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Letter to the editor
The epidemiology of glioma in
adults: a “state of the science”
review
This is a wide-ranging and comprehensive study.1
However, the
section “Nonionizing Radiation: Cellular Phones” has serious de-
ficiencies. It cites 3 incidence time trend studies,2 – 4
2 cohort
studies,5,6
and 1 case control study.7
Incidence Time Trend Studies
Late ascertainment and poor histological concordance are
common accuracy problems. Late ascertainment results in an
underestimation of incidence rates in recently reported years. A
paper reported: “Results: Initial incidence case counts . . . ac-
counted for only 88%–97% of . . . final counts; it would take
4–17 years for 99% or more of the cancer cases to be reported.”8
Another study reported that the histological concordance by 4
neuropathologists reviewing gliomas was “52% all 4 reviewers,
any 3 reviewers, 60%; 2 reviewers, 70%.”9
The study by Deltour and colleagues2
reported that glioma
rates were stable among the 40–59 age group from 1979 to
2008.2
The Ostrom authors1
failed to report a significant in-
crease, ages 20–79, annual percent change (APC) ¼ 0.4%,
95% CI ¼ 0.1%–0.6% in men and APC ¼ 0.3%, 95% CI ¼
0.1%–0.5% in women.2
It received funding via a “firewall”
from the cellphone companies Telia-Sonera, Telenor, and Erics-
son.10
During the years of this study (1979 to 1994; 53% of
the duration), cellphones did not exist or the prevalence was
very low; in 1998 the prevalence was 44%; by 2005 prevalence
had reached 100%. With incidence trends over a 30-year period
where in most of the years there was almost no cellphone use
and with only 3 years of 100% prevalence, how can one con-
clude whether or not cellphone use was affecting incidence?
The US study by Little and colleagues3
was for the years
1992–2008.3
In 1992 cellphone prevalence was 1% and by
2008 it was 84%.11
A 2013 report noted that the Veterans Ad-
ministration hospitals had ceased from 2005 to 2014 to report
cancer cases diagnosed among military veterans.12
The result
was that 3%–8% of all male cancer cases were missing. In
1992, only 1% of the population were using cellphones, where-
as by 2008, use was at 84%. With 3%–8% of male cancers not
reported, combined with late ascertainment, how could a
change in glioma incidence rates be expected? In spite of
these issues, Little et al reported a significantly increased
APC in temporal lobe glioma, APC ¼ 0.73%, 95% CI ¼
0.23%–1.23%. The temporal lobe absorbs the largest
proportion of cellphone radiation of any anatomic region of
the brain.13
The title of the third incidence time trend study cited,
“Changes in Brain Glioma Incidence and Laterality Correlates
With Use of Mobile Phones—a Nationwide Population Based
Study” (emphasis added),4
is in direct contradiction to the as-
sertions in the deficient section.
Incidence Time Trend Studies not Cited
A US paper examined cancer incidence across 3 cancer regis-
tries for the years 1992–2006.14
It reported: “Data from 3
major cancer registries demonstrate increased [APC] incidences
of GBMs in the frontal lobe, temporal lobe, and cerebellum.”
These 3 anatomic regions absorb between 81% (900 MHz)
and 86% (1800 MHz) of all the cellphone radiation absorbed
by the brain.13
An Australian paper with 2000–2008 data,15
though cited in
the Ostrom study,1
was not cited for its time trend results, brain
cancer APC ¼ 3.9%, 95% CI ¼ 2.4–5.5.15
The same team re-
ported: “A significant increasing incidence in glioblastoma mul-
tiforme . . . was observed in the study period [APC ¼ 2.5%, 95%
CI ¼ 0.4–4.6], particularly after 2006.”16
For the years 2003–2012 the Danish Cancer Registry report-
ed an increased incidence of male and female brain cancers of
41.2% and 46.1%, respectively.17
Cohort Studies
The Ostrom study cited 2 cohort studies as evidence that cell-
phone use is not a risk for glioma.5,6
For rare diseases, case con-
trol studies are essential. Cohort studies are incapable of
determining risks.18
It is axiomatic that absence of evidence
is not evidence of absence. Both studies found significant re-
duced risks for various cancers.
Case Control Study
A single case control study was cited, noting that its odds ratios
(ORs) “were markedly elevated in all categories of use.”7
Case Control Studies not cited
The Hardell team’s significant findings are consistent with what
would be expected if wireless phones (cell and cordless) were
causing brain cancer:
(i) The higher the cumulative hours of use, the higher the
risk.7,19
Received 13 December 2014; accepted 14 December 2014
# The Author(s) 2015. Published by Oxford University Press on behalf of the Society for Neuro-Oncology. All rights reserved.
For permissions, please e-mail: journals.permissions@oup.com.
Neuro-Oncology
Neuro-Oncology 2015; 0, 1–2, doi:10.1093/neuonc/nou358
1 of 2
Neuro-Oncology Advance Access published January 20, 2015
byguestonJanuary20,2015http://neuro-oncology.oxfordjournals.org/Downloadedfrom
(ii) The longer the time since first use, the higher the risk.7,19–21
(iii) The higher the radiated power, the higher the risk.7,19 –21
(iv) Ipsilateral risk is higher than contralateral risk.7,19,20,22
Another study reported brain cancer risk with 1640+ hours of
cellphone use compared with ,5 hours of use, OR ¼ 1.82, 95%
CI ¼ 1.15–2.89; and for 10+ years since use compared with
1–1.9 years since first use, OR ¼ 2.18, 95% CI ¼ 1.43–3.31.23
The CERENAT study reported “heavy mobile phone use”
(≥896 hours), OR ¼ 2.89, 95% CI ¼ 1.41–5.93; with 5+ years
since first use, OR ¼ 5.30, 95% CI ¼ 2.12–13.23, P , .001; and
for use exclusively in urban areas, OR ¼ 8.20, 95% CI ¼ 1.37–
49.07.24
In conclusion, the authors’ statement that the “evidence
published since the IARC monograph in 2011 does not support
an association between cellular phone use and the risk of glio-
ma in adults1
” requires revision.
L. Lloyd Morgan
Environmental Health Trust, Berkeley, California
Corresponding Author: L Lloyd Morgan, BS EE, Environmental
Health Trust, 2022 Francisco Street, Berkeley, CA 94709, USA
(lloyd.l.morgan@gmail.com).
References
1. Ostrom QT, Bauchet L, Davis FG, et al. The epidemiology of glioma
in adults: a “state of the science” review. Neuro Oncol. 2014;16(7):
896–913.
2. Deltour I, Auvinen A, Feychting M, et al. Mobile phone use and
incidence of glioma in the Nordic countries 1979–2008:
consistency check. Epidemiology. 2012;23(2):301–307.
3. Little MP, Rajaraman P, Curtis RE, et al. Mobile phone use and
glioma risk: comparison of epidemiological study results with
incidence trends in the United States. BMJ. 2012;344:e1147.
4. Barchana M, Margaliot M, Liphshitz I. Changes in brain glioma
incidence and laterality correlates with use of mobile phones—a
nationwide population based study in Israel. Asian Pac J Cancer
Prev. 2012;13(11):5857–5863.
5. Frei P, Poulsen AH, Johansen C, et al. Use of mobile phones and risk
of brain tumours: update of Danish cohort study. BMJ. 2011;343:
d6387.
6. Benson VS, Pirie K, Schu¨z J, et al. Mobile phone use and risk of brain
neoplasms and other cancers: prospective study. Int J Epidemiol.
2013;42(3):792–802.
7. Hardell L, Carlberg M, So¨derqvist F, et al. Case-control study of the
association between malignant brain tumours diagnosed
between 2007 and 2009 and mobile and cordless phone use.
Int J Oncol. 2013;43(6):1833–1845.
8. Clegg LX, Feuer EJ, Midthune DN, et al. Impact of reporting delay
and reporting error on cancer incidence rates and trends. J Natl
Cancer Inst. 2002;94(20):1537–1545.
9. Coons SW, Johnson PC, Scheithauer BW, et al. Improving
diagnostic accuracy and interobserver concordance in the
classification and grading of primary gliomas. Cancer. 1997;
79(7):1381–1393.
10. Danish Strategic Research Council (grant number 2064-04-0010).
http://www.thecosmosproject.org/funding.php. Accessed 12
December 2014.
11. CTIA’s Semi-Annual Wireless Industry Survey Results: December
1985–December 2008. 2009 CTIA–The Wireless Association.
12. Ostrom QT, Gittleman H, Farah P, et al. CBTRUS statistical report:
primary brain and central nervous system tumors diagnosed in
the United States in 2006–2010. Neuro Oncol. 2013;15(Suppl 2):
ii1–i56.
13. 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;53:2771–2783.
14. Zada G, Bond AE, Wang YP, et al. Incidence trends in the anatomic
location of primary malignant brain tumors in the United States:
1992–2006. World Neurosurg. 2012;77(3–4):518–524.
15. Dobes M, Shadbolt B, Khurana VG, et al. A multicenter study of
primary brain tumor incidence in Australia (2000–2008). Neuro
Oncol. 2011;13(7):783–790.
16. Dobes M, Khurana VG, Shadbolt B, et al. Increasing incidence of
glioblastoma multiforme and meningioma, and decreasing
incidence of Schwannoma (2000–2008): findings of a multicenter
Australian study. Surg Neurol Int. 2011;2:176. Epub 2011 Dec 13.
17. Cancerregisteret. 2012. http://www.ssi.dk/Aktuelt/Nyheder/2013/~/
media/Indhold/DK%20-%20dansk/Sundhedsdata%20og%20it/
NSF/Registre/Cancerregisteret/Cancerregisteret%202012.ashx.
Accessed 12 December 2014.
18. Kundi M. Failure to detect a link between mobile phone use and
brain tumours in a large Danish cohort study: but findings may
be due to bias. Evid Based Med. 2012;17(5):165–166.
19. Hardell L, Carlberg M. Using the Hill viewpoints from 1965 for
evaluating strengths of evidence of the risk for brain tumors
associated with use of mobile and cordless phones. Rev Environ
Health. 2013;28(2–3):97–106.
20. Hardell L, Carlberg M, Hansson Mild K. Use of cellular telephones
and brain tumour risk in urban and rural areas. Occup Environ
Med. 2005;62(6):390–395.
21. Hardell L, Carlberg M, Mild KH. Pooled analysis of two case-control
studies on use of cellular and cordless telephones and the risk of
malignant brain tumours diagnosed in 1997–2003. Int J Oncol.
2006;28:509–518.
22. 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 tumors diagnosed during 1997–2003. Int
Arch Occup Environ Health. 2006;28:509–518.
23. 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(3):675–694.
24. Coureau G, Bouvier G, Lebailly P, et al. Mobile phone use and brain
tumours in the CERENAT case-control study. Occup Environ Med.
2014;71(7):514–522.
Letter to the editor
2 of 2 Neuro-Oncology
byguestonJanuary20,2015http://neuro-oncology.oxfordjournals.org/Downloadedfrom

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Ostrom Letter to the Editor 1-20-15

  • 1. Letter to the editor The epidemiology of glioma in adults: a “state of the science” review This is a wide-ranging and comprehensive study.1 However, the section “Nonionizing Radiation: Cellular Phones” has serious de- ficiencies. It cites 3 incidence time trend studies,2 – 4 2 cohort studies,5,6 and 1 case control study.7 Incidence Time Trend Studies Late ascertainment and poor histological concordance are common accuracy problems. Late ascertainment results in an underestimation of incidence rates in recently reported years. A paper reported: “Results: Initial incidence case counts . . . ac- counted for only 88%–97% of . . . final counts; it would take 4–17 years for 99% or more of the cancer cases to be reported.”8 Another study reported that the histological concordance by 4 neuropathologists reviewing gliomas was “52% all 4 reviewers, any 3 reviewers, 60%; 2 reviewers, 70%.”9 The study by Deltour and colleagues2 reported that glioma rates were stable among the 40–59 age group from 1979 to 2008.2 The Ostrom authors1 failed to report a significant in- crease, ages 20–79, annual percent change (APC) ¼ 0.4%, 95% CI ¼ 0.1%–0.6% in men and APC ¼ 0.3%, 95% CI ¼ 0.1%–0.5% in women.2 It received funding via a “firewall” from the cellphone companies Telia-Sonera, Telenor, and Erics- son.10 During the years of this study (1979 to 1994; 53% of the duration), cellphones did not exist or the prevalence was very low; in 1998 the prevalence was 44%; by 2005 prevalence had reached 100%. With incidence trends over a 30-year period where in most of the years there was almost no cellphone use and with only 3 years of 100% prevalence, how can one con- clude whether or not cellphone use was affecting incidence? The US study by Little and colleagues3 was for the years 1992–2008.3 In 1992 cellphone prevalence was 1% and by 2008 it was 84%.11 A 2013 report noted that the Veterans Ad- ministration hospitals had ceased from 2005 to 2014 to report cancer cases diagnosed among military veterans.12 The result was that 3%–8% of all male cancer cases were missing. In 1992, only 1% of the population were using cellphones, where- as by 2008, use was at 84%. With 3%–8% of male cancers not reported, combined with late ascertainment, how could a change in glioma incidence rates be expected? In spite of these issues, Little et al reported a significantly increased APC in temporal lobe glioma, APC ¼ 0.73%, 95% CI ¼ 0.23%–1.23%. The temporal lobe absorbs the largest proportion of cellphone radiation of any anatomic region of the brain.13 The title of the third incidence time trend study cited, “Changes in Brain Glioma Incidence and Laterality Correlates With Use of Mobile Phones—a Nationwide Population Based Study” (emphasis added),4 is in direct contradiction to the as- sertions in the deficient section. Incidence Time Trend Studies not Cited A US paper examined cancer incidence across 3 cancer regis- tries for the years 1992–2006.14 It reported: “Data from 3 major cancer registries demonstrate increased [APC] incidences of GBMs in the frontal lobe, temporal lobe, and cerebellum.” These 3 anatomic regions absorb between 81% (900 MHz) and 86% (1800 MHz) of all the cellphone radiation absorbed by the brain.13 An Australian paper with 2000–2008 data,15 though cited in the Ostrom study,1 was not cited for its time trend results, brain cancer APC ¼ 3.9%, 95% CI ¼ 2.4–5.5.15 The same team re- ported: “A significant increasing incidence in glioblastoma mul- tiforme . . . was observed in the study period [APC ¼ 2.5%, 95% CI ¼ 0.4–4.6], particularly after 2006.”16 For the years 2003–2012 the Danish Cancer Registry report- ed an increased incidence of male and female brain cancers of 41.2% and 46.1%, respectively.17 Cohort Studies The Ostrom study cited 2 cohort studies as evidence that cell- phone use is not a risk for glioma.5,6 For rare diseases, case con- trol studies are essential. Cohort studies are incapable of determining risks.18 It is axiomatic that absence of evidence is not evidence of absence. Both studies found significant re- duced risks for various cancers. Case Control Study A single case control study was cited, noting that its odds ratios (ORs) “were markedly elevated in all categories of use.”7 Case Control Studies not cited The Hardell team’s significant findings are consistent with what would be expected if wireless phones (cell and cordless) were causing brain cancer: (i) The higher the cumulative hours of use, the higher the risk.7,19 Received 13 December 2014; accepted 14 December 2014 # The Author(s) 2015. Published by Oxford University Press on behalf of the Society for Neuro-Oncology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com. Neuro-Oncology Neuro-Oncology 2015; 0, 1–2, doi:10.1093/neuonc/nou358 1 of 2 Neuro-Oncology Advance Access published January 20, 2015 byguestonJanuary20,2015http://neuro-oncology.oxfordjournals.org/Downloadedfrom
  • 2. (ii) The longer the time since first use, the higher the risk.7,19–21 (iii) The higher the radiated power, the higher the risk.7,19 –21 (iv) Ipsilateral risk is higher than contralateral risk.7,19,20,22 Another study reported brain cancer risk with 1640+ hours of cellphone use compared with ,5 hours of use, OR ¼ 1.82, 95% CI ¼ 1.15–2.89; and for 10+ years since use compared with 1–1.9 years since first use, OR ¼ 2.18, 95% CI ¼ 1.43–3.31.23 The CERENAT study reported “heavy mobile phone use” (≥896 hours), OR ¼ 2.89, 95% CI ¼ 1.41–5.93; with 5+ years since first use, OR ¼ 5.30, 95% CI ¼ 2.12–13.23, P , .001; and for use exclusively in urban areas, OR ¼ 8.20, 95% CI ¼ 1.37– 49.07.24 In conclusion, the authors’ statement that the “evidence published since the IARC monograph in 2011 does not support an association between cellular phone use and the risk of glio- ma in adults1 ” requires revision. L. Lloyd Morgan Environmental Health Trust, Berkeley, California Corresponding Author: L Lloyd Morgan, BS EE, Environmental Health Trust, 2022 Francisco Street, Berkeley, CA 94709, USA (lloyd.l.morgan@gmail.com). References 1. Ostrom QT, Bauchet L, Davis FG, et al. The epidemiology of glioma in adults: a “state of the science” review. Neuro Oncol. 2014;16(7): 896–913. 2. Deltour I, Auvinen A, Feychting M, et al. Mobile phone use and incidence of glioma in the Nordic countries 1979–2008: consistency check. Epidemiology. 2012;23(2):301–307. 3. Little MP, Rajaraman P, Curtis RE, et al. Mobile phone use and glioma risk: comparison of epidemiological study results with incidence trends in the United States. BMJ. 2012;344:e1147. 4. Barchana M, Margaliot M, Liphshitz I. Changes in brain glioma incidence and laterality correlates with use of mobile phones—a nationwide population based study in Israel. Asian Pac J Cancer Prev. 2012;13(11):5857–5863. 5. Frei P, Poulsen AH, Johansen C, et al. Use of mobile phones and risk of brain tumours: update of Danish cohort study. BMJ. 2011;343: d6387. 6. Benson VS, Pirie K, Schu¨z J, et al. Mobile phone use and risk of brain neoplasms and other cancers: prospective study. Int J Epidemiol. 2013;42(3):792–802. 7. Hardell L, Carlberg M, So¨derqvist F, et al. Case-control study of the association between malignant brain tumours diagnosed between 2007 and 2009 and mobile and cordless phone use. Int J Oncol. 2013;43(6):1833–1845. 8. Clegg LX, Feuer EJ, Midthune DN, et al. Impact of reporting delay and reporting error on cancer incidence rates and trends. J Natl Cancer Inst. 2002;94(20):1537–1545. 9. Coons SW, Johnson PC, Scheithauer BW, et al. Improving diagnostic accuracy and interobserver concordance in the classification and grading of primary gliomas. Cancer. 1997; 79(7):1381–1393. 10. Danish Strategic Research Council (grant number 2064-04-0010). http://www.thecosmosproject.org/funding.php. Accessed 12 December 2014. 11. CTIA’s Semi-Annual Wireless Industry Survey Results: December 1985–December 2008. 2009 CTIA–The Wireless Association. 12. Ostrom QT, Gittleman H, Farah P, et al. CBTRUS statistical report: primary brain and central nervous system tumors diagnosed in the United States in 2006–2010. Neuro Oncol. 2013;15(Suppl 2): ii1–i56. 13. 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;53:2771–2783. 14. Zada G, Bond AE, Wang YP, et al. Incidence trends in the anatomic location of primary malignant brain tumors in the United States: 1992–2006. World Neurosurg. 2012;77(3–4):518–524. 15. Dobes M, Shadbolt B, Khurana VG, et al. A multicenter study of primary brain tumor incidence in Australia (2000–2008). Neuro Oncol. 2011;13(7):783–790. 16. Dobes M, Khurana VG, Shadbolt B, et al. Increasing incidence of glioblastoma multiforme and meningioma, and decreasing incidence of Schwannoma (2000–2008): findings of a multicenter Australian study. Surg Neurol Int. 2011;2:176. Epub 2011 Dec 13. 17. Cancerregisteret. 2012. http://www.ssi.dk/Aktuelt/Nyheder/2013/~/ media/Indhold/DK%20-%20dansk/Sundhedsdata%20og%20it/ NSF/Registre/Cancerregisteret/Cancerregisteret%202012.ashx. Accessed 12 December 2014. 18. Kundi M. Failure to detect a link between mobile phone use and brain tumours in a large Danish cohort study: but findings may be due to bias. Evid Based Med. 2012;17(5):165–166. 19. Hardell L, Carlberg M. Using the Hill viewpoints from 1965 for evaluating strengths of evidence of the risk for brain tumors associated with use of mobile and cordless phones. Rev Environ Health. 2013;28(2–3):97–106. 20. Hardell L, Carlberg M, Hansson Mild K. Use of cellular telephones and brain tumour risk in urban and rural areas. Occup Environ Med. 2005;62(6):390–395. 21. Hardell L, Carlberg M, Mild KH. Pooled analysis of two case-control studies on use of cellular and cordless telephones and the risk of malignant brain tumours diagnosed in 1997–2003. Int J Oncol. 2006;28:509–518. 22. 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 tumors diagnosed during 1997–2003. Int Arch Occup Environ Health. 2006;28:509–518. 23. 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(3):675–694. 24. Coureau G, Bouvier G, Lebailly P, et al. Mobile phone use and brain tumours in the CERENAT case-control study. Occup Environ Med. 2014;71(7):514–522. Letter to the editor 2 of 2 Neuro-Oncology byguestonJanuary20,2015http://neuro-oncology.oxfordjournals.org/Downloadedfrom