Biological Effects of RF Energy

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NEUROLOGICAL EFFECTS OF RADIOFREQUENCY ELECTROMAGNETIC RADIATION
 
Bioelectromagnetics Research
 
Laboratory, Department of Bioengineering, School of
Medicine and College of Engineering, University of
Washington, Seattle, Washington, USA
 
Paper presented to the Workshop on possible
biological and health effects of RF electromagnetic
fields. 
 
Mobile Phones and
Health, Symposium, October 25-28, 1998,
University of Vienna, Austria.
 
Reproduced with
permission of Henry Lai 
 
INTRODUCTION
 
Radiofrequency electromagnetic radiation (RFR), a
form of energy between 10 KHz-300 GHz in the
electromagnetic spectrum, is used in wireless
communication and emitted from antennae of mobile
telephones (handys) and from cellular masts. RFR can
penetrate into organic tissues and be absorbed and
converted into heat. One familiar application of this
energy is the microwave ovens used in cooking.
 
The close proximity of a mobile telephone antenna to
the userís head leads to the deposition of a
relatively large amount of radiofrequency energy in
the head. The relatively fixed position of the
antenna to the head causes a repeated irradiation of
a more or less fixed amount of body tissue. Exposure
to RFR from mobile telephones is of a short-term,
repeated nature at a relatively high intensity,
whereas exposure to RFR emitted from cell masts is of
long duration but at a very low intensity. The
biological and health consequences of these exposure
conditions need further understanding.
 
Formal research on the biological effects of RFR
began more than 30 years ago. In my opinion, the
research has been of high quality, innovative, and
intelligent. All of us who work in this field should
be proud of it. However, knowledge of the possible
health effects of RFR is still inadequate and
inconclusive. I think the main barrier in
understanding the biological effects of RFR is caused
by the complex interaction of the different exposure
parameters in causing an effect. An independent
variable of such complexity is unprecedented in any
other field of biological research.
 
In this paper, I have briefly summarized the results
of experiments carried out in our laboratory on the
effects of RFR exposure on the nervous system of the
rat. But, before that, I will discuss and point out
some of the general features and concerns in the
study of the biological effects of RFR.
 
EXPOSURE CONDITIONS AND BIOLOGICAL RESPONSES
 
The intensity (or power intensity) of RFR in the
environment is measured in units such as mW/cm2.
However, the intensity provides little information on
the biological consequence unless the amount of
energy absorbed by the irradiated object is known.
This is generally given as the specific absorption
rate (SAR), which is the rate of energy absorbed by a
unit mass (e.g., one kg of tissue) of the object, and
usually expressed as W/kg. We may liken the intensity
of RFR to a quantity of aspirin tablets. Lets say,
there are 100 mg of aspirin per tablet (i.e., the
intensity). This information tells us
nothing about the efficacy of the tablets unless the
amount taken is also known, e.g., take 2 tablets
every 4 hrs (or 200 mg every 4 hrs) (analogous to the
SAR). The amount of a drug absorbed into the body is
the main determinant of its effect. Thus, in order to
understand the effect of RFR, one should also know
the SAR.
 
Unfortunately, RFR does not behave as simply as a
drug. The rate of absorption and the distribution of
RFR energy in an organism depend on many factors.
These include: the dielectric composition (i.e.,
ability to conduct electricity) of the irradiated
tissue, e.g., bones, with a lower water content,
absorb less of the energy than muscles; the size of
the object relative to the wavelength of the RFR
(thus, the frequency); shape, geometry, and
orientation of the object; and configuration of the
radiation, e.g., how close is the object from the RFR
source? These factors make the distribution of energy
absorbed in an irradiated organism extremely complex
and non-uniform, and also lead to the formation of so
called 'hot spots' of concentrated energy in the
tissue. For example, an experiment reported by Chou
et al. [1985], measuring local energy absorption
rates (SARs) in different areas of the brain in a rat
exposed to RFR, has shown that two brain regions less
than a millimeter apart can have more than a two-fold
difference in SAR. The rat was stationary when it was
exposed. The situation is more complicated if an
animal is moving in an RF field. Depending on the
amount of movement of the animal, the energy
absorption pattern in its body could become either
more complex and unpredictable or more uniform. In
the latter situation, we are all familiar with the
case that a microwave oven with a rotating carousel
provides more uniform heating of the food than one
without. However, the distribution of energy in the
head of a user of a mobile telephone is more discrete
because of the relatively stationary position of the
phone. 'Hot spots' may form in certain areas of the
head. As a reference, from theoretical calculations
[e.g., Dimbylow 1993; Dimbylow and Mann 1994; Martens
et al. 1995], peak (hot spot) SAR in head tissue of a
user of mobile telephone can range from 2 to 8 W/kg
per watt output of the device. The peak energy output
of mobile telephones can range from 0.6-1 watt,
although the average output could be much smaller. 
 
Thus, in summary, the pattern of energy absorption
inside an irradiated body is non-uniform, and
biological responses are dependent on distribution of
energy and the body part that is affected [Lai et
al., 1984a, 1988]. Related to this is that we [Lai et
al., 1989b] have found that different areas of the
brain of the rat have different sensitivities to RFR.
This further indicates that the pattern of energy
absorption could be an important determining factor
of the nature of the response.
 
Two obviously important parameters are the frequency
and intensity of RFR. Frequency is analogous to the
color of a light bulb, and intensity is its wattage.
There is a question of whether 'the effects of RFR of
one frequency is different from those of another
frequency.' The question of frequency is vital
because it dictates whether existing research data on
the biological effects of RFR can apply to the case
of mobile telephones. Most previous research studied
frequencies different from those used in wireless
communication. Frequency is like the color of an
object. In this case, one is basically asking the
question ''Are the effects of red light different
from those of green light?" The answer to this
is that it depends on the situation. They are
different: if one is looking at a traffic light,
'red' means 'stop' and 'green' means 'go'. But, if
one is going to send some information by Morse code
using a light (on and off, etc.), it will not matter
whether one uses a red or green light, as long as the
receiver can see and decode it. We don't know which
of these two cases applies to the biological effects
of RFR.
 
It must be pointed out that data showing different
frequencies producing different effects, or an effect
was observed at one frequency and not at another, are
sparse. An example is the study by Sanders et al
[1984] who observed that RFR at frequencies of 200
and 591 MHz, but not at 2450 MHz, produced effects on
energy metabolism in neural tissue. There are also
several studies that showed different frequencies of
RFR produced different effects [D'Andrea et al.,
1979, 1980; de Lorge and Ezell, 1980; Thomas et al.,
1975]. However, it is not certain whether these
differences were actually due to differences in the
distribution of energy absorption in the body of the
exposed animal at the varous frequencies. In
addition, some studies showed frequency-window
effects, i.e., effect is only observed at a certain
range of frequencies and not at higher or lower
ranges [Bawin et al., 1975; Blackman et al., 1979,
1980a,b, 1989; Chang et al., 1982; Dutta et al.,
1984, 1989, 1992; Lin-Liu and Adey, l982; Oscar and
Hawkins, 1977; Sheppard et al., 1979]. These results
may suggest that the frequency of an RFR can be a
factor in determining the biological outcome of
exposure.
 
On the other hand, there are more studies showing
that different frequencies can produce the same
effect. For example, changes in blood-brain barrier
have been reported after exposure to RFRs of 915 MHz
[Salford et al., 1944]; 1200 MHz [Frey et al., 1975],
1300 MHz [Oscar and Hawkin, 1977], 2450 and 2800 MHz
[Albert, 1977], and effects on calcium have been
reported at 50 MHz [Blackman et al., 1980b], 147 MHz
[Bawin et al., 1975; Blackman et al., 1980a; Dutta et
al., 1989], 450 MHz [Sheppard et al., 1979], and 915
MHz [Dutta et al., 1984]. If there is any difference
in effects among different frequencies, it is a
difference in quantity and not quality.
 
An important question regarding the biological
effects of RFR is whether the effects are cumulative,
i.e., after repeated exposure, will the nervous
system adapt to the perturbation and, with continued
exposure, when will homeostasis break down leading to
irreparable damage? The question of whether an effect
will cumulate over time with repeated exposure is
particularly important in considering the possible
health effects of mobile telephone usage, since it
involves repeated exposure of short duration over a
long period (years) of time. Existing results
indicate changes in the response characteristics of
the nervous system with repeated exposure, suggesting
that the effects are not 'forgotten' after each
episode of exposure. Depending on the responses
studied in the experiments, several outcomes have
been reported. (1) An effect was observed only after
prolonged (or repeated) exposure, but not after one
period of exposure [e.g., Baranski, 1972; Baranski
and Edelwejn, 1974; Mitchell et al., 1977; Takashima
et al., 1979]; (2) an effect disappeared after
prolonged exposure suggesting habituation [e.g.,
Johnson et al., 1983; Lai et al., 1992a]; and (3)
different effects were observed after different
durations of exposure [e.g., Baranski, 1972; Dumanski
and Shandala, 1974; Grin, 1974; Lai et al., 1989a;
Servantie et al., 1974; Snyder, 1971]. As described
in a later section, we found that a single episode of
RFR exposure increases DNA damage in brain cells of
the rat. Definitely, DNA damage in cells is
cumulative. Related to this is that various lines of
evidence suggest that responses of the central
nervous system to RFR could be a stress response
[Lai, 1992; Lai et al., 1987a]. Stress effects are
well known to cumulate over time and involve first
adaptation and then an eventual break down of
homeostatic processes when the stress persists.
 
Another important conclusion of the research is that
modulated or pulsed RFR seems to be more effective in
producing an effect. They can also elicit a different
effect when compared with continuous-wave radiation
of the same frequency [Arber and Lin, 1985; Baranski,
1972; Frey and Feld, 1975; Frey et al., 1975; Lai et
al., 1988; Oscar and Hawkins, 1977; Sanders et al.,
1985]. This conclusion is important since mobile
telephone radiation is modulated at low frequencies.
This also raises the question of how much do low
frequency electric and magnetic fields contribute to
the biological effects of mobile telephone radiation.
Biological effects of low frequency (< 100Hz)
electric and magnetic fields are quite well
established [see papers by Blackman, and Von Klitzing
in this symposium].
 
Therefore, frequency, intensity, exposure duration,
and the number of exposure episodes can affect the
response to RFR, and these factors can interact with
others and produce different effects. In addition, in
order to understand the biological consequence of RFR
exposure, one must know whether the effect is
cumulative, whether compensatory responses result,
and when homeostasis will break down.
 
EFFECTS OF VERY LOW INTENSITY RFR
 
For those who have questions on the possible health
effects of exposure to radiation from cell masts,
there are studies that show biological effects at
very low intensities. The following are some
examples: Kwee and Raskmark [1997] reported changes
in cell proliferation (division) at SARs of 0.000021-
0.0021 W/kg; Magnras and Xenos [1997] reported a
decrease in reproductive functions in mice exposed to
RFR intensities of 160-1053 nW/square cm (the SAR was
not calculated); Ray and Behari [1990] reported a
decrease in eating and drinking behavior in rats
exposed to 0.0317 W/kg; Dutta et al. [1989] reported
changes in calcium metabolism in cells exposed to RFR
at 0.05-0.005 W/kg; and Phillips et al. [1998]
observed DNA damage at 0.024-0.0024 W/kg. Most of the
above studies investigated the effect of a single
episode of RFR exposure. As regards exposure to cell
mast radiation, chronic exposure becomes an important
factor. Intensity and exposure duration do interact
to produce an effect. We [Lai and Carino, In press]
found with extremely low frequency magnetic fields
that 'lower intensity, longer duration exposure' can
produce the same effect as from a 'higher intensity,
shorter duration exposure'. A field of a certain
intensity, that exerts no effect after 45 min of
exposure, can elicit an effect when the exposure is
prolonged to 90 min. Thus, as described earlier, the
interaction of exposure parameters, the duration of
exposure, whether the effect is cumulative,
involvement of compensatory responses, and the time
of break down of homeostasis after long-term
exposure, play important roles in determining the
possible health consequence of exposure to radiation
emitted from cell masts.
 
THERMAL AND NONTHERMAL EFFECTS
 
When RFR is absorbed, it is converted into heat. A
readily understandable mechanism of effect of RFR is
tissue heating (thermal effect). Biological systems
alter their functions as a result of change in
temperature. However, there is also a question on
whether 'nonthermal' effects can occur from RF
exposure. There can be two meanings to the term
'nonthermal' effect. It could mean that an
effect occurs under the condition of no apparent
change in temperature in the exposed animal or
tissue, suggesting that physiological or exogenous
mechanisms maintain the exposed object at a constant
temperature. The second meaning is that somehow RFR
can cause biological effects without the involvement
of heat energy (or temperature independent). This is
sometime referred to as 'athermal effect'. For
practical reasons, I think it is futile to make these
distinctions simply because it is very difficult to
rule out thermal effects in biological responses to
RFR, because heat energy is inevitably released when
RFR is absorbed.
 
In some experiments, thermal controls (i.e., samples
subjected to direct heating) have been studied.
Indeed, there are reports showing that 'heating
controls' do not produce the same effect of RFR
[D'Inzeo et al., 1988; Johnson and Guy, 1971; Seaman
and Wachtel, 1978; Synder, 1971; Wachtel et al.,
1975]. These were taken as an indication of
non/a-thermal effects. However, as we discussed
earlier, it is difficult to reproduce the same
pattern of internal heating of RFR by external
heating, as we know that a conventional oven cooks
food differently than a microwave oven. And pattern
of energy distribution in the body is important in
determining the effect of RFR [e.g., Frey et al.,
1975; Lai et al., 1984a, 1988]. Thus, 'heating
controls do not produce the same effect of RFR' does
not really support the existence of nonthermal
effects.
 
On the other hand, even though no apparent change in
body temperature during RFR exposure occurs, it
cannot really rule out a ' thermal effect'. In one of
our experiments [Lai et al., 1984a], we have shown
that animals exposed to a low SAR of 0.6 W/kg are
actively dissipating the energy absorbed. This
suggests that the brain system involved in body
temperature regulation is activated. The physiology
of body temperature regulation is complicated and can
involve many organ systems. Thus, changes in
thermoregulatory activity can indirectly affect
biological responses to RFR.
 
Another difficulty in eliminating the contribution of
thermal effects is that it can be 'micro-thermal'. An
example of this is the auditory effect of pulsed RFR.
We can hear RFR delivered in pulses. An explanation
for this 'hearing' effect is that it is caused by
thermoelastic expansion of the head of the
'listener.' In a classic paper by Chou et al. [1982],
it was stated that "... one hears sound because
a miniscule wave of pressure is set up within the
head and is detected at the cochlea when the absorbed
microwave pulse is converted to thermal energy."
The threshold of hearing was determined to be
approximately 10 microjoule/gm per pulse, which
causes an increment of temperature in the head of one
millionth of a degree centigrade! Lebovitz [1975]
gives another example of a microthermal effect of
RFR on the vestibulocochlear apparatus, an organ in
the inner ear responsible for keeping body balance
and sensing of movement. He proposed that an uneven
distribution of RFR absorption in the head can set up
a temperature gradient in the semicircular canals,
which in turns affect the function of the vestibular
system. The semicircular canals are very minute
organs in our body.
 
What about in vitro experiments in which isolated
organs or cells are exposed to RFR? Generally, these
experiments are conducted with the temperature
controlled by various regulatory mechanisms. However,
it turns out that the energy distribution in culture
disks, test tubes, and flasks used these studies are
very uneven. Hotspots are formed. There is a question
of whether the temperature within the exposed samples
can be efficiently controlled.
 
In any case, my argument is not about whether a
non/a-thermal effect can occur. The existence of
intensity-windows, reports of modulated fields
producing stronger or different effects than
continuous-wave fields, and the presence of effects
that occur at very low intensity described in the
previous section could be indications of
non/a-thermal effects. My argument is that it may not
be practical to differentiate these effects
experimentally due to the difficulty of eliminating
thermal effects.
 
I propose the use of the term 'low-intensity'
effects, which is based on the exposure guideline of
your community. By multiplying the guideline level
with the safety factor used to determine the
guideline, one would get a level that supposedly
causes an effect(s). Any experiment/exposure done
below that level would be considered 'low-intensity'.
For example, if the safety guideline is an SAR of 0.4
W/kg for whole body exposure, and a safety factor of
10 has been used to determine the guideline, then,
the level at which effects should occur would be 4.0
W/kg. Any exposure below 4 W/kg would be considered a
'low-intensity' exposure. Any effect found at
'low-intensities' could conceivably contribute to the
setting of future guidelines.
 
OUR RESEARCH ON NEUROLOGICAL EFFECTS OF RFR
 
When the nervous system or the brain is disturbed,
e.g., by RFR, morphological, electrophysiological,
and chemical changes can occur. A significant change
in these functions will inevitably lead to a change
in behavior. Indeed, neurological effects of RFR
reported in the literature include changes in
blood-brain-barrier, morphology, electrophysiology,
neurotransmitter functions, cellular metabolism,
calcium efflux, responses to drugs that affect the
nervous system, and behavior [for a review of these
effects, see Lai, 1994 and Lai et al., 1987a].
 
Our research on the effects of RFR exposure on the
nervous system covers topics from DNA damage in brain
cells to behavior. My research in this area began in
1980 when I investigated the effects of brief
exposure to RFR on the actions of various drugs that
act on the nervous system. We found that the actions
of several drugs- amphetamine, apomorphine, morphine,
barbituates, and ethyl alcohol- were affected in rats
after 45 min of exposure to RFR [Lai et al., 1983;
1984 a,b]. One common feature of these responses was
that they seemed to be related to the activity of a
group of neurotransmitters in the brain known as the
endogenous opioids [Lai et al., 1986b]. These are
compounds that are generated by the brain and behave
like morphine. We proposed that exposure to RFR
activates endogenous opioids in the brain of the rat
[Lai et al., 1984c]. One interesting finding was that
RFR could inhibit morphine withdrawal in rats [1986a,
which led me to speculate as to whether low-intensity
RFR could be used to treat morphine withdrawal and
addiction in humans. When I was in Leningrad, USSR in
1989, a scientist informed me that he had read my
paper on 'RFR decreased morphine withdrawal in rats',
and he had been using RFR to treat morphine
withdrawal in humans. Also, unknown to us at that
time was that the 'endogenous opioid hypothesis'
could actually explain the increase of alcohol
consumption in RFR-exposed rats that we reported in
1984 [Lai et al., 1984b]. In the summer of 1996, the
United States Food and Drug Administration approved
the use of the drug naloxone for the treatment of
alcoholism. Naloxone is a drug that blocks the action
of endogenous opioids. Increase in endogenous opioid
activity in the brain can somehow cause
alcohol-drinking behavior. In addition, our finding
that RFR exposure alters the effect of alcohol on
body temperature of the rat [Lai et al., 1984b] was
replicated by Hjeresen et al. [1988, 1989] at an SAR
half of what we used.
 
Interactions between RFR with drugs could have
important implications on the health effects of RFR.
They suggest that certain individuals in the
population could be more susceptible to the effects
of RFR. For example, an important discovery in this
aspect is that ophthalmic drugs used in the treatment
of glaucoma can greatly increase the damaging effects
of RFR on the eye [Kues et al., 1992].
 
Subsequently, we carried out a series of experiments
to investigate the effect of RFR exposure on
neurotransmitters in the brain of the rat. The main
neurotransmitter we investigated was acetylcholine, a
ubiquitous chemical in the brain involved in numerous
physiological and behavioral functions. We found that
exposure to RFR for 45 min decreased the activity of
acetylcholine in various regions of the brain of the
rat, particularly in the frontal cortex and
hippocampus. Further study showed that the response
depends on the duration of exposure. Shorter exposure
time (20 min) actually increased, rather than
decreasing the activity. Different brain areas have
different sensitivities to RFR with respect to
cholinergic responses [Lai et al., 1987b, 1988b,
1989a,b]. In addition, repeated exposure can lead to
some rather long lasting changes in the system: the
number of acetylcholine receptors increase or
decrease after repeated exposure to RFR to 45 min and
20 min sessions, respectively [Lai et al., 1989a].
Changes in acetycholine receptors are generally
considered to be a compensatory response to repeated
disturbance of acetylcholine activity in the brain.
Such changes alter the response characteristic of the
nervous system. Other studies have shown that
endogenous opioids are also involved in the effect of
RFR on acetylcholine [Lai et al., 1986b, 1991, 1992b,
1996].
 
At the same time, we speculated that biological
responses to RFR are actually stress responses, i.e.,
RFR is a stressor (see Table I in Lai et al., 1987a).
A series of experiments was carried out to compare
the effects of RFR on brain acetylcholine with those
of two known stressors: loud noise and body restraint
[Lai, 1987, 1988; Lai and Carino, 1990a,b, 1992; Lai
et al., 1986d, 1989c]. We found that the responses
are very similar. Two other bits of information also
support the notion that RFR is a stressor. We found
that RFR activates the stress hormone, corticotropin
releasing factor [Lai et al., 1990], and affect
benzodiazepine receptors in the brain [Lai et al.,
1992a]. Benzodiazepine receptors mediate the action
of antianxiety drugs, such as Valium and Librium, and
are known to change when an animal is stressed.
 
Another interesting finding is that some of the
effects of RFR are classically conditionable [Lai et
al., 1986b,c, 1987c]. Conditioning processes,
which connect behavioral responses with events
(stimuli) in the environment, are constantly
modifying the behavior of an animal. In a situation
known as classical conditioning, a 'neutral' stimulus
that does not naturally elicit a certain response is
repeatedly being presented in sequence with a
stimulus that does elicit that response. After
repeated pairing, presentation of the neutral
stimulus (now the conditioned stimulus) will elicit
the response (now the conditioned response). You may
have heard of the story of "Pavlov's dogî. A
bell was rung when food was presented to a dog. After
several pairing of the bell with food, ringing the
bell alone could cause the dog to salivate.
 
We found that biological effects of RFR can be
classically conditioned to cues in the exposure
environment. In earlier experiments, we reported that
exposure to RFR attenuated amphetamine-induced
hyperthermia [Lai et al., 1983] and decreased
cholinergic activity in the frontal cortex and
hippocampus [Lai et al., 1987b] in the rat. In the
conditioning experiments, rats were exposed to RFR in
ten daily sessions (45 min per session). On day 11,
animals were sham-exposed (i.e., subjected to the
normal procedures of exposure but the RFR was not
turned on) and either amphetamine-induced
hyperthermia or cholinergic activity in the frontal
cortex and hippocampus was studied immediately after
exposure. In this paradigm, the RFR was the
unconditioned stimulus and cues in the exposure
environment were the neutral stimuli, which after
repeated pairing with the unconditioned stimulus
became the conditioned stimulus. Thus on the 11th day
when the animals were sham-exposed, the conditioned
stimulus (cues in the environment) alone would elicit
a conditioned response in the animals. In the case of
amphetamine-induced hyperthermia [Lai et al., 1986b],
we observed a potentiation of the hyperthermia in the
rats after the sham exposure. Thus, the conditioned
response (potentiation) was opposite to the
unconditioned response (attenuation) to RFR. This is
known as 'paradoxical conditioning' and is seen in
many instances of classical conditioning. We found in
the same experiment that, similar to the
unconditioned response, the conditioned response
could be blocked by the drug naloxone, implying the
involvement of endogenous opioids. In the case of
RFR-induced changes in cholinergic activity in the
brain, we [Lai et al., 1987c] found that conditioned
effects also occurred in the brain of the rat. An
increase in cholinergic activity in the hippocampus
(paradoxical conditioning) and a decrease in the
frontal cortex were observed after the session of
sham exposure on day 11. In additon, we [Lai et al.,
1984c] observed an increase in body temperature
(approximately 1.0 oC) in the rat after exposure to
RFR, and found that this RFR effect was also
classically conditionable and involved endogenous
opioids [Lai et al., 1986c].
 
Conditioned effects may be related to the
compensatory response of an animal to the disturbance
of RFR and whether it can habituate to repeated
challenge of the radiation. For example, the
conditioned effect on cholinergic activity in the
hippocampus is opposite to that of its direct
response to RFR (paradoxical conditioning), whereas
that of the frontal cortex is similar to its direct
response. We found that the effect of RFR on
hippocampal cholinergic activity habituated after 10
sessions of exposure. On the other hand, the effect
of RFR on frontal cortical cholinergic activity did
not habituate after repeated exposure [Lai et al.,
1987c].
 
Since acetylcholine in the frontal cortex and
hippocampus is involved in learning and memory
functions, we carried out experiments to study
whether exposure to RFR affects these behavioral
functions in the rat. Two types of memory functions:
spatial 'working' and 'reference' memories were
investigated. Acetylcholine in the brain, especially
in the hippocampus, is known to play an important
role in these behavioral functions.
 
In the first experiment, 'working' memory (short-term
memory) was studied using the 'radial arm maze'. This
test is very easy to understand. Just imagine you are
shopping in a grocery store with a list of items to
buy in your mind. After picking up the items, at the
check out stand, you find that there is one chicken
at the top and another one at the bottom of your
shopping cart. You had forgotten that you had already
picked up a chicken at the beginning of your shopping
spree and picked up another one later. This is a
failure in short-term memory and is actually very
common in daily life and generally not considered as
being pathological. A distraction or a lapse in
attention can affect short-term memory. This analogy
is similar to the task in the radial-arm maze
experiment. The maze consists of a circular center
hub with arms radiating out like the spokes of a
wheel. Rats are allowed to pick up food pellets at
the end of each arm of the maze. There are 12 arms in
our maze, and each rat in each testing session is
allowed to make 12 arm entries. Re-entering an arm is
considered to be a memory deficit. The results of our
experiment showed that after exposure to RFR, rats
made significantly more arm re-entries than unexposed
rats [Lai et al., 1994]. This is like finding two
chickens, three boxes of table salt, and two bags of
potatoes in your shopping cart.
 
In another experiment, we studied the effect of RFR
exposure on 'reference' memory (long-term memory)
[Wang and Lai, submitted for publication].
Performance in a water maze was investigated. In this
test, a rat is required to locate a submerged
platform in a circular water pool. It is released
into the pool, and the time taken for it to land on
the platform is recorded. Rats were trained in
several sessions to learn the location of the
platform. The learning rate of RFR-exposed rats was
slower, but, after several learning trials, they
finally caught up with the control (unexposed) rats
(found the platform as fast). However, the story did
not end here. After the rats had learned to locate
the platform, in a last session, the platform was
removed and rats were released one at a time into the
pool. We observed that unexposed rats, after being
released into the pool, would swim around circling
the area where the platform was once located, whereas
RFR-exposed rats showed more random swimming
patterns. To understand this, let us consider another
analogy. If I am going to sail from the west coast of
the United States to Australia. I can learn to read a
map and use instruments to locate my position, in
latitude and longitude, etc. However, there is an
apparently easier way: just keep sailing southwest.
But, imagine, if I sailed and missed Australia. In
the first case, if I had sailed using maps and
instruments, I would keep on sailing in the area that
I thought where Australia would be located hoping
that I would see land. On the other hand, if I sailed
by the strategy of keeping going southwest, and
missed Australia, I would not know what to do. Very
soon, I would find myself circumnavigating the globe.
Thus, it seems that unexposed rats learned to locate
the platform using cues in the environment (like
using a map from memory), whereas RFR-exposed rats
used a different strategy (perhaps, something called
'praxis learning', i.e., learning of a certain
sequence of movements in the environment to reach a
certain location. It is less flexible and does not
involve cholinergic systems in the brain). Thus, RFR
exposure can completely alter the behavioral strategy
of an animal in finding its way in the environment.
 
In summary, RFR apparently can affect memory
functions at least in the rat. The effects are most
like reversible and transient. Does this have any
relevance to health? The consequence of a behavioral
deficit is situation dependent. What is significant
is that the effects persist for sometime after RFR
exposure. If I am reading a book and receive a call
from a mobile phone, it probably will not matter if I
cannot remember what I has just read. However, the
consequence would be much serious, if I am an
airplane technician responsible for putting screws
and nuts on airplane parts. A phone call in the
middle of my work can make me forget and miss several
screws. Another adverse scenario of short-term memory
deficit is that a person may overdose himself on
medication because he has forgotten that he has
already taken the medicine.
 
Lastly, I like to briefly describe the experiments we
carried out to investigate the effects of RFR on DNA
in brain cells of the rat. We [Lai and Singh 1995,
1996; Lai et al., 1997] reported an increase in DNA
single and double strand breaks, two forms of DNA
damage, in brain cells of rats after exposure to RFR.
DNA damages in cells could have an important
implication on health because they are cumulative.
Normally, DNA is capable of repairing itself
efficiently. Through a homeostatic mechanism, cells
maintain a delicate balance between spontaneous and
induced DNA damage. DNA damage accumulates if such a
balance is altered. Most cells have considerable
ability to repair DNA strand breaks; for example,
some cells can repair as many as 200,000 breaks in
one hour. However, nerve cells have a low capability
for DNA repair and DNA breaks could accumulate. Thus,
the effect of RFR on DNA could conceivably be more
significant on nerve cells than on other cell types
of the body. Cumulative damages in DNA may in turn
affect cell functions. DNA damage that accumulates in
cells over a period of time may be the cause of slow
onset diseases, such as cancer. One of the popular
hypotheses for cancer development is that DNA
damaging agents induce mutations in DNA leading to
expression of certain genes and suppression of other
genes resulting in uncontrolled cell growth. Thus,
damage to cellular DNA or lack of its repair could be
an initial event in developing a tumor. However, when
too much DNA damage is accumulated over time, the
cell will die. Cumulative damage in DNA in cells also
has been shown during aging. Particularly, cumulative
DNA damage in nerve cells of the brain has been
associated with neurodegenerative diseases, such as
Alzheimer's, Huntington's, and Parkinson's diseases.
 
Since nerve cells do not divide and are not likely to
become cancerous, more likely consequences of DNA
damage in nerve cells are changes in functions and
cell death, which could either lead to or accelerate
the development of neurodegenerative diseases. Double
strand breaks, if not properly repaired, are known to
lead to cell death. Indeed, we have observed an
increase in apoptosis (a form of cell death) in cells
exposed to RFR (unpublished results). However,
another type of brain cells, the glial cells, can
become cancerous, resulting from DNA damage.
 
This type of response, i.e., genotoxicity at low and
medium cumulative doses and cell death at higher
doses, would lead to an inverted-U response function
in cancer development and may explain recent reports
of increase [Repacholi et al., 1997], decrease [Adey
et al., 1996], and no significant effect [Adey et
al., 1997] on cancer rate of animals exposed to RFR.
Understandably, it is very difficult to define and
judge what constitute low, medium, and high
cumulative doses of RFR exposure, since the
conditions of exposure are so variable and complex in
real life situations.
 
Interestingly, RFR-induced increases in single and
double strand DNA breaks in rat brain cells can be
blocked by treating the rats with melatonin or the
spin-trap compound N-t-butyl-a-phenylnitrone [Lai and
Singh, 1997]. Since both compounds are potent free
radical scavengers, this data suggest that free
radicals may play a role in the genetic effect of
RFR. If free radicals are involved in the RFR-induced
DNA strand breaks in brain cells, results from his
study could have an important implication on the
health effects of RFR exposure. Involvement of free
radicals in human diseases, such as cancer and
atherosclerosis, has been suggested. As a consequence
of increase in free radicals, various cellular and
physiological processes can be affected including
gene expression, release of calcium from
intracellular storage sites, cell growth, and
apoptosis. Effects of RFR exposure on free radicals
in cells could affect these cellular functions.
 
Free radicals also play an important role in aging
processes, which have been ascribed to be a
consequence of accumulated oxidative damage to body
tissues [Forster et al., 1996; Sohal and Weindruch,
1996], and involvement of free radicals in
neurodegenerative diseases, such as Alzheimer's,
Huntington's, and Parkinson's, has been suggested
[Borlongan et al., 1996; Owen et al., 1996].
Furthermore, the effect of free radicals could depend
on the nutritional status of an individual, e.g.,
availability of dietary antioxidants [Aruoma, 1994],
consumption of alcohol [Kurose et al., 1996], and
amount of food consumption [Wachsman, 1996]. Various
life conditions, such as psychological stress [Haque
et al., 1994] and strenuous physical exercise
[Clarkson, 1995], have been shown to increase
oxidative stress and enhance the effect of free
radicals in the body. Thus, one can also speculate
that some individuals may be more susceptible to the
effects of RFR exposure.
 
CONCLUDING REMARKS
 
It is difficult to deny that RFR at low intensity can
affect the nervous system. However, data available
suggest a complex reaction of the nervous system to
RFR. Exposure to RFR does produce various effects on
the central nervous system. The response is not
likely to be linear with respect to the intensity of
the radiation. Other parameters of RFR exposure, such
as frequency, duration, waveform, frequency- and
amplitude-modulation, etc, are important determinants
of biological responses and affect the shape of the
dose (intensity)-response relationship. In order to
understand the possible health effects of exposure to
RFR from mobile telephones, one needs first to
understand the effects of these different parameters
and how they interact with each other.
 
Therefore, caution should be taken in applying the
existing research results to evaluate the possible
effect of exposure to RFR during mobile telephone
use. It is apparent that not enough research data is
available to conclude whether exposure to RFR during
the normal use of mobile telephones could lead to any
hazardous health effect. Research studying RFR of
frequencies and waveforms similar to those emitted
from cellular telephones and intermittent exposure
schedule resembling the normal pattern of phone use
is needed. At this point, since not much is known on
the biological effects of mobile telephone use but
there is indication that the radiation from the
phones can cause biological effects which could lead
to detrimental health effects, prudent usage should
be taken as a logical guideline.
 
ACKNOWLEDGMENT
 
I thank Cindy Sage for her insightful comments and
discussion in the preparation of this manuscript. She
tried, maybe in vain, to edit my scientific jargon
and mundaneness of scientific narration.
 
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