Over 80 million Americans currently use wireless communications devices (e.g., cellular
phones) with about 25 thousand new users daily. This translates into a potentially
significant public health problem should the use of these devices even slightly increase
the risk of adverse health effects. Currently cellular phones and other wireless
communication devices are required to meet the radio frequency radiation (RFR)
exposure guidelines of the Federal Communications Commission (FCC), which were
most recently revised in August 1996. The existing exposure guidelines are based on
protection from acute injury from thermal effects of RFR exposure, and may not be
protective against any non-thermal effects of chronic exposures. Animal exposure
research reported in the literature suggests that low level exposures may increase the risk
of cancer by mechanisms yet to be elucidated, but the data is conflicting and most of this
research was not conducted with actual cellular phone radiation. In one study transgenic
mice exposed to a digital phone signal developed more than twice as many non-lymphoblastic
lymphomas as the unexposed control group, a statistically significant
increase. These results suggest a potential carcinogenic effect from the digital phone
signal using this animal model. There is wide agreement within the international
scientific community regarding the types of research needed to assess whether RFR from
wireless communications poses a health risk to users. Research needs have been
articulated by a number of groups, including the European Commission and the World
Health Organization International EMF Project. Animal experiments are crucial because
meaningful data will not be available from epidemiological studies for many years due to
the long latency period between exposure to a carcinogen and the diagnosis of a tumor.
Studies must also be performed in animals that are genetically predisposed to cancer and
endpoints other than cancer, such as ocular damage and neurological effects, must also be
examined. High priority must be given to replication of prior studies that indicate
adverse effects, such as the transgenic mice model mentioned above. There is currently
insufficient scientific basis for concluding either that wireless communication
technologies are safe or that they pose a risk to millions of users. A significant research
effort, involving large well-planned animal experiments is needed to provide the basis to
assess the risk to human health of wireless communications devices.
A. Summary of Biological Effects - Wireless Telephone Radiation
As noted above, the use of wireless communications devices (e.g., cellular phones) is
increasing rapidly. FDA concluded over five years ago that little was known about the
possible health effects of repeated or long-term exposure to low levels of RFR of the
types emitted by such devices. However, some scientific articles suggest a potential
cancer risk may exist. While some other studies did not find evidence of carcinogenicity
for RFR, data from long-term animal studies with a multi-dose exposure paradigm are
unavailable. Properly conducted scientific research is needed to address these issues and
fill in the gaps in our understanding of the biological effects of exposure to RFR.
B. Physical Properties of Wireless Telephone Radiation
Personal (cellular) telecommunications is a rapidly evolving technology that uses
microwave radiation to communicate between a fixed base station and a mobile user.
Presently, most systems employ analog technology, where the low frequency speech
signals are directly modulated on to a high frequency carrier in a manner similar to a
frequency-modulated (FM) radio. The power level is effectively constant during the
modulation, although some power control may occur. However, the recently introduced
second-generation systems in Europe, USA and Japan employ digital technology, where
the low frequency speech is digitally coded prior to modulation. There is a strong trend
towards hand-held cellular telephones, which means that the radiating antenna is close to
the head of the user. In the relatively near future the use of digital systems will
The electric and magnetic fields surrounding a cellular telephone handset near a person's
head are complicated functions of the design and operating characteristics of the handset
and its antenna and the electric and magnetic fields vary considerably from point to point.
Microwave radiation absorption occurs at the molecular, cellular, tissue and whole-body
levels. The dominant factor for net energy absorption by an entire organism is related to
the dielectric properties of bulk water, which ultimately causes transduction of
electromagnetic energy into heat. For laboratory experiments, exposure conditions can
be classified as thermal or non-thermal. There are no strict boundaries for these different
exposure regimens because a number of factors may influence the characteristics of
exposure. Thermal effects are well established and form the biological basis for
restricting exposure to RF fields. In contrast, non-thermal effects are not well established
and, currently, do not form a scientifically acceptable basis for restricting human
exposure to microwave radiation at those frequencies used by hand-held cellular
telephones. A large number of biological effects have been reported in cell cultures and
in animals, often in response to exposure to relatively low-level fields, which are not well
established but which may have health implications and are, hence, the subject of on-going
research. It is not scientifically possible to guarantee those non-thermal levels of
microwave radiation, which do not cause deleterious effects for relatively short
exposures, will not cause long-term adverse health effects.
C. Human Exposure
For the purpose of radiation protection, dosimetric quantities are needed to estimate the
absorbed energy and its distribution inside the body. A dosimetric quantity that is widely
adopted for microwaves is the Specific Absorption Rate (SAR). SAR is defined as the
time derivative of the incremental energy, absorbed by or dissipated in an incremental
mass contained in a volume element of a given density. SAR is expressed in the unit watt
per kilogram (W kg
). Numerical calculations, based upon coupling from handsets to an
anatomically realistic numerical phantom of the head have been performed. Such
calculations have shown that, during normal operation, a radiated power of 1 W gives rise
to a maximum SAR of 2.1 W kg
at 900 MHz and 3.0 W kg
at 1.8 GHz averaged over
any 10 g of tissue. Typical handset powers are 0.6 W. To enable communication with
locations not easily reachable with land networks, satellite communication systems have
been recently designed and implemented. New systems will involve small portable units
and hand-held sets similar to current cellular telephones. In these special cases, higher
power classes can be envisioned.
Digital cellular telephones transmit information in bursts of power. The power is turned
on and off, and the equipment transmits for a fraction of the time only and then is silent
for the remaining part of the burst period. The basic repetition frequency is 217 Hz for
GSM and DCS 1800 systems and 100 Hz for DECT; however, the spectrum also contains
a number of higher harmonics due to the narrow pulse, so there are also frequencies in
the kilohertz region. Owing to the complexity of these communications systems, there
are also 2 and 8 Hz components in the signal, apart from multiples of 100 and 217 Hz.
D. Regulatory Status
As described previously, when tissues are exposed to microwave fields strong enough to
raise the temperature, the resulting biological effects are said to be thermal. There is
currently a general consensus in the scientific and standards community that the most
significant parameter, in terms of biologically relevant effects of human exposure to RF
electromagnetic fields, is the SAR in tissue. SAR values are of key importance when
validating possible health hazards and in setting standards.
Possible thermal effects in the eye are also important. The latter is regarded as
potentially sensitive to heating because of the limited cooling ability of the lens caused by
the lack of a blood supply and the tendency to accumulate damage and cellular debris.
Effects of electromagnetic radiation on the three major eye components essential for
vision, the cornea, lens and retina, have been investigated, the largest number of studies
being concerned with cataracts. It has been established that lens opacities can form after
exposure to microwave radiation above 800 MHz; however, below about 10 GHz cataract
induction requires long exposures at an incident power density exceeding 10
SARs in the lens large enough to produce temperatures in the lens greater than 41
required. Effects on the retina have been associated with levels of microwave radiation
above 500 Wm
. All these data suggest that thermal effects will probably only occur in
people subjected to whole body or localized heating sufficient to increase tissue
temperatures by more than 1
C. These various effects are well-established and form the
biological basis for restricting exposure to RF fields. In contrast, non-thermal effects are
not well-established and, currently, do not form a scientifically acceptable basis for
restricting human exposure to microwave radiation at those frequencies used by handheld
cellular telephones and base stations.
The setting of safety limits for human exposure to RF electromagnetic fields is currently
performed in two steps. First, basic limits (or restrictions) for SARs inside the body are
specified from biological considerations in terms of whole-body SAR and SAR averaged
over a small mass of tissue. Then relationships between SAR values and unperturbed
field strengths are used to set derived limits (or reference or investigation levels) for field
strengths and power density to be used in assessing compliance with the adopted
standard. Studies to relate core temperature rise with whole-body averaged SARs (Elder
and Cahill, 1984) suggested that the 1-4 W Kg
range is the threshold at which
significant core temperature rise occurs. Another approach to identify thresholds of
whole body thermal effects is based on the change in animal behavior exposed to RF
fields. A review of animal data indicates a threshold for behavioral responses in the same
1-4 W kg
range. Another review of animal data also concluded that the threshold of RF
exposure in terms of the whole body SAR is 4 W kg
(IEEE, 1991). Based on the
estimated threshold and a safety factor of 10, the whole body averaged SAR of 0.4 W kg
has been widely accepted as the basic restriction for occupational exposures under
controlled environmental conditions (IEEE, 1991). For the general public under
uncontrolled environmental conditions, a five times smaller value of 0.08 W kg
often been adopted as the basic restriction. In order to avoid excessive local exposures,
maximum local SARs are limited as one of the basic restrictions in safety guidelines.
Basic restrictions for partial body exposure are given in terms of maximum local SARS.
Local SAR values change spatially within the body depending on the depth of
penetration, shape of the body part, and tissue homogeneity. It is therefore important to
define the mass of tissue taken to evaluate average local body SARS. The limit values of
local SARs have not been unified between various standards or guidelines. However, a
local SAR limit of 8 W kg
averaged over a mass of 1g has also been adopted (IEEE,
Currently cellular phones and other wireless communication devices are required to meet
the RFR exposure guidelines of the Federal Communications Commission (FCC), which
were most recently revised in August 1996. Since the FCC is not a health agency, it
sought and received guidance from the federal health agencies including the
Environmental Protection Agency, the National Institute of Occupational Health and
Safety, the Occupational Safety and Health Administration, and the FDA. These
exposure guidelines incorporated the most recent exposure standards of the National
Commission for Radiation Protection and the American National Standards Institute, and
are subject to continuing review and revision as new scientific information which could
define a better basis for such exposure guidelines becomes available. As noted above, the
existing exposure guidelines are based entirely on protection from acute injury from
thermal effects of RF exposure, and may not be protective against any non-thermal
effects of chronic exposures.
E. Toxicological Data
The evidence for a clastogenic (chromosome breaking) or genetic effect of microwave
radiation exposure is contradictory and, overall, it may be concluded that RF/microwave
radiation is not genotoxic. Therefore, it may also be concluded that RF/microwave
radiation is not a tumor initiator and that, if it is somehow related to carcinogenicity, this
has to be by some other mechanism (e.g., by influencing tumor promotion). Tumor
promotion may be influenced by increases in cell proliferation rate via effects mediated
through changes in proliferative signaling pathways, leading to enhanced transcription
and DNA synthesis.
According to a series of papers, low level, low frequency, amplitude-modulated
microwave radiation may affect intracellular activities of enzymes involved in neoplastic
promotion without measurable influence on overall DNA synthesis. For example, a
number of investigations showed some evidence of an effect on intracellular levels of
ornithine decarboxylase (ODC) an enzyme implicated in tumor promotion. Tumor
promoters increase ODC synthesis. Where such effects have been observed with
microwave exposure, they have been much weaker and have occurred only for certain
modulations of the carrier wave.
Assays of cell transformation were performed in order to detect changes consistent with
carcinogenesis. For example, Balcer-Kubiczek and Harrison (1991) exposed cells to 120
Hz modulated microwave radiation followed by treatment with a phorbol ester tumor
promoter. Cell transformation was induced in a dose-dependent way (increase with
increasing SAR value). Overall, these results are in agreement with those from earlier
studies, although there are also some inconsistencies. To date, the significance of these
results is not clear in terms of in vivo carcinogenesis.
Along with investigations carried out in vitro, a number of in vivo investigations have
also been performed. Of particular interest is, for example, the study conducted by
Szmigielski et al (1983), who observed faster development of benzo(a)pyrene-induced
skin tumors in mice that were exposed for some months to sub-thermal 2450 MHz
Also of interest is a study where 100 rats were exposed from 2 to 27 months of age to
pulsed microwave radiation (0.4 W kg
) (Guy et al, 1985). The exposed group had a
significant increase in primary malignant lesions compared with the control group when
lesions were pooled regardless of their location in the body, but no single type of
malignant tumor was enhanced. Overall the incidence of primary malignancies was
similar to that reported elsewhere in rats of this type. If the incidence of primary
malignant lesions was pooled without regard to site or cause of death, however, the
exposed group had a significantly higher incidence compared with the control group.
Also, primary malignancies occurred early in the exposed group compared with the sham
exposed group. While interesting, these data do not provide clear evidence of an increase
in tumor incidence as result of microwave exposure. The incidence of benign tumors did
not appear enhanced in the exposed group compared with the controls, nor was any
particular type of neoplasm in the exposed group significantly elevated compared with
the values reported in stock rats of this strain. Yet, overall, there was no clear evidence
of an increase in tumor incidence as a result of exposure to microwave radiation.
In another study, the effects of exposure to electromagnetic fields were investigated in a
rat brain glioma model. The exposure consisted of 915 MHz microwave radiation, both
as continuous wave and ELF-modulated radiation (Salford, et al, 1993). The extensive
daily exposure did not cause tumor promotion. However, the experimental model has
sometimes been questioned as the experimental animals had a high rate of spontaneous
tumors. In another investigation in which cancer cells (B 16 melanoma) were injected
into animals, a lack of effect of exposure to continuous wave and pulsed RFR on tumor
progression was observed (Santini et al, 1988). Overall, evidence for a co-carcinogenic
effect of microwave radiation on tumor progression is not substantiated. The few
positive results which do exist are, however, sufficiently indicative to merit further
Repacholi et al (Repacholi, et al 1997) using Pim-l transgenic mice that are moderately
predisposed to develop lymphoma spontaneously, conducted a more recent study of the
co-carcinogenic potential of RFR. One hundred mice were exposed for two thirty-minute
periods per day for up to 18 months to 900 MHz RFR with modulation characteristics
and SAR similar to those of some wireless telephones. The mice exposed to RFR
developed over twice as many lymphomas as the sham-exposed group of mice. A study
of 50 Hz magnetic fields in these same transgenic mice conducted by the same
investigators (Repacholi et al, 1998) did not result in greater numbers of lymphomas in
the exposed mice, suggesting that the earlier positive result in RFR exposed mice is
unlikely to be artifactual.
There is wide agreement within the international scientific community regarding the
types of research needed to assess whether RFR from wireless communications poses a
health risk to users. Research needs have been articulated by a number of groups,
including the European Commission and the World Health Organization International
EMF Project. Animal experiments are crucial because meaningful data will not be
available from epidemiological studies for many years due to the long latency period
between exposure to a carcinogen and the diagnosis of a tumor. Studies must also be
performed in animals that are genetically predisposed to cancer and endpoints other than
cancer, such as ocular damage and neurological effects, must also be examined. High
priority must be given to replication of prior studies that indicate adverse effects, such as
the transgenic mice model mentioned above. These research needs are similar to those
identified by the VVEO EMF Project.
There is currently insufficient scientific basis for concluding either that wireless
communication technologies are safe or that they pose a risk to millions of users. A
significant research effort, including well-planned animal experiments, is needed to
provide the basis to assess the risk to human health of wireless communications devices.
1. Balcer-Kubiczek EK, Harrison GH (1985). Evidence for microwave carcinogenicity
in vitro. Carcinogenesis 6: 859-864.
2. Balcer-Kubiczek EK, Harrison GH (1989). Induction of neoplastic transformation in
C3H/IOT cells by 2.45 GHz microwaves and phorbol ester. Radiation Res. 17:531-537.
3. Balcer-Kubiczek EK, Harrison GH (1991). Neoplastic transformation of C3H/I OT
cells following exposure to 120 Hz modulated 2.45 GHz microwaves and phorbol ester
tumor promoter. Radiat Res. 126: 65-72.
4. Byus CV, Lundak RL, Fletcher RM, Adey WR (1984). Alterations in protein kinase
activity following exposure of cultured human lymphocytes to modulated microwave
fields. Bioelectromagnetics 5: 341-51.
5. Byus CV, Kartun K, Pieper S, Adey WR (1988). Increased orinthine decarboxylase
activity in cultured cells exposed to low energy modulated microwave fields and phorbol
ester tumor promoters. Cancer Res. 48: 4222-6.
6. Chou CK, Guy AW, Kunz LL, Johnson RF, Crowley JJ, Krupp JH (1992). Long-term
low-level microwave irradiation of rats. Bioelectromagnetics 13: 469-96.
7. Cleary SF, Cao G, Liu L-M (1996). Effects of isothermal 2.45 GHz microwave
radiation on the mammalian cell cycle: comparison with effects of isothermal 27 MHz
radiofrequency radiation exposure. Bioelectrochem. Bioenerget. 39: 167-73.
8. Cleary SF, Liu L-M, Garber F (1985).Viability and phagocytosis of neutrophils
exposed in vitro to 1 00 MHz radiofrequency radiation. Bioelectromagnetics 6: 5 3 -60.
9. Cleary SF, Liu L-M, Merchant RE (1990a). Glioma proliferation modulated in vitro
by isothermal radiofrequency radiation exposure. Radiat Res. 121: 38-45.
10. Cleary SF, Liu L-M, Merchant RE (1990b). In vitro lymphocyte proliferation
induced by radiofrequency electromagnetic radiation under isothermal conditions.
Bioelectromagnetics 11: 47-56.
11. Elder JA, Cahill DF, eds. (1984). Biological effects of radiofrequency radiation. US
Environmental Protection Agency: EPA-600/8-83-026.
12. Guy AW, Chou C-K, Kunz LL, Crowley J, Krupp J (1985). Effects of long-term
low-level radiofrequency radiation exposure on rats. Vol 9: Summary. Texas, Brooks
Air Force Base, USAF School of Aerospace Medicine: ASAFSAM-TR-85-11.
13. ICNIRP (1996). Health issues related to the use of hand-held radiotelephones and
base transmitters. Health Phys. 70: 587-93.
14. IEEE (1991). IEEE Standard for safety levels with respect to human exposure to
radiofrequency electromagnetic fields, 3 kHz to 300 GHz. New York; Institute of
Electrical and Electronic Engineers: C95. 1.
15. IRPA/INIRC (1988). Guidelines on limits of exposure to radiofrequency
electromagnetic fields in the frequency range from I 00 kHz to 3 00 GHz. Health Phys;
54: 11 5 -23.
16. Krause D, Brent JA, Mullins JM, Penafiel LM, Nardone RM (1990). Enhancement
of orinithine decarboxylase activity in L929 cells by amplitude modulated microwaves.
In: Proceedings of Bioelectromagnetics Society 12th Annual Meeting, San Antonio,
Texas: 94 (abstract).
17. Krause D, Penafield LM, Desta A, Litovitz T, Mullins JM (1996). Role of
modulation on the effect of microwaves on orinithine decarboxylase activity in L929
Bioelectromagnetics. In press.
18. Kues HA, Monohan JC, D'Anna SA, McLeod DS, Lutty GA, Koslov S (1992).
Increased sensitivity of the non-human primate eye to microwave radiation following
ophthalmic drug pretreatment. Bioelectromagnetics 13 (5): 379-393.
19. Kunz LL, Johnson RB, Thompson D, Crowley J, Chou C-K, Guy AW (1985).
Effects of long-term low-level radiofrequency radiation exposure on rats. Vol 8:
Evaluation of longevity, cause of death, and histopathological findings. Texas, Brooks
Air Force Base, USAF School of Aerospace Medicine, ASAFSAM-TR-85-11.
20. Lai H, Singh NP (1995). Acute low-intensity microwave exposure increases DNA
single-strand breaks in rat brain cells. Bioelectromagnetics 16: 207-10.
21. Lai H, Singh NP (1996). Single- and double-strand DNA breaks in rat brain cells
after acute exposure to radiofrequency electromagnetic radiation. Int J Radiat Biol 69:
22. Litovitz TA, Penafiel M, Mullins JM, Krause D (1996). ELF magnetic noise fields
inhibit the effect of cellular phone radiation on the activity of orinithine decarboxylase.
In: Proceedings of Bioelectromagnetics Society 18th Annual Meeting, Victoria, Canada
23. NCRP (1986). Biological effects and exposure criteria for radiofrequency
electromagnetic fields. Bethesda, MD. National Council on Radiation Protection and
Measurements: NCRP Report No 86.
24. Prausnitz S, Susskind C (1962). Effects of chronic microwave irradiation on mice.
IRE Trans Biomed Electron 9: 104.
25. Salford LG, Brun A, Persson BRR, Eberhardt J (1993). Experimental studies of
brain tumor development during exposure with continuous and pulsed 915 MHz
radiofrequency radiation. Bioelectrochem Bioenerget 30: 313-8.
26. Salford LS, Brun A, Sturesson K, Eberhardt JL, Persson BRR (1994). Permeability
of the blood-brain barrier induced by 915 MHz electromagnetic radiation, continuous
wave and modulated at 8, 50, and 200 Hz. Microscopy Res Tech 27: 535-42.
27. Santini R, Honsi M, Deschaux P, Pacheco H (1988). B 16 melanoma development
in black mice exposed to low-level microwave radiation. Bioelectromagnetics 9: 105-7.
28. Szrnigielski S, Szudzinski A, Pietraszek A, Bielec M, Wrembel JK (1982).
Accelerated development of spontaneous and bennzo(a)pyrene-induced skin cancer in
mice exposed to 2450 MHz microwave radiation. Bioelectromagnetics 3: 179.
29. UNEP/WHO/IRPA (1993). Electromagnetic fields (300 Hz-300 GHz). Geneva:
World Health Organization; Environmental Health Criteria #137.