a priori
to have been at the highest risk if RF exposure were tumourigenic. This was not the
case however for either glioma (OR 1.34 (95% CI 0.90-2.01)) or meningioma (OR
0.95 (95% CI 0.56-1.63)) (INTERPHONE Study Group, 2010). Instead it appeared
that the very few individuals who started regular use only 1-4 years ago, yet whose
cumulative call time fell in the highest decile, due to their reported recent heavy use,
carried the greatest risk of both tumour types: for glioma OR 3.77 (1.25-11.4) and for
meningioma OR 4.80 (1.49-15.4), with no dose-response. The similarity of the results
for meningioma and glioma suggests that shared recall bias exists, since such a short-
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term usage period should have little or no bearing on the pathogenesis of meningioma,
which tends to have a long latent period.
The magnitudes of relative risk of glioma and meningioma found in the top decile of
cumulative use of phones were not large (1.40 and 1.15, respectively), and are on the
margins of what epidemiology can detect. It is at a level at which the errors and biases
identified in the study data provide a plausible, indeed at present a more plausible,
alternative explanation of the findings than does causation. Furthermore the analyses
were derived from a very large number of comparisons investigated (some reported in
the paper, the great majority not), and hence there was the potential for selective
emphasis in presentation of the results.
In summary, Interphone and the literature overall have methodological deficiencies
but do not demonstrate greater risk of either glioma or meningioma with longer or
greater use of mobile phones, although the longest period since first use examined is
<15 years.
Anatomical distribution of the tumours compared with anatomical distribution of
RF exposure during mobile phone use is highly attenuated within a few centimetres in
the brain, and therefore exposure is largely to the side of the brain, and to the
anatomical area, closest to the antenna. It has been reported that on the side of the
brain where the phone is used, 50-60% of the total RF energy is absorbed in the
temporal lobe and the average specific absorption rate (SAR) is highest in the
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temporal lobe and the cerebellum (Cardis et al. 2008). Thus examination of location
of the tumour in relation to location of exposure is of interest.
If there were a causal association between mobile phone use and brain tumour risk,
one would expect an increased risk on the same side of the head as the phone is held,
and a null finding on the opposite side. On the other hand, if some brain tumour
patients believed that mobile phone use had caused their tumour, and consequently
over-reported use on the affected side, this would result in an apparent risk increase
on the same side of the head accompanied by a decreased risk on the opposite side.
(The same bias is not possible for controls, who do not have a tumour side).
Furthermore, if there were a causal relationship, one would expect an effect of
laterality to occur after a sufficient induction period, not for solely recent use (unless
there were a very rapid and substantial promotional effect of mobile phones, which
presumably would be detectable easily and rapidly from population incidence trends).
ORs for glioma and meningioma in the Interphone study tended to be greater in
subjects who reported usual phone use on the same side of the head as their tumour
than on the opposite side for most categories of duration of use, cumulative call time
and cumulative number of calls. Most ipsilateral ORs were not above unity, however,
and there was no dose-response trend, although the greatest ORs tended to be for the
top decile of ipsilateral exposure.
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There are currently no validation studies of retrospective self-reported side of use, and
there is no evidence of consistency over time in the preferred side of use. Overall, the
greater risk for reported ipsilateral than contralateral use would be compatible with
causation or bias as an explanation, but the finding that contralateral risks and many
of the ipsilateral risks were generally below unity, with no consistent pattern of
greater ipsilateral/contralateral ratios with greater exposure (except for cumulative
number of calls and risk of glioma), would favour bias as the explanation.
The risk of glioma in the temporal lobe for regular use and for most categories of
exposure was reduced and not different from that in other lobes. ORs for long term
use and highest cumulative call time, however, were somewhat greater in the temporal
lobe than in other lobes: this is the pattern one would expect if there were a causal
effect, although there was no suggestion of a dose-response effect for temporal
tumours, which would also be expected if there were causality. No coherent pattern
was observed for meningioma, for which the OR for temporal lobe tumours for
regular use was somewhat lower than for other lobes and there was no evidence of
greater risk in the temporal than other lobes in other categories of use.
Exact anatomical location of the tumour
Interphone collected neuroradiological information on the exact locations of brain
tumours in the study. Although this has not been published for the study overall, it has
been published for glioma for many of the study centres and meningioma for one
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centre. These analyses gave no indication of an association of tumour risk to
proximity of the tumour to the exposure source (Larjavaara et al., 2011; Takebayashi
et al. 2008).
In summary, among the three types of data on anatomical location, the results for
laterality of phone use are the least interpretable. They are compatible with bias, or at
least partly with causation, but do not give firm evidence for either. The evidence on
lobe of glioma, but not of meningioma, is inconsistently in the direction that would be
expected with causality, but not decisively so. The evidence on exact location of the
tumour, which one would expect to give the most rigorous analysis since it has greater
precision without bias, does not support a causal association.
Data on tumour risk in relation to type of mobile phone, and hence of exposure, have
not suggested a relation (Supplemental Material, page 2).
Other relevant evidence
The biological literature on RF and cancer does not support an aetiological effect –
extensive research has not established any biological mechanism by which
radiofrequency fields, which are not mutagenic, could cause cancer, and animal
experiments have given no replicable evidence for cancer causation in animals
(SCENIHR 2009).
The major biases and uncertainties in interpretation of the Interphone study are similar
to those in other interview-based case-control studies of brain tumours and mobile
phones. The exceptional size of the Interphone study has not proved to be a critical
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strength – issues of bias and misclassification have proved far more important than
tightness of confidence intervals. Therefore, more studies of the same basic design as
Interphone, based on recall of phone use, no matter how carefully designed and
conducted are unlikely to add materially to our knowledge. There are other
epidemiological designs that do not share these weaknesses (although they have
others), whose results need consideration in relation to the uncertainties remaining
after Interphone: studies of the effects of occupational and residential RF exposures;
record linkage-based case-control and cohort studies of phone use; and trend analyses
of brain tumour incidence rates in the general population.
The occupational studies, and those of cancer risk in relation to residential proximity
to RF broadcasting towers, have not indicated any cancer risk although they have
been methodologically weak (Ahlbom et al., 2004). Studies that have linked private
non-corporate telephone subscription records to cancer registry records (in certain
Nordic countries) (Auvinen et al., 2002; Schuz et al., 2006) or death records (in the
US) (Dreyer et al., 1999) have the strengths that they avoid recall bias and
misclassification, and avoid participation bias. They have the weaknesses, however,
not present in interview case-control studies such as Interphone, that the subscription
data exclude corporate subscriptions, which in the early years were likely often to
have been held by heavy users, and that the named subscriber is not necessarily the
user. These problems are likely to have diluted any true association. A US cohort
study (Dreyer et al.1999) was halted one year after recruitment, so was essentially
uninformative. A national records-based case-control study in Finland (Auvinen et al.
2002) based on very short durations of use found a borderline significantly raised risk
of glioma in ever-users with some evidence for a relation to analogue not digital
Page 16 of 21
phone use. A Danish cohort study (Schuz et al. 2006) followed 420,000 phone
subscribers over a period of 7-21 years and gave no indicationof raised risk of glioma
or meningioma nor any trend in risk with duration since first use.
Analyses of secular trends in brain tumour incidence, in countries that have had good
quality diagnostic facilities and cancer registration, can give powerful evidence
constraining what can reasonably be proposed as an aetiological relationship. The
dramatic rise in mobile phone use over a relatively short period of time provides an
unusual opportunity to assess the potential for a causal effect on cancer occurrence
through high quality, unbiased descriptive epidemiological data. As substantial
misclassification is inevitable in recall-based exposure information from the
Interphone interviews, it follows that if the raised relative risk observed in the top
decile of users in the Interphone study were causally due to phone use, not chance or
artefact, then the true effect would likely be much larger, and therefore more easily
detectable in population cancer incidence trends. However, data from the Nordic
countries 1974-2003 (Deltour et al, 2009), children in the Nordic Countries 1985-
2006 (Schmidt et al, 2011), Switzerland 1969-2002 (Roosli et al, 2007), England
1998-2007 (de Vocht et al, 2011) and the US 1992-2006 (Inskip et al, 2010) and
1987-2007 (Kohler et al, 2011) showed no indication of increases in brain tumour
incidence in relation to the introduction and growing use of mobile phones, up to 20
years after their introduction and 10 years after their use became widespread.
Page 17 of 21
This does not appear compatible with the greatest risk shown in the Interphone study
– the odds ratios of about 4 within 5 years of first use for individuals using a phone
for ≥1,640 hours cumulatively, nor with the risk estimates using a ‘low user’ baseline
group, in the Appendix of the Interphone paper.
The Interphone levels of exposure were those in the population in 2003 and earlier,
since when prevalence and probably levels of use have increased greatly. Future
examination of cancer incidence trend data over the next few years, especially by age
of occurrence and anatomical location of tumours, should greatly clarify whether
mobile phones cause brain tumours: if there are no apparent effects on trends in the
next few years, after almost universal exposure to mobile phones in Western
countries, it will become increasingly implausible that there is a material causal effect.
Conversely, if there are unexplained rising trends, there will be a case to answer.
Supplemental Material Figure 1 shows the most recently available data, up to 2009,
from Sweden, one of the earliest adopters of mobile phones; the data give evidence
against an impact of mobile phone use on brain tumour occurrence.
Interphone is an impressively large study with multiple indices of exposure.
However, it has some methodological deficits, largely inevitable in recall-based casecontrol
studies, which limit interpretation of its findings. Such evidence as it provides,
combined with the results of biological and animal studies, other epidemiological
studies, and brain tumour incidence trends, suggest that within the first 10-15 years
after first mobile phone use there is unlikely to be a material increase in risk of adult
Page 18 of 21
brain tumours resulting from mobile phone use. At present there are no data on risk of
childhood tumours.
The deficiencies of exposure measurement, because of recall misclassification in
studies such as Interphone, and because of mis-identification of users in records-based
studies such as the published cohorts, leave it doubtful that either study type could
reliably detect a small effect, if one existed. Both for this reason, and because research
cannot in principle prove the complete absence of an effect, but only place limits on
its possible magnitude, there is bound to remain some uncertainty for many years to
come. The limited duration of data yet available, which is mainly for up to 10 years of
exposure and to a lesser extent for a few years beyond this, also leave uncertainty
because of the potential for long lag period effects, especially for meningioma which
is generally slower growing than glioma. The possibility of a small or a longer term
effect thus cannot be ruled out. Nevertheless, while one cannot be certain, the trend in
the accumulating evidence is increasingly against the hypothesis that mobile phone
use causes brain tumours.
Page 19 of 21
Ahlbom, A., Green, A., Kheifets, L.I., Savitz, D., Swerdlow, A., 2004. Epidemiology
of health effects of radiofrequency exposure. ICNIRP (International Commission for
Non-Ionizing Radiation Protection) Standing Committee on Epidemiology. Environ
Health Perspect 112, 1741-1754.
Ahlbom A, Feychting M, Green A, Kheifets L, Savitz DA, Swerdlow AJ. 2009.
Epidemiologic evidence on mobile phones and tumor risk: a review. Epidemiology
Auvinen A, Hietanen M, Luukkonen R, Koskela R-S. 2002. Brain tumors and salivary
gland cancers among cellular telephone users. Epidemiology 13:356-359.
Cardis E, Deltour I, Mann S, Moissonnier M, Taki M, Varsier N, et al. 2008.
Distribution of RF energy emitted by mobile phones in anatomical structures of the
brain. Phys. Med. Biol. 53:2771-2783.
Deltour I, Johansen C, Auvinen A, Feychting M, Klaeboe L, Schuz J 2009 Time
trends in brain tumor incidence rates in Denmark, Finland, Norway, and Sweden,
1974-2003. J Natl Cancer Inst. 101: 1721-1724
de Vocht F, Burstyn I, Cherrie JW 2011 Time trends (1998-2007) in brain cancer
incidence rates in relation to mobile phone use in England. Bioelectromagnetics. 32:
Dreyer NA, Loughlin JE, Rothman KJ. 1999. Cause-specific mortality in cellular
telephone users. JAMA 282:1814-1816.
Hardell L, Carlberg M, Hansson MK, 2006a. Pooled analysis of two case-control
studies on the use of cellular and cordless telephones and the risk of benign brain
tumours diagnosed during 1997-2003. Int. J. Oncol. 28:509-518.
Hardell L, Carlberg M, Hansson MK, 2006b. Pooled analysis of two case-control
studies on use of cellular and cordless telephones and the risk for malignant brain
tumours diagnosed in 1997-2003. Int. Arch. Occup. Environ. Health 79:630-639.
IEGMP (Independent Expert Group on Mobile Phones) 2000. Mobile Phones and
Health. , IEGMP, Chilton.
Inskip PD, Tarone RE, Hatch EE, Wilcosky TC, Shapiro WR, Selker RG, et al. 2001.
Cellular-telephone use and brain tumors. N Engl J Med 344:79-86.
Inskip PD, Hoover RN, Devesa SS, 2010. Brain cancer incidence trends in relation to
cellular telephone use in the United States. Neuro. Oncol. 12:1147-1151.
International Telecommunication Union. Accessed 16 May 2011. D/ict/statistics/at_glance/KeyTelecom.html
Page 20 of 21
INTERPHONE Study Group. 2010. Brain tumour risk in relation to mobile telephone
use: results of the INTERPHONE international case-control study. Int. J. Epidemiol.
Kohler BA, Ward E, McCarthy BJ, Schymura MJ, Ries LAG, Eheman C, Jemal A,
Anderson RN, Ajani UA, Edwards BK. 2011. Annual Report to the Nation on the
Status of Cancer, 1975-2007, Featuring Tumors of the Brain and Other Nervous
System. JNCI 103:1-23.
Larjavaara S, Schüz J, Swerdlow A, Feychting M, Johansen C, Lagorio S, et al. 2011.
Location of gliomas in relation to mobile phone use: a case-case and case-specular
analysis. Am. J. Epidemiol.174:2-11.
Muscat JE, Malkin MG, Thompson S, Shore RE, Stellman SD, McRee D, et al. 2000.
Handheld cellular telephone use and risk of brain cancer. JAMA 284:3001-3007.
Roosli M, Michel G, Kuehni CE, Spoerri A. 2007. Cellular telephone use and time
trends in brain tumour mortality in Switzerland from 1969 to 2002. Eur. J. Cancer
Prev. 16:77-82.
SCENIHR (Scientific Committee on Emerging and Newly Identified Health Risks)
2009. Health Effects of EMF. , EC, Brussels.
Schmidt LS, Schmiegelow K, Lahteenmaki P, Trager C, Stokland T, Grell K,
Gustafson G, Sehested A, Raashou-Nielsen O, Johansen C, Schuz J. Incidence of
Childhood Central Nervous System Tumors in the Nordic Countries. Pediatr Blood
Cancer 2011. 56:65-69.
Schuz J, Jacobsen R, Olsen JH, Boice JD, Jr., McLaughlin JK, Johansen C. 2006.
Cellular telephone use and cancer risk: update of a nationwide Danish cohort. J. Natl.
Cancer Inst. 98:1707-1713.
Takebayashi T, Varsier N, Kikuchi Y, Wake K, Taki M, Watanabe S, et al. 2008.
Mobile phone use, exposure to radiofrequency electromagnetic field, and brain
tumour: a case-control study. Br. J. Cancer 98:652-659.
Vrijheid M, Armstrong BK, Bedard D, Brown J, Deltour I, Iavarone I, et al. 2009.
Recall bias in the assessment of exposure to mobile phones. J. Expo. Sci. Environ.
Epidemiol. 19:369-381.
Vrijheid M, Cardis E, Armstrong BK, Auvinen A, Berg G, Blaasaas KG, et al. 2006.
Validation of short term recall of mobile phone use for the Interphone study. Occup.
Environ. Med. 63:237-243.

Mobilni telefoni, tumori mozga i interfon studija:”Gde smo sada?”








Anthony J. Swerdlow (АЈС), Maria Feychting (МФ), Adele C Green, Leeka Kheifets, David A Savitz

1 July 2011

Изјава о сукобу интереса

Средства за истраживања предузете од стране МФ и Ајс обезбеђена су из многобројних извора, укључујући

– Европску Пети оквир Програма;

– Међународне уније против рака, која добија средства од форума Мобилних произвођача и ГСМ Асоцијације;

– од програма мобилна телекомуникација здравство и истраживања;

– Шведски истраживачки савет;

– AFA осигурање и

– VINNOVA (шведске Владина Агенција за иновације система). VINNOVA добиjа средства од Телиа Сонера, Ерицсон Б, и         Теленор-а .

Сва средства из комерцијалних извора су зааштићена и преко заштитних менеханизама обезбеђена. Аутори су  потврдили  да је њихова слобода за пројектовање, понашања, тумачи и објављује истраживање није компромитован на било који контролише спонзора. Ајс има акције у телекомуникацискиме компанијама кабловским и бежичним широм света и кабловским и бежичним Комуникације. Ајс ‘супруга има акције у БТ Гроуп, глобална телекомуникационих услуга компаније.

МФ, АЦГ, а Ајс су чланови Међународне комисије за заштиту од нејонизујућих зрачења(ICNIRP), које је независно тело постављања смерница за не-јонизујуће зрачења. МФ и Ајс служе као саветници бројних  група које управљају истраживањима у вези потенцијалних здравствених ефеката приликом  излагања нејонизујућегм зрачењу.

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