1. Modulation of Electromagnetic Radiation
Known and Unknown Health Hazards
General Overview
Modulation of electromagnetic radiation (EMR) is very important but little is
known about its importance in the context of cancer risk (see below).
We know, all else being equal, that documented biological effects are larger with
modulation (mostly adverse, but some evidence of therapeutic effects as well) than
non-modulated (CW—continuous wave) EMR.
There is strong evidence that the Specific Absorption (SA) measured in Joules per
kilogram (J/kg), that is, the cumulative hours of exposure is the most important
exposure metric though in the case of cancer this is mitigated by the latency time
between first exposure and diagnosis. The SA can be thought of as the average
absorbed power multiplied by time.
Importance of Modulation
To my knowledge, the only paper to discuss the risk of glioma (brain cancer) by
modulation is the pooled glioma study by the Hardell teami. This study examines
the risk from use of specific wireless phone types (analog, 2G—GSM modulated,
3G—UMTS modulated, and cordless—modulation unstated).
In Table 2, years since first use, for the same category of years of use [limited to
>5 to 10 years because of the relatively recent use of UMTS modulated phones]
the statistically significant Odds Ratios (ORs) are: GSM modulation, OR=1.7;
UMTS modulation, OR=4.1, and cordless phone modulation, OR=1.4.
In Table 3, the risk per 100 hours of cumulative hour of years the risk is consistent
with Table 2. GSM modulation, OR=1.047, GSM modulation and cordless phone
modulation, OR=1.014.
The average radiated power of GSM modulated phone is 10s of mW; UMTS
modulated is 10 of µW, and for cordless phones, 10 mw in Europe.
In other words, with a 3 orders of magnitude less radiated power from UMTS
modulated phone the risk of brain cancer after >5-10 years since first use is 240%
higher risk (4.1/1.7=2.4) than GSM modulated phones are 290% higher risk than

2. cordless phones; similarly for risk of brain cancer per 100 cumulative hours of use,
UMTS modulated phones are 336% higher risks than GSM or cordless phones.
Previous Evidence of Higher Risk of UMTS Compared to GSM Modulation
The Hardell paper cites three studies by Igor Belyaev and other authors:
Of certain interest is the higher risk we observed for 3G mobile phone use
compared with other types. However, this observation was based on short
latency and rather low numbers of exposed subjects. Contrary to 2G GSM,
3G universal global telecommunications system (UMTS) mobile phones
emit wide-band microwave (MW) signals. Hypothetically, UMTS MWs
may result in higher biological effects compared to GSM signal because of
eventual “effective” frequencies within the wideband [32, 33]. To our
knowledge, there are only two mechanistic studies, which compare effects of
2G and 3G signals using the same experimental approach under well-defined
conditions of exposure [32, 34]. UMTS MWs affected chromatin and inhibit
formation of DNA double-strand breaks (DSB) co-localizing
53BP1/gamma-H2AX DNA repair foci in human lymphocytes from
hypersensitive and healthy persons [32]. The data were in line with the
hypothesis that the type of signal, UMTS MWs, may have higher biological
efficiency and possibly larger health risk effects compared to GSM radiation
emissions. The effects of UMTS MWs and GSM-915 MHz MWs on the
formation of the DNA repair foci, were statistically different for
hypersensitive but not for control subjects [32].
[32] I.Y. Belyaev, E. Markova, L. Hillert, L.O.G. Malmgren, B.R.R.
Persson, Microwaves from UMTS/GSM mobile phones induce long-lasting
inhibition of 53BP1/-H2AX DNA repair foci in human lymphocytes,
Bioelectromagnetics 30 (2009) 129–141.
[33] I. Belyaev, Dependence of non–thermal biological effects of
microwaves on physical and biological variables: implications for
reproducibility and safety standards, in: L. Giuliani, M. Soffritti (Eds.),
European J. Oncol.—Library Non–Thermal Effects and Mechanisms of
Interaction between Electromagnetic Fields and Living Matter, 5, Ramazzini
Institute, Bologna, Italy, 2010, pp. 187–218 (An ICEMS Monograph)
http://www.icems.eu/papers.htm?f=/c/a/2009/12/15/MNHJ1B49KH.DTL
(accessed 14.10.21).
[34] E. Markova, L.O.G. Malmgren, I.Y. Belyaev, Microwaves from mobile
phones inhibit 53BP1 focus formation in human stem cells more strongly
than in differentiated cells: possible mechanistic link to cancer risk, Environ.
Health Perspect. 118 (2010) 394–399.

3. Not cited in the Hardell paper were two in vitro studies from the E. U. REFLEX
studies on the genotoxicity risk of human fibroblast cells exposed to EMR. These
two studies reported the threshold to detect genotoxic effects was found at
SAR=0.3 W/kg (Final Report, Risk Evaluation of Potential Environmental Hazards
From Low Frequency Electromagnetic Field Exposure Using Sensitive in vitro
Methods [REFLEX] pdf page 140) from a GSM modulated exposure and
SAR=0.05 W/kg (Schwarz C, Kratochvil E, Pilger A, Kuster N, Adlkofer F,
Rüdiger HW. Radiofrequency electromagnetic fields (UMTS, 1,950 MHz) induce
genotoxic effects in vitro in human fibroblasts but not in lymphocytes from a
UMTS modulated exposure. [Int Arch Occup Environ Health. 2009 Jan;82(2):279-
83.] In other words genotoxic effects from a 6-fold lower SAR were induced from
a UMTS modulated exposure compared to a GSM modulated exposure.
While these results are far from definitive, they certainly hint that UMTS
modulation is far more biologically active than GSM modulation.
Meanwhile additional modulation technologies have been introduced including
Wi-Fi in its myriad modes and the 4th generation LTE. Additional modulation
technologies are under development.
It is reasonable to suspect that when risks are compared between different
modulation technologies that additional hazards may be found.
L. Lloyd Morgan
Sr. Research Fellow, Environmental Health Trust
Lloyd.L.Morgan@gmail.com
14 September 2015
i Hardell L, Carlberg M. Mobile phone and cordless phone use and the risk for glioma - Analysis of pooled case-
control studies in Sweden, 1997-2003 and 2007-2009. Pathophysiology.2015 Mar;22(1):1-13.