ArticlePDF Available

Risk of brain tumours in relation to estimated RF dose from mobile phones: Results from five Interphone countries

Authors:
  • National Institute of Occupational Safety and Health, Cincinnati, United States

Abstract and Figures

The objective of this study was to examine the associations of brain tumours with radio frequency (RF) fields from mobile phones. Patients with brain tumour from the Australian, Canadian, French, Israeli and New Zealand components of the Interphone Study, whose tumours were localised by neuroradiologists, were analysed. Controls were matched on age, sex and region and allocated the 'tumour location' of their matched case. Analyses included 553 glioma and 676 meningioma cases and 1762 and 1911 controls, respectively. RF dose was estimated as total cumulative specific energy (TCSE; J/kg) absorbed at the tumour's estimated centre taking into account multiple RF exposure determinants. ORs with ever having been a regular mobile phone user were 0.93 (95% CI 0.73 to 1.18) for glioma and 0.80 (95% CI 0.66 to 0.96) for meningioma. ORs for glioma were below 1 in the first four quintiles of TCSE but above 1 in the highest quintile, 1.35 (95% CI 0.96 to 1.90). The OR increased with increasing TCSE 7+ years before diagnosis (p-trend 0.01; OR 1.91, 95% CI 1.05 to 3.47 in the highest quintile). A complementary analysis in which 44 glioma and 135 meningioma cases in the most exposed area of the brain were compared with gliomas and meningiomas located elsewhere in the brain showed increased ORs for tumours in the most exposed part of the brain in those with 10+ years of mobile phone use (OR 2.80, 95% CI 1.13 to 6.94 for glioma). Patterns for meningioma were similar, but ORs were lower, many below 1.0. There were suggestions of an increased risk of glioma in long-term mobile phone users with high RF exposure and of similar, but apparently much smaller, increases in meningioma risk. The uncertainty of these results requires that they be replicated before a causal interpretation can be made.
Content may be subject to copyright.
Risk of brain tumours in relation to estimated RF dose
from mobile phones: results from five
Interphone countries
E Cardis,
1
B K Armstrong,
2
J D Bowman,
3
G G Giles,
4,5
M Hours,
6
D Krewski,
7
M McBride,
8
M E Parent,
9
S Sadetzki,
10,11
A Woodward,
12
J Brown,
2
A Chetrit,
10
J Figuerola,
1
C Hoffmann,
11,13
A Jarus-Hakak,
10
L Montestruq,
6
L Nadon,
9
L Richardson,
14
R Villegas,
1
M Vrijheid
1
ABSTRACT
Objectives The objective of this study was to examine
the associations of brain tumours with radio frequency
(RF) fields from mobile phones.
Methods Patients with brain tumour from the
Australian, Canadian, French, Israeli and New Zealand
components of the Interphone Study, whose tumours
were localised by neuroradiologists, were analysed.
Controls were matched on age, sex and region and
allocated the ‘tumour location’ of their matched case.
Analyses included 553 glioma and 676 meningioma
cases and 1762 and 1911 controls, respectively. RF dose
was estimated as total cumulative specific energy
(TCSE; J/kg) absorbed at the tumour’s estimated centre
taking into account multiple RF exposure determinants.
Results ORs with ever having been a regular mobile
phone user were 0.93 (95% CI 0.73 to 1.18) for glioma
and 0.80 (95% CI 0.66 to 0.96) for meningioma. ORs for
glioma were below 1 in the first four quintiles of TCSE
but above 1 in the highest quintile, 1.35 (95% CI 0.96 to
1.90). The OR increased with increasing TCSE 7+ years
before diagnosis (p-trend 0.01; OR 1.91, 95% CI 1.05 to
3.47 in the highest quintile). A complementary analysis in
which 44 glioma and 135 meningioma cases in the most
exposed area of the brain were compared with gliomas
and meningiomas located elsewhere in the brain showed
increased ORs for tumours in the most exposed part of
the brain in those with 10+ years of mobile phone use
(OR 2.80, 95% CI 1.13 to 6.94 for glioma). Patterns for
meningioma were similar, but ORs were lower, many
below 1.0.
Conclusions There were suggestions of an increased
risk of glioma in long-term mobile phone users with high
RF exposure and of similar, but apparently much smaller,
increases in meningioma risk. The uncertainty of these
results requires that they be replicated before a causal
interpretation can be made.
INTRODUCTION
Rapid increases in mobile phone use have generated
concerns about possible health effects of exposure
to radio frequency (RF) electromagnetic elds. A
multinational caseecontrol study, Interphone,
1
aimed to evaluate the association of brain, acoustic
nerve and parotid gland tumours with RF exposure
from mobile phone use. Most epidemiological
studies, including Interphone, have only reported
risk in relation to mobile phone use history.
2e20
For numbered affiliations see
end of article.
Correspondence to
Professor E Cardis, Centre for
Research in Environmental
Epidemiology (CREAL), Hospital
del Mar Research Institute
(IMIM), CIBER Epidemiologia y
Salud Pu
´blica (CIBERESP),
Doctor Aiguader 88, 08003
Barcelona, Spain;
ecardis@creal.cat
Accepted 20 May 2011
Published Online First
9 June 2011
This paper is freely available
online under the BMJ Journals
unlocked scheme, see http://
oem.bmj.com/site/about/
unlocked.xhtml
What this paper adds
<Previous epidemiological studies of mobile
phone use and brain cancer risk have used
information on mobile phone use as a proxy
measure of exposure to radio frequency fields
from mobile phones.
<Most studies have not observed increased ORs
in relation to ever having been a mobile phone
user. There were suggestions, however, of an
increased risk of glioma in long-term and heavy
users, though biases and errors prevent a causal
interpretation.
<The relationship between radio frequency
energy absorbed at the tumour location and
mobile phone use history is complex. In addition
to amount of use, it depends on phone type,
network properties, conditions of use and
tumour location. The present paper is the first
to use estimates of radio frequency energy
deposition at the centre of tumours in the brain
as a measure of radio frequency dose.
<An increased risk of glioma was seen in
individuals at the highest quintile of radio
frequency dose, though reduced risks were
seen in the four lower quintiles. When risk was
examined as a function of dose received in
different time windows before diagnosis, an
increasing trend was observed with increasing
radio frequency dose (p¼0.01) for exposures
7 years or more in the past.
<Caseecase analyses, made possible by tumour
localisation, indicated an increased risk in the
most exposed region of the brain compared with
other areas among long-term users.
<Patterns of risk for meningioma in relation to
radio frequency dose were similar, although
increases in risk were much smaller than for
glioma, and not statistically significant.
<Our results suggest that there may be an
increase in risk of glioma in the most exposed
area of the brain among long-term and heavy
users of mobile phones. These results are
uncertain (in light of the uncertainties associated
with tumour centre localisation, radio frequency
dose estimation and sample size) and require
replication before they can be taken to indicate
a causeeeffect relationship.
Occup Environ Med 2011;68:631e640. doi:10.1136/oemed-2011-100155 631
Original article
The relationship between RF energy absorbed at the tumour
location and mobile phone use history is complex.
21e23
In
addition to amount of use, it depends on phone type, network
properties, conditions of use and tumour location.
24
Thus,
Interphone attempted a systematic and detailed evaluation and
quantication of factors thought to inuence RF dose from
mobile phones in different brain locations. This necessitated
identication of probable determinants of RF Specic Absorp-
tion Rate (SAR) during protocol development and questionnaire
design and collection and analysis of information to evaluate the
importance of each factor. An algorithm was developed to
evaluate total RF dose absorbed at specic locations in the
brain
24
and applied to Interphone study subjects in ve countries
to estimate RF dose at the tumour location. This paper presents
the results of analysis of associations of glioma and meningioma
risk with these dose estimates.
MATERIALS AND METHODS
Analyses used data from the ve Interphone countriesd
Australia, Canada, France, Israel and New Zealanddthat agreed
to transfer their data to Barcelona when EC, the Interphone
Principal Investigator, relocated there. Interphone is an
international, population-based caseecontrol study based on
a common protocol.
1 25
Definition of cases and controls
Cases were patients aged 30e59 years with brain glioma or
meningioma diagnosed between 2000 and 2004. Cases were
ascertained actively from neurosurgical and oncological facilities,
and completeness of ascertainment checked through secondary
sources.
1
All diagnoses were histologically conrmed or based on
unequivocal diagnostic imaging.
The original Interphone protocol called for selection of one
control per case from a locally appropriate population-based
sampling frame. Matching variables were age (within 5 years), sex,
region of residence and, in Israel, country of birth. Controls tended
to be interviewed later than cases.
1
As mobile phone use increased
during the study period, later interviews could have spuriously
increased exposure prevalence among controls. To minimise
resulting bias, controls in all countries were post-hoc matched
to cases with tumour localisation using an algorithm that opti-
mised matching on interview time and age within strata dened
by sex, region and, in Israel, country of birth. Date of case diag-
nosis was used as the reference date for cases and controls in
each matched set. Each control was assigned the tumour location
of his or her matched case as a reference location. To maximise
statistical power, all interviewed and eligible controls were
matched to glioma and meningioma cases separately, provided
they had been interviewed within 1 year of the of the cases
interview; 1439 controls are thus included in both glioma
and meningioma analyses. Number of controls per case varied
from 1 to 19 (median 3) for glioma and 1 to 23 (median 2) for
meningioma.
Collection of information
Detailed information on past mobile phone use was collected
by interview with study subjects or proxies.
1
This included
amount, timing and conditions of mobile phone use, phone
models and operators. A catalogue of phones was used to assist
subjects in identifying phones they had used. In each country,
historical information was obtained from mobile phone
operators on communication systems and frequencies used,
introduction of adaptive power control and use of discontinuous
transmission.
Tumour localisation
Since intracranial RF energy deposition from mobile phones
is non-uniform, with most of the energy absorbed near the
phone,
23
each tumours centre was estimated so that RF dose at
that location could be estimated. Neuroradiologists in each
centre reviewed radiological images (MRI and CT scans) when
possible and recorded tumour location and their best guess
at the tumour centre (referred to as centre estimated by
neuroradiologist) on a generic three-dimensional (3-D) grid
map of the human brain, the Gridmaster, made up of 1 cm
cubes.
26
A detailed methodological description will be published
separately.
27
When images were not available, neuroradiologists used
radiology reports to prepare a 3-D representation of the tumour
volume in the Gridmaster (all cases in Israel and 12% of cases
elsewhere) (table AI). We then developed a computer algorithm
to estimate tumour centre (referred to as centre estimated by
computer algorithm). For glioma cases, the Euclidean distances
from each Gridmaster cube of the tumour s 3-D representation
to the others were calculated and the cube(s) at the shortest
distance(s) from others (the centre of gravity) chosen as the
centre. For meningioma, tumours were separated into those on
the surface of the meninges close to the skull and others. For the
second, the process was as described for glioma; for the rst, it
included only cubes in the outermost Gridmaster layer. The
program was validated on subjects for whom a neuroradiologist
estimated the centre, with good agreement, particularly for
glioma.
27
RF dose algorithm
An algorithm was developed to estimate dose as cumulative
specic energy (CSE
l,f,s
), in joules per kilogram, absorbed at
a given location in the brain (l) for a given frequency band (f)
and communication system (s) (eg, AMPS, Advanced Mobile
Phone System; GSM, Global System for Mobile).
24
CSE
l,f,s
was
calculated as the sum, over all phones the subject used, of the
product of estimated average SAR received at the tumour s
location and total call duration in this frequency band and
communication system. Modifying factors were taken into
account: laterality of use, hands-free devices, network charac-
teristics and, where appropriate, frequency of use in urban and
rural settings. Total cumulative specic energy (TCSE) at the
location was then calculated as the sum, over all frequency
bands and communication systems, of the frequency- and
communication-system-specic CSEs.
If the subject reported a preferred side of use, 90% of phone
use was assigned to that side of the head and 10% to the other. If
the subject could not answer, or said he or she used it on both
sides, 50% of use was assigned to each side.
Statistical analyses
Analyses were limited to cases with tumour localisation data.
The main analyses used unconditional logistic regression,
stratied on the matching variables (age, sex and region) and
adjusted for education level and the interaction between study
region and time period of interview (6-month intervals). As the
matching was on variables that were explicitly measured (and
therefore could be controlled in an unconditional analysis),
stratied unconditional logistic regression was conducted, rather
than conditional logistic regression based on matched sets, to
maximise the number of informative strata in the analyses. This
was important for analyses by time windows as many matched
sets would have been dropped out of these analyses if
conditional logistic regression had been used.
632 Occup Environ Med 2011;68:631e640. doi:10.1136/oemed-2011-100155
Original article
For the main analyses, the reference category for ORs was
subjects who reported that they had never used mobile phones
regularly. Sensitivity analyses restricted to regular users, with
the lowest users as the reference category, were also conducted.
Dose variables included TCSE averaged over the estimated
tumour centre (generally one to two cubes of the Gridmaster),
TCSE averaged over the entire tumour volume and CSE for
individual systems dened by frequency band (800e900 and
1800e1900 MHz) and technology type (analogue and digital). In
each analysis, TCSE or CSE was censored 1 year before the
reference date to allow a minimum latent period between rst
exposure and tumour diagnosis.
Categorical analyses were conducted in quintiles of TCSE or
CSE among regular user controls. In analyses of specic systems,
mobile phone users who had not used that system were assigned
a CSE of 0 and included in a separate category (eg, non
800e900 MHzfor analyses of 800e900 MHz). To allow
comparisons with the 13-country Interphone analyses of mobile
phone use,
28
we also analysed quintiles of cumulative call time
(data were too sparse for analyses by deciles).
The main analyses were based on TCSE at the tumour centre
estimated by neuroradiologists when available or by computer
algorithm and took into account laterality of use. We also
assessed the possible effect of RF exposure in different time
periods, by tting a model in which we considered TCSE
<3 years before the reference date, 3e6 years before and 7+
years before, based on reported mobile phone use in these
periods. As previous studies have raised the issue of risk 10 years
or more after exposure, we originally intended to analyse TCSE
in periods 0e4, 5e9 and 10+ years before the reference date but
could not because of small numbers of subjects in different
TCSE categories in the 10+ years period.
Sensitivity analyses were conducted restricting analyses to
subjects with probable centre estimated by a neuroradiologist;
not taking into account laterality of phone use (50% of CSE was
assigned to each side for all subjects); averaging CSE over the
entire tumour volume; and excluding proxy interviews, subjects
with very high levels of reported phone use (5 h or more per day
in any period) or subjects who reported use of 450 MHz tele-
phones (with little information on spatial SAR distribution, see
Cardis et al
24
).
Finally, caseecase analyses were conducted in which mobile
phone use was compared between cases whose probable tumour
centre was in the most exposed brain region and cases whose
tumour centre was elsewhere, using unconditional logistic
regression adjusted for age, sex and region. The most exposed
area was dened as the area with the highest RF SAR from
mobile phones,
23
falling within the 3 dB exposure volume (gure
AI), without taking into account reported laterality of use or
self-reported amount of mobile phone use. It comprised 230 of
the 1431 Gridmaster cubes, a region comprising about 16% of
the brain volume and absorbing over 50% of the SAR from
mobile phones.
RESULTS
The ve Interphone countries contributing to this analysis
ascertained 1302 cases of glioma, 1199 cases of meningioma and
4838 controls eligible for the study (table AI).
1
Of these, 809
glioma cases and 842 meningioma cases were interviewed and
could be matched to at least one control (table AI). Information
on tumour localisation, communication systems and frequency
bands used was available for 553 glioma cases (42.4% of glioma
cases) and 1762 matched controls (36% of controls), and 676
meningioma cases (56.4% of meningioma cases) and 1911
matched controls (39.5% of controls); these were the subjects
of the primary analyses of RF exposure. The mean age of glioma
cases was 47.2 years and 62% were men; the mean age of
meningioma cases was 49.7 years and 26% were men. The
respective matched controls had similar age and sex
distributions.
We calculated ORs for regular phone use and cumulative call
time without use of hands-free devices in all interviewed
subjects who could be matched to relate results of this ve-
country analysis to those of Interphone as a whole.
28
For glioma,
the OR for regular phone use was 0.92 (95% CI 0.75 to 1.13) and
that for the top category of cumulative call time (735+ h of use)
was 1.17 (95% CI 0.88 to 1.56) (table 1). The most closely
corresponding Interphone results were, respectively, 0.81 (95%
CI 0.70 to 0.94) and, for 735e1639.9 and 1640+ h of use
together, 1.00 (95% CI 0.80 to 1.22). For meningioma, the OR
for regular phone use was 0.80 (95% CI 0.66 to 0.96) and that for
735+ h of use was 1.01 (95% CI 0.75 to 1.36) (table 1) compared
with Interphone results of, respectively, 0.79 (95% CI 0.68 to
0.91) and, for 735e1639.9 and 1640+ h of use together, 0.93
(95% CI 0.73 to 1.19). Results of similar analyses in subjects
with localisation data were not greatly different from those in
all interviewed subjects (table 1). ORs for glioma in subjects
whose tumour centre was also estimated by a neuroradiologist
were higherd1.06 (95% CI 0.77 to 1.47) in regular users and 1.72
(95% CI 1.07 to 2.77) in 735+ h of call time, mainly due to
exclusion of subjects from Israel. Israel contributed 73% of
excluded glioma cases and its ORs for glioma were 0.67 (95% CI
0.43 to 1.05) in regular users and 0.57 (95% CI 0.30 to 1.74) in
735+ h of call time.
TCSE was highly skewed in cases and controls (gure AII).
Higher proportions of glioma cases than controls had TCSE
above 3500 J/kg. Though there was moderate agreement
between categorisation of subjects by TCSE and cumulative call
time (weighted
k
0.68), misclassication was non-negligible,
particularly at higher frequency bands.
24
ORs for glioma and
meningioma were below 1 in the rst four quintiles of TCSE. In
the highest quintile, the OR for glioma was 1.35 (95% CI 0.96 to
1.90) in subjects with tumour localisation and 1.66 (95% CI 1.03
to 2.67) in subjects with centre estimated by a neuroradiologist
(table 2). Corresponding ORs for meningioma were 0.90 (95%
CI 0.66 to 1.24) and 1.01 (95% CI 0.63 to 1.62).
In analyses of TCSE in different time intervals before the
reference date, an increased OR was seen for glioma in the
highest category of TCSE 7+ years before diagnosis (OR 1.91,
95% CI 1.05 to 3.47), with an irregular but reasonably consistent
trend across TCSE categories (p¼0.01). There was no evidence of
increased risk for more recent exposures. Results for meningioma
were similar, but without evidence of a trend with TCSE for
exposure 7+ years before diagnosis (p¼0.24) (table 3).
Table 4 shows the results of sensitivity analyses for associa-
tions of brain tumours with the highest quintile of TCSE. Using
tumour centre estimated by computer algorithm for all subjects
had little impact on the results. The ORs for glioma and
meningioma fell slightly when reported laterality was not taken
into account. Excluding subjects with improbable reported use
(>5 h/day) or with reported use of 450 MHz phones had no
effect on ORs in the highest quintile, while excluding subjects
with proxy interviews increased them slightly, particularly for
glioma. The OR in the highest quintile was greatest in analyses
excluding non-regular users (using the lowest quintile of TCSE
as the reference categorydsee also table AII) and analyses
restricted to subjects for whom images were available for
tumour localisation.
Occup Environ Med 2011;68:631e640. doi:10.1136/oemed-2011-100155 633
Original article
Considering frequency band and technology type (analogue or
digital) (table 4), ORs were increased somewhat for glioma in
the highest quintile of CSE in the 800e900 MHz frequency
range and the highest two quintiles in the 1800e1900 MHz
range. The OR for meningioma was also elevated in the highest
quintile in the 800e900 MHz range, but much reduced in the
highest quintile in the 1800e1900 MHz range. There was little
evidence of increased risk when considering analogue and digital
technologies separately, except possibly for analogue signals
with meningioma. These analyses are not independent,
however, as many subjects had used several different frequency
bands or technologies. Data were too sparse for meaningful
analyses of subjects who only used one frequency band or
system. ORs for glioma were above 1 in all countries except
Israel; CIs were wide; however, the p value for heterogeneity
across countries was 0.37. Country-specic ORs for meningioma
were more variable. There was little evidence of differences in
ORs between men and women.
For the caseecase analyses, there were 44 glioma cases and
135 meningioma cases located in the most exposed area of the
brain and 512 and 537 cases, respectively, located elsewhere.
Knowledge of SAR was used to dene the two case groups, thus
Table 1 ORs for brain tumours with regular use of a mobile phone and cumulative mobile phone call time in all eligible subjects, subjects with tumour
localisation data and subjects with tumour centre estimated by a neuroradiologist*
All subjects matched to controls or case
interviewed within 1 year
Subjects with tumour centre estimated by
a neuroradiologist or computer algorithmy
Only subjects with tumour centre estimated
by a neuroradiologist
Cases Controls OR (95% CI) Cases Controls OR (95% CI) Cases Controls OR (95% CI)
Glioma
Regular use
Never regular user 266 834 1.00 196 617 1.00 117 361 1.00
Regular user 542 1629 0.92 (0.75 to 1.13) 355 1103 0.93 (0.73 to 1.18) 209 565 1.06 (0.77 to 1.47)
Cumulative call time without hands-free devices (h)
Never regular user 266 834 1.00 196 617 1.00 117 361 1.00
<13.0 69 234 0.88 (0.63 to 1.24) 44 174 0.83 (0.55 to 1.26) 25 102 0.81 (0.46 to 1.42)
13.0e60.9 103 327 0.93 (0.69 to 1.25) 68 223 0.93 (0.65 to 1.32) 46 134 1.11 (0.71 to 1.75)
61.0e199.9 110 383 0.74 (0.55 to 0.99) 63 264 0.66 (0.46 to 0.96) 39 136 0.81 (0.5 to 01.33)
200e734.9 123 367 0.94 (0.71 to 1.26) 90 237 1.07 (0.76 to 1.50) 46 110 1.03 (0.64 to 1.67)
735+ 137 318 1.17 (0.88 to 1.56) 90 205 1.25 (0.88 to 1.77) 53 83 1.72 (1.07 to 2.77)
Meningioma
Regular use
Never regular user 356 807 1.00 294 643 1.00 157 398 1.00
Regular user 486 1 541 0.80 (0.66 to 0.96) 381 1153 0.77 (0.63 to 0.95) 186 648 0.77 (0.58 to 1.03)
Cumulative call time without hands-free devices (h)
Never regular user 356 807 1.00 294 643 1.00 157 398 1.00
<13.0 102 247 0.86 (0.64 to 1.15) 80 198 0.84 (0.60 to 1.16) 43 117 0.87 (0.56 to 1.34)
13.0e60.9 101 301 0.79 (0.60 to 1.04) 82 225 0.80 (0.59 to 1.10) 46 137 0.80 (0.53 to 1.22)
61.0e199.9 97 347 0.71 (0.53 to 0.94) 73 257 0.64 (0.46 to 0.89) 35 156 0.61 (0.39 to 0.96)
200e734.9 89 349 0.69 (0.51 to 0.93) 67 265 0.63 (0.45 to 0.88) 29 141 0.57 (0.35 to 0.94)
735+ 97 297 1.01 (0.75 to 1.36) 79 208 1.06 (0.75 to 1.48) 33 97 1.30 (0.79 to 2.15)
*Analyses based on unconditional logistic regression stratified on age, sex and region and adjusted for education and timing of interview.
yOrigin is as estimated by a neuroradiologist when available or as estimated by computer algorithm otherwise.
Table 2 ORs for brain tumours with level of total cumulative specific radio frequency energy (total
cumulative specific energy) (in joules per kilogram)*
Subjects with tumour centre estimated by
a neuroradiologist or computer algorithmy
Only subjects with tumour centre estimated
by a neuroradiologist
Cases Controls OR (95% CI) Cases Controls OR (95% CI)
Glioma
Never regular user 196 617 1.00 117 361 1.00
<76.7 67 265 0.76 (0.53 to 1.09) 36 150 0.84 (0.51 to 1.36)
76.7e68 227 0.94 (0.66 to 1.35) 43 128 1.00 (0.62 to 1.60)
284.1e60 207 0.80 (0.54 to 1.18) 39 102 1.15 (0.69 to 1.90)
978.9e57 197 0.89 (0.61 to 1.30) 34 99 0.92 (0.55 to 1.53)
3123.9+ 103 207 1.35 (0.96 to 1.90) 57 86 1.66 (1.03 to 2.67)
Meningioma
Never regular user 294 643 1.00 156 396 1.00
<76.7 103 261 0.90 (0.67 to 1.21) 51 150 0.86 (0.57 to 1.29)
76.7e71 199 0.74 (0.53 to 1.04) 47 127 0.95 (0.62 to 1.44)
284.1e56 233 0.56 (0.39 to 0.80) 29 136 0.53 (0.32 to 0.87)
978.9e62 209 0.72 (0.51 to 1.02) 23 117 0.55 (0.32 to 0.93)
3123.9+ 88 251 0.90 (0.66 to 1.24) 35 114 1.01 (0.63 to 1.62)
*Analyses based on unconditional logistic regression stratified on age, sex and region and adjusted for education and timing of
interview.
yCentre is as estimated by a neuroradiologist when available or as estimated by computer algorithm otherwise.
634 Occup Environ Med 2011;68:631e640. doi:10.1136/oemed-2011-100155
Original article
only mobile phone use was compared between them. The ORs
for glioma in the highest exposed area were higher in long-term
users than in short-term users (OR 2.80, 95% CI 1.13 to 6.94 for
10 years or more of use). While OR for glioma tended to increase
with increasing call time to the fourth quintile, it was 0.99 in
the highest quintile (table 5). For meningioma, ORs were
highest in long-term and heavy users, but CIs were wide.
DISCUSSION
We have presented results of a rst attempt to analyse brain
tumour risk in relation to amount of RF absorbed by the brain
from use of a mobile phone held to the ear. In principle,
a measure of absorbed RF should be a more accurate indicator of
RF exposure to neural tissue than just mobile phone use and
enhance our ability to detect causal associations that might exist
between exposure to mobile phone RF elds and brain tumours.
Although our estimate of RF dose takes into account reported
phone use (which is subject to recall bias and uncertainties
28
), it
also incorporates objective parameters (location of tumour,
frequency band and characteristics of communication systems),
not inuenced by the interviewees recall, which affect the
amount of RF energy received at the tumour location.
24
The
localisation of tumours, necessary for accurate estimation of
relevant RF absorption, made our caseecase analysis by regions
of the brain possible.
Overall, there was weak evidence of stronger associations of
glioma and meningioma when a comprehensive estimate of RF
dose rather than just mobile phone use was used in the casee
control analysis. For glioma, the OR for the highest quintile of
TCSE was 1.35; that for the highest quintile of cumulative call
time was 1.25. There was a similar pattern for meningioma.
There are several possible explanations for this comparative lack
of increase in ORs using TCSE: observations of increased brain
tumour risk with mobile phone use are due to biases, and there
is no true association between mobile phone RF and brain
tumours; the associations of brain tumours with TCSE are
greatly weakened by sources of uncertainty in our dose esti-
mates; or a metric other than the absorbed energy better reects
the carcinogenic mechanism.
24
Furthermore, the small increases
observed could be due to confounding of RF absorption with
pulsed extremely low frequency (ELF) magnetic elds from
digital phones.
24
There is little support for this, though, when
we compare ORs for analogue and digital systems (table 4) or in
our caseecase analyses in which the most exposed region was
dened on the basis of RF absorption, which is much more
localised than ELF absorption. With respect to the performance
of TCSE as a dose measure, it should be noted that while
cumulative call time contributed to the calculation of TCSE and
there was moderate agreement between the two measures, there
was important residual variation due to the inclusion of
measures of RF absorption in TCSE.
24
It is thus possible that
investigation of different dose metrics and quantication of
related uncertainties may yet improve RF dose estimation.
24
The results of our caseecase analysis show a moderately
strong association of glioma with mobile phone use that started
10+ years before diagnosis, OR 2.80, and little increase with
shorter latency. Because of the nature of the caseecase analyses,
bias due to differential participation of cases and controls is ruled
out; systematic differences in recall between cases with tumours
in the heavily exposed region of the brain and those with
tumours in the less heavily exposed region seem improbable
since cases are not aware of exact tumour location and its
meaning regarding exposure. The comparatively small number
of subjects from ve countries on which this analysis is based
makes the results of the present caseecase analysis much more
uncertain than they would be if based on Interphone as a whole.
We also observed evidence of increased glioma risk with a long
latent period after rst use of a mobile phone in our standard
caseecontrol study analysis. The OR for glioma in the highest
quintile of TCSE was 1.91 for exposure beginning 7+ years in
the past (numbers of subjects by quintile of TCSE were too small
for meaningful analyses of exposures 10+ years in the past), and
Table 3 ORs for glioma and meningioma with level of total cumulative specific energy exposure (in joules per kilogram) in different windows of time
before diagnosis of the case in subjects with probable tumour centre estimated by a neuroradiologist or computer algorithm*
Glioma Meningioma
Cases Controls OR (95% CI) Cases Controls OR (95% CI)
<3 years in the past
Never regular user in this time period 206 647 1.00 300 667 1.00
<76.7 111 350 0.88 (0.61 to 1.26) 128 353 0.81 (0.59 to 1.11)
76.7e72 271 0.63 (0.41 to 0.96) 84 252 0.79 (0.54 to 1.14)
284.1e75 224 0.73 (0.46 to 1.16) 67 259 0.69 (0.46 to 1.04)
978.9e40 141 0.56 (0.32 to 0.99) 51 144 0.92 (0.57 to 1.47)
3123.9+ 47 87 1.29 (0.68 to 2.47) 46 126 0.86 (0.49 to 1.53)
3e6 years in the past
Never regular user in this time period 270 917 1.00 417 962 1.00
<76.7 60 218 1.05 (0.69 to 1.61) 79 211 1.09 (0.75 to 1.56)
76.7e64 170 1.36 (0.88 to 2.11) 41 168 0.73 (0.46 to 1.15)
284.1e51 167 1.04 (0.62 to 1.75) 45 180 0.93 (0.58 to 1.50)
978.9e49 132 1.14 (0.65 to 2.01) 48 132 1.08 (0.65 to 1.78)
3123.9+ 57 116 0.97 (0.49 to 1.93) 46 148 0.76 (0.40 to 1.43)
7+ years in the past
Never regular user in this time period 421 1445 1.00 586 1493 1.00
<76.7 20 63 1.11 (0.61 to 2.02) 28 81 1.07 (0.64 to 1.78)
76.7e23 53 1.53 (0.85 to 2.78) 8 49 0.74 (0.33 to 1.67)
284.1e24 53 1.50 (0.81 to 2.78) 17 68 0.88 (0.47 to 1.64)
978.9e25 49 1.69 (0.91 to 3.13) 16 59 1.00 (0.52 to 1.92)
3123.9+ 38 57 1.91 (1.05 to 3.47) 21 51 2.01 (1.03 to 3.93)
*Unconditional logistic regression analyses stratified on age, sex and region and adjusted for education and timing of interview. Centre is taken to be as estimated by a neuroradiologist where
available and as estimated by computer algorithm otherwise. Associations in each time window are adjusted for associations in each other window.
Occup Environ Med 2011;68:631e640. doi:10.1136/oemed-2011-100155 635
Original article
there was evidence of a trend towards increasing risk with
increasing exposure. Lack of such a trend has been a consistent
feature of Interphone analyses of risk of glioma and may suggest
that increased ORs in the highest cumulative mobile phone use
category are due to observed greater overestimation of more
distant past mobile phone use by cases than controls.
29
The
apparent doseeresponse relationship for exposure 7+ years ago,
however, suggests that bias is not a sufcient explanation for the
increased OR in the highest TCSE category, at least in this
exposure period, and suggests that the increased OR seen in the
highest category of use in the Interphone report is valid. These
results also suggest that if there is a real effect of RF on brain
tumour risk, a combination of a minimum latent period and
amount of exposure may be needed for an increased risk to be
observable (it is of note that the highest category of use in this
study, 735 h or more corresponds to about 12e13 min of use
a day over 10 years).
A number of caseecontrol studies, including Interphone,
28
have reported stronger associations with phone use on the
side of the head with the tumour. We dealt with exposure
laterality in the present analysis by allocating 90% of reported
phone use to the preferred side of phone use and 10% to the
other side when there was a preferred side (87% of cases and
91% of controls); otherwise, 50% was allocated to each side. In
a sensitivity analysis in which we allocated 50% to each side
in all subjects, the ORs for glioma and meningioma in the
highest quintile of TCSE averaged over the whole tumour
were only slightly reduced (table 4). Like comparisons of ORs
for RF absorption with cumulative mobile phone use, this
lack of marked change in OR may indicate that estimation of
RF absorption has not greatly improved overall exposure
ascertainment in this study. It also suggests that the increased
glioma ORs are not sensitive to errors in recall of laterality
of mobile phone use, which is suggested also by our casee
case analyses in which laterality of use was not taken into
account.
Associations observed with higher levels of TCSE exposure
are much weaker for meningioma than glioma, being barely
evident with TCSE in the caseecontrol analyses except in the
highest category in those rst exposed 7+ years before diag-
nosis (table 3). The ORs for meningioma in intermediate TCSE
exposure categories are also sometimes much less than those for
glioma (tables 2 and 3) and below unity. We have no certain
explanation for these differences, except that they could
suggest biases affecting results for both tumours (more for
meningioma), a causal association of mobile phone RF with
both (stronger for glioma than for meningioma) or, perhaps,
a shorter latency for glioma occurrence.
Table 4 Results of sensitivity analyses on ORs for glioma and meningioma with radio frequency exposure in the highest quintile of total cumulative
specific energy (TCSE)
Factors included in sensitivity analyses
Glioma Meningioma
Cases Controls OR (95% CI) Cases Controls OR (95% CI)
All subjects with tumour localisation
TCSE at centre of tumour
Estimated by neuroradiologists when available, predicted by computer
algorithm otherwisedmain analysis
103 207 1.35 (0.96 to 1.90) 88 251 0.90 (0.66 to 1.24)
Predicted by computer algorithm for all subjects 99 206 1.32 (0.93 to 1.86) 93 253 0.93 (0.68 to 1.27)
Estimated by neuroradiologists when available, predicted by computer
algorithm otherwise not taking account of tumour laterality
105 241 1.23 (0.89 to 1.72) 94 288 0.84 (0.62 to 1.15)
TCSE averaged over the entire tumour
Taking into account reported tumour laterality 107 224 1.28 (0.92 to 1.80) 93 253 0.92 (0.69 to 1.24)
Not taking into account tumour laterality 111 254 1.21 (0.87 to 1.68) 94 291 0.84 (0.61 to 1.15)
Effect of exclusion of
Subjects with very high reported use (>5 h/day) 93 188 1.34 (0.94 to 1.91) 81 235 0.91 (0.66 to 1.26)
Subjects with proxy response 94 207 1.43 (0.99 to 2.05) 87 249 0.93 (0.68 to 1.27)
Subjects reporting use of 450 MHz telephones 101 202 1.35 (0.96 to 1.91) 88 246 0.92 (0.67 to 1.26)
Never regular users (using the lowest quintile of TCSE as
reference category)
103 195 1.93 (1.26 to 2.96) 88 237 1.04 (0.71 to 1.53)
By frequency band
800e900 MHz 100 197 1.36 (0.96 to 1.93) 88 240 1.35 (0.74 to 2.44)
1800e1900 MHz 22 57 1.45* (0.80 to 2.63) 6 59 0.28 (0.10 to 0.79)
By communication system
Analogue 43 82 1.22 (0.77 to 1.92) 27 109 1.29 (0.71 to 2.34)
Digital 79 194 1.22 (0.84 to 1.76) 87 214 0.87 (0.45 to 1.67)
Only subjects with centre estimated by neuroradiologists
Using centre estimated by neuroradiologist 57 86 1.66 (1.03 to 2.67) 35 114 1.01 (0.63 to 1.62)
Using centre predicted by computer algorithm for all subjects 53 85 1.58 (0.98 to 2.57) 39 118 1.02 (0.64 to 1.61)
Only subjects for whom images were available (ie, excluding Israel) 70 109 1.82 (1.20 to 2.76) 33 113 1.23 (0.76 to 2.00)
Country-specific estimates
Australia 30 49 1.15 (0.56 to 2.38) 19 67 0.75 (0.38 to 1.48)
Canada 21 27 3.48 (1.63 to 7.43) 7 33 1.51 (0.58 to 3.93)
France 11 29 1.39 (0.56 to 3.49) 7 29 0.77 (0.30 to 1.98)
Israel 33 98 0.74 (0.40 to 1.37) 50 116 0.74 (0.47 to 1.17)
New Zealand 8 4 3.69 (0.78 to 17.5) 5 6 5.52 (0.98 to 31.2)
Sex-specific estimates
Men 85 133 1.33 (0.87 to 2.03) 41 151 0.98 (0.58 to 1.65)
Women 18 74 1.30 (0.69 to 2.47) 47 100 0.88 (0.58 to 1.34)
*OR in fourth quintile: 1.86, 95% CI 1.07 to 3.22 (29 cases and 54 controls).
636 Occup Environ Med 2011;68:631e640. doi:10.1136/oemed-2011-100155
Original article
A major strength of this paper is improved ascertainment of
relevant exposure, which we presume to be mobile phone RF
energy absorbed at the tumour location when the phone is in use
near the ear. It is a weakness, though, that tumour localisation
was only available for about half the cases. Small increases in
strengths of associations when comparing results for TCSE with
those for cumulative phone use suggest that there was a small
increase in measurement accuracy (assuming a causal associa-
tion) from estimation of RF dose at the tumourscentres. This
suggestion is supported by the further increases in ORs when
only tumours for which a neuroradiologist had estimated the
centre were included in analyses. However, this analysis
excluded Israeli subjects, for which the OR for any use of
a mobile phone was less than that for the other four centres (OR
without Israel 1.06), which weakens this inference. Further-
more, when neuroradiologists estimates of the centre were
replaced by computer generated estimates, the OR for glioma in
the highest category of TCSE fell only from 1.66 to 1.58. Thus
neuroradiologistslocalisations of the centre at the tumours
centre of gravity may have been no more accurate than the
computer algorithms.
The association of glioma with estimated TCSE seemed to be
robust against subjectsrecall of implausibly high mobile
phone use: exclusion of those with use >5 h reduced the OR
minimally from 1.35 to 1.34. In contrast, in Interphone as
a whole, the reduction was from 1.40 to 1.27. While this
difference might be due to different exposure measures, it could
also be due to the use of a subset of Interphone countries in this
analysis.
Generally speaking, results of our analyses are similar to
comparable analyses based on all Interphone centres.
28
One
other study, from Sweden, has investigated associations of
mobile phone use with brain tumour risk based on tumours
diagnosed over a period, 2000 to 2003, nearly the same as
Interphone, 2000 to 2004.
9
That study found increased risks of
malignant brain tumours (mostly gliomas) with any use of
analogue or digital mobile phones or cordless phones; risk was
generally increased in both low- and high-exposure categories,
evident with exposure 1e5 years before diagnosis and increasing
with intensity of exposure in time intervals more distant from
diagnosis. Our results are different from this studys results
with respect to the apparent limitation of an association
between exposure and glioma in our data to higher exposures
and exposures occurring 7+ or 10+ years before diagnosis.
Our use of estimates of RF energy absorbed in the brain as
indicators of dose in analyses of associations of brain tumour
occurrence with mobile phone use may have increased the
strength of some positive associations otherwise observable
between these tumours and estimated cumulative use of a
mobile phone. Although subject to considerable uncertainty, our
analyses suggest that there is an increase in glioma risk with
higher levels of RF dose in people whose brain has absorbed
high levels of RF energy from mobile phone use and that this
risk may only be evident in people who began mobile phone
use 7e10 years or more before diagnosis. There is a possibility
also of similar, but apparently much smaller, increases in
meningioma risk. Uncertainties around these results require that
they are replicated before they can be considered to be real. The
best way to replicate them would be to repeat this analysis in
data from the other eight Interphone countries and in future
studies with longer latency periods and higher cumulative
exposures.
Author affiliations
1
Centre for Research in Environmental Epidemiology (CREAL), Hospital del Mar
Research Institute (IMIM), CIBER Epidemiologia y Salud Pu
´blica (CIBERESP),
Barcelona, Spain
2
Sydney School of Public Health, The University of Sydney, Sydney, Australia
3
Engineering and Physical Hazards Branch, National Institute for Occupational Safety
and Health (NIOSH), Cincinnati, Ohio, USA
4
Cancer Epidemiology Centre, Cancer Council Victoria, Melbourne, Australia
5
Centre for MEGA Epidemiology, School of Population Health, The University of
Melbourne, Melbourne, Australia
6
Universite
´de Lyon, Institut franc¸ais des sciences et technologies des transports, de
l’ame
´nagement et des re
´seaux, Institut national de Veille Sanitaire, Unite
´Mixte de
Recherche e
´pide
´miologique et de Surveillance Transports Travail Environnement, Lyon,
France
7
McLaughlin Centre for Population Health Risk Assessment, University of Ottawa,
Ottawa, Canada
Table 5 Results of caseecase analyses of glioma and meningioma by time since start of use of mobile phones and cumulative call time comparing
cases* originating in the region of the brain within the 3 dB exposure volume (w16% of brain volume receiving 50% of the total absorbed energy) to
casesyoriginating in other areas of the brainz
Glioma Meningioma
Centre within most
exposed area*
Centre outside most
exposed areayOR (95% CI)
Centre within most
exposed area*
Centre outside most
exposed areayOR (95% CI)
Regular user
Never regular user 14 178 1.00 66 221
Ever regular user 30 334 1.35 (0.64 to 2.87) 69 316 0.74 (0.49 to 1.11)
Time since start of use (years)
Never regular user 14 178 1.00 66 221 1.00
1e4 12 133 1.37 (0.59 to 3.19) 38 179 0.67 (0.41 to 1.07)
5e9 7 147 0.72 (0.27 to 1.90) 22 112 0.75 (0.42 to 1.34)
10+ 11 54 2.80 (1.13 to 6.94) 9 25 1.34 (0.55 to 3.25)
Cumulative call time without hands-free devices (h)
Non-regular 14 178 1.00 66 221 1.00
<39 6 65 1.19 (0.40 to 3.51) 16 97 0.55 (0.29 to 1.02)
39e4 67 0.93 (0.27 to 3.14) 21 78 0.93 (0.51 to 1.68)
220e5 68 1.38 (0.42 to 4.53) 9 52 0.52 (0.23 to 1.14)
520e10 66 2.55 (0.94 to 6.91) 10 52 0.67 (0.30 to 1.48)
1147+ 5 68 0.99 (0.30 to 3.27) 13 37 1.41 (0.66 to 3.02)
*Treated as ‘cases’.
yTreated as ‘controls’.
zQuintiles of cumulative call time among ‘controls’ (glioma cases with tumour centre outside the most exposed area). Centre is as estimated by a neuroradiologist when available or as
estimated by computer algorithm otherwise. Unconditional logistic regression analyses were done, stratified on age, sex and region and adjusted for education and timing of interview.
Occup Environ Med 2011;68:631e640. doi:10.1136/oemed-2011-100155 637
Original article
8
BC Cancer Research Centre, BC Cancer Agency, Vancouver, Canada
9
INRS-Institut Armand-Frappier, Universite
´du Que
´bec, Laval, Canada
10
Cancer and Radiation Epidemiology Unit, Gertner Institute, Chaim Sheba Medical
Center, Tel-Hashomer, Israel
11
Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel
12
School of Population Health, University of Auckland, Auckland, New Zealand
13
Department of Diagnostic Imaging, Chaim Sheba Medical Center, Tel Hashomer,
Israel
14
Department of Population health, Hospital Research Centre (CRCHUM) University of
Montreal, Montreal, Canada
Acknowledgements The authors acknowledge
<The important work of N. Varsier and J Wiart (France Telecom RD, France),
M Taki (Tokyo Metropolitan University and National Institute of Information and
Communications Technology, Japan), K. Wake (National Institute of Information
and Communications Technology, Japan), I Deltour (Danish Cancer Centre,
Copenhagen), S. Mann (Health Protection Agency, Japan), L. Ardoino (Italy) and
P. Vecchia (National Institute of Health, Italy) in the development of the RF dose
algorithm;
<The outstanding contribution of the neuroradiologists: Ken Faulder (Australia),
William Miller, Genevieve Matte and Rafael Glickstein (Canada), Marc Hermier
(Lyon) and Jacques Doyon (France) (who participated in the review of cases and
also in the development and testing of the localisation protocol); Chen Hoffman
(Israel) and Glen Thomson (Auckland, New Zealand) made in reviewing images
and records and recording the location and origins of brain tumours in the
Gridmaster;
<The collaboration of all the clinicians in the five countries who permitted access
to their patients;
<The excellent work of Monika Moissonnier, He
´le
`ne Tardy and Emilie Combarlot
(IARC, Lyon) in the design and validation of the international database, as well
as, for MM, precious assistance in the development and testing of the RF
algorithm.
In addition, the authors thank Professor Jack Siemiatycki for allowing the use of
Montreal data in these analyses. The Australian team would like to acknowledge too
the overall support given to study design and implementation by Associate Professor
Michael Besser and Professor Andrew Kaye; and to thank fieldwork staff in
MelbournedMonique Kilkenny, Georgina Marr, Tracey McPhail, Fiona Phillips,
Hayley Shaw, Yvonne Torn-Broers; and SydneydMatthew Carroll, Sally Dunlop,
Virginia MacDonald and Elizabeth Willowsdthe many interviewers for their hard
work, and the NSW and Victorian Cancer Registries for aiding case identification.
We also thank Angus Cook (University of Western Australia) and Neil Pearce
(London School of Hygiene and Tropical Medicine) who, together with AW, were
responsible for the conduct of the Interphone Study in New Zealand. The
Canada-Ottawa centre gratefully acknowledges the work of Lynn Pratt and Daniel
Be
´dard for their leading roles in study coordination. The Canada-Montreal team
acknowledges the diligent work of fieldwork staff including Marie-Claire Goulet,
Sylvie Plante, Sally Campbell and the interviewer team. The following hospitals and
physicians in Montreal permitted access to their patients: CHUMdHo
ˆpital
Notre-Dame (Dr Wieslaw Michel Bojanowski, Dr Jean Jacques Dufour, Dr Franc¸ois
Lavigne, Dr Robert A Moumdjian); Neurological Institute of Montreal (Dr Rolando
Del Maestro, Dr Richard Leblanc); Ho
ˆpital du Sacre
´-Coeur de Montre
´al (Dr Marc
F Giroux); The Jewish General Hospital (Dr Gerard Mohr, Dr Jamie Miles Rappaport).
The Canada-Vancouver centre wishes to acknowledge the work carried out by
Dr Alison Pope, Patricia Nelson, Nelson Ha, Dr Kaushik Bhagat and the interviewer
team. The French team to thank the French fieldwork team, Mary-Pierre Herrscher,
Fatima Lamri, Agne
`s Boidart, He
´le
`ne Gire, Juliette Krassilchik, Judith Lenti, Delphine
Maillac, Fre
´de
´rique Sonnet, Flore Taguiev, Julie Frantz, France Castay, Florian Gay,
for their excellent work. The Israeli team acknowledge the diligent work of the
fieldwork and office staff including Etti Aviezer, Tehila Ben-Tal, Meirav Dolev, Yonit
Deutch, Tamara Rodkin, Ahuva Zultan and the interviewer team.
Funding Funding for the Interphone Study was provided by the European Fifth
Framework Program, ‘Quality of Life and Management of Living Resources’ (contract
QLK4-CT-1999901563), the International Union against Cancer (UICC). The UICC
received funds for this purpose from the Mobile Manufacturers’ Forum and GSM
Association. Provision of funds to the Interphone Study investigators via the UICC was
governed by agreements that guaranteed Interphone’s complete scientific
independence. The terms of these agreements are publicly available at http://www.
iarc.fr/en/research-groups/RAD/RCAd.html Specific additional funds were provided for
the development and analysis of the radio frequency exposure gradient and by the
Fondation Sante
´et Radiofre
´quences, France and the Bundesamt fuer Strahlenschutz,
Germany. The Australian centre was supported by the National Health and Medical
Research Council (EME grant 219129); BKA was supported by the University of
Sydney Medical Foundation Program Grant and Julianne Brown by an Australian
Postgraduate Award. The Cancer Council NSW and the Cancer Council Victoria
provided most of the infrastructure for the project in Australia. The Canada-Montre
´al
data collection was funded by a grant from the Canadian Institutes of Health Research
(project MOP-42525). Additionally, Dr Siemiatycki’s research team was partly funded
by the Canada Research Chair programme and by the Guzzo-CRS Chair in Environment
and Cancer. Dr. Parent had salary support from the Fonds de recherche en sante
´du
Que
´bec. The other Canadian centres were supported by a universityeindustry
partnership grant from the Canadian Institutes of Health Research (CIHR), the latter
including partial support from the Canadian Wireless Telecommunications Association.
The CIHR universityeindustry partnerships program also includes provisions that
ensure complete scientific independence of the investigators. DK is the
NSERC/SSHRC/McLaughlin Chair in Population Health Risk Assessment at the
University of Ottawa. Additional funding for the study in France was provided by
l’Association pour la Recherche sur le Cancer (ARC) (contract 5142) and three
network operators (Orange, SFR, Bouygues Te
´le
´com). The funds provided by the
operators represented 5% of the total cost of the French study and were governed by
contracts guaranteeing the complete scientific independence of the investigators. In
New Zealand, funding was provided by the Health Research Council, Hawkes Bay
Medical Research Foundation and the Cancer Society of New Zealand. The findings
and conclusions in this paper have not been formally disseminated by the National
Institute for Occupational Safety and Health and should not be construed to represent
any agency determination or policy.
Competing interests BKA’s travel expenses to give two invited lecture were paid by
the Australian Centre for Radio frequency Bioeffects Research, which identifies Telstra
Australia as a participating institution.
Patient consent Consent was obtained from patient or next of kin if patient was too
ill or deceased and next of kin responded as a proxy.
Ethics approval This study was conducted with the approval of the ethical
committee of the International Agency for Research on Cancer (IARC) and appropriate
local and national Institutional Review Boards (IRBs).
Contributors All authors participated in the conception and design, analysis and
interpretation of data, the drafting of the article or its critical revision for important
intellectual content and approved the version to be published.
Provenance and peer review Not commissioned; externally peer reviewed.
REFERENCES
1. Cardis E, Richardson L, Deltour I, et al. The INTERPHONE study: design,
epidemiological methods, and description of the study population. Eur J Epidemiol
2007;22:647e64.
2. Dreyer NA, Loughlin JE, Rothman KJ. Cause-specific mortality in cellular telephone
users. JAMA 1999;282:1814e16.
3. Johansen C, Boice J Jr, McLaughlin J, et al. Cellular telephones and cancerea
nationwide cohort study in Denmark. J Natl Cancer Inst 2001;93:203e7.
4. Schu
¨zJ,Jacobsen R, Olsen JH, et al. Cellular telephone use and cancer risk: update
of a nationwide Danish cohort. J Natl Cancer Inst 2006;98:1707e13.
5. Auvinen A, Hietanen M, Luukkonen R, et al. Brain tumors and salivary gland cancers
among cellular telephone users. Epidemiology 2002;13:356e9.
6. Christensen HC, Schu
¨z J, Kosteljanetz M, et al. Cellular telephones and risk for
brain tumors: a population-based, incident case-control study. Neurology
2005;64:1189e95.
7. Hardell L, Na
¨sman A, Pa
˚hlson A, et al. Use of cellular telephones and the risk for
brain tumours: A case-control study. Int J Oncol 1999;15:113e16.
8. Hardell L, Carlberg M, Hansson Mild K. Pooled analysis of two case-control
studies on the use of cellular and cordless telephones and the risk of benign brain
tumours diagnosed during 1997e2003. Int J Oncol 2006;28:509e18.
9. Hardell L, Carlberg M, Hansson Mild K. Pooled analysis of two case-control
studies on use of cellular and cordless telephones and the risk for malignant
brain tumours diagnosed in 1997e2003. Int Arch Occup Environ Health
2006;79:630e9.
10. Hardell L, Mild KH, Carlberg M, et al. Tumour risk associated with use of cellular
telephones or cordless desktop telephones. World J Surg Oncol 2006;4:74.
11. Hepworth SJ, Schoemaker MJ, Muir KR, et al. Mobile phone use and risk of glioma
in adults: case-control study. BMJ 2006;332:883e7.
12. Hours M, Bernard M, Montestrucq L, et al. [Cell Phones and Risk of brain and
acoustic nerve tumours: the French INTERPHONE case-control study] (In French).
Rev Epidemiol Sante
´Publique 2007;55:321e32.
13. Inskip PD, Tarone RE, Hatch EE, et al. Cellular-telephone use and brain tumors.
N Engl J Med 2001;344:79e86.
14. Lahkola A, Auvinen A, Raitanen J, et al. Mobile phone use and risk of glioma in
5 North European countries. Int J Cancer 2007;120:1769e75.
15. Lahkola A, Salminen T, Raitanen J, et al. Meningioma and mobile phone useda
collaborative case-control study in five North European countries. Int J Epidemiol
2008;37:1304e13.
16. Lo¨nn S, Ahlbom A, Hall P, et al. Long-term mobile phone use and brain tumor risk.
Am J Epidemiol 2005;161:526e35.
17. Muscat JE, Malkin MG, Thompson S, et al. Handheld cellular telephone use and risk
of brain cancer. JAMA 2000;284:3001e7.
18. Schuz J, Bohler E, Berg G, et al. Cellular phones, cordless phones, and the risks of
glioma and meningioma (Interphone Study Group, Germany). Am J Epidemiol
2006;163:512e20.
638 Occup Environ Med 2011;68:631e640. doi:10.1136/oemed-2011-100155
Original article
19. Klaeboe L, Blaasaas KG, Tynes T. Use of mobile phones in Norway and risk of
intracranial tumours. Eur J Cancer Prev 2007;16:158e64.
20. Takebayashi T, Varsier N, Kikuchi Y, et al. Mobile phone use, exposure to
radiofrequency electromagnetic field, and brain tumour: a case-control study. Br J
Cancer 2008;98:652e9.
21. Kainz W, Christ A, Kellom T, et al. Dosimetric comparison of the specific
anthropomorphic mannequin (SAM) to 14 anatomical head models using
a novel definition for the mobile phone positioning. Phys Med Biol
2005;50:3423e45.
22. Wiart J, Mittra R, Chaillou S, et al. The analysis of human head interaction with
a hand-held mobile using the non-uniform FDTD, In Proceedings IEEE AP-S Wireless
Commun. Conf., Nov. 1998, pp. 77e80.
23. Cardis E, Deltour I, Mann S, et al. Distribution of RF energy emitted by
mobile phones in anatomical structures of the brain. Phys Med Biol
2008;53:2771e83.
24. Cardis E, Varsier N, Bowman JD, et al. Estimation of RF energy absorbed in the
brain from mobile phones in the Interphone study. Occup Environ Med
2011;68:686e93.
25. Cardis E, Kilkenny M. International Case-Control Study of Cancers of Brain and
Salivary GlanddReport of the Feasibility Study. 99/004. Lyon: International Agency
for Research on Cancer (IARC), 1999. IARC Internal Reports.
26. GridMaster Computer Program.Du
¨sseldorf: Vompras, 2007.
27. Vrijheid M, Cardis E, Varsier N, et al. Tumour localisation in the Interphone
international study of mobile phone radiofrequency exposure and brain tumour risk.
(in preparation).
28. The Interphone Study Group. Brain tumour risk in relation to mobile telephone use:
results of the INTERPHONE international case-control study. Int J Epidemiol
2010;39:675e94.
29. Vrijheid M, Armstrong BK, Be
´dard D, et al. Recall bias in the assessment of
exposure to mobile phones. J Expo Sci Environ Epidemiol 2009;19:369e81.
APPENDIX
Table AI Distributions of glioma and meningioma cases and controls ascertained, interviewed and matched and with data available for analysis
Glioma
Total
ascertained Interviewed
Matched to case or
controls interviewed
within 1 year
Cases with tumour localisation data and their matched controls
Centre estimated by
neuroradiologist or
computer algorithm
As in preceding column
and have information about
communication system
and frequency band
Centre estimated
by neuroradiologist
As in preceding column
and have information about
communication system
and frequency band
Cases
Total 1302 829 809 567 553 339 329
Australia 536 301 295 142 142 141 141
Canada 273 170 170 158 144 110 100
France 155 94 94 68 68 56 56
Israel 206 180 168 163 163 0 0
New Zealand 132 84 82 36 36 32 32
Controls
Total 4838 2565 2496 1877 1762 1032 958
Australia 1608 669 669 328 317 327 316
Canada 1330 653 633 581 492 348 296
France 639 472 459 331 328 294 291
Israel 911 599 587 566 562 0 0
New Zealand 350 172 148 71 63 63 55
Meningioma
Total
ascertained Interviewed
Matched to controls
or case interviewed
within 1 year
Cases with tumour localisation data and their matched controls
Tumour centre
estimated by
neuroradiologist or
computer algorithm
As in preceding column
and have information about
communication system
and frequency band
Tumour centre
estimated by
neuroradiologist
As in preceding column
and have information about
communication system
and frequency band
Cases
Total 1199 895 842 688 676 349 343
Australia 413 254 250 158 158 155 155
Canada 134 94 94 82 71 56 50
France 190 145 144 116 116 109 109
Israel 390 350 306 303 302 0 0
New Zealand 72 52 48 29 29 29 29
Controls
Total 4838 2565 2464 2015 1911 1213 1142
Australia 1608 669 667 431 413 417 400
Canada 1330 653 613 540 466 342 295
France 639 472 458 379 376 358 356
Israel 911 599 591 569 565 0 0
New Zealand 350 172 135 96 91 96 91
Occup Environ Med 2011;68:631e640. doi:10.1136/oemed-2011-100155 639
Original article
Figure AI Spatial deposition of radio frequency (RF) energy in the
Gridmaster cellsdthe light cubes identify the most exposed region of
the brain, that is, that with the highest specific absorption rate of RF
energy from mobile phones. The dark cubes identify the less exposed
area of the brain. The most exposed area (light cubes) correspond to
about 16% of the brain volume and absorbs >50% of the total RF energy
in the brain from mobile phones used at the ear.
Figure AII Distribution of glioma
cases and controls by level of total
cumulative specific energy (TCSE) (in
joules per kilogram) at the estimated
centre of the tumour; centre is taken to
be as estimated by neuroradiologist,
where available, and as estimated by
computer algorithm otherwise.
Table AII ORs for brain tumours with level of total cumulative specific
RF energy (TCSE) exposure (in joules per kilogram) in subjects with
tumour centre estimated by a neuroradiologist or computer algorithm,
excluding non-regular users. n these analyses, the lowest quintile of
TCSE is used as the reference category
Subjects with tumour centre estimated by
a neuroradiologist or computer algorithm
Cases Controls OR (95% CI)
Glioma
<76.7 65 241 1.00
76.7e68 213 1.34 (0.86 to 2.08)
284.1e60 198 1.13 (0.71 to 1.79)
978.9e57 191 1.22 (0.77 to 1.93)
3123.9+ 103 195 1.93 (1.26 to 2.96)
Meningioma
<76.7 96 231 1.00
76.7e71 194 0.86 (0.58 to 1.27)
284.1e56 221 0.63 (0.41 to 0.95)
978.9e62 199 0.87 (0.58 to 1.31)
3123.9+ 88 237 1.04 (0.71 to 1.53)
PAGE fraction trail=10
640 Occup Environ Med 2011;68:631e640. doi:10.1136/oemed-2011-100155
Original article
... Epidemiological studies were conducted to determine whether there was an association between exposure to RF-EMF and brain tumours. The most famous is the Interphone study, which was initiated as an international set of case control studies looking for different types of tumours (Cardis et al., 2011). Globally, the results of this study showed no increase in the risk of glioma or meningioma from the use of mobile phones, however, the authors suggested an increased risk of glioma at the highest exposure levels among long-term users. ...
Thesis
Full-text available
Avec l'utilisation sans cesse grandissante du téléphone portable, de plus en plus d'inquiétudes sont formulées concernant leurs effets potentiels sur la santé humaine, dont de possibles effets sur l'EEG de repos. Il n'y a pas à ce jour de réponses vraiment concluantes à ces questions. Nous avons réalisé pour la première fois dans ce domaine un protocole de magnétoencéphalographie et d'électroencéphalographie caractérisé par une très haute résolution temporelle et spatiale, afin de déterminer les régions corticales qui seraient impliquées dans ces effets. Des sujets sains jeunes adultes ont été exposés à des champs électromagnétiques à l'aide de deux téléphones issus du commerce, dont l'un a délivré une exposition "réelle" de radiofréquences à 900 MHz et l'autre une exposition factice ou "sham". Ces conditions d'exposition ont été définies par un ordre croisé, randomisé et contrebalancé en double-aveugle. L'analyse des données de magnétoencéphalographie enregistrées avant et après exposition a principalement montré une diminution de la densité de puissance spectrale des bandes alpha basse (8–10 Hz) et haute (10–12 Hz). Les régions corticales impliquées étaient dépendantes de la condition d'enregistrement "yeux ouverts" ou "yeux fermés". L'analyse des données EEG enregistrées en même temps que l'exposition n'a pas confirmé ces résultats sur la bande alpha (8–12 Hz) ni sur la bande de fréquence alpha individuelle. L'analyse de certains paramètres de contrôle, tels que le niveau de stress et la consommation de caféine, nous a permis d'exclure de potentiels biais sur nos résultats concernant les modulations des ondes alpha
... The more it distributes, the more likely can be subject to, hackers, and other possible risks such as identity theft including financial identity theft, Insurance Identity Theft, Medical Identity Theft, Mail-Identity Theft [8,9,10], which might threaten a personal information privacy and could lead to potential privacy and security users privacy from being violated. By applying proposed model, we can achieve higher privacy-preserving by providing an alternative virtual mobile number that associates with a user actual mobile number. ...
Article
Full-text available
The importance of personal mobile numbers has dramatically increased in recent years. Most of social network’s apps today required a validated personal mobile number to register in their services. Publishing a person’s mobile number may lead to a privacy and security violation. In this paper, we describe how a person’s mobile number could easily be used to violate a user’s privacy. We study possible concerns and risks associated with publishing a user’s mobile number, and we propose an alternative: Virtual Mobile Number Model (VMNM) that links a user’s real mobile number with a virtual mobile number to help secure individual privacy. Telecommunication Service Provider (TSP) present privacy management system that sets up the connection between callers. Finally, we evaluate the model and explain how it helps to protect the user’s privacy as well as prevent personal data from being violated.
... Actually, all studies relevant for the current systematic review have used indirect measures of exposure, based on self-reported histories of mobile phone use or on mobile phone subscriber lists (Deltour and Schüz 2014). Estimates of absorbed RF energy were used in two studies (Cardis et al., 2011a;Takebayashi et al., 2008); the modelled brain absorption was based on various input variables, but the self-reported call time was the dominating parameter, while other factors gave a very small contribution to variation in estimated values (Cardis et al., 2011b). ...
Article
Full-text available
Background The World Health Organization (WHO) has an ongoing project to assess potential health effects of exposure to radiofrequency electromagnetic fields (RF-EMF) in the general and working population. Here we present the protocol for a systematic review of the scientific literature on cancer hazards from exposure to RF-EMF in humans, commissioned by the WHO as part of that project. Objective To assess the quality and strength of the evidence provided by human observational studies for a causal association between exposure to RF-EMF and risk of neoplastic diseases. Eligibility criteria We will include cohort and case-control studies investigating neoplasia risks in relation to three types of exposure to RF-EMF: near-field, head-localized, exposure from wireless phone use (SR-A); far-field, whole body, environmental exposure from fixed-site transmitters (SR-B); near/far-field occupational exposures from use of handheld transceivers or RF-emitting equipment in the workplace (SR-C). While no restriction on tumour type will be applied, we will focus on selected neoplasms of the central nervous system (brain, meninges, pituitary gland, acoustic nerve) and salivary gland tumours (SR-A); brain tumours and leukaemias (SR-B, SR-C). Information sources Eligible studies will be identified through Medline, Embase, and EMF-Portal. Risk-of-bias assessment We will use a tailored version of the OHAT's tool to evaluate the study's internal validity. Data synthesis We will consider separately studies on different tumours, neoplasm-specific risks from different exposure sources, and a given exposure-outcome pair in adults and children. When a quantitative synthesis of findings can be envisaged, the main aims of the meta-analysis will be to assess the strength of association and the shape of the exposure–response relationship; to quantify the degree of heterogeneity across studies; and explore the sources of inconsistency (if any). When a meta-analysis is judged inappropriate, we will perform a narrative synthesis, complemented by a structured tabulation of results and appropriate visual displays. Evidence assessment Confidence in evidence will be assessed in line with the GRADE approach. Funding This project is supported by the World Health Organization. Co-financing was provided by the New Zealand Ministry of Health; the Istituto Superiore di Sanità in its capacity as a WHO Collaborating Centre for Radiation and Health; ARPANSA as a WHO Collaborating Centre for Radiation Protection. Registration PROSPERO CRD42021236798.
... Phones emit radiofrequency-electromagnetic waves (RF-EMWs), a low-level RF between 800 and 2200 MHz that can be absorbed by the human body and have potential adverse effects on the brain, heart, endocrine system, and reproductive function (Al-Bayyari, 2017a). Currently, the association between mobile phone use and the risk of development of several cancers, including childhood cancer, has not been clearly established (Benson et al., 2013;Cardis et al., 2007Cardis et al., , 2011Frei et al., 2011;Grell et al., 2016;Group, 2010;Johansen et al., 2001;Larjavaara et al., 2011;Schoemaker et al., 2005;Schüz et al., 2006). A recent systemic review reported that long-term cell phone use for more than 10 years might increase the risk of brain tumor (Prasad et al., 2017). ...
Article
Background Mobile phones emit radiofrequency (RF) electromagnetic waves (EMWs), a low-level RF that can be absorbed by the human body and exert potential adverse effects on the brain, heart, endocrine system, and reproductive function. Owing to the novel findings of numerous studies published since 2012 regarding the effect of mobile phone use on sperm quality, we conducted a systematic review and updated meta-analysis to determine whether the exposure to RF-EMWs affects human sperm quality. Methods This study was conducted in accordance with the PRISMA guidelines. The outcome measures depicting sperm quality were motility, viability, and concentration, which are the most frequently used parameters in clinical settings to assess fertility. Results We evaluated 18 studies that included 4280 samples. Exposure to mobile phones is associated with reduced sperm motility, viability, and concentration. The decrease in sperm quality after RF-EMW exposure was not significant, even when the mobile phone usage increased. This finding was consistent across experimental in vitro and observational in vivo studies. Discussion Accumulated data from in vivo studies show that mobile phone usage is harmful to sperm quality. Additional studies are needed to determine the effect of the exposure to EMWs from new mobile phone models used in the present digital environment.
Article
The MOBI-Kids case-control study on wireless phone use and brain tumor risk in childhood and adolescence included the age group 10–24 years diagnosed between 2010 and 2015. Overall no increased risk was found although for brain tumors in the temporal region an increased risk was found in the age groups 10–14 and 20–24 years. Most odds ratios (ORs) in MOBI-Kids were <1.0, some statistically significant, suggestive of a preventive effect from RF radiation; however, this is in contrast to current knowledge about radiofrequency (RF) carcinogenesis. The MOBI-Kids results are not biologically plausible and indicate that the study was flawed due to methodological problems. For example, not all brain tumor cases were included since central localization was excluded. Instead, all brain tumor cases should have been included regardless of histopathology and anatomical localization. Only surgical controls with appendicitis were used instead of population-based controls from the same geographical area as for the cases. In fact, increased incidence of appendicitis has been postulated to be associated with RF radiation which makes selection of control group in MOBI-Kids questionable. Start of wireless phone use up to 10 years before diagnosis was in some analyses included in the unexposed group. Thus, any important results demonstrating late carcinogenesis, a promoter effect, have been omitted from analysis and may underestimate true risks. Linear trend was in some analyses statistically significant in the calculation of RF-specific energy and extremely low frequency (ELF)-induced current in the center of gravity of the tumor. Additional case-case analysis should have been performed. The data from this study should be reanalyzed using unconditional regression analysis adjusted for potential confounding factors to increase statistical power. Then all responding cases and controls could be included in the analyses. In sum, we believe the results as reported in this paper seem uninterpretable and should be dismissed.
Article
Wireless phones (both mobile and cordless) emit not only radiofrequency (RF) electromagnetic fields (EMF) but also extremely low frequency (ELF) magnetic fields, both of which should be considered in epidemiological studies of the possible adverse health effects of use of such devices. This paper describes a unique algorithm, developed for the multinational case-control MOBI-Kids study, that estimates the cumulative specific energy (CSE) and the cumulative induced current density (CICD) in the brain from RF and ELF fields, respectively, for each subject in the study (aged 10–24 years old). Factors such as age, tumour location, self-reported phone models and usage patterns (laterality, call frequency/duration and hands-free use) were considered, as was the prevalence of different communication systems over time. Median CSE and CICD were substantially higher in GSM than 3G systems and varied considerably with location in the brain. Agreement between RF CSE and mobile phone use variables was moderate to null, depending on the communication system. Agreement between mobile phone use variables and ELF CICD was higher overall but also strongly dependent on communication system. Despite ELF dose distribution across the brain being more diffuse than that of RF, high correlation was observed between RF and ELF dose. The algorithm was used to systematically estimate the localised RF and ELF doses in the brain from wireless phones, which were found to be strongly dependent on location and communication system. Analysis of cartographies showed high correlation across phone models and across ages, however diagonal agreement between these cartographies suggest these factors do affect dose distribution to some level. Overall, duration and number of calls may not be adequate proxies of dose, particularly as communication systems available for voice calls tend to become more complex with time.
Article
Full-text available
In recent decades, the possibility that use of mobile communicating devices, particularly wireless (mobile and cordless) phones, may increase brain tumour risk, has been a concern, particularly given the considerable increase in their use by young people. MOBI-Kids, a 14-country (Australia, Austria, Canada, France, Germany, Greece, India, Israel, Italy, Japan, Korea, the Netherlands, New Zealand, Spain) case-control study, was conducted to evaluate whether wireless phone use (and particularly resulting exposure to radiofrequency (RF) and extremely low frequency (ELF) electromagnetic fields (EMF)) increases risk of brain tumours in young people. Between 2010 and 2015, the study recruited 899 people with brain tumours aged 10 to 24 years old and 1,910 controls (operated for appendicitis) matched to the cases on date of diagnosis, study region and age. Participation rates were 72% for cases and 54% for controls. The mean ages of cases and controls were 16.5 and 16.6 years, respectively; 57% were males. The vast majority of study participants were wireless phones users, even in the youngest age group, and the study included substantial numbers of long-term (over 10 years) users: 22% overall, 51% in the 20–24-year-olds. Most tumours were of the neuroepithelial type (NBT; n = 671), mainly glioma. The odds ratios (OR) of NBT appeared to decrease with increasing time since start of use of wireless phones, cumulative number of calls and cumulative call time, particularly in the 15–19 years old age group. A decreasing trend in ORs was also observed with increasing estimated cumulative RF specific energy and ELF induced current density at the location of the tumour. Further analyses suggest that the large number of ORs below 1 in this study is unlikely to represent an unknown causal preventive effect of mobile phone exposure: they can be at least partially explained by differential recall by proxies and prodromal symptoms affecting phone use before diagnosis of the cases. We cannot rule out, however, residual confounding from sources we did not measure. Overall, our study provides no evidence of a causal association between wireless phone use and brain tumours in young people. However, the sources of bias summarised above prevent us from ruling out a small increased risk.
Article
Currently the fifth generation, 5G, for wireless communication is about to be rolled out worldwide. Many persons are concerned about potential health risks from radiofrequency radiation. In September 2017, a letter was sent to the European Union asking for a moratorium on the deployment until scientific evaluation has been made on potential health risks (http://www.5Gappeal.eu). This appeal has had little success. The Health Council of the Netherlands released on September 2, 2020 their evaluation on 5G and health. It was largely based on a World Health Organization draft and report by the Swedish Radiation Safety Authority, both criticized for not being impartial. The guidelines by the International Commission on Non-Ionizing Radiation Protection were recommended to be used, although they have been considered to be insufficient to protect against health hazards (http://www.emfscientist.org). The Health Council Committee recommended not to use the 26 GHz frequency band until health risks have been studied. For lower frequencies, the International Commission on Non-Ionizing Radiation Protection guidelines were recommended. The conclusion that there is no reason to stop the use of lower frequencies for 5G is not justified by current evidence on cancer risks as commented in this article. A moratorium is urgently needed on the implementation of 5G for wireless communication.
Article
A significant share of the technology that has emerged over the past several decades produces electromagnetic field (EMFR) radiation. Communications devices, household appliances, industrial equipment, and medical equipment and devices all produce EMFR with a variety of frequencies, strengths, and ranges. Some EMFR, such as Extremely Low Frequency (ELF), Radio Frequency (RF), and Ionizing Range (IR) radiation have been shown to have harmful effects on human health. Depending on the frequency and strength of the radiation, EMFR can have health effects at the cellular level as well as at brain, nervous, and cardiovascular levels. Health authorities have enacted regulations locally and globally to set critical values to limit the adverse effects of EMFR. By introducing a more comprehensive field of EMFR study and practice, architects and designers can design for a safer electromagnetic (EM) indoor environment, and, as building and construction specialists, will be able to monitor and reduce EM radiation. This paper identifies the nature of EMFR in the built environment, the various EMFR sources, and its human health effects. It addresses European and US regulations for EMFR in buildings and provides a preliminary action plan. The challenges of developing measurement protocols for the various EMFR frequency ranges and determining the effects of EMFR on building occupants are discussed. This paper argues that a mature method for measuring EMFR in building environments and linking these measurements to human health impacts will foster occupant health and lead to the adequate development of safeguards for occupants of buildings in future research.
Article
Full-text available
The use of cellular telephones has increased dramatically during the 1990's in the world. In the 1980's the analogue NMT system was used whereas the digital GSM system was introduced in early 1990's and is now the preferred system. Case reports of brain tumours in users initiated this case-control study on brain tumours and use of cellular telephones. Also other exposures were assessed. All cases, both males and females, with histopathologically verified brain tumour living in Uppsala-Örebro region (1994-96) and Stockholm region (1995-96) aged 20-80 at the time of diagnosis and alive at start of the study were included, 233 in total. Two controls to each case were selected from the Swedish Population Register matched for sex, age and study region. Exposure was assessed by questionnaires supplemented over the phone. The analyses were based on answers from 209 (90%) cases and 425 (91%) controls. Use of cellular telephone gave odds ratio (OR) = 0.98 with 95% confidence interval (CI) = 0.69-1.41. For the digital GSM system OR = 0.97, CI = 0.61-1.56 and for the analogue NMT system OR = 0.94, CI = 0.62-1.44 were calculated. Dose-response analysis and using different tumour induction periods gave similar results. Non-significantly increased risk was found for tumour in the temporal or occipital lobe on the same side as a cellular phone had been used, right side OR = 2.45, CI = 0.78-7.76, left side OR = 2.40, CI = 0.52-10.9 Increased risk was found only for use of the NMT system. For GSM use the observation time is still too short for definite conclusions. An increased risk for brain tumour in the anatomical area close to the use of a cellular telephone should be especially studied in the future.
Article
Full-text available
The objective of this study was to develop an estimate of a radio frequency (RF) dose as the amount of mobile phone RF energy absorbed at the location of a brain tumour, for use in the Interphone Epidemiological Study. We systematically evaluated and quantified all the main parameters thought to influence the amount of specific RF energy absorbed in the brain from mobile telephone use. For this, we identified the likely important determinants of RF specific energy absorption rate during protocol and questionnaire design, we collected information from study subjects, network operators and laboratories involved in specific energy absorption rate measurements and we studied potential modifiers of phone output through the use of software-modified phones. Data collected were analysed to assess the relative importance of the different factors, leading to the development of an algorithm to evaluate the total cumulative specific RF energy (in joules per kilogram), or dose, absorbed at a particular location in the brain. This algorithm was applied to Interphone Study subjects in five countries. The main determinants of total cumulative specific RF energy from mobile phones were communication system and frequency band, location in the brain and amount and duration of mobile phone use. Though there was substantial agreement between categorisation of subjects by cumulative specific RF energy and cumulative call time, misclassification was non-negligible, particularly at higher frequency bands. Factors such as adaptive power control (except in Code Division Multiple Access networks), discontinuous transmission and conditions of phone use were found to have a relatively minor influence on total cumulative specific RF energy. While amount and duration of use are important determinants of RF dose in the brain, their impact can be substantially modified by communication system, frequency band and location in the brain. It is important to take these into account in analyses of risk of brain tumours from RF exposure from mobile phones.
Article
Full-text available
The BJC is owned by Cancer Research UK, a charity dedicated to understanding the causes, prevention and treatment of cancer and to making sure that the best new treatments reach patients in the clinic as quickly as possible. The journal reflects these aims. It was founded more than fifty years ago and, from the start, its far-sighted mission was to encourage communication of the very best cancer research from laboratories and clinics in all countries. The breadth of its coverage, its editorial independence and it consistent high standards, have made BJC one of the world's premier general cancer journals. Its increasing popularity is reflected by a steadily rising impact factor.
Article
Full-text available
Background: Use of cellular telephones is increasing exponentially and has become part of everyday life. Concerns about possible carcinogenic effects of radiofrequency signals have been raised, although they are based on limited scientific evidence. Methods: A retrospective cohort study of cancer incidence was conducted in Denmark of all users of cellular telephones during the period from 1982 through 1995. Subscriber lists from the two Danish operating companies identified 420 095 cellular telephone users. Cancer incidence was determined by linkage with the Danish Cancer Registry. All statistical tests are two-sided. Results: Overall, 3391 cancers were observed with 3825 expected, yielding a significantly decreased standardized incidence ratio (SIR) of 0.89 (95% confidence interval [CI] = 0.86 to 0.92). A substantial proportion of this decreased risk was attributed to deficits of lung cancer and other smoking-related cancers. No excesses were observed for cancers of the brain or nervous system (SIR = 0.95; 95% CI = 0.81 to 1.12) or of the salivary gland (SIR = 0.72; 95% CI = 0.29 to 1.49) or for leukemia (SIR = 0.97; 95% CI = 0.78–1.21), cancers of a priori interest. Risk for these cancers also did not vary by duration of cellular telephone use, time since first subscription, age at first subscription, or type of cellular telephone (analogue or digital). Analysis of brain and nervous system tumors showed no statistically significant SIRs for any subtype or anatomic location. Conclusions: The results of this investigation, the first nationwide cancer incidence study of cellular phone users, do not support the hypothesis of an association between use of these telephones and tumors of the brain or salivary gland, leukemia, or other cancers.
Article
Full-text available
Use of mobile telephones has been suggested as a possible risk factor for intracranial tumours. To evaluate the effect of mobile phones on risk of meningioma, we carried out an international, collaborative case-control study of 1209 meningioma cases and 3299 population-based controls. Population-based cases were identified, mostly from hospitals, and controls from national population registers and general practitioners' patient lists. Detailed history of mobile phone use was obtained by personal interview. Regular mobile phone use (at least once a week for at least 6 months), duration of use, cumulative number and hours of use, and several other indicators of mobile phone use were assessed in relation to meningioma risk using conditional logistic regression with strata defined by age, sex, country and region. Risk of meningioma among regular users of mobile phones was apparently lower than among never or non-regular users (odds ratio, OR = 0.76, 95% confidence interval, CI 0.65, 0.89). The risk was not increased in relation to years since first use, lifetime years of use, cumulative hours of use or cumulative number of calls. The findings were similar regardless of telephone network type (analogue/digital), age or sex. Our results do not provide support for an association between mobile phone use and risk of meningioma.
Article
Context A relative paucity of data exist on the possible health effects of using cellular telephones.Objective To test the hypothesis that using handheld cellular telephones is related to the risk of primary brain cancer.Design and Setting Case-control study conducted in 5 US academic medical centers between 1994 and 1998 using a structured questionnaire.Patients A total of 469 men and women aged 18 to 80 years with primary brain cancer and 422 matched controls without brain cancer.Main Outcome Measure Risk of brain cancer compared by use of handheld cellular telephones, in hours per month and years of use.Results The median monthly hours of use were 2.5 for cases and 2.2 for controls. Compared with patients who never used handheld cellular telephones, the multivariate odds ratio (OR) associated with regular past or current use was 0.85 (95% confidence interval [CI], 0.6-1.2). The OR for infrequent users (<0.72 h/mo) was 1.0 (95% CI, 0.5-2.0) and for frequent users (>10.1 h/mo) was 0.7 (95% CI, 0.3-1.4). The mean duration of use was 2.8 years for cases and 2.7 years for controls; no association with brain cancer was observed according to duration of use (P = .54). In cases, cerebral tumors occurred more frequently on the same side of the head where cellular telephones had been used (26 vs 15 cases; P = .06), but in the cases with temporal lobe cancer a greater proportion of tumors occurred in the contralateral than ipsilateral side (9 vs 5 cases; P = .33). The OR was less than 1.0 for all histologic categories of brain cancer except for uncommon neuroepitheliomatous cancers (OR, 2.1; 95% CI, 0.9-4.7).Conclusions Our data suggest that use of handheld cellular telephones is not associated with risk of brain cancer, but further studies are needed to account for longer induction periods, especially for slow-growing tumors with neuronal features.
Article
Methods An interview-based case-control study with 2708 glioma and 2409 meningioma cases and matched controls was conducted in 13 countries using a common protocol. Results A reduced odds ratio (OR) related to ever having been a regular mobile phone user was seen for glioma [OR 0.81; 95% confidence interval (CI) 0.70-0.94] and meningioma (OR 0.79; 95% CI 0.68-0.91), possibly reflecting participation bias or other methodological limitations. No elevated OR was observed >= 10 years after first phone use (glioma: OR 0.98; 95% CI 0.76-1.26; meningioma: OR 0.83; 95% CI 0.61-1.14). ORs were < 1.0 for all deciles of lifetime number of phone calls and nine deciles of cumulative call time. In the 10th decile of recalled cumulative call time, >= 1640 h, the OR was 1.40 (95% CI 1.03-1.89) for glioma, and 1.15 (95% CI 0.81-1.62) for meningioma; but there are implausible values of reported use in this group. ORs for glioma tended to be greater in the temporal lobe than in other lobes of the brain, but the CIs around the lobe-specific estimates were wide. ORs for glioma 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. Conclusions Overall, no increase in risk of glioma or meningioma was observed with use of mobile phones. There were suggestions of an increased risk of glioma at the highest exposure levels, but biases and error prevent a causal interpretation. The possible effects of long-term heavy use of mobile phones require further investigation.
Article
The use of cellular telephones has increased dramatically during the 1990's in the world. In the 1980's the analogue NMT system was used whereas the digital GSM system was introduced in early 1990's and is now the preferred system. Case reports of brain tumours in users initiated this case-control study on brain tumours and use of cellular telephones. Also other exposures were assessed. All cases, both males and females, with histopathologically verified brain tumour living in Uppsala-Orebro region (1994-96) and Stockholm region (1995-96) aged 20-80 at the time of diagnosis and alive at start of the study were included, 233 in total. Two controls to each case were selected from the Swedish Population Register matched for sex, age and study region. Exposure was assessed by questionnaires supplemented over the phone. The analyses were based on answers from 209 (90%) cases and 425 (91%) controls. Use of cellular telephone gave odds ratio (OR) = 0.98 with 95% confidence interval (CI) = 0. 69-1.41. For the digital GSM system OR = 0.97, CI = 0.61-1.56 and for the analogue NMT system OR = 0.94, CI = 0.62-1.44 were calculated. Dose-response analysis and using different tumour induction periods gave similar results. Non-significantly increased risk was found for tumour in the temporal or occipital lobe on the same side as a cellular phone had been used, right side OR = 2.45, CI = 0.78-7.76, left side OR = 2.40, CI = 0.52-10.9 Increased risk was found only for use of the NMT system. For GSM use the observation time is still too short for definite conclusions. An increased risk for brain tumour in the anatomical area close to the use of a cellular telephone should be especially studied in the future.