| Executive
Summary
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 predominate.
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-1). 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-1 at
900 MHz and 3.0 W kg-1 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 103
Wm-2. SARs in the lens large enough to produce temperatures
in the lens greater than 41o C are required. Effects on the
retina have been associated with levels of microwave radiation above
500 Wm-2. 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 1o
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-1 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-1 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-1 (IEEE,
1991). Based on the estimated threshold and a safety factor of 10, the
whole body averaged SAR of 0.4 W kg-1 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-1
has 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-1 averaged over a mass of 1g has
also been adopted (IEEE, 1991).
Currently cellular
phones and other wireless communication devices are required to
meetthe 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 microwave radiation.
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-1) (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
investigation.
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.
F. References
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 cells. 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 69:51321.
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 (abstract).
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.
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