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NEUROLOGICAL
EFFECTS OF RADIOFREQUENCY
ELECTROMAGNETIC RADIATION
Henry Lai
Bioelectromagnetics Research Laboratory,
Department of Bioengineering,
School of Medicine and College of Engineering,
University of Washington, Seattle, Washington, USA
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 user's 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/cm2.1 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.2 We may liken the
intensity of RFR to a quantity of aspirin tablets. Let's 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 dog". 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, 2000]. 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. 3 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 likely 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 had just read. However,
the consequence would be much more 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 would 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 damage 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 constitutes 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-?-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 this
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 increases 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 radical formation
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, available data 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 curve. 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 insufficient research data are available to
conclude whether exposure to RFR during the normal use of mobile telephones
could lead to any hazardous health effects. 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, little is known about the biological effects of mobile
telephone use, but since there are indications that the radiation from these
phones can cause biological effects that could be detrimental to health,
prudent usage should be taken as a logical guideline.
Please send correspondence to:
Henry Lai
Department of Bioengineering, Box 357962
University of Washington
Seattle, WA 98195-7962
USATelephone: 1-206-543-1071
FAX: 1-206-685-3925
e-mail: hlai@u.washington.edu
1. It can also be given in other units, e.g., ?W/cm2 (= 0.001 mW/cm2); W/m2 (=
0.1 mW/cm2).
2. mW/g (=W/kg); mW/kg (= 0.001 W/kg)
3. By the way, it is not a surprise that one can miss Australia by sailing
southwest from the west coast of the United States. The part of the Pacific
Ocean between southeast Australia and northwest New Zealand is called the
Tasman sea. I was told that the Dutch explorer Abel Janszoon Tasman, who
discovered New Zealand and the island Tasmania, sailed around and missed the
big continent of Australia. He named that part of the ocean the Tasman sea.
CELLPHONE HEALTH WARNING: PITTSBURGH
CANCER INSTITUTE WARNS OF CELL PHONE-CANCER HIGH RISK, DEFYING PREVIOUSLY
PUBLISHED RESEARCH! –
By Jennifer C. Yates and Seth Borenstein, Associated Press Writers,
Thursday, July 24, 2008, 11:14 p.m.
PDT
PITTSBURGH (AP) – The head of a prominent
cancer research institute issued an unprecedented warning to his faculty and
staff Wednesday:
Limit cell phone use because of the possible risk of cancer.
The warning from Dr. Ronald B. Herberman,
director of the University of Pittsburgh Cancer Institute, is contrary to
numerous studies that don't
find a link between cancer and cell phone use, and a public lack of worry by
the U.S. Food and Drug Administration.
Herberman is basing his alarm on early
unpublished data. He says it takes too long to get answers from science and he
believes people should take action now — especially when it comes to children.
"Really at the heart of my concern is
that we shouldn't wait for a definitive study to come out, but err on the side
of being safe rather
than sorry later," Herberman said.
No other major academic cancer research
institutions have sounded such an alarm about cell phone use. But Herberman's
advice is sure to raise concern among many cell phone users and especially
parents. In the memo he sent to about 3,000 faculty and staff Wednesday, he
says children should use cell phones only for emergencies because their brains
are still developing.
Adults should keep the phone away from the
head and use the speakerphone or a wireless headset, he says. He even warns
against using cell phones in public places like a bus because it exposes others
to the phone's electromagnetic fields. The issue that concerns some scientists
— though nowhere near a consensus — is electromagnetic radiation, especially
its possible effects on children. It is not a major topic in conferences of
brain specialists.
A 2008 University of Utah analysis looked at
nine studies — including some Herberman cites — with thousands of brain tumor
patients and
concludes "we found no overall increased risk of brain tumors among
cellular phone users. The potential elevated risk of brain tumors after
long-term cellular phone use awaits confirmation by future studies."
Studies last year in France and Norway concluded the same thing.
"If there is a risk from these products
— and at this point we do not know that there is — it is probably very
small," the Food and Drug
Administration says on an agency Web site.
Still, Herberman cites a "growing body
of literature linking long-term cell phone use to possible adverse health
effects including cancer."
"Although the evidence is still
controversial, I am convinced that there are sufficient data to warrant issuing
an advisory to share some
precautionary advice on cell phone use," he wrote in his memo.
A driving force behind the memo was Devra Lee
Davis, the director of the university's center for environmental oncology.
"The question is do you want to play
Russian roulette with your brain," she said in an interview from her cell
phone while using the hands-free
speaker phone as recommended. "I don't know that cell phones are
dangerous. But I don't know that they are safe."
Of concern are the still unknown effects of
more than a decade of cell phone use, with some studies raising alarms, said
Davis, a former health
adviser in the Clinton Administration.
She said 20 different groups have endorsed
the advice the Pittsburgh cancer institute gave, and authorities in England,
France and India have
cautioned children's use of cell phones. Herberman and Davis point to a massive
ongoing research project known as Interphone, involving
scientists in 13 nations, mostly in Europe. Results already published in
peer-reviewed journals from this project aren't so alarming, but
Herberman is citing work not yet published.
The published research focuses on more than
5,000 cases of brain tumors. The National Research Council in the U.S., which
isn't participating in the Interphone project, reported in January that the
brain tumor research had "selection bias." That means it relied on
people with cancer to remember how often they used cell phones. It is not
considered the most accurate research approach. The largest published study,
which appeared in the Journal of the National Cancer Institute in 2006, tracked
420,000 Danish cell phone users, including thousands that had used the phones
for more than 10 years. It found no increased risk of cancer among those using
cell phones.
A French study based on Interphone research
and published in 2007 concluded that regular cell phone users had "no
significant increased
risk" for three major types of nervous system tumors. It did note,
however, that there was "the possibility of an increased risk among the
heaviest users" for one type of brain tumor, but that needs to be verified
in future research.
EARLIER RESEARCH ALSO FOUND NO CONNECTION
Joshua E. Muscat of Penn State University,
who has studied cancer and cell phones in other research projects partly funded
by the cell phone
industry, said there are at least a dozen studies that have found no
cancer-cell phone link. He said a Swedish study cited by Herberman as
support for his warning was biased and flawed.
"We certainly don't know of any
mechanism by which radiofrequency exposure would cause a cancerous effect in
cells. We just don't know
this might possibly occur," Muscat said.
Cell phones emit radiofrequency energy, a
type of radiation that is a form of electromagnetic radiation, according to the
National Cancer
Institute. Though studies are being done to see if there is a link between it
and tumors of the brain and central nervous system, there is
no definitive link between the two, the institute says on its Web site.
"By all means, if a person feels
compelled that they should take precautions in reducing the amount of
electromagnetic radio waves
through their bodies, by all means they should do so," said Dan Catena, a
spokesman for the American Cancer Society. "But at the same time, we have
to remember there's no conclusive evidence that links cell phones to cancer,
whether it's brain tumors or other forms of cancer."
Joe Farren, a spokesman for the CTIA-The
Wireless Association, a trade group for the wireless industry, said the group
believes there is a risk
of misinforming the public if science isn't used as the ultimate guide on the
issue.
"When you look at the overwhelming
majority of studies that have been peer reviewed and published in scientific
journals around the world, you'll find no relationship between wireless usage
and adverse health affects," Farren said.
Frank Barnes, who chaired the January report
from the National Research Council, said Wednesday that "the jury is
out" on how hazardous long-term cell phone use might be.
Speaking from his cell phone, the professor
of electrical and computer engineering at the University of Colorado at Boulder
said he takes no
special precautions in his own phone use. And he offered no specific advice to
people worried about the matter.
It's up to each individual to decide what if
anything to do. If people use a cell phone instead of having a land line,
"that may very well be
reasonable for them," he said. Susan Juffe, a 58-year-old Pittsburgh
special education teacher, heard about Herberman's cell phone advice on the
radio earlier in the day.
"Now, I'm worried. It's scary," she
said. She says she'll think twice about allowing her 10-year-old daughter Jayne
to use the cell phone.
"I don't want to get it (brain cancer)
and I certainly don't want you to get it," she explained to her daughter.
Sara Loughran, a 24-year-old doctoral student
at the University of Pittsburgh, sat in a bus stop Wednesday chatting on her
cell phone with her mother. She also had heard the news earlier in the day, but
was not as concerned.
"I think if they gave me specific
numbers and specific information and it was scary enough, I would be
concerned," Loughran said, planning to
call her mother again in a matter of minutes. "Without specific numbers,
it's too vague to get me worked up."
------------------------------------------
Jennifer Yates reported from Pittsburgh. Science Writer Seth Borenstein
reported from Washington. Reporter Ramit Plushnick-Masti contributed
from Pittsburgh and Science Writer Malcolm Ritter contributed from New York.
ON THE INTERNET:
Advice from the University of Pittsburgh
Cancer Institute:
