2 IEEE JOURNAL OF ELECTROMAGNETICS, RF, AND MICROWAVES IN MEDICINE AND BIOLOGY, VOL. 1, NO.
1, JUNE 2017
Cancer Occurrences in Laboratory Rats From
Exposure to RF and Microwave Radiation
James C. Lin
(Invited Paper)
Abstract—The health effects of radio-frequency (RF) and mi-
crowave radiation have been a subject of scientific inquiry and
public interest of late because of widespread global usage of mo-
bile communication devices by billions of people everywhere. A
minute increase in health risks such as cancer from RF radiation
might lead to significant consequences for the health of the gen-
eral public. A recent U.S. government announcement about the
discovery of rare cancers in rats exposed to RF radiation is an im-
portant occurrence. Note that any new or single report should not
be viewed in isolation. The U.S. government project was organized
to confront the weaknesses of prior laboratory rodent studies on
the potential of RF exposure to impact human health such as cancer
in controlled environments. Indeed, several published reports on
animal cancer investigations involving prolonged exposure to RF
radiation are contentious and perplexing. The discrepancies have
presented ambiguity in assessing public health threats from RF
exposure. It is the objective of this review to provide a critical and
analytical synopsis and assessment on current progress in cancers
in rats exposed to lifelong RF and microwave radiation. Its focus is
on laboratory studies involving cancer production and promotion,
as well as the survival of experimental rats. Of special interest is
carcinogenesis in the head—cancer development in the head. The
question of whether RF exposure from wireless and mobile devices
and systems poses a health risk will likely remain equivocal and
controversial for some time to come.
Index Terms—Animal study, brain tumor, carcinogenesis, elec-
tromagnetic radiation, health risk, mobile communication, wireless
technology.
I. INTRODUCTION
IOLOGICAL effects of radio-frequency (RF) and mi-
B crowave radiation have been subjects of scientific inquiry
since shortly after the first laboratory generation of electro-
magnetic radiation more than a century ago. Since then, scien-
tific knowledge concerning their health impacts has improved
steadily. Nevertheless, they have become a focus of current
devotion because of swift expansion and enhanced use of mi-
crowave and RF radiation for wireless communication over the
past two decades.
Microwave and RF electromagnetic radiation provide the
channels for all wireless communication networks and systems
Manuscript received April 28, 2017; accepted June 2, 2017. Date of publica-
tion August 2, 2017; date of current version October 30, 2017. The associate
editor coordinating the review of this paper and approving it for publication was
Prof. Changzhi Li.
The author is with the Department of Electrical and Computer Engineer-
ing, University of Illinois at Chicago, Chicago, IL 60607-7053 USA (e-mail:
lin@uic.edu).
Digital Object Identifier 10.1109/JERM.2017.2721427
2469-7249 © 2017 IEEE. Personal use is permitted, but republication/redistribution requires IEEE permission.
See http://www.ieee.org/publications standards/publications/rights/index.html for more information.
, Life Fellow, IEEE
through which conversations, data, pictures, and text are trans-
mitted and received. In recent years, all regions of the world
have seen rapid growth in demand for wireless access and has
been anticipated to remain so for many more years. Sustain-
ing that mandate would necessarily give rise to greater human
exposure to microwave and RF radiation.
There are two facets of these systems pushing the reemer-
gence of scientific attention toward public health. Namely, the
pervasive base station antennas of different types across many
metropolitan and outlying scenarios and the elevation of en-
vironmental levels of RF and microwave radiation in office,
school, and residential settings. Also, never before in human
history have ubiquitous sources of RF and microwave electro-
magnetic radiation been positioned in close proximity to the
head and body of such a large number of users—nearly the
entire human population—at any time or in any place.
Moreover, aside from primary intended roles, RF and mi-
crowave radiation can produce other effects that may impact the
life activities of biological systems. The modifications generated
would depend on many biological and physical circumstances.
They may or may not be grossly visible and discernable quickly
after exposure of the living system.
Scientific investigations of biological interactions and health
consequences of RF and microwave radiation began in the
1940s, shortly after the introduction of radar, and recommen-
dations for restraining exposure to RF and microwave electro-
magnetic radiation were first published in the late 1960s with
the aim of providing protection against known adverse health
effects, specifically, induced tissue temperature elevation. Since
then, guidelines have been occasionally revised and updated.
In 2011, the International Agency for Research on Cancer
(IARC) of the World Health Organization classified exposure
to RF radiation as a possible carcinogen to humans. The IARC
evaluated available scientific studies and decided that while ev-
idence was limited and incomplete, especially in terms of find-
ings from animal investigations, epidemiological studies de-
scribing elevated chances for brain cancer (gliomas) and au-
ditory nerve tumors (acoustic neuromas) for prolonged use or
among heavy users of cellular mobile telephones are amply
convincing to justify a classification of RF radiation as possibly
cancer-causing in humans [1], [2].
In May 2016, a U.S. government study announced findings of
rare cancers in laboratory rats exposed to mobile-phone RF and
microwave radiation [3]. It is a singularly large animal health
LIN: CANCER OCCURRENCES IN LABORATORY RATS FROM EXPOSURE TO RF AND MICROWAVE RADIATION
impact research carried out, to date, by the National Toxicology
Program (NTP). Its aim was to furnish a key input of scientific
data on a significant issue to human health because a minute
rise in cancer incidences from exposure to mobile phone RF
radiation might lead to significant consequences of the health of
the general public. Adoption of cellular communication devices,
especially mobile phones, has become worldwide [3]. Thus, the
NTP project was organized to confront the weaknesses of prior
laboratory rodent studies on the potential of RF exposure to
impact human health such as cancer in controlled environments.
The announcement of rat cancers resulting from NTP’s large RF
animal research was an important event. However, it should be
noted that a new or any single study should not be viewed in
isolation.
As previously mentioned, published animal cancer inves-
tigations involving prolonged exposures to RF radiation are
contentious and perplexing. The discrepancies have presented
ambiguity in assessing public health threats from RF exposure.
It is the objective of this review to provide a critical and
analytical synopsis and assessment of current status on cancers
in experimental rats subjected to lifelong RF and microwave
radiation exposure. It focuses on laboratory research involving
cancer production and promotion, as well as survival of RF- and
microwave-exposed laboratory rats, especially carcinogenesis
in the brain—cancer development in the brain.
This review will begin with a brief account of current guide-
lines for safe human exposure and description of results from
human epidemiology that served as the basis of IARC’s classi-
fication.
II. EXPOSURE GUIDELINES FOR HUMANS
Current safety guidelines in the RF and microwave frequency
range impose limits on exposure to preclude total-body heat
stress and overheating of localized tissue. The guidelines are
intended to prevent hazardous effects associated with an induced
body temperature elevation greater than 1 °C over any 6-min
period for 300 MHz to 6 GHz [4], [5]. This degree of temperature
elevation may result from exposure of human adults to a total-
body specific energy absorption rate (SAR) of around 4 W/kg
for about 30 min, under moderate environmental conditions.
The average SAR of 0.4 W/kg was chosen as the restriction
to afford a reasonable safeguard for occupational exposure. An
extra factor of 5 was incorporated for exposure of the general
population, which ends up with a total-body SAR restriction of
0.08 W/kg.
Note that 1.6 and 2.0 W/kg, in any 1 and 10 g, respectively,
are limiting local tissue SAR standards set up by the Federal
Communications Commission (FCC) in Washington, DC, USA,
and the International Commission on Nonionizing Radiation
Protection (ICNIRP) in Munich, Germany [31].
III. MODULATION CHARACTERISTICS AND SCHEMES OF
RF SIGNALS
While this paper focuses on cancer risks of RF radiation
used in mobile communication and wireless technologies, this
section will provide a brief synopsis on various cellular mobile
3
communication technologies since they are the platforms or
sources of RF exposure employed for the rat studies. Although
there are distinctions among various generations of related
technologies, in some cases, the distinction is blurring.
Digital communication systems have become the foremost
wireless service worldwide [6]. However, system architectures
differ from region to region. The prevailing system around
the world, i.e., most regions in Asia, Europe, and North and
South America, is the Global System for Mobile Communi-
cations (GSM) system. It is based on RF carrier frequencies
between 850 and 1900 MHz and an operating bandwidth of
250 kHz and a data rate of 9.6 kbit/s. It employs a Time Division
Multiple Access (TDMA) technique—a cell phone is “on” for
0.58 ms or 4.615/8 ms—and comes back periodically at a rate
of 217 Hz. The remaining 7/8 of the available timeframe is as-
signed to other phones. So from the perspective of RF power
delivery, it is burst-mode transmission. There are also power
variations at rates of 2 and 8 Hz due to a variety of control and
system signals, in addition to the access frequency of 217 Hz
and its harmonics.
The IS-95 standard is a direct-sequence spread spectrum sys-
tem, known in North America as Code Division Multiple Ac-
cess (CDMA). The CDMA scheme differs considerably from
the GSM technique. Its phones are “on” concurrently, but di-
vided by distinct codes, which are ‘spread’ on the RF carrier to
a broader bandwidth than is imposed by the un-spread scheme.
The chip rate or spreading speed for CDMA is 1.2288 Mchip/s
over a bandwidth of 1.25 MHz. A direct result is the absence of
pulsing variations common in TDMA systems.
There are two third-generation (3G) versions of CDMA sys-
tems: the North American CDMA-2000 network, which varies
mainly from W-CDMA in network architecture. The family of
3G standards also includes Universal Mobile Telecommunica-
tion System (UMTS) networks. However, W-CDMA functions
as the air interface for UMTS. It remains as the underlying stan-
dard and supports two 5-MHz channels: 1900-MHz for uplink
from user to base station and 2100-MHz for downlink. On the
other hand, CDMA-2000 relies on 1.25-MHz channels for trans-
mission. Thus, W-CDMA requires a broader bandwidth and
supports up to 2 Mbit/s data transfer rate, although most users
can anticipate 64 kbit/s performance in a heavily congested sys-
tem. However, it is much faster than GSM’s 14.4 kbit/s single
data channel and can provide economical access to the World
Wide Web from cellular mobile devices.
The Personal Digital Cellular (PDC) system is a TDMA sys-
tem used mainly in Japan. It operates in the 800-MHz and
1.5-GHz bands and offers packet transmission capability
through a PDC-Packet (PDC-P) subsystem. The radio charac-
teristics are similar, namely 3-channel TDMA. PDC-P provides
9.6 kbit/s packet access with one TDMA time slot and 28.8 kbit/s
with three time slots.
Digital Enhanced Cordless Telecommunication (DECT) is a
globally adopted digital system, but with its origins in Europe.
The DECT standard operates in the 1880 to 1900 MHz RF band
with Gaussian-frequency-shift-keying (GFSK) modulation for
wireless communication. It is a flexible system for homes, of-
fices, and public settings. It is compatible with many types of
4 IEEE JOURNAL OF ELECTROMAGNETICS, RF, AND MICROWAVES IN MEDICINE AND BIOLOGY, VOL. 1, NO. 1, JUNE 2017
telecommunications networks. The system is known for high
voice quality voice communication, but it has widespread appli-
cations such as Internet access and offers interoperability with
other fixed or wireless services. In fact, many DECT-based de-
vices are available for on-demand services.
IV. IARC CLASSIFICATION OF RF RADIATION AS A POSSIBLE
HUMAN CARCINOGEN
The classification of RF radiation as a possible cancer-causing
agent to humans is medium among IARC’s categorization of
five groups of carcinogens in humans [2]. The highest class is
Group 1, which is designation for agents that are “carcinogenic
to humans.” The next is Group 2A: defined as “probably car-
cinogenic to humans;” followed by 2B: designated as “possibly
carcinogenic to humans;” after that Group 3: labeled as “not
classifiable as to its carcinogenicity to humans;” and finally,
Group 4: named as “probably not carcinogenic to humans.”
The IARC determination that while evidence from human
epidemiological studies is limited and imperfect, it is reasonably
robust to warrant a categorization of “possibly carcinogenic
to humans” for RF electromagnetic radiation. It specifically
recognized some reported scientific studies suggesting elevated
odds ratios for glioma types of cancer and auditory nerve tumors
(acoustic neuromas) for prolonged use or among “heavy mobile
phone users” [1], [2].
The IARC report mentioned that among hundreds of
scientific articles examined, four reports had most prominent
roles in its decision. They included the Interphone international
case-control study [7], [8], a pooled analysis of malignant brain
tumors [9], and a case-case study of acoustic neuroma risks
[10]. The international study disclosed elevated odds ratios
of 40% for gliomas. The increase for “heavy” users tended to
be higher in study participants who typically positioned cell
phones on the same side of the head as detected cancer.
The pooled analysis observed a 270% rise in risk for astro-
cytoma (a more common type of glioma) for long-term mobile
phone use. It also observed a heightened risk for acoustic neu-
roma, although the number of cases was noticeably lower for
glioma. The case-case study obtained indications of elevated
risks for acoustic neuroma (10% to 300%) with mobile phone
users. IARC recognized that human epidemiological studies are
potentially vulnerable to bias and confounding as well as pro-
cedural flaws such as detection mistake, recall error, selection
prejudice, and participant preconception. Nevertheless, it de-
cided that the outcomes could not be dismissed as exhibiting
bias and confounding alone, and that a contributory explanation
between mobile communication RF radiation and cancer in the
head is a possibility.
V. BRAIN CANCERS OR TUMORS IN HUMANS
Astrocytoma and glioblastoma multiforme are the most com-
mon and aggressive malignant brain cancers in human adults.
These cancers invade and infiltrate widely and lack distinct
borders, and cells reproduce rapidly. They develop a necrotic
core of dead cells in the center of the tumor that is hypoxic or
deficient in oxygen. These cancers also stimulate the creation of
new blood vessels to sustain their aggressive growth. Primary
brain tumors that grow slowly often are benign or the least ma-
lignant, and their symptoms tend to take a long time to appear.
These brain tumors are frequently related to prolonged survival.
Currently, the prediction or prognosis for life expectancy of the
most aggressive brain tumors is extremely poor. Outlook for sur-
vival could be as short as one month for expectant management,
and better than one year with surgery and radiation treatment,
but improves further when combined with chemotherapy.
At present, the projected freshly diagnosed primary malignant
and non-malignant brain tumors are 79,270 per year in the U.S.
This includes an estimated 26,070 primary and 53,200 non-
malignant cases [11]. In 2013, the estimated number of people
living with brain and other nervous system cancers was 152,
751 in the U.S. [12]. The total U.S. populations were 316.5 and
323.1 million in 2013 and 2016, respectively [13].
VI. CANCERS IN RF-EXPOSED LABORATORY RATS
Many controlled laboratory rat cancer studies have been con-
ducted and reported during the past quarter century to appraise
the potential health hazards. A majority of the laboratory in-
vestigations were conducted in academic research laboratory
or good laboratory practice (GLP) conditions using both female
and male rats. The studies commonly followed prescribed meth-
ods and procedures that are typical of commercial product or
pharmaceutical testing.
It should be noted that laboratory results obtained from rodent
studies have repeatedly demonstrated the same organ damage
in rodents and humans by many known cancer-causing agents,
although there are anatomical and physiological differences.
This review will begin with a brief account of an earlier
investigation and two short-term studies involving laboratory
rats. Specifically, the short-term studies include a brain tumor
study in rats that died two to three weeks following implantation
of glioma cells and microwave exposure [14] and a short-term
liver bioassay [15].
A. Preliminary Investigations
The experiments conducted by Kunz et al. [16] were aimed
to investigate biological effects of RF radiation on grown ani-
mals targeting on general health status and survival. (Chou et al.
paper [17] later published an abbreviated version of the Kunz
et al. report.) Assays conducted included comprehensive serum
chemistries, hematology, protein panel, thyroxine, plasma cor-
ticosterone, open-field behavioral activity, and immunologi-
cal competence. Beginning at 8 weeks of age and continued
daily for 21.5 h/day, male Sprague-Dawley (SD) rats (100 each
for exposure and sham control) were exposed individually to
0.15–0.4 W/kg of whole-body averaged SARs, in circularly
polarized waveguide exposure chambers for up to 25 months.
Pulsed power (0.144 W, 2450-MHz, 10-μs wide pulse at
800 pps, modulated at 8 Hz) was delivered to each exposure
chamber. A statistically significant increase in primary cancers
was observed at death: 18 in RF-exposed rats vs. five in sham-
exposed controls. Overall, lifelong exposure did not show any
noteworthy changes in the general health of RF-exposed rats.
LIN: CANCER OCCURRENCES IN LABORATORY RATS FROM EXPOSURE TO RF AND MICROWAVE RADIATION
RF- and sham-exposed rats had essentially undistinguishable
survival rates during the rats’ lifetime.
To assess any relationship between microwave and RF radi-
ation and brain cancer promotion late in the carcinogenic pro-
cess, Salford et al. [14] exposed Fischer 344 rats (150–250 g) of
both sexes, implanted with RG2 and N32 rat glioma models to
915 MHz microwaves at levels that did not elevate body temper-
ature. The growth rate of ethylnitrosourea (ENU)-induced RG2
glioma cells was approximately twice that of N32 cancer cells.
Cancer cells in nutrient solution were injected stereotaxically
into the right caudate nucleus in the heads of 37 experimental
rats and 37 matched, sham controls. Exposure of un-anesthetized
animals, individually, in well-ventilated transverse electromag-
netic (TEM) exposure chambers commenced 5 days after inocu-
lation for 7 h/day, 5 d/wk for two to three weeks (typical duration
over which rats died after glioma cell implantation). Control rats
were in an identical TEM exposure chamber but without RF ra-
diation. For RF exposure, 1W, 0.57 ms pulses at 0, 4, 8.33, 16,
50, or 217 Hz generated SARs of 0.008–0.4 W/kg. However at
50 Hz, 6.67 ms pulses with a peak power of 2 W produced an
SAR of 1.0 W/kg [14]. Tumor size measurement and histopatho-
logical examination revealed that exposure to pulsed 915 MHz
radiation did not accelerate growth of implanted gliomas outside
their typical course.
Promotion of cancer by local absorption of pulse modulated
RF radiation was the objective of a short-term rat liver carcino-
genesis experiment [15]. A single dose of diethylnitrosamine
(DEN, 200 mg/kg, I.P.) was delivered to six-week-old male
Fischer 344 rats (48 exposed and 48 sham-exposed). Another
24 rats only received DEN and partial hepatectomy, served as
controls. Two weeks later, it was followed by RF exposure
of the mid-lateral body section to 929.2 MHz TDMA modu-
lated PDC radiation from the near field of a monopole antenna.
The 90 min/day and five d/wk exposure regime continued for
six weeks. The maximum local SAR in the liver was 1.7 to
2.0 W/kg. (Although less relevant, the whole-body SAR was
0.58 to 0.80 W/kg.) Rats were killed after the 6-week exposure
period when the rats were 14 weeks of age. Carcinogenesis was
recorded by numbers and areas of glutathione S-transferase pla-
cental form (GST-P) positive foci in the livers. There were no
meaningful variances between the exposed and sham-exposed
young rats due to local body exposure from 929.2 MHz radiation
with PDC signals.
B. Research Studies Using Chronically Exposed Rats
To date, including the three papers mentioned above, there
are 18 published reports on carcinogenic and co-carcinogenic
potentials of two-year or lifelong exposure of laboratory rats to
RF and microwave radiation. Rats tested include three differ-
ent laboratory strains: eight studies used Fischer 344, 3 studies
tapped Wistar, and seven studies involved Sprague-Dawley rats.
In many cases, rats were restrained during exposure but some
were not, which potentially complicates interpretation of results.
RF and microwave exposure scenarios include both plane-wave
and near-field exposure environments. Specific information on
key parameters associated with each study is given in Table I.
5
The following descriptions are organized in terms of various an-
imal models utilized in these long-term studies under a variety
of exposure scenarios and conditions.
Fischer 344 Rats
Among published studies on RF carcinogenic and co-
carcinogenic potentials in rats, eight studies used the Fischer
344 strain of laboratory rats in six different types of RF systems.
TDMA-836 MHz: Spontaneous carcinogenicity and occur-
rence of central nervous system (CNS) cancers caused by a
carcinogen, ENU, in utero and subsequent pulse modulated
836 MHz TDMA exposure were the subjects of a study involv-
ing pregnant Fischer 344 rats and offspring. It included both
plane-wave and near-field exposures [18]. Plane-wave exposure
began on gestational day 19 for pregnant dams, and followed
with offspring in their cage until weaning at 21 days of age.
Near-field exposure commenced after weaning with each rat
in individual restraints and continued for the next 22 months,
two h/day, and four consecutive days weekly. Dams and pups
were free to move about their cages. The system was circularly
polarized to reduce orientation-dependent RF absorption. The
plane-wave power density at the center was 26 ± 5.0 W/m2
and was within 1.6 dB across the cage. It is not obvious whether
cage-control animals formed a part of this study, since related
data analyses were not provided.
Exposures took place in three shifts to accommodate 360
experimental and sham control rats. To billet 120 rats (60 ex-
posed, 60 sham) for simultaneous exposure, the study employed
12 carousel type near-field system. Each carousel had 10 rats
oriented radially, facing a central antenna. A plastic holder re-
strained each rat for the entire exposure duration to ease dosime-
try. Average SAR was 1.0 to 1.6 W/kg in the brain of rats whose
mass ranged from 250 to 450 g. It is emphasized that this study
took meticulous care of dosimetry, involving both experimental
and numerical approaches, and validated each by an independent
method.
Rats did not all survive; survivors (182 or 77%) went through
thorough histopathological analysis. The results did not reveal
any carcinogenic effects in rat brains from TDMA-modulated
836 MHz RF exposure; however, some evidence of exposure-
related cancer prevention (“protective effect”) was observed.
TDMA-exposed rats trended to a lower rate of spontaneous
brain cancers (P < 0.16) and ENU-initiated brain cancers (P
< 0.16), but in rats that died from primary brain cancers (54
or 23%) during the study, exposure to TDMA-radiation con-
siderably decreased the occurrence of ENU-initiated brain can-
cers (P < 0.03). The “protective” effect of TDMA exposure
was unexpected. Aside from the small numbers of cancers and
cancer-bearing rats, the “protective” finding was clouded by
animal stress presented by restraining rats and lack of cage con-
trols. Nonetheless, the results suggested that TDMA-modulated
836 MHz RF exposure of Fischer 344 rats from late pregnancy
through 24 months of life has little effect on occurrence rate of
either spontaneous primary or ENU-initiated brain cancers.
FM-836 MHz: A related study from the same laboratory that
exposed Fischer 344 rats to 836 MHz, frequency-modulated
(FM) RF radiation with computer-generated cell phone conver-
sation showed that the incidence rate and histopathological type
6 IEEE JOURNAL OF ELECTROMAGNETICS, RF, AND MICROWAVES IN MEDICINE AND BIOLOGY, VOL. 1, NO. 1, JUNE 2017

TABLE I
CANCER INITIATION OR PROMOTION IN LABORATORY RATS EXPOSED TO RF RADIATION (UPDATED AND ADOPTED FROM [33] WITH PERMISSION)

Reference Signal, Rats Co-carcinogen Exposure SAR(W/kg) Tumor Type, Study

Modulation, (number) System (Whole-body, Location Design
Exposure Regime local peak) (Results)

[14] 915 MHz GSM Fischer 344 (male Implanted RG2 TEM chamber 0.008–1.0 Brain (No Promotion; RF
Pulse 7 h/day, and female; 37 and N32 (Partially difference) and Sham control
5 d/wk, 2-3 wk exposed, 37 sham) Restrained) only
[15] 929.2 MHz TDMA Fischer 344 (male; Diethyl- Monopole 0.58-0.8 wb ave; Liver (No Promotion; RF
90 min/day, 5 d/wk 48 exposed, 48 nitrosamine Near-field 6.6-7.2 peak wb: difference) and Sham only
6 wk sham; 24 DEN (DEN) (Partially 1.7-2.0 peak in
control) Restrained) liver
[18] 836 MHz TDMA Fischer 344 (236 N-Ethyl- Plane Wave Horn 0.27–0.72 Brain or CNS (No Initiation and
2 h/day, 4 d/wk, 2 yr offspring; in 4 nitrosourea (ENU, in utero and Whole-body; overall difference; Promotion; RF,
groups of 60:30 4 mg/kg) in utero offsprings; (0.74-1.6 in brain) Reduction w/o Sham, No cage
female/30 male), Carousel after ENU) controls
ENU/RF (26 weaning
female/30 male) (Restrained)
[19] 836 MHz FM 2 Fischer 344 (102 ENU 4 mg/kg in Plane wave Horn 0.27–0.72 Brain or CNS (No Initiation and
h/day, 4 d/wk, 2 yr pregnant dams; utero for Pregnant dams Whole-body; overall difference) Promotion; RF,
540 offspring in 6 and offspring; (0.74-1.6 in brain) Sham, and Cage
groups: 45 female Carousel after control
and 45 males/ weaning
group) (Restrained)
[20] 1.44 GHz TDMA, Fischer 344 (500 ENU 4 mg/kg in Carousel <0.4 Whole-body Brain or CNS (No Cancer
1.5 h/day, 5 d/wk, 2 5-wk old pups; 50 utero (Restrained with 4 (0.67 and 2.0 overall difference) Promotion; RF,
yr female and 50 sizes of holders) brain ave) Sham, Cage
male per group) control
[21] 1.95 GHz Fischer 344 (500 ENU 4 mg/kg in Carousel <0.4 Whole-body Brain or CNS (No Cancer
W-CDMA, 5-wk old pups; 50 utero (Restrained with 4 (0.67 and 2.0 overall difference) Promotion; RF,
1.5 h/day, 5 d/wk female and 50 sizes of holders) brain ave) Sham, Cage
for 2 yr male per group) control
[22] 836 MHz FM or Fischer 344 (480 None Carousel 1.3 Brain ave (0.5 Brain or organs Initiation RF,
848 MHz CDMA, 6-wk old; 80 (Restrained) and 2.5 local (No difference in Sham, No cage
4h/day, 5 d/wk, 2 yr female and 80 brain) any tumor in any controls
male per group) organ)
[23] 1.62 GHz Iridium Fischer 344 (102 None Parallel plate, 0.036 to 0.077 Brain or organs Initiation RF,
2h/day, 4 d/wk, 2 yr pregnant dams; Plane wave for Whole-body (0.16 (No difference in Sham, Cage
540 offspring in 6 Pregnant dams and 1.6 brain ave) treatment groups.) controls
groups: 45 female and offspring; Not reported for
and 45 Carousel after cage control.
males/group) weaning
(Unrestrained)
[24] 900 MHz GSM Wistar (288 Co-carcinogen Radial 0.3 (0.07–1.2) and Tumor type or Promotion RF,
2h/day, female 7-wk old in 3-chloro-4- Transmission Line 0.9 (0.21–3.6) incidence, No Sham, Cage
5 d/wk, 2 yr 4 groups of 72) (dichloromethyl)- TEM plane wave Whole-body ave effect control
5-hydroxy-2(5H)- (Unrestrained)
furanone (MX),
1.7 mg/kg
Oral daily
[25] 902 MHz GSM Wistar 500 (7-wk None Waveguide 0.44, 1.33, and 4.0 Primary tumor or Initiation RF,
2h/day, old in 5 groups of Wheel Whole-body ave neoplastic lesion Sham, Cage
5 d/wk, 2 yr 50 females and 50 (Restrained) No effect control
males/group)
[25] 1747 MHz DCS Wistar 500 (7-wk None Exposure Wheel 0.44, 1.33, and 4.0 Primary tumor No Initiation RF,
2h/day, old in 5 groups of waveguides Whole-body ave effect Sham, Cage
5 d/wk, 2 yr 50 females and 50 (Restrained) control
males/group)
[26] 860 MHz FM or SD (900 pups in ENU (0, 2.5, 10 Carousel with 0.27–0.42 Brain or organs Initiation and
MiRS pulsed, 15 groups of 30 mg/kg) in utero different size Whole-body ave (No difference), Promotion RF,
6h/day, females and 30 wedge or tube (1.0 brain ave) Trend in high Sham, Cage
5 d/wk, 2 yr males/group) holders ENU controls
(Restrained)
[27] 900 MHz GSM CW SD (360 female DMBA (50 Plane wave 0.017–0.13 Breast (No Promotion RF,
exposure until 51-day old in 6 mg/kg) chamber Whole-body ave difference) Sham, No cage
tumors developed in groups of 60) (Unrestrained) (low-level) control
150-280 days
[28] 900 MHz GSM SD (128 female DMBA (10 mg Plane wave 0.1, 0.7, 1.4, 2.2, Breast (No Promotion RF,
2h/day, 55-day old in 8 total) chamber and 3.5 difference) Trend Sham, No cage
5 d/wk, 9 wk groups of 16) (Restrained) Whole-body ave in low SAR control
LIN: CANCER OCCURRENCES IN LABORATORY RATS FROM EXPOSURE TO RF AND MICROWAVE RADIATION 7

TABLE I
CONTINUED

Reference Signal, Modulation, Rats Co-carcinogen Exposure SAR(W/kg) Tumor Type, Study
Exposure Regime (number) System (Whole-body, Location Design
local peak) (Results)

[29] 900 MHz GSM SD (500 female DMBA (35 Waveguide Wheel 0.44, 1.33, and 4.0 Breast (No Promotion RF,
4h/day, 5 d/wk, 26 wk 48-day old in 5 mg/kg) (Restrained) Whole-body ave sham/exposed Sham, Cage
groups of 100) difference; but in control
cage control)
[30] 902 MHz GSM SD (500 female DMBA (17 Waveguide Wheel 0.44, 1.33, and 4.0 Breast (Many Promotion RF,
4h/day, 5 d/wk, 26 wk 47-day old in 5 mg/kg, oral) (Restrained) Whole-body ave differences but no Sham, Cage
groups of 100) dose response control
relation)
[3], [31] 900 MHz GSM SD (In utero in 14 None Multimode 1.5, 3.0, and 6.0 Male brain RF, Sham, No
CDMA 9h/day, 7d/wk groups of 90) Chamber Whole-body ave gliomas and heart cage control
before birth thru 2yr (Unrestrained) schwannomas

of either spontaneous or ENU-initiated brain cancers did not
change with RF exposure [19]. Results from these two studies
from the same laboratory appear to indicate there might be a re-
lationship between specific schemes of RF radiation modulation
and carcinogenesis in Fisher 344 rats.
TDMA-1.44 GHz: In this study, pups of Fischer 344 dams
treated with an injection of ENU dose in utero were exposed
to 1.44 GHz, TDMA-modulated radiation from a PDC system
[20]. The exposure used a carousel configuration and individual
restraining holders with the rats’ noses pointing toward the radi-
ating antenna at the center. The protocol called for plastic holders
of four different sizes to manage body mass increase during the
two-year experiment. The whole-body SAR was 0.4 W/kg for
average SARs of 0.67 and 2.0 W/kg in the brain.
Pups were assigned to five groups: three groups of ENU +
RF (sham exposure, 0.67 W/kg and 2.0 W/kg); ENU alone,
and untreated cage controls. Each group consisted of 50 rats
of each sex. An additional 63 females and 63 males served as
replacement rats to fill vacancies due to death to maintain equal
number of rats for each exposure condition.
The increase in body mass of RF-exposed rats was similar
to that of unexposed controls of both sexes. Group values and
variances were small in body mass, food consumption, or sur-
vival rates; likewise, incidence rate or number of brain or CNS
cancers in RF-exposed groups were comparable. In addition,
observed cancer types were similar. However, rat restraint was
associated with curtailed growth in male rats but only after 18
months of age in female rats. Therefore, lifelong exposure to
TDMA-modulated 1.44 GHz, RF radiation at brain SARs of
0.67 and 2.0 W/kg did not display a promotional response for
ENU-initiated CNS carcinogenesis. Note that this experiment
used four different-sized restraining holders to accommodate
growth in rats’ body mass. This procedure barred smaller rats
from turning inside the holder and helped to improve dosimetry.
However, body restraints may also heighten stress.
W-CDMA-1.95 GHz: The RF exposure system mentioned in
the above investigation was applied to study the co-carcinogenic
effect of two-year exposure to W-CDMA radiation as a promoter
of ENU-initiated cancer [21]. A monopole antenna was attuned
to operate at 1.95 GHz. On gestational day 18, an injection of
ENU dose was given to pregnant Fisher 344 rats. Pups (500)
were separated into five groups as in the TDMA-1.44 GHz in-
vestigation, and each group consisted of 50 females and 50
males. The study did not show any significant elevation in num-
ber or incidence rate of cancers in these rats. Likewise, there
were no clear variations in brain cancer types. However, the
study suggested that brain cancer development in female Fisher
344 rats exposed to W-CDMA 1.95 GHz, RF field had a slight
tendency to rise.
FDMA-836 and CDMA-848 MHz: Spontaneous carcinogene-
sis without ENU initiation was studied for frequency-modulated
continuous-wave (FMCW) radiation at 836 MHz with frequency
division multiple access (FDMA) in a carousel exposure appa-
ratus [22]. The study also included a protocol using CDMA-
modulated 848 MHz. It involved 480 young Fischer 344 rats of
both sexes (six weeks old when RF exposure began); 80 females
and 80 males were placed in one of three experimental groups:
CDMA, FDMA, and sham. Rats were placed in holders and
exposed for four h/day, five d/wk during the two-year investiga-
tion. Sentinel rats to screen for infectious diseases were kept in
the same room. It appeared that cage-control rats were absent
from this study. Data reported indicated that two-year exposures
to 848 MHz CDMA or 836 MHz FDMA RF radiation did not
influence spontaneous brain cancer development in these young
Fischer 344 rats.
IRIDIUM-1.6 GHz: The Iridium system—a satellite-based,
1.6 GHz, digital, wireless, personal communication network—
uses differentially encoded quaternary phase shift keying (DE-
QPSK) RF modulation. A study of Iridium RF exposure on car-
cinogenic potential involved pregnant rats and their offspring
(Fischer 344) from 19th day of gestation [23]. Whole-body,
plane-wave exposure was done in a parallel-plate system at a
power density of 4.3 W/m2 and whole-body average SAR of
0.036 to 0.077 W/kg (0.10 to 0.22 W/kg in the brain). Rats were
exposed for two h/day, seven d/wk until weaning. Thereafter,
female and male offspring were exposed, individually and head-
first, to near-field radiation for two h/day, five d/wk in a carousel
system for two years. In this case, SARs in the brain were either
0.16 or 1.6 W/kg.
The protocol also included cage control and concurrent sham-
exposed animals. The 150 pregnant female rats were assigned to
three groups: 72 RF exposures, 36 sham controls, and 42 cage
8 IEEE JOURNAL OF ELECTROMAGNETICS, RF, AND MICROWAVES IN MEDICINE AND BIOLOGY, VOL. 1, NO. 1, JUNE 2017
controls. Each female rat was singly accommodated, or with
their pups in the same cage throughout the plane-wave expo-
sure phase until weaning. During near-field exposure, rats of
the same sex from the same exposure group were accommo-
dated three per cage. Pups (700) were assigned to four sets
comprised of three groups each of 90 males and 90 females
for 0.16 W/kg, 1.6 W/kg, and sham, respectively, as well as
80 males and 80 females as cage controls. Litter size, weaning
mass, survival rate, and histopathological evidence of cancer did
not indicate any statistically significant results among any of the
groups. While end-of-experiment survival rates were compara-
ble among male groups, a significantly reduced survival rate and
time were seen in females of the cage-control group. It is worthy
of note that reporting of histopathological data was inconsistent.
Specifically, brain cancer incidence in cage controls was not pro-
vided. Instead, observed brain cancer incidence was reported to
be similar to those of historical control incidence for Fischer
344 rats.
Wistar Rats
There were two reported studies on carcinogenic and co-
carcinogenic potentials of cell phone RF radiation using Wistar
rats as subjects.
GSM-900 MHz: The potent bacterial mutagen, 3-chloro-4-
(dichloromethyl)-5-hydroxy-2(5H)-furanone (MX) is a multi-
site carcinogen in Wistar rats. The first one investigated co-
carcinogenesis induced by MX in drinking water (average daily
dose of 1.7 mg MX/kg body mass). Rats were exposed, unre-
strained, in individual cages installed in a radial transmission
line system [24]. They were free to move about inside the cages
and food was always available. Water bottle was taken away
during RF exposure to GSM-modulated 900 MHz radiation at
whole-body SARs of 0.0 (sham), 0.3, and 0.9 W/kg. Female
Wistar rats, which were seven weeks old at the beginning of the
experiment, were assigned to 4 groups of 72 animals: three MX
groups and a cage-control group. MX rats were exposed two
h/day, five d/wk for two years. There were no statistically sig-
nificant differences in mortality. Histopathological results did
not indicate any GSM exposure-related changes in incidence or
type of cancer in MX-exposed rats.
GSM-902 and DCS-1747 MHz: The carcinogenic potential
in rats exposed to GSM at 902 MHz and DCS at 1747 MHz
was the subject of two double-blinding studies [25]. RF expo-
sure was accomplished using the waveguide wheel—an array of
waveguides excited in the center via a circularly-polarized loop
antenna. In addition to cage and sham controls, 500, seven-
week-old Wistar rats (five groups of 50 females and 50 males
per group) were exposed for two h/day, five d/wk for up to
two years at whole-body SARs of 0.44, 1.33, and 4.0 W/kg,
respectively, for each radiation type.
Besides average SARs, the report gave spatial peak and
organ-specific SARs. Specifically, the brain-averaged SAR was
1.5 W/kg for GSM-902 compared to 7.6 W/kg for DCS. It
clearly demonstrated differences in frequency-dependent distri-
bution of RF absorptions. Moreover, this investigation reported
SAR averaged over the entire exposure period. While 4 W/kg
was attained for DCS, SAR had to be reduced for GSM because
growth rate in body mass was greater than expected so that the
power of RF sources was inadequate to support 4 W/kg. The
whole-body SAR for GSM averaged over the entire exposure
period was 3.7 W/kg.
This research did not report any statistically significant RF-
associated findings in the incidence, latency, multiplicity, or type
of any primary cancers in combined female and male rats. Note
that cancer incidence in females was higher than in males, with
the highest occurring in sham control females both for GSM-
902 and DCS-1474. Also, histopathology was not performed
for cage-control rats. There were several statistically signifi-
cant macroscopic findings. For example, the number of liver
foci in 1.33 W/kg GSM males and skin nodules in 0.44 W/kg
DCS males were significantly higher, but for 1.33 and 4.0 W/kg
GSM males, the number of foci in lachrymal glands was lower.
However, authors of the report regarded these as isolated, trivial
observations unrelated to RF radiation [25].
Sprague-Dawley (SD) Rats
The carcinogenic and co-carcinogenic potentials of RF radi-
ation, especially with regard to CNS and breast cancers, were
investigated using SD rats.
PRF/FM-860 MHz: In a reported study [26], Motorola Inte-
grated Radio Service (MiRS) sources were used to energize a
carousal system and expose SD rats to FM (CWRF) or pulsed
RF (PRF) 860 MHz radiation. Rats were placed into 15 groups
of 60 rats (30 females and 30 males). Each RF exposure group
was matched to a sham-exposure group. Rats were held in iden-
tical compartments during exposure (at average brain SAR of
1.0 W/kg for six h/day, five d/wk from two months to two years
of age). Some groups were treated with a 0, 2.5, or 10 mg/kg
dose of ENU (i.v.) for brain cancer induction. In general, PRF or
CWRF exposure did not initiate cancer in SD rats. There was no
sign of RF promotion of brain or neural cancers. Also, there was
no statistically noteworthy upsurge in size, site, incidence rate,
histological type of brain cancer, or mortality. However, authors
indicated there was a higher incidence trend for the high ENU
dose group, when exposed to PRF, to form fatal brain cancers.
GSM-900 MHz: To explore an animal model for hu-
man breast cancer development from RF radiation, 7,12-
dimethylbenz[α]anthracene (DMBA)-initiated breast cancers in
female SD rats were tested in four co-carcinogenic studies. In
one investigation, three experiments were replicated twice by
starting the two subsequent experiments on the same day of
the two following years using female SD rats under the same
conditions [27]. Rats (120 plus 60 sham, 51-day-old, 150 g
SD) were administered a 50 mg/kg dose of DMBA in each
experiment. Plane-wave exposure chambers with circularly po-
larized 900 MHz GSM radiation produced a power density of
100 μW/cm2 at the bottom of rat exposure cages. Exposure was
continuous, except for brief cleaning periods, until all rats had
developed breast cancers. Rats were free to move about within
the cage. The beginning whole-body SAR was between 0.033
and 0.13 W/kg. For an adult female 300-g SD rat, the SAR
was 0.017–0.070 W/kg but declined continuously, due to body-
resonant RF absorption, during the experiment. It was found
that the latency for induction of breast cancers was consider-
ably longer for RF rats compared to sham controls (278 vs. 145
median days) in the first experiment. However, this disparity
LIN: CANCER OCCURRENCES IN LABORATORY RATS FROM EXPOSURE TO RF AND MICROWAVE RADIATION
was not revealed in two subsequent experiments. In general,
the combined results of all three experiments were that low
power GSM-900 RF radiation had very little impact on latency
to cancer onset, and the cumulative DMBA-initiated breast can-
cer incidence was unchanged. Thus, GSM-900 radiation did not
reveal a promotional ability on DMBA-initiated breast cancers
in SD rats.
Another study on the promotional significance of exposure
to GSM-900 radiation over a wide range of SARs on DMBA-
initiated cancers in SD rats was comprised of two separate exper-
iments [28]. Breast cancers were initiated in 55-day-old female
SD rats by ingesting a 10-mg dose of DMBA. Plane-wave RF
exposure began 10 days later for nine months on a schedule of
two h/day, five d/wk. Rats (128 in 8 groups of 16) were exposed
with the electric-field vector parallel to the long body axis at
SARs of 0.0 (sham), 0.1, 0.7, 1.4, 2.2, and 3.5 W/kg. There
were two 1.4 W/kg groups of rats, in which the exposures were
separated in time by one month. A group of eight rats served
as cage controls (not included in data analysis). Overall, study
results showed no significant disparities in cancer mass, latency,
or multiplicity among the groups. For cancer incidence, results
were erratic compared to sham exposure. A reduction incidence
trend of DMBA-initiated breast cancer was suggested for GSM-
900 rats at 1.4 W/kg or lower. It is noteworthy that the number
of rats per group (16 and 128 total) is relatively small for this
type of study.
There is one more study that examined the promotional capac-
ity of GSM-900 MHz radiation in SD rats. It used an “exposure
wheel” system comprised of a circular array of 17 sector waveg-
uides with a loop antenna at the center to launch RF radiation
[29]. In an effort to even RF exposure, the position of each rat
was rotated weekly by one position on the wheel throughout
the 26-week exposure experiment. Five hundred SD rats were
assigned to five groups: 0.0 (sham), 0.44, 1.33, and 4.0 W/kg,
respectively, and cage controls. The 26-week, GSM-900 RF ex-
posure began one day after DMBA injection (35 mg/kg) for
four h/day and five d/wk. Each rat was examined weekly for the
presence of breast cancers. In general, a significant variation in
breast cancer incidence, latency, mass, or multiplicity was ab-
sent between GSM 900- and sham-exposed SD rats. However, a
significant difference was found in benign mammary tumors and
body mass between all exposure groups and cage-control rats. In
fact, they were considerably lower than cage-control rats. Also,
the latency to benign mammary tumor onset was significantly
longer in the exposure groups than the cage-control group. It is
noteworthy that for cage-control rats, food and water were avail-
able ad libitum throughout the 26-week experiment. In contrast,
exposure rats (including sham) were deprived of food and water
during exposure (4.5–5.0 h per exposure day). It is well-known
that chronic food deprivation restrains mammary tumor growth
in rats. Changes detected in DMBA-initiated mammary tumors
in female experimental SD rats are probably related to dietary
deprivation.
The same “exposure wheel” system used in the above-
mentioned study [29] supported the protocol of a rare, parallel
investigation of DMBA-initiated breast cancers in female SD
rats [30]. Basically, results showed that cage-control rats had
9
significantly more malignant breast cancers and benign tumors
compared to exposure groups—likely for the same reasons
as already mentioned. However, among the exposure groups,
there were several noteworthy differences—although they did
not yield a clear dose-response outcome. In theory, differences
between sham-exposed and RF-exposed rats may be interpreted
as indicative of an RF exposure response. Nevertheless, authors
had opined that the differences were incidental because of high
data variability.
GSM AND CDMA-900 MHz: Recently, a U.S. government
project reported finding two rare kinds of cancers in SD rats ex-
posed to RF radiation: malignant gliomas and cardiac schwan-
nomas [3]. The study was the biggest and most complicated
animal study carried out by NTP, which is a part of the Na-
tional Institutes of Health (NIH). While the paper has yet to
be published in a peer-reviewed scientific journal, results were
reviewed by experts from NTP and NIH.
The study involved lifelong (two-year) whole-body exposures
in “multimode reverberation chamber” furnished with mode
stirrers and shims to help produce more even distribution of
RF radiation throughout the inner space of cavity. GSM and
CDMA 900 MHz power sources were used to produce the RF
radiation. The whole-body SARs were set at 1.5, 3, or 6 W/kg.
The RF exposure field in reverberation chambers were tuned to
accommodate growth in body mass to maintain preset SARs.
Body temperature in exposed rats was kept below 1 °C.
RF exposures began in utero with pregnant dams and contin-
ued throughout gestation. Following birth, dams and pups were
exposed and housed in the same cage until weaning. Dams were
then removed and RF exposure of 90 pups per sex per group
persisted for up to 106 weeks. Daily exposures were performed
seven d/wk for approximately 18 h with 10-min on and off for
a cumulative exposure duration of nine h/day. Single, common,
sham control groups of each sex were housed in identical re-
verberation chambers without RF radiation. The environmental
conditions in exposure chambers were similarly regulated in-
cluding a 12-h light/dark cycle.
The specific results were two rare types of cancers—
malignant gliomas and cardiac schwannomas in male SD rats
exposed to GSM and CDMA 900 radiation. It is noteworthy
that while historical control incidences in NTP studies were
provided in this report, this study did not include cage-control
rats. NTP historical controls may or may not be identical to
cancer incidences for local laboratory cage-control rats.
The report suggested a significant positive SAR-dependent
trend in the incidence rate of malignant gliomas in the brain
(p < 0.05) for CDMA RF radiation (see Table II). Statistically,
there was no noteworthy difference among exposed male rats of
the RF groups. A low incidence (2%) of malignant gliomas was
reported in exposed males, but no malignant gliomas were seen
in controls. Moreover, historical incidence for control SD rats
in all NTP studies is also 2.0%. Malignant gliomas were found
in three RF-exposed female rats (0.55%); none were observed
in any female controls. At NTP, historical incidence for control
females is 0.18%.
For both GSM- and CDMA RF radiation, schwannomas of the
heart were observed in male SD rats of all exposure groups (4%);
10 IEEE JOURNAL OF ELECTROMAGNETICS, RF, AND MICROWAVES IN MEDICINE AND BIOLOGY, VOL. 1, NO. 1, JUNE 2017

TABLE II What follows will be separate discussions of co-

INCIDENCE RATES OF GLIOMAS IN SD RATS EXPOSED TO GSM OR CDMA RF
RADIATION (DATA FROM [3])
carcinogenesis and carcinogenesis in the two-year or lifelong rat
studies. In general, these studies did not yield unambiguous indi-
cations of a rise in the promotion of brain, breast, or CNS cancer,
Female
or RF-induced primary cancer over those of sham-exposed rats.
Modul. Scheme Control GSM CDMA

Number of Rats 90 90 90 90 90 90 90
A. Cancer Promotion or Co-Carcinogenic Investigations
SAR (W/kg) 0.0 1.5 3.0 6.0 1.5 3.0 6.0 Among the promotional cancer studies involving co-
Glioma, 0 0 0 1 2 (2.2%) 0 0
Number (%) (1.1%) carcinogens, six did not show any statistically significant obser-
Male vation, while two studies reported different findings in female
SD rats (see Table IV).
Modul. Scheme Control GSM CDMA
Among Fischer 344 rat studies, four involved promotion of
Number of Rats 90 90 90 90 90 90 90
SAR (W/kg) 0 1.5 3.0 6.0 1.5 3.0 6.0
ENU-induced cancer. RF carrier frequencies ranged from 836
Gliomas, 0 3 3 (3.3%) 2 0 0 3 (3.3%) to 1950 MHz with different modulations. Nevertheless, none
Number (%) (3.3%) (2.2%) showed increase in ENU-initiated brain cancer promotion. It
should be noted that restraining rats in the carousel system likely
TABLE III have presented a stress factor, complicating result evaluations.
INCIDENCE RATE OF SCHWANNOMAS IN SD RATS EXPOSED TO GSM OR A solitary promotional study, in which unrestrained, MX
CDMA MODULATED RF RADIATION (DATA FROM [3])
mutagen-treated Wistar rats were exposed to GSM-900 plane
waves, also provided null results with regard to any cancer type
Female [24].
Modul. Scheme Control GSM CDMA The DMBA breast cancer model in female SD rats formed the
basis for four studies employing GSM-900 radiation (Table IV).
Number of Rats 90 90 90 90 90 90 90 The Bartsch et al. investigation [27] was a self-replicated study
SAR (W/kg) 0.0 1.5 3.0 6.0 1.5 3.0 6.0
Schwannoma, 0 0 2(2.2%) 0 2(2.2%) 0 2(2.2%) using unrestrained rats. It found no statistically significant dif-
Number (%) ference between sham and exposed rats. Note that this study did
Male not include cage controls.
Number of Rats 90 90 90 90 90 90 90
However, a parallel set of investigations using GSM-900 ra-
SAR (W/kg) 0 1.5 3.0 6.0 1.5 3.0 6.0 diation and matching “waveguide-wheel” systems to provide
Schwannoma, 0 2 1 (1.1%) 5 2 (2.2%) 3 6 (6.6%) SARs showed very different results for breast cancer incidence
Number (%) (2.2%) (5.5%) (3.3%)
[29], [30]. While one showed little difference between sham-
and RF-exposed rats, benign tumors in cage controls were con-
siderably higher [29]. The onset latency to breast cancer in cage
none were observed in control animals (see Table III). There was controls was also appreciably shorter than in exposed rats. This
also a significant trend in SAR dependency for schwannomas difference could be associated with food deprivation imposed on
(p < 0.05). Furthermore, schwannomas in the 6-W/kg male rats exposed rats. Moreover, cage-control rats in the other study had
were considerably higher in CDMA-exposed rats. the highest incidence [30]. There were several substantial vari-
The response of Schwann cells to GSM- and CDMA RF ances among different exposure groups. While this may point
radiation seems to be identified with the heart tissue of male to an effect of RF exposure, the findings did not produce a
SD rats. The study did not find any RF-related observations on clear dose-response correlation, rendering it tenuous in arriving
incidence rate of schwannomas in the heart or combined with at a firm decision. Moreover, the DMBA breast cancer model
other tissue sites in female SD rats. is susceptible to varying results, especially if DMBA dose and
delivery are different.
VII. DISCUSSION AND CONCLUSION
The carcinogenic and co-carcinogenic research assessed in- B. Carcinogenic or Cancer Induction Investigations
cludes 18 reports of rats exposed to RF radiation from a diverse As summarized in Table V, there are seven carcinogenic or
set of mobile telecommunication systems. The studies involved spontaneous cancer induction investigations of rats exposed life-
three different strains of rats as biological subjects: SD, Wistar, long to RF radiation. Sources ranged in frequency from 836 to
and Fischer 344. Most studies had rats restrained in holders and 2450 MHz and had involved common wireless communication
underwent either near-field or plane-wave equivalent exposure schemes. The studies included three using Fischer 344, two Wis-
scenarios. Also, most exposures were lifelong or two years in tar, and two SD rats. In sum, three studies showed a carcinogenic
duration, except for two. One exposed Fischer 344 rats following effect, including the most recent report [3], and no effect was
glioma cell implantation using GSM-900 radiation for two to seen in four of the seven carcinogenic effect studies.
three weeks until death [14]. Another was a six-week liver study One ENU project [19] had included a non-ENU group [19].
of Fischer 344 rats subjected to TDMA-900 radiation [20]. Nei- It showed a drop in cancer rate for TDMA 836 MHz radiation.
ther study showed any significant influence from RF radiation. While it may be regarded as suggestive of a cancer “protective”
LIN: CANCER OCCURRENCES IN LABORATORY RATS FROM EXPOSURE TO RF AND MICROWAVE RADIATION 11

TABLE IV
CO-CARCINOGENESIS OR CANCER PROMOTION IN RATS FROM 2-YR RF EXPOSURE

Reference Radio Rat Type Restraint SAR(W/kg) Significant

Frequency Holder (Whole-body/Local tissue) Findings (Results)

[18] 836 MHz TDMA Fischer 344 Yes 0.27–0.72 Whole-body; (0.74-1.6 Brain or CNS (No overall
in brain) difference)
[19] 836 MHz FM Fischer 344 Yes 0.27–0.72 Whole-body; Brain or CNS (No overall
(0.74–1.6 in brain) difference)
[20] 1.44 GHz TDMA Fischer 344 Yes <0.4 Whole-body (0.67 and 2.0 Brain or CNS (No overall
brain ave) difference)
[21] 1.95 GHz W-CDMA Fischer 344 Yes <0.4 Whole-body (0.67 and 2.0 Brain or CNS (No overall
brain ave) difference)
[24] 900 MHz GSM Wistar No 0.3 (0.07–1.2) and 0.9 (0.21–3.6) Cancer type or incidence, No
Whole-body ave effect
[26] 860 MHz FM or MiRS Sprague-Dawley Yes 0.27–0.42 Whole-body ave (1.0 Brain or organs (No difference)
brain ave) Trend in high ENU
[27] 900 MHz GSM CW Sprague-Dawley No 0.017–0.13 Whole-body ave Breast (No difference)
exposure until tumor (low-level)
developed in 150-280
days
[29] 900 MHz GSM Sprague-Dawley Yes 0.44, 1.33, and 4.0 Whole-body Breast (No sham/exposed
ave difference; but higher in cage
control)
[30] 902 MHz GSM Sprague-Dawley Yes 0.44, 1.33, and 4.0 Whole-body Breast (Many differences but no
ave dose response relation)

TABLE V
CARCINOGENESIS OR CANCER INDUCTION IN RATS FROM 2-YR RF EXPOSURE

Reference Radio Rat Type Restraint SAR (W/kg) Significant

Frequency Holder (Whole- body/Local tissue) Finding (Results)

[18] 836 MHz TDMA Fischer 344 Yes 0.27–0.72 Whole-body; Brain or CNS (Cancer Reduction)
(0.74–1.6 in brain)
[22] 836 MHz FM or Fischer 344 Yes 1.3 Brain ave (0.5 and 2.5 Brain or organs (No cancer effect)
848 MHz CDMA, local brain)
[23] 1.62 GHz Iridium Fischer 344 No 0.036 to 0.077 Whole-body Brain or organs (No cancer effect)
(0.16 and 1.6 brain ave)
[25] 902 MHz GSM Wistar Yes 0.44, 1.33, and 4.0 Primary cancers No effect
Whole-body ave
[25] 1747 MHz DCS Wistar Yes 0.44, 1.33, and 4.0 Primary cancers No effect
Whole-body ave
[17] 2,450 MHz Pulsed Sprague-Dawley No 0.15, and 0.4 Whole-body ave Primary cancers
[3], [31] 900 MHz GSM CDMA Sprague-Dawley No 1.5, 3.0, and 6.0 Whole-body Male brain glioma and cardiac
ave schwannoma

effect, this explanation is not as robust as it appears, since cage-
control Fisher 344 rats were not included in this project.
Restrained Wistar rats were chosen as subjects in a car-
cinogenic investigation to study RF cancer induction from the
near field of a GSM-900 waveguide-wheel [25]. The paper
also reported results for DCS at 1747 MHz. Histopathological
examination of cage-control rats was not performed. For GSM
exposures across all groups, reported combined female and
male cancer incidences were similar. However, the macroscopic
results suggested several noteworthy occurrences comparing
sham controls with GSM-exposed rats. Moreover, the study
showed that incidence rate in female rats was higher, with the
highest incidence occurring in sham control females for both
GSM-900 and DCS-1474 exposures.
One of the SD rat studies listed in Table V was actually
completed about 30 years ago, well before the rest of studies
reviewed. It was a study targeting the impact of microwave
exposure on general health in adult rats [16], [17]. Pulsed-
modulated, 2450-MHz microwaves at 0.15–0.4 W/kg of whole-
body SARs were observed to have a reliable rise in number
of primary malignancies at the end of the study. However, the
project did not observe any significant effects on the overall
health of RF-exposed SD rats, and the survival curves were
undistinguishable for microwave and sham SD rats.
The NTP project was planned to confront shortcomings of
prior rodent studies on RF radiation to produce major health
issues such as cancer under controlled conditions. Its objective
was to tender a strategic contribution of scientific information
on a significant human health matter. Findings from this study
revealed heightened hazards of rare cancers, especially gliomas
in the brain and schwannomas of the heart in male SD rats
subjected to lifelong GSM and CDMA RF radiation, but no in-
creased risk was found among female SD rats. To be sure, a new
or single report should not be viewed in isolation, even though
12 IEEE JOURNAL OF ELECTROMAGNETICS, RF, AND MICROWAVES IN MEDICINE AND BIOLOGY, VOL. 1, NO. 1, JUNE 2017
the study was the biggest and most complicated laboratory an-
imal project associated with exposure to RF radiation. These
findings surely augment other published animal cancer studies
on RF radiation.
Of particular note is that gliomas were also reported in hu-
man brains in research on RF exposure from mobile phone use.
Interestingly, schwannomas in rat hearts and acoustic neuromas
in human brains were separately reported for two dissimilar
mammalian organ sites. Conceivably, a link could exist since
Schwann cells surround nerve tissues along the auditory path-
ways and in the heart.
In summary, combining all co-carcinogenic and carcinogenic
investigations in laboratory rats exposed to two-year RF radia-
tion, there are 10 reported studies showing a noteworthy variance
in incidence rates of cancer between RF-exposed and sham-
exposed rats. Clearly, there are more reported studies showing
no carcinogenic effect than showing effect, regardless of their
study merit, design, experimental quality, or flaws, shortcom-
ings, limitations, or methodological weakness. Moreover, few
studies were designed or performed as an extant, independent
replication or confirmation. Most of them are one-of-a-kind
investigations—a paltry four projects were planned as confir-
mation or replication studies.
Research findings and/or reporting of findings have been in-
consistent and fraught with omissions in some cases. Thus, it is
difficult to come to a complete or unequivocal decision. It is a
notable flaw that many projects did not involve cage-control rats
as part of the project or the data were not incorporated in the
statistical analyses. Moreover, restraining rats in holders during
prolonged exposure to RF radiation may contribute to enhanced
stress in restrained rats. The stress factor confounds understand-
ing of reported results, since stress is linked to cancer initiation
in rodents.
The effect of RF exposure on carcinogenesis thus remains
tentative. The inconsistencies continue to pose uncertainty
to calculations of risks to public health from exposure to RF
radiation. The question of whether RF exposure from wireless
and mobile devices and systems pose a health risk would
likely remain equivocal and controversial for some time to
come.
REFERENCES
[1] R. Baan et al., “WHO international agency for research on cancer mono-
graph working group. Carcinogenicity of radiofrequency electromagnetic
fields,” Lancet Oncol. vol. 12, 624–626, 2011.
[2] IARC Working Group on the Evaluation of Carcinogenic Risks to Humans,
“Non-ionizing radiation, Part 2: Radiofrequency electromagnetic fields,”
IARC Monographs Eval. Carcinogenic Risks Humans, vol. 102, no. pt. 2,
pp. 1–460, 2013.
[3] M. Wyde et al., “Report of partial findings from the national toxicology
program carcinogenesis studies of cell phone radiofrequency radiation in
Hsd: Sprague Dawley SD rats (whole body exposure),” bioRxiv, May 26,
2016, [Online]. Available: http://dx.doi.org/10.1101/055699
[4] International Commission on Non-Ionizing Radiation Protection (IC-
NIRP), “Guidelines for limiting exposure to time-varying electric, mag-
netic, and electromagnetic fields (up to 300 GHz),” Health Phys., vol. 74,
pp. 494–522, 1998.
[5] Standard For Safety Levels With Respect To Human Exposure To Radio
Frequency Electromagnetic Fields, 3 kHz to 300 GHz. IEEE Std. C95.1-
2005, 2005.
[6] J. C. Lin et al., “ICNIRP statement on EMF-emitting new technologies,”
Health Phys. vol. 94, pp. 376–392, 2008.
[7] E. Cardis and the Interphone Study Group, “Brain tumour risk in relation
to mobile telephone use: Results of the INTERPHONE international case-
control study,” Int. J. Epidemiol., vol. 39, no. 3, pp. 675–694, 2010.
[8] E. Cardis and the Interphone Study Group, “Acoustic neuroma risk in rela-
tion to mobile telephone use: Results of the INTERPHONE international
case-control study,” Cancer Epidemiol., vol. 35, no. 5, pp. 453–464, 2011.
[9] L. Hardell, M. Carlberg, and K. Mild-Hansson, “Pooled analysis of case-
control studies on malignant brain tumours and the use of mobile and
cordless phones including living and deceased subjects,” Int. J. Oncol.,
vol. 38, no. 5, pp. 1465–1474, 2011.
[10] Y. Sato, S. Akiba, O. Kubo, and N. Yamaguchi, “A case-case study of
mobile phone use and acoustic neuroma risk in Japan,” Bioelectromagn.,
vol. 32, no. 2, pp. 85–93, 2011.
[11] CBTRUS, “Central brain tumor registry of the U.S. incidence rates
and estimated new cases,” Central Brain Tumor Registry of the United
States, Hinsdale, IL, USA. [Online]. Available: http://www.cbtrus.
org/factsheet/factsheet.html. Accessed on: Jan. 27, 2017.
[12] SEER, “Cancer stat facts: Brain and other nervous system cancer,”
[Online]. Available: https://seer.cancer.gov/statfacts/html/brain.html.
Accessed on: Jan. 27, 2017.
[13] U.S. Census, “The total U.S. populations,” U.S. Census, Washington, DC,
USA. [Online]. Available: http://www.census.gov/popclock/. Accessed:
Jan. 27, 2017.
[14] L. G. Salford, A. Brun, B. R. R. Persson, and J. L. Eberhardt, “Experimen-
tal studies of brain tumour development during exposure to continuous and
pulsed 915 MHz radiofrequency radiation,” Bioeletrochem. Bioenergetics,
vol. 30, pp. 313–318, 1993.
[15] K. Imaida et al., “Lack of promotion of 7,12-dimethylbenz[a]anthracene-
initiated mouse skin carcinogenesis by 1.5 GHz electromagnetic near
fields,” Carcinogenesis vol. 22, no. 11, pp. 1837–1841, 2001.
[16] L. L. Kunz, R. B. Johnson, D. Thompson, J. Crowley, C-K Chou, and A. W.
Guy,, “Effects of long-term low-level radiofrequency radiation exposure
on rats. Vol 8: Evaluation of longevity, cause of death, and histopatholog-
ical findings,” US Air Force Sch. Aerospace Medicine, Brooks Air Force
Base, TX, USA, Rep. ASAFSAM-TR-85-11, 1985.
[17] C. K. Chou, A. W. Guy, L. L. Kunz, R. B. Johnson, J. J. Crowley, and J.
H. Krupp. “Long term, low-level microwave irradiation of rats,” Bioelec-
tromagn., vol. 13, pp. 469–496, 1992.
[18] W. R. Adey et al., “Spontaneous and nitrosourea-induced primary tumors
of the central nervous system in Fischer 344 rats chronically exposed to
836 MHz modulated microwaves,” Radiat. Res., vol. 152, pp. 293–302,
1999.
[19] W. R. Adey et al., “Spontaneous and nitrosourea-induced primary tumors
of the central nervous system in Fischer 344 rats exposed to frequency-
modulated microwave fields,” Cancer Res., vol. 60, pp. 1857–1863, 2000.
[20] T. Shirai et al., “Chronic exposure to a 1.439 GHz electromagnetic field
used for cellular phones does not promote N-ethylnitrosourea induced
central nervous system tumors in F344 rats,” Bioelectromagn., vol. 26, pp.
59–68, 2005.
[21] T. Shirai et al., “Lack of promoting effects of chronic exposure to 1.95-
GHz W-CDMA signals for IMT-2000 cellular system on development of
N-ethylnitrosourea-induced central nervous system tumors in F344 rats,”
Bioelectromagn., vol. 28, no. 7, pp. 562–572, 2007.
[22] M. La Regina, E. G. Moros, W. F. Pickard, W. L. Straube, J. Baty, and J.
L. Roti Roti, “The effect of chronic exposure to 835.62 MHz FDMA or
847.74 MHz CDMA radiofrequency radiation on the incidence of spon-
taneous tumors in rats,” Radiat. Res. vol. 160, no. 2, pp. 143–151, 2003.
[23] L.E. Anderson, D. M. Sheen, B. W. Wilson, S. L. Grumbein, J. A. Creim,
and L. B. Sasser, “Two-year chronic bioassay study of rats exposed to a 1.6
GHz radiofrequency signal,” Radiat. Res., vol. 162, no. 2, pp. 201–210,
2004.
[24] P. Heikkinen et al., “No effects of radiofrequency radiation on 3-chloro-
4-(dichloromethyl)-5-hydroxy-2(5H)-furanone-induced tumorigenesis in
female Wistar rats,” Radiat. Res., vol. 166, no. 2, pp. 397–408, 2006.
(Erratum in: Radiat. Res., vol. 167, no. 1, pp. 124–125, 2007).
[25] P. Smith, N. Kuster, S. Ebert, and H. J. Chevalier, “GSM and DCS wireless
communication signals: combined chronic toxicity/carcinogenicity study
in the Wistar rat,” Radiat. Res., vol. 168, no. 4, pp. 480–492, 2007.
[26] B. C. Zook, and S. J. Simmens, “The effects of 860 MHz radiofrequency
radiation on the induction or promotion of brain tumors and other neo-
plasms in rats,” Radiat. Res. vol. 155, no. 4, pp. 572–583, 2001.
[27] H. Bartsch et al., “Chronic exposure to a GSM-like signal (mobile phone)
does not stimulate the development of DMBA-induced mammary tumors
in rats: Results of three consecutive studies,” Radiat. Res., vol. 157, no. 2,
pp. 183–190, 2002.
LIN: CANCER OCCURRENCES IN LABORATORY RATS FROM EXPOSURE TO RF AND MICROWAVE RADIATION
[28] R. Anane, P. E. Dulou, M. Taxile, M. Geffard, F. L. Crespeau, and
B. Veyret, “Effects of GSM-900 microwaves on DMBA-induced mam-
mary gland tumors in female Sprague-Dawley rats,” Radiat. Res. vol. 160,
no. 4, pp. 492–497, 2003.
[29] D. Yu, Y. Shen, N. Kuster, Y. Fu, and H. Chiang, “Effects of 900 MHz GSM
wireless communication signals on DMBA-induced mammary tumors in
rats,” Radiat. Res. vol. 165, no. 2, pp. 174–180, 2006.
[30] R. Hruby, G. Neubauer, N. Kuster, and M. Frauscher, “Study on potential
effects of “902-MHz GSM-type Wireless Communication Signals” on
DMBA-induced mammary tumours in Sprague-Dawley rats,” Mutation
Res., vol. 649, no. 1/2, pp. 34–44, 2008.
[31] J. C. Lin, “Changing the conversation on cell phone RF radiation car-
cinogenesis,” IEEE Microw. Mag., vol. 17, no. 10, pp. 21–23, Oct. 2016.
(Comment: vol. 18, no. 1, p. 138, 2017).
[32] J. C. Lin, “The NTP cell phone radio frequency radiation health effects
project,” IEEE Microw. Mag., vol. 18, no. 1, pp. 15–17, Jan./Feb. 2017.
[33] J. C. Lin, “Carcinogenic effect of wireless communication radiation in
rodents,” Advances in Electromagnetic Fields in Living Systems, vol. 5,
New York, NY, USA: Springer, pp. 35–82, 2009.
13
James C. Lin (S’65–M’67–SM’77–F’86– LF’07)
received B.S., M.S., and Ph.D. degrees in electri-
cal engineering from the University of Washington,
Seattle, WA, USA.
He is currently a Professor Emeritus at the Univer-
sity of Illinois at Chicago, Chicago, IL, USA, where
he was the Head of the Bioengineering Department,
the Director of the Robotics and Automation Lab-
oratory, and the Director of Special Projects in the
College of Engineering. He has authored or edited
13 books, authored 380+ book chapters and articles
in journals and magazines, and has made 280+ conference presentations. In ad-
dition to fundamental scientific contributions to electromagnetics in biology and
medicine, he has pioneered several medical applications of RF and microwave
energies, including invention of minimally invasive microwave ablation treat-
ment for cardiac arrhythmia, noncontact and noninvasive microwave sensing of
physiological signatures and vital signs, and microwave thermoacoustic (ther-
moelastic) tomography and imaging.
Prof. Lin is a Fellow of AAAS, AIMBE, and URSI. He held an NSC Research
Chair from 1993 to 1997 and was an IEEE-EMBS Distinguished Lecturer. He
received the d’Arsonval Medal from the Bioelectromagnetics Society, IEEE
EMC Transactions Prize Paper Award, IEEE COMAR Recognition Award, and
CAPAMA Outstanding Leadership and Service Awards. He was a member of
the U.S. President’s Committee for National Medal of Science (1992–1993).
He has served in leadership positions of several scientific and professional or-
ganizations, including President of the Bioelectromagnetics Society, Chairman
of the International Scientific Radio Union Commission on Electromagnet-
ics in Biology and Medicine, Chairman of the IEEE Committee on Man and
Radiation, Vice President of the U.S. National Council on Radiation Protec-
tion and Measurements, and a member of the International Commission on
Nonionizing Radiation Protection. He also served on numerous advisory com-
mittees and panels for the U.S. Congress, Office of the U.S. President, National
Academy of Sciences, National Research Council, National Science Founda-
tion, National Institutes of Health, Marconi Foundation, and the World Health
Organization. He has chaired several international conferences, including IEEE,
BEMS, URSI, and ICST (founding chairman of Wireless Mobile Communica-
tion and Healthcare—MobiHealth). Since 2006, he has been the Editor-in-Chief
of the Bioelectromagnetics journal and has served as Guest Editor and Member
of editorial boards of several journals. He is a member of Sigma Xi, Phi Tau
Phi, Tau Beta Pi, and Golden Key honorary societies. He was listed in American
Men and Women of Science, Who’s Who in America, Who’s Who in Engineering,
Who’s Who in the World, and Men of Achievement, among others.