Betreff: Re: Sensitivity of Neurons to Weak Electric Fields
Von: "Iris Atzmon"
Datum: Tue, 16 Nov 2004 22:49:52 +0200
An: "Robert Riedlinger"
CC: "Milt Bowling" , "Bernd" , "Blake Levitt" , "DECT Victima" , "Don Maisch" , "Federico Zanasi" , , "Hans Karow" , "Jean Marie Danze" , "Joanne Muller" , "Klaus Rudolph" , "Libby Kelley" , "Lothar Geppert" , "Louis Slesin" , "Marcus Relton" , "Miguel" , "Olle Johansson" , "Penny Hargreaves" , "Raule" , "Robert Riedlinger" , "Roger Santini" , "Shivani" , "Siannette Kwee" , "teslabelg"

Sensitivity of Neurons to Weak Electric Fields -- Francis et al. 23 (19): 7255 -- Journal of Neuroscience
If I say "I am a good person" 10 times a day, does it prove that I am a good person?
Of course that's ridiculus. The same is Repacholi's answer, who's trying to present himself 
as "evidence based" just by writing maximum times the word "science". Well, we have done some reading, we learnt of his history, we have collected kgs of researchs, it's a pity that Repacholi is not updated with the scientific advances, even IARC is more updated.  Repeating "we base our claims on science" many times in a short answer is nothing but abusing and disrespect for science, and if we talk about pity, then it's a pity that Repacholi thinks that we are all stupid.  Dr. Niel Cherry, Prof Goldsmith, Don Maisch, Dr. Hyland, Dr. Philips and many other scientists that are the leading scientists in this field, exposed the fraud of what Repacholi calls "science".
Doing business with the industry, hiding his own findings, ignoring from the evidence about childhood leukemia and IARC classification, being in the WHO and in the ICNIRP at the same time and claiming to be "objective", and running the whole world through remote control by seeding ignorance and irradiationg the whole world is
not science, it's pure fraud.  
----- Original Message -----
From: Robert Riedlinger
To: Hans Karow
Cc: Milt Bowling ; Iris Atzmon ; Marc and Lisa ; Imelda Oconnor
Sent: Tuesday, November 16, 2004 8:06 PM
Subject: Fw: Sensitivity of Neurons to Weak Electric Fields

 I AM BUSY MAKING UP A REPLY TO THE FOLLOWING LETTER FROM MR REPACHOLI.I COULD USE SOME HELP Regards Robert
----- Original Message -----
From: repacholim@who.int
To: r_riedlin@telus.net
Cc: Art_Thansandote@hc-sc.gc.ca ; imeldaoconnor@hotmail.com
Sent: Sunday, November 14, 2004 11:33 PM
Subject: RE: Sensitivity of Neurons to Weak Electric Fields

Robert WHO bases its decision on the science...if the science does not support your position this is not my problem. It is a cheap shot to say that because the WHO position is the same an an industry position that we are in bed with industry...this is patently untrue and it does you no good to even suggest it..
 
Our Director General claimed to be hypersensitive...this does not mean that we should base our decisions on anything but the valideated evidence..
 
Pity is that people such as yourself wont listen to the science...it is one of our greatest resources...all successful countries reply on it.


From: Robert Riedlinger [mailto:r_riedlin@telus.net]
Sent: 09 November 2004 02:35
To: repacholim
Cc: Art Thansandote; Imelda Oconnor
Subject: Sensitivity of Neurons to Weak Electric Fields

IS  ELECTRO- MAGNETIC SENSITIVITY REAL or a psycho's dream??
 
 
Mr Repacholi
Dr William J. Rea of Environmental Health Center, Dallas claims that he is himself is sensitive to electromagnetic fields.Would  you class him as a psycho or a dreamer along with the rest of us that are EHS/ I am amazed at your inability to look beyond the industrial sponsored and funded research. Regards Robert
 

 
J. Neurosci. 

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The Journal of Neuroscience, August 13, 2003, 23(19):7255-7261

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Sensitivity of Neurons to Weak Electric Fields

Joseph T. Francis,1,4 Bruce J. Gluckman,1,2 and Steven J. Schiff1,3,4

1Krasnow Institute for Advanced Studies and Departments of 2Physics and Astronomy and 3Psychology, George Mason University, Fairfax, Virginia 22030, and 4Neuroscience Program, The George Washington University, Washington, DC 20037


   Abstract
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
 
Weak electric fields modulate neuronal activity, and knowledge of the interaction threshold is important in the understanding of neuronal synchronization, in neural prosthetic design, and in the public health assessment of environmental extremely low frequency fields. Previous experimental measurements have placed the threshold between 1 and 5 mV/mm, although theory predicts that elongated neurons should have submillivolt per millimeter sensitivity near 100 ÁV/mm. We here provide the first experimental confirmation that neuronal networks are detectably sensitive to submillivolt per millimeter electrical fields [Gaussian pulses 26 msec full width at half-maximal, 140 ÁV/mm root mean square (rms), 295 ÁV/mm peak amplitude], an order of magnitude below previous findings, and further demonstrate that these networks are more sensitive than the average single neuron threshold (185 ÁV/mm rms, 394 ÁV/mm peak amplitude) to field modulation.

Key words: electric field; neuron; threshold; synchrony; ephaptic; hippocampus


   Introduction
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
 
Weak electric fields modulate neuronal activity (Jefferys, 1995), and knowledge of the interaction threshold is important in the understanding of neuronal synchronization, in neural prosthetic design, and in the public health assessment of environmental extremely low frequency (ELF) fields.

Previous experimental measurements have placed the threshold for neuronal interaction with electric fields between 1 and 5 mV/mm (field strength applied to tissue). In mammalian brain, direct current (DC) electric fields 5-10 mV/mm cause changes in neuronal evoked population spikes in hippocampal slices (Jefferys, 1981). In experiments that used both sinusoidal input fields and added noise, stochastic resonance, Gluckman et al. (1996b) detected field interactions as low as 2.5 mV/mm root mean square (rms) in the CA1 region of the hippocampal slice. More recently, Ghai et al. (2000) demonstrated the ability to modify activity in low calcium hippocampal slices with electric fields as low as 1 mV/mm.

Theory, however, predicts that elongated neurons should have submillivolt per millimeter sensitivity (Weaver et al., 1998). Significant interaction with an electric field requires an effect on cellular biochemical processes greater than the "molecular shot noise" driven by macromolecular thermal fluctuations. Based on an elongated neuron model with thermal noise, the threshold for electric field interaction was estimated near 100 ÁV/mm (Weaver et al., 1998).

The mammalian hippocampus has several unique features that render it particularly sensitive to electric fields. Cellular packing is so dense that it can display epileptiform events even in the absence of functioning chemical synapses (Jefferys and Haas, 1982; Taylor and Dudek, 1982), a condition under which electric fields likely play a significant role in ensemble activity. Hippocampal pyramidal cells have somata asymmetrically placed with respect to their dendritic trees, and the sensitivity of a neuron to firing rate modulation from an imposed electric field is related to the amount of positional asymmetry of the soma with respect to the dendritic tree (Chan and Nicholson, 1986; Chan et al., 1988). In addition, the individual pyramidal cells are aligned such that adjacent cells have parallel dendrites, which favor interaction with fields aligned along the collective somatodendritic axes (Rushton, 1927). These oriented low amplitude effects are distinct from the depolarization block seen with unoriented fields of higher amplitude and frequency (Bikson et al., 2001).

In the experiments that are described here, we used a longitudinal hippocampal slice to maximize alignment of CA1 or CA3 neurons with the parallel electric field lines generated from parallel plate electrodes. We also used an electric field waveform with similarities to natural CA3 population extracellular fields, mimicking the low frequency characteristics of CA3 population activity local field potentials. We examined the effect of weak fields both on network responses and single neurons.


   Materials and Methods
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
 
Slice preparation. Hippocampal slices were prepared from 45-to 80-d-old Sprague Dawley rats that were anesthetized deeply with diethyl-ether and decapitated. Slices (350 Ám thick) were cut longitudinally with a tissue chopper and placed in an interface type perfusion chamber at 34░C. Consistently healthy longitudinal slices were obtained if slices were placed into the chamber at room temperature before being warmed with the temperature control circuit. Slices were perfused for 90 min with artificial CSF (ACSF) composed of (in mM): 155 Na+, 136 Cl-, 3.5 K+, 1.2 Ca 2+, 1.2 Mg 2+, 1.25 PO4 2-, 24 HCO3-, 1.2 SO42-, and 10 dextrose. To generate synchronous population events in the hippocampal slice, we then replaced the perfusate with elevated potassium ACSF containing 8.5 mM K+ and 141 mM Cl - (Rutecki et al., 1985). Slices were allowed to acclimate to the elevated K+ for 1-1.5 hr.

Recording methods. All neuronal activity was recorded with the use of saline-filled micropipette electrodes (1-3 M{Omega} for recording population bursts and 9-15 M{Omega} for single-unit recording), which were amplified differentially (Grass model P16, Grass Instruments, Quincy, MA) with respect to a saline agar bridge reference electrode (75 K{Omega}). This bridge electrode contained agar prepared with 8.5 mM KCl as the solvent. To minimize the stimulation artifact, we placed the reference electrode on an isopotential of the applied field, manipulating it with respect to the recording electrode to minimize a test sinusoidal electric field (Gluckman et al., 1996b).

In the presence of elevated K+ the hippocampal slices exhibit population burst firing activity in the CA3 region (Rutecki et al., 1985). CA1 activity from longitudinal slices in elevated K+ consists of smaller population events than seen in CA3 and prominent single-unit activity. This differs from transverse slice CA1 dynamics in elevated K+ because the CA1 effectively is disconnected from the CA3 in this longitudinal preparation. We used a simple threshold-crossing technique to detect the onset times of the CA3 population bursts and CA1 neuronal activity. Single-unit spike extraction was performed with Common Processing and Autocut software (DataWave Technologies, Longmont, CO).

Electric field production. Slices were placed between two field-generating Ag-AgCl parallel plate electrodes submerged in the perfusate. The electric field was generated in the chamber from driving current between two 12-mm-wide parallel Ag-AgCl plates, spaced 17 mm apart, embedded within the chamber floor. To compensate for electrode polarization, we feedback-controlled the current that was applied by using a four-electrode technique (Fig. 1 A) such that the electrical potential between two 1-mm-in-diameter sensing electrodes placed 12 mm apart was proportional to a control signal (Gluckman et al., 2001). The resulting electric field in the central 1 cm 2 region, where the slices were placed, was mapped by using sinusoidal applied fields to establish electric field uniformity and to calibrate the stimulation electronics. The stimulation electronics were constructed such that the potentials of the stimulation electrodes could float with respect to measurement ground. The final current-generating stage was battery powered, based on an Analog Devices Amp01 instrumentation amplifier (Wilmington, MA), with an additional operational amplifier stage. Additionally, the input stage of the stimulation amplifier contained a zeroing offset, used to set the electric field to zero when the control signal was zero. In practice, this offset was adjusted at the beginning of each experiment until the differentially measured potential difference between micropipette electrodes placed within the chamber 5-10 mm apart in the direction of the field was minimized, yielding a baseline DC field with a magnitude <10 ÁV/mm.



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Figure 1. A, Schematic of the electrode configuration used to generate electric fields. B, Typical network activity from the CA1 region. Calibration: 0.04 mV, 100 msec. Dashed lines indicate the positive and negative thresholds used to detect events (see Materials and Methods). C, D, Shown are the power spectral densities (PSDs) of the natural (E) and simulated (F) CA3 bursts. Scaled versions of waveform F were used as the electric field input in the experiments.

 

To stimulate the slices, we used simulated burst stimulus waveforms (Fig. 1 F) that had a Gaussian profile (26 msec full width at half-maximal) and a low frequency spectrum with a similar distribution (Fig. 1C,D) to that of a CA3 population burst (Fig. 1 E). The stimulus waveform was generated at 10 kHz on a PC, producing an analog signal via a digital-to-analog circuit (M16-E National Instruments, Austin, TX). This analog signal was low-pass-filtered (<1.5 kHz) to reduce artifacts from the digital-to-analog conversion. Because such waveforms differ significantly from the typical square wave stimuli used in previous electric field threshold experiments, we will report both the peak amplitude and the rms amplitude of these simulated burst waveforms. The rms amplitude of stimulus waveforms was calculated over a window of 90 msec. All amplitudes that appear in the figures are in units of rms.

CA3 experimental protocol. In experiments conducted on the CA3, we chose slices that both exhibited robust population bursting and could be entrained fully by input fields with a maximum peak of 10 mV/mm. This excluded slices that were insensitive to electric field modulation, presumably because of the variability of the slicing procedure. Because of our alignment of the reference electrode along an isopotential, the stimulation artifacts from fields as large as 10 mV/mm were small with respect to the CA3 population burst activity and allowed for straightforward burst time extraction by using a simple threshold crossing. CA3 data were low-pass-filtered below 500-1000 Hz (recorded in true DC).

At the beginning of each CA3 experiment the mean interburst interval (IBI) of the slice was established over a 2 min period. A periodic input time series of simulated bursts was generated, with inter-event intervals 12% faster than the mean rate of the slice for slices with decreasing IBI and 10% faster for slices with increasing or stable IBI. The mean IBI rate of the slice was recalculated after each trial to ensure that the mean input frequency used for the stimulus remained faster than the new intrinsic mean of the slice. If after a trial the slice had a mean intrinsic IBI faster than that of the stimulus, then the data were discarded, because this implied that at some time during the experiment the rate of the input and slice were the same. Such identical frequencies would generate spurious cross-correlation, which could not be distinguished from true synchronization because of coupling between the two systems.

In an effort to reduce further the spurious cross-correlation because of shared frequency content, the phase of the input field was perturbed randomly (see Fig. 2 B) at least once per minute. Recordings during stimulation were 7 min in length, a time chosen as a compromise in obtaining sufficient data for statistical analysis while minimizing drift in the intrinsic mean IBI.



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Figure 2. Data taken from a CA3 experiment. The thick lines pointing downward in A and B indicate the times of the input stimuli (shown in Fig. 1 F). The thin traces are voltage recordings of population burst activity from CA3. A, Data from an experiment with an rms peak electric field strength of 3.9 mV/mm. B, Data from the corresponding sham experiment. Stimulus artifact (SA) and phase perturbations (PP) are marked. C, D, Raster plots from experiments in A and B showing entrainment and lack of entrainment, respectively.

 

Sham experiments were conducted with the field electronics turned off and were interspersed with the field experiments. These sham experiments were used to generate statistical confidence limits for the field stimulation experiments.

CA1 experimental protocol. Experiments conducted on the CA1 were taken from slices that showed robust cellular activity in this region and that retained little or no anatomic CA3 after slicing. Such slices therefore were devoid of large-scale population burst firing events from the CA3, which minimized endogenous electric field or synaptic input to the CA1 that would have complicated interpretation of the results. Small spontaneous population responses and single-cell activity were observed. Stimulation frequency of 1-2 Hz was used for CA1 experiments.

All of the CA1 data were bandpass-filtered (250-2000 Hz) before data analysis. This bandpass served to capture multiple and single-unit activity well and, when applied to recordings of the stimuli from the chamber without a slice present, nearly eliminated the stimulus waveform. The same phase perturbations and sham experiments discussed above also were used for CA1 experiments.

However, because of the smaller signal-to-noise ratio of CA1 activity, we remained cautious of spurious stimulus artifacts and therefore generated two peri-stimulus time histograms (PSTHs) that used both upper and lower threshold crossings (Fig. 1 B). Because of the asymmetry of the input field with respect to zero voltage, we would expect mirror image changes in these two PSTH values from stimulus artifact contamination. The sum of these PSTHs was calculated for each bin so that field artifacts would sum to zero, giving distributions similar to the sham experiments. Biological activity that synchronized to the fields, either excitatory or inhibitory, would give asymmetric PSTH distributions after such dual-threshold PSTHs were combined.


   Results
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
 
CA3 activity
Raw data from a CA3 experiment are shown in Figure 2. In Figure 2, A and B, the top traces (thick lines) mark the timing of the stimulus field inputs, and the bottom trace (thin lines) shows the simultaneously recorded neuronal activity. At the beginning of the epoch shown in Figure 2A, the stimulus and CA3 activity start out of phase and remain unsynchronized for several stimulus cycles. This illustrates the subthreshold nature of small input fields, which are not able to produce arbitrarily large phase resets for the population bursts. However, once the stimulus phase comes into close alignment with the CA3 population phase, it captures and entrains the network (by pulse 4) at this field strength of 3.9 mV/mm rms (6.8 mV/mm peak). The residual stimulus artifact (SA) shown in Figure 2 is the largest we observed in these experiments after properly aligning the reference electrode close to an isopotential. The amplitude disparity between CA3 bursts and such residual SA made use of a simple threshold adequate to discriminate population firing times from SA in CA3 experiments without errors. Figure 2B illustrates data from the corresponding sham experiment in which the independent nature of the signals can be observed readily. An example of a phase perturbation (PP) is shown at the beginning of the epoch in Figure 2B.

Raster plots of the population events shown in Figure 2, A and B, are shown in Figure 2, C and D, respectively. It is clear that in Figure 2C the neuronal data are synchronized strongly to the stimulus input. Note that the neuronal activity escapes entrainment near the 45th stimulus, followed by steady advance of the phase difference between the stimulus and the neuronal activity until capture again is effected. No entrainment is seen in the raster plot from the sham experiment in Figure 2D. The raster plots in Figure 2 represent just over 3 min of recording.

CA3 synchronization at smaller field strengths from one experiment is illustrated in Figure 3. The left column demonstrates synchronization between an electric field stimulus and CA3 population burst activity with field strengths as low as 560 ÁV/mm rms (1.2 mV/mm peak amplitude) in Figure 3, E and G. On the right side of the figure are the corresponding sham experimental results. Figure 3, A and C, demonstrates strong synchronization at a field strength of 1.68 mV/mm rms (3.6 mV/mm peak), whereas the weaker synchronization remains visually evident in the raster and histogram plots in Figure 3, E and G. The dotted lines in Figure 3 indicate 2 SD above the mean histogram bin values.



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Figure 3. Raster plots from a CA3 electric field experiment (A, E) and the corresponding shams (B, F) are shown with corresponding peri-stimulus time histograms (PSTHs), using 20 msec bins (C, D, G, H). Dashed horizontal lines are the mean of the histogram values plus 2 SD. The input stimulus rms amplitudes are indicated.

 

To estimate the electric field threshold that would cause statistically reliable synchronization, we examined all of the data from slices that would synchronize completely with the input field at a peak strength of 10 mV/mm. This relatively large field (Terzuolo and Bullock, 1956; Jefferys, 1981; Gluckman et al., 1996a,b; Ghai et al., 2000) would synchronize more than one-half of the slices that were tested.

For individual experiments (see supplementary data; available at www.jneurosci.org), significant consecutive histogram peaks just after stimulation were observed for three of 10 slices at 460 ÁV/mm rms (979 ÁV/mm peak). For random variables drawn from a normal distribution, consecutive histogram values >2SD should occur with frequencies <0.0025. We observed a significant consecutive histogram peak in only one of six experiments at 370 ÁV/mm rms (787 ÁV/mm peak).

Such simple threshold statistics do not reflect the broader histogram deviations just after stimulation, with values below 2 SD evident in these experiments. To better estimate a population threshold, we therefore pooled data from all of the experiments. The pooled and averaged results for 35 slices from six rats at a selection of field strengths are illustrated in Figure 4. In each panel the means (thin solid line) ▒ 2 SD (dashed lines) of the pooled and averaged sham experiments are indicated. We sought to match the number of bursts in the sham experimental groups to the number of bursts in the respective field experimental groups. If the total number of events in a given experimental group was less than the total number of sham events, we would resample the sham experiments randomly. Using the sham results to establish statistical confidence, we found that the lowest field strength that produced statistically significant pooled synchronization results in CA3 experiments was 370 ÁV/mm rms (787 ÁV/mm peak amplitude).



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Figure 4. PSTHs (20 msec bins) from data pooled and averaged over all of the CA3 experiments. The electric field orientation, excitatory, is illustrated in the top left inset. Solid horizontal line is the mean of the number-matched sham data, and the dashed horizontal lines are ▒ 2 SD of the sham data. The input stimulus rms amplitudes are indicated. Significant synchronization is observed at 370 ÁV/mm rms (787 ÁV/mm rms peak). The bottom right panel (0 mV/mm) was generated from pooling and averaging all of the CA3 sham data.

 

CA1 network activity
Synchronization between CA1 network activity and the electric field stimulus is illustrated in Figure 5 for experiments from one slice. At the top of the figure is an example of raw CA1 network data with small population and multiunit activity (calibration 0.04 mV, 1000 msec), stimulated with the Gaussian-shaped field indicated in the bottom trace, with an excitatory field of 1.75 mV/mm rms. The expanded insets show the Gaussian profile of the slight residual field artifact and the increased CA1 network activity responding with small time lags to the onset of each stimulus field. The raster plots and histograms of the left column of Figure 5 illustrate an experiment in which the electric field was excitatory (top left inset), and the right column illustrates data in which the electric field was inhibitory (top right inset). Each panel shows the mean ▒ 2 SD of the histogram (10 msec bins). Evidence of synchronization is present for each field strength that is shown. At the larger field strengths in Figure 5, the histogram peaks easily can be seen reflected in the raster plots.



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Figure 5. PSTHs (10 msec bins) generated from threshold crossing times of CA1 network activity at time lags relative to the stimulus waveform. Inset at the top of the figure illustrates a sample of CA1 network data with small population and multiunit activity (calibration: 0.04 mV, 1000 msec), stimulated with Gaussian-shaped field indicated in bottom trace with an excitatory field of 1.75 mV/mm rms. The expanded insets show the Gaussian profile of the slight residual field artifact and the increased CA1 network activity responding with small time lags to the onset of each stimulus field. The raster plots and histograms of the left column represent data taken with the electric field oriented such that it causes excitation, and the right column represents data with the electric field oriented in the opposite direction such that it causes suppression. Each right-left pair of histograms was taken from the same slice within 10 min of each other. Solid horizontal line is the mean of the histogram bin counts, and the dashed lines are ▒ 2 SD of the mean. The input stimulus rms amplitudes are indicated.

 

To estimate the electric field threshold limit that would cause statistically reliable synchronization, we examined all of the data from slices that would synchronize significantly with the input field at a peak strength of 1 mV/mm. This was in contrast to 10 mV/mm used for the CA3, because the CA1 was much more sensitive to electric fields. Almost every slice that exhibited robust CA1 cellular activity met this criterion.

For individual experiments (see supplementary data) significant consecutive histogram values just after stimulation were observed (from 6 slices) for three of five excitatory (+) and two of four inhibitory (-) experiments at 140 ÁV/mm rms (298 ÁV/mm peak).

Figure 6 shows the pooled and averaged results from 18 experiments on five rats, using seven slices with two field strengths: 290 ÁV/mm and 140 ÁV/mm (rms). The field orientations correspond to the excitatory (top) and inhibitory (bottom) orientations. In each plot the PSTHs are a combination of the upper and lower threshold crossings, with the mean ▒ 2 SD for event number-matched shams plotted as solid and dotted lines, respectively (sham data histograms are plotted as insets). The lowest field strength used that produced significant synchronization in these averaged CA1 experiments was 140 ÁV/mm rms (298 ÁV/mm peak amplitude).



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Figure 6. PSTHs (10 msec bins) of data pooled and averaged over all of the CA1 experiments. Thick curve illustrates results that use an input field of 290 ÁV/mm rms (596 ÁV/mm peak), and the thin curve data are from experiments with an input field of 140 ÁV/mm rms (298 ÁV/mm peak). Solid horizontal line is the mean of a number-matched sham, and dashed lines are ▒ 2 SD of that sham distribution. Insets show the CA1 sham distributions. The top panel illustrates results that use the excitatory field orientation, whereas the bottom reflects the inhibitory field.

 

CA1 single-unit activity
Figure 7A shows 10 sec of bandpass-filtered recording (250-2000 Hz) from an experiment observing a single unit in CA1 (further illustrated in Fig. 8). Note the absence of stimulus artifact. A single-unit trace is shown as an inset at an expanded time base in Figure 7A. Figure 7B shows an overlay of all of the first spike waveforms from the bursts from this experiment, confirming that this was indeed a single unit.



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Figure 7. A, Bandpass-filtered (250-2500 Hz) data (10 sec) from a single CA1 unit, with one burst expanded in the inset. B, An overlay of all of the primary (first) spikes from each burst event from this experiment, the overlap confirming that this was indeed a single unit.

 


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Figure 8. Raster plots generated from CA1 single-unit activity from two different hippocampal slices along with the corresponding PSTH (20 msec bins). Dashed horizontal lines are the mean of the histograms ▒ 2 SD. The input stimulus rms amplitudes are indicated.

 

Raster plots from two separate single-unit experiments are shown in Figure 8, A, B, E, and F, along with the corresponding PSTH in Figure 8, C, D, G, and H. Figure 8, E and G, demonstrates data from the solitary observed case of a single unit synchronizing with a field of 140 ÁV/mm rms (298 ÁV/mm peak amplitude), along with the corresponding sham experiment in Figure 8, F and H. Once again the dashed lines in the histograms are the mean histogram value ▒ 2 SD. Although frequent network synchronization was observed at this field strength, this was the only single unit observed to synchronize at such low field intensity.

For individual experiments (see supplementary data) significant consecutive histogram peaks just after stimulation were observed in three of 11 experiments of single-unit modulation at 185 ÁV/mm rms (394 ÁV/mm peak) and a single significant result for one of 14 slices at 140 ÁV/mm rms (298 ÁV/mm peak).

Most single units demonstrated burst firing activity as shown in Figure 7. If the electrodes were pushed against the cells during positioning, burst firing often would convert transiently to singlet activity. After electrodes were positioned, most cells would switch spontaneously from burst to singlet firing during recording at some point during the experiment, although burst firing remained the predominant mode of activity (>80%). Single-cell data were pooled from both singlet and burst firing modes, and all spikes were used for the analysis shown here. When only the first spike in a burst was used for analysis, the electric field interaction threshold appeared to be unchanged (data not shown).

Figure 9 illustrates averaged results for a selection of excitatory field strengths for CA1 single-unit activity. Event number-matched sham data averaged for each experimental group are indicated (thin lines) along with ▒ 2 SD of the sham mean (dashed lines). The lowest field strength that produced significant synchronization in pooled and averaged data (15 experiments on 4 rats, using 6 slices) was 185 ÁV/mm rms (393 ÁV/mm peak).



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Figure 9. PSTHs (10 msec bins) generated from the pooled and averaged CA1 single-unit data from all of the experiments. Field is oriented such that it causes excitation. Thick lines are the PSTH from the data, and thin lines are from the number-matched sham experiments. Significant modulation is observed for 185 ÁV/mm rms (394 ÁV/mm peak) for these pooled data, but not for 140 ÁV/mm rms (298 ÁV/mm peak). Solid horizontal line is the mean from the sham experiments, and dashed lines are ▒ 2 SD from the sham mean. The input stimulus rms amplitudes are indicated.

 


   Discussion
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
 
Our findings are the first experimental evidence that neurons are indeed capable of synchronizing to weak electric fields below 1 mV/mm, and our results demonstrate thresholds for electrical field interactions close to the best available theoretical limits. CA1 pyramidal cell networks were sensitive to fields with rms amplitudes as small as 140 ÁV/mm. In addition, we have shown the first experimental demonstration that neuronal networks appear to respond to fields with more sensitivity than single neurons.

We observed both excitation and suppression of network activity in CA1 at the lowest field strengths that were used (140 ÁV/mm rms). Such weak interaction thresholds are important for several reasons: the potential use of weak electric fields for neuronal modulation in prosthetic device design (Gluckman et al., 1996a, 2001; Ghai et al., 2000; Richardson et al., 2003), the environmental ELF field threshold for interaction with biological systems (Adair, 1991; Weaver et al., 1998), or consideration of the significance of endogenous field interactions within the intact nervous system (Jefferys and Haas, 1982; Snow and Dudek, 1984a,b, 1986; Traub et al., 1985a,b; Dudek et al., 1986; Vigmond et al., 1997).

The CA1 networks were more sensitive to the electric fields than the CA3 networks. Anatomic evidence suggests that the CA1 pyramidal cells are more consistent in their total dendritic lengths from one area of the CA1 to the next, in contrast to CA3 (Ishizuka et al., 1995). The pyramidal cells of the CA1 region also have a smaller extracellular-to-intracellular volume ratio than that of the CA3 region (McBain et al., 1990), and such tight packing of neurons increases the electrical impedance and field interactions between cells (Vigmond et al., 1997).

The observation that weak perturbations can synchronize oscillatory physical systems is centuries old (Huygenii, 1673). In vivo measurements of hippocampal sharp waves can be as large as 8-14 mV/mm (Buzsaki, 1986), nearly two orders of magnitude larger than needed to observe the effects seen in our experiments. Our findings suggest that endogenous local field potentials are large enough to play a role in the synchronization of neuronal networks in the intact brain (Traub et al., 1985a,b). Because small fields can modulate neuronal excitability in a subthreshold manner, network activity could modulate the excitability of cells that are not spiking and of cells not connected synaptically to the firing neurons producing the electrical fields. Examples of place cells (Skaggs et al., 1996) and odor recognition (Wehr and Laurent, 1996), in which the phase of the rhythmic local field potential is important in neural encoding, are situations in which endogenous electric fields could play a role.

Recent work predicts that the theoretical limit for the threshold to detect a response in an elongated cell (25 x 1000 Ám) to ELF electric fields would be ~100 ÁV/mm (Weaver et al., 1998). This estimation is based on the assumption that the electric field must produce effects larger than the stochastic fluctuations relevant to biological membranes such as voltage-gated ion channels and their associated ion fluxes, the so-called molecular shot noise (Astumian et al., 1995). Our findings of a threshold for the CA1 networks and single cells between 100 and 200 ÁV/mm are the first experimental data consistent with this predicted limit (Weaver et al., 1998).

In addition, to our knowledge, this is the first demonstration that neuronal networks respond to fields more sensitively than single neurons. Whether this is a manifestation of simply increasing the numbers of neuronal detectors or is from array-enhanced signal detection caused by coupling (Linder et al., 1995; Gailey, 2000; Krawiecki et al., 2000) remains to be determined.

We made no attempt to optimize the stimulus waveforms that were used. Instead, we selected the field temporal profiles to mimic naturally occurring population burst profiles from CA3. Optimizing waveforms to incorporate neuronal resonant frequencies (Hutcheon and Yarom, 2000) might decrease further the field strength required to observe synchronization. The use of white noise electric field stimulation with spike-triggered averaging of the preceding electric field (Bryant and Segundo, 1976) could serve as a useful tool for optimizing the electric field morphology.

Modulation by small fields has advantages in control devices that use electric fields to modulate neuronal networks (Gluckman et al., 2001; Richardson et al., 2003). Designing such devices to operate at the smallest possible field strengths will minimize the potential for unwanted functional effects or tissue damage from long-term chronic stimulation.

Whether weak environmental ELF fields affect neuronal firing will be a function of the reduction in ambient field by the anatomic layers surrounding the brain and the neuronal modulation threshold. Estimates suggest that typical ambient fields will be attenuated below the thresholds we have determined (Adair, 1991). We view it as important to fill in two remaining experimental gaps in our knowledge of ELF field effects: to verify experimentally the predicted attenuation of fields and, in the manner described here, to measure the synchronization threshold for 50-60 Hz fields.


   Footnotes
 
Received Mar. 20, 2003; revised May. 9, 2003; accepted May. 13, 2003.

This work was supported by National Institutes of Health Grants K02MH01493 and R01MH50006 and the Whitaker Foundation.

Correspondence should be addressed to Steven J. Schiff, Krasnow Institute, Mail Stop 2A1, George Mason University, Fairfax, VA 22030. E-mail: sschiff@gmu.edu.

J. T. Francis' present address: State University of New York Downstate Medical Center, Brooklyn, NY 11203.

Copyright ę 2003 Society for Neuroscience 0270-6474/03/237255-07$15.00/0


   References
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
 

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M. Bikson, M. Inoue, H. Akiyama, J. K. Deans, J. E. Fox, H. Miyakawa, and J. G. R. Jefferys
Effects of uniform extracellular DC electric fields on excitability in rat hippocampal slices in vitro
J. Physiol., May 15, 2004; 557(1): 175 - 190.
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Repacholi's circus


The world health organization's team, and especially Repacholi, must be
thinking they are running a circus, and that the public is some kind of
a circus animal, something that you can throw today to the right,
tomorrow to the left, to juggle with, and still, at the end of the day
it is expected to lick your hand and say "thank you".

Otherwise, how can this behaviour can be explained (Microwave News
May/June issue): (Repacholi wanted to provoke comments - I hope he will
get now rain of comments.) WHO Flip-Flops on EMFs, Precautionary
Principle Now Revoked

June 5, 2003 - The World Health Organization has decided not to invoke
the precautionary principle for electromagnetic fields (EMFs), Dr.
Michael Repacholi has told Microwave News.

Less than three months after the WHO EMF project told participants at
its workshop on the precautionary principle that there is "sufficient
evidence" to apply the principle to power-frequency EMFs and
radiofrequency and microwave radiation, Repacholi, who runs the project,
said that the earlier statement was only a trial balloon.

"The draft we submitted to the Luxembourg workshop was purely a
discussion draft to provoke comment....It was very successful at that,"
Repacholi said.

The move took many of those who had attended the February workshop by
surprise. We have full coverage --including reactions of those who went
to Luxembourg-- in our May/June 2003 issue.

(More in the new microwave news)
A proposal from the IEEE's International Committee on Electromagnetic
Safety to relax the limits for mobile phone radiation has come in for
criticism. The May/June issue explains why.

Exposure to power-frequency magnetic fields at work increased the risk
prostate cancer among utility workers.

The U.K. government has announced an $8 million long-term study of the
possible health effects of radiation from TETRA digital radios, which
police throughout the country will soon be using.

In the U.K., Dr. David de Pomerai of the University of Nottingham has
shown that very weak microwave radiation can change the shape of
proteins, prompting them to clump together or form long strands called
fibrils. De Pomerai argues that these changes in turn trigger the
production of heat shock proteins, previously reported by his and other labs.

Informant: Iris Atzmon

de Pomerai DI, Smith B, Dawe A, North K, Smith T, Archer DB, Duce IR,
Jones D, Candido EP.

School of Life and Environmental Sciences, University of Nottingham,
University Park, NG7 2RD, Nottingham, UK

Exposure to microwave radiation enhances the aggregation of bovine serum
albumin in vitro in a time- and temperature-dependent manner.

Microwave radiation also promotes amyloid fibril formation by bovine
insulin at 60 degrees C. These alterations in protein conformation are
not accompanied by measurable temperature changes, consistent with
estimates from field modelling of the specific absorbed radiation (15-20 mW kg(-1)).

Limited denaturation of cellular proteins could explain our previous
observation that modest heat-shock responses are induced by microwave
exposure in Caenorhabditis elegans. We also show that heat-shock
responses both to heat and microwaves are suppressed after RNA
interference ablating heat-shock factor function.

FEBS Lett. 2003 May 22;543(1-3):93-7.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=
PubMed&list_uids=12753912&dopt=Abstract

Informant: Reinhard Rueckemann


EXTREME LOW FREQUENCY MAGNETIC FIELDS AND EEG ENTRAINMENT

Recent well-documented research suggests that between 25% and 75% of
human and animal subjects exhibit psychophysiological sensitivity to
magnetic and electrical fields in the extreme low frequency (ELF) ranges
corresponding to brainwave spectra.

Neuronal synchronization/desynchronization and brainwave entrainment can
be demonstrated clinically in cats, monkeys, and human sensitives in the
presence of ELF oscillations of both natural and man-made signals,
including pulse-modulated radio frequency carriers.

http://www.elfis.net/elfol8/e8elfeeg1.htm

Informant: Romy


My ES Symptoms - Like Evidence required

I am from Australia.

I suffer from:-
Chronic Fatigue Syndrome
Multiple Chemical Sensitivity
EMR Hyper-Sensitivity

All the above (though at different stages) was initailly triggered by
exposure to a mobile phone base station antenna over a duration of 10
minutes. I was within 6 - 8 meters most of the time of the antennas. For
a very short while I was closer. And later trying to work whilst ill
(with computers & on phone calls for long hours & with mobile phones in
workplace everywhere).

My current ES Symptoms vary.

I am affected by:-

CRT Computer Monitor's
Mobile Phones
Cordless Phones
The earpeice of a standard telephone
22kV & above power lines

Typical symptoms are:-

Foggy head
Pressure pain throughout head, particularly around the temple area
Tingling sensation all over head
Dizzy & spaced out feeling
slight balance defect
Headpain (unlike normal headache)
can't think clearly
memory effected

There is also sometimes labarinyth symptoms.

Can anybody who has similar symptoms or anybody who has research that
duplicates or can explain these symptoms please e-mail me. I would be
VERY PLEASED to hear from you. I am in the process of a health claim &
possible court action & need all the evidence I can get. I've been told
to see a pychirchirst also, so I need good hard evidence that ES is not
an immaginary pych illness.

PLEASE E-MAIL ME: My future depends upon it. I had to give up my work
some years ago due to my symptoms.

Thanking you kindly.

Dom

 

 
Electromagnetic Field Sensitivity

William J. Rea, MD, FACS
Environmental Health Center, Dallas
8345 Walnut Hill Lane, Suite 205
Dallas, TX 75231

Yaqin Pan, MD
Dept. of Allergy, Beijing Union Medical College Hospital Beijing, PRC

Ervin J. Yenyves, PhD
Dept. of Physics, University of Texas at Dallas

Iehiko Sujisawa, MD. and Hideo Suyama, MD
Dept. of Ophthamology, Kitasato University Kitasato, Japan

Nasrola Samadi, PhD
Jacksonville State University, Jacksonville, Florida
 
Gerald H. Ross, M.D., CCFP
Environmental Health Center, Dallas

Source: This article was first published in 1991 in the Journal of Bioelectricity, 10(1&2), 241-256. Figure 1is not included here, but can be obtained by writing Dr. W. J. Rea at the Environmental Health Center, Dallas, 8345 Walnut Hill Lane, Suite 205, Dallas, TX 75231.

Abstract
A multiphase study was performed to find an effective method to evaluate electromagnetic field (EMF) sensitivity of patients. The first phase developed criteria for controlled testing using an environment low in chemical, particulate, and EMF pollution. Monitoring devices were used in an effort to ensure that extraneous EMF would not interfere with the tests. A second phase involved a single-blind challenge of 100 patients who complained of EMF sensitivity to a series of fields ranging from 0 to 5 MHz in frequency, plus 5 blank challenges. Twenty-five patients were found who were sensitive to the fields, but did not react to the blanks. These were compared in the third phase to 25 healthy naive volunteer controls. None of the volunteers reacted to any challenge, active or blank, but 16 of the EMF-sensitive patients (64%) had positive signs and symptoms scores, plus autonomic nervous system changes. In the fourth phase, the 16 EMF-sensitive patients wer rechallengd twice to the frequencies to which they were most sensitive during the previous challenge. The active frequency was found to be positive in 100% of the challenges, while all of the placebo tests were negative. We concluded that this study gives strong evidence that electromagnetic field sensitivity exists, and can be elicited under environmentally controlled conditions.

Introduction
Interaction mechanisms that underlie the health and biological effects of electromagnetic fields (EMF) on humans have been studied by many authors.1,2,3,4,5,6 This subject was reviewed recently at the 1990 spring meeting of the American Physical Society .7 Choy et. al.8 investigated individuals with multiple sensitivities who reported reactions to various types of electrical equipment, including power lines, electronic office equipment such as typewriters and computer terminals, video display terminals, household appliances (such as hair dryers), and fluorescent lights.

This paper presents preliminary data on electromagnetic field tests using a square wave generator to evaluate the EMF sensitivity of patients reporting such sensitivities under environmentally controlled and monitored conditions.

Materials and Methods
This study was carried out in four phases.

I. The tests were carried out in an environmentally controlled area with porcelain-on-steel walls to minimize airborne chemical pollution which might interfere with the testing procedure. This type of construction also acted to decrease external electromagnetic fields. Portable EMF monitoring devices were used to find an area that would minimize background EMF which might disturb double-blind challenges and interfere with the testing process. The low-pollution room had a background of 0-100 V/m electric field and 20-200 nT (Tesla) magnetic field. The immediate test site of the patients had unmeasurable electrical fields and magnetic fields in the vicinity of 20 nT.

The major emphasis of this phase of the studies was the evaluation of the effects of the magnetic field generated by a coil fed from a sweep/function generator (Model 3030, B.K. Precision Dynascan Corp.). This equipment allowed us to test square wave frequencies from 0.1 Hz to 5 MHz.

The patients were tested while they were sitting comfortably upright in a chair with the generator on a desk at least 2 m away, with its output connected to a coil 6 cm in diameter and 15 cm tall, made of 35 m of cable and positioned on the floor with its center approximately 0.3 m from the feet of the person tested. The mean values of the alternating magnetic field generated by this arrangement were approximately 2900 nT at floor level, approximately 350 nT at the level of the chair seat and patients' knees, and about 70 nT at hand level. The exposure period lasted approximately 3 minutes per challenge.
 
Before the EMF challenge, blood pressure, pulse rate, respiratory rate, temperature, sign and symptom scores, and autonomic nervous system functions were tested. The autonomic nervous system function was tested with a binocular iriscorder (Model C2515, Hamamatsu Photonics), which measured pupil area, time at which constriction and dilation occurred, and rate of constriction/dilation.9

All patients had been previously evaluated and treated for biological inhalant, food, and chemical sensitivities in order to minimize possible confusion from coexisting problems. The patients were stabilized on a healthy diet in a constant low-pollution environment. In addition, they had their overall body load reduced and stabilized in a controlled environment.

II. This was a single-blind screening of 100 patients who cornplained of being EMF-sensitive. They were challenged under low-pollution conditions using the sweep/function generator at 0.1, 0.5, 1, 2.5, 5, 10, 20, 40, 50, 60, and 100 Hz; then at 1, 5, 10, 20, 35, 50, 75, and 100 KHz; and finally at I and 5 MHz. There were twenty-one active challenges and five blanks (placebos) per person, giving a total of 2600 challenges. When the number and/or intensity of symptoms were 20% over baseline, the result was considered positive, and were recorded as such under the various criteria used. A change in the iriscorder readings more than two standard deviations from baseline was also recorded as a positive result.

III. Twenty-five patients who were found to be positive in phase II challenges and who had no more than one placebo reaction were then selected for a third phase of the study. In addition, 25 healthy naive volunteers were challenged. Double-blind EMF challenges and placebos using the aforementioned parameters were performed. There were 1300 total challenges, of which 1050 were active and 250 were blanks. The tests averaged 21 active frequencies and 5 blanks per subject.

IV. Sixteen patients who reacted in phase III were then rechallenged on two separate occasions in a double-blind manner, using only the frequencies to which they had responded most strongly. For each subject, the frequency of maximum sensitivity was inserted randomly into a series of 5 placebo challenges. Thus, there were a total of 32 active challenges and 160 blanks.

Results
Phase I. The EMF measurements were quite reproducible. We found that the lights. and air handling equipment had to be off during the tests because of their electromagnetic field output. Baseline studies on patients were completed without remarkable result.
Phase II. Of the total of 100 patients tested in the single-blind study, 50 reacted to several of the placebos in addition to the active challenges, and were excluded from further study. Twenty-five subjects who did not react to any active challenges were also excluded. A final 25 subjects who did react to active challenges, but not to blanks, were selected for the third phase of the study (Table 1).

Phase III. The 25 subjects selected from phase II were rechallenqed, and 16 (64%) reacted positively to the active challenges. The total number of positive reactions to the 336 active challenges in the 16 patients was 179 (53%), as compared to 6 positive reactions out of 60 blanks (7.5%). There were no reactions to any challenge, active or placebo, in the volunteer group of naive subjects (Table 2).

When evaluating frequency response, 75% of the 16 patients reacted to 1 Hz, 75% to 2.5 Hz, 69% to 5 Hz, 69 % to 10 Hz, 69% to 20 Hz, and 69% to 10 KHz (Table 3). No patient reacted to all 21 of the active frequencies in the challenges. The average was 11 reactive frequencies per patient, with a range of 1 to 19 positive responses.

The principal signs and symptoms produced were neurological (tingling, sleepiness, headache, dizziness, unconsciousness), musculoskeletal (pain, tightness, spasm, fibrillation), cardiovascular (palpitation, flushing, tachycardia, edema), oral/respiratory (pressure in earss tooth pains, tightness in chest, dyspnea), gastrointestinal (nausea, belching), ocular (burning), and dermal (itching, burning5 prickling pain) (Table 4). Most reactions were neurological.

Phase IV. In the 16 patients again rechallenged in a double-blind manner, using only the single frequency to which they were most sensitive, all reported reactions to the active frequencies when challenged. None reacted to the placebos (Table 5). Signs and symptoms in all 16 patients were positive as was the autonomic nervous system dysfunction, as measured by the iriscorder (Table 6, Figure 1). Examples of changes were a 20% decrease in pulmonary function and a 40% increase in heart rate. In the 16 patients with positive reactions to EMF challenges, two had delayed reactions; gradually became depressed and finally became unconscious. Eventually, they awoke without treatment. Symptoms lasted from 5 hours to 3 days.

Discussion
Since it has been found that electromagnetic fields can affect health, researchers have investigated these phenomena in vivo and in vitro, in animals10,11,12 and humans.1,2,3,4,5,6,7 No individual had been specifically challenged in an attempt to reproduce acute symptoms until Smith and Monro5 followed by Choy, Monro, and Smith,8 who used a series of oscillators of varying frequency to trigger symptoms in electrically sensitive patients. We modified this procedure by developing controlled environmental area, where baselines were constantly monitored for particulates, pollutants, and extraneous fields. Here, controlled EMF output was applied so that data would be more reproducible.

 Several factors have led us to believe that we have reproducible results. Meticulous construction of environmental rooms made a great difference in the reproducibility of test results. Prior to the use of such facilities and careful monitoring, a variety of factors, such as diet, exposure to chemicals, EMF, or dust gave rise to symptoms which would have been mistaken for placebo reactions. Such effects were minimized here, as evidenced by the sinail number of placebo reactions. A few patients reacted to the tields generated by the monitoring devices (Iriscorder, EKG, and computers) and had to be dropped from the study as too fragile for accurate analysis. Some patients reacted to the fields generated by the fluorescent lights, and others did not present the same signs and symptoms at each challenge, even though the reactions were significant when contrasted with the blank responses. The Iriscorder data were objective, however, and were always reproducible (Figure 1).

We also noted that patients sometimes had delayed or prolonged responses. Therefore, care had to be taken to be certain that the patient had returned to baseline before the next challenge. This carry-over was first noted when evaluating responses to placebo challenges. Such a response could usually be explained and eliminated by use of longer intervals between challenges.

In this study, of the 100 patients who expressed suspicion of EMF sensitivity, 75 actually responded to fields, whereas none of the controls did. Of the 75, 25 had no reactions to blanks, whereas 50 did, and thus were discarded from the study; even though we felt that some of the reactions to blanks might be evidence of delayed reaction to previous frequencies, or prolonged response to the previous positive challenge, as well as true placebo reactions.

We learned that challenge with 21 frequencies was impossible on many sensitive patients. They were often unwell for several hours or days, which confused the data from repeat challenges on subsequent days. Hence, we selected the one frequency of maximum sensitivity for repeat challenges in the phase IV studies.

When one compares the various groups to controls, it is clear that there is a group of patients who have unstable response systems which appear different from those of the individuals who acted as controls. These studies show that EMF sensitivity could be elicited under environmentally controlled conditions. As a result of the weak field levels and short exposure time, the responses were mild except in two patients whose symptoms were so severe (e.g., drop attack, severe itching) that they received intravenous vitamin C, magnesium, and oxygen as a result of the prolonged and delayed reactions.

Signs and symptoms appeared similar to those seen in food or chemically sensitive patients at the Environmental Health Center-Dallas, and included neurological, musculoskeletal, cardiovascular, respiratory, gastrointestinal, dermal, and ocular changes. The neurological symptoms were most comon. Similar responses have been recorded by others in the literature.5,6,7,6,13,14 In 1972, after the Soviets reported that electrical utility workers were suffering from listlessness, fatigue, and nausea, Subrohmangam and coworkers13 investigated and reported decisive changes in cardiac function and bioamine levels when pulses of 0.01 and 0.1 Hz were used. They found significant changes in the hypothalamus in response to the EMF fields.

In these studies, the preponderance of reactions occurred at one to 10 Hz, which accords well with their observations. However, many reactions also occurred at 50 and 60 Hz, as well as some up to 5 MHz. We conclude that in any given individual susceptibility may develop to any frequency and produce reactions.

Static magnetic fields are known to cause increased blood pressure on some individuals.14 Choy and coworkers8 found that EMF reactions in EMF sensitive patients were not limited to the nervous system, but occurred in the same systems as in these studies, which basically corroborate theirs, though neurological symptoms predominated in our experiments.

Over the past 30 years, numerous investigations with animals and a few epidemiological studies of human populations have been devoted to assessing the relationship of microwave exposure to cataract development. The severity and speed of formation depends not only on intensity, but also on wavelength and duration of exposure.16-21 McCally et al.22 reported damage to corneal epithelium in Cynomolgus monkeys after 2.45 GHz irradiation for 6everal hours at only 20-30 mW/cm2 (CW) or even 10-15 mW/cm2 with pulsed fields. Therefore, the results of Paz23 strongly suggests that the potential for eye injury exists in surgery where EMF fields are present.

In our experience, the patients' clinical responses could not always be reproduced completely, but the objective Iriscorder, EKG, and respirometer could be. However, the responses were definitely different from controls or placebo challenges. In our experience over the years, we have found partial reproduction of symptoms on repeat challenge to be as significant as total reproduction. Therefore, significant differences from controls in objective ineasurementa were deemed valid.

There are several explanations for lack of exact reproducibility. These are the following: (a) the patients' total body loads were different at different exposure periods. For example, some patients may only respond to EMF when in a reactive hypersensitive state;5,8 (b) tissue resistance could influence the effect of the EMF. Zimerman24 reported that electrical resistance of skin decreased with increasing temperature and increased with progressive drying, as might be expected; (c) injections of antigen neutralizing substances prior to test may have reduced the response to EMF. One patient with asthma was sensitive to high voltage power lines a well as low voltage house wiring. He experienced muscle spasms in head, neck, arms, and legs. This patient was also sensitive to dust, weeds, dust mites, and some foods. He reacted in our tests to 2.5 and 60 Hz and to 5 and 50 KHZ with tightness in the chest. He then received an antigen shot to neutralize his hypersensitivity reactions. Five months later, he was unreactive to EMF; (d) weather changes might affect the results, since we know that the weather can influence the propagation of EMF, as may alterations in the geomagnetic fields. Since humidity, pollution, temperature, etc. can affect resistance and total body load, weather should perhaps affect the results. Adverse weather (inversions, for example) may increase pollution load, while good weather lessens it. There is some evidence of resonance between geomagnetic fields and an applied ac magnetic field,25 which implies that the results may depend in part at least upon the strength and orientation of the geomagnetic field in the test area; and (e) different wave forms might cause different responses. In these experiments, we used only square wave inputs to the coils. Consequently, we do not know whether other wave forms (sine, sawtooth, triangular, etc.) might induce different types or intensities of reactions.

Thus far, definitive information has not been sufficient to identify a plausible mechanism for EMF interactions with biological tissue. Interactions appear to take place at the cell surface, perhaps acting on receptor sites and altering ion and molecular transport across the membranes.25 Further work remains to be done in the field.

It is clear that EMF sensitivity is a real phenomenon in some environmentally sensitive patients, because some had consistent reactions while none of the controls did. This study must be considered as only preliminary, but the evidence clearly points to sensitivity in some people.

In conclusion, it is evident that EMF testing is at a rudimentary stage; but clearly EMF sensitivity exists and can be elicited under environmentally controlled conditions. Further studies are needed to investigate the effects of EMF fields on human health.

References
1. Ravitz, L. J. (1982). History, measurement, and applicability of periodic changes in the electromagnetic field in health and disease. Ann. N.Y. Acad. Sci., 98, 1144-1201.

2. Wever, R. A. (1973). Human circadian rhythms under the influence of weak electric fields and the different aspects of these studies. Int. J. Biometeor., 17, 227-232.

3. Smith, C. W. (1985). Superconducting areas in living systems. In R. K. Mishra (Ed.), The living state II (pp. 404-420). Singapore: World Scientific.

4. Phillips, R. D. (1986, Sept.). Health effects of ELM fields: Research and communications regulation. Toronto, Int'l Utilities Symp.

5. Smith, C. W., Jafarg-Asl, A. H., Choy, R.Y.S., & Monro, J.A. (Year?). The emission of low-intensity electromagnetic radiation from multiple allergy patients and other biological systems. In B. Jezowska-Trzebiatowska, B. Kochel, J. Slawinski, and W. Streck (Eds.) Proc. int'l. symp. on photon emission from biological systems (pp. 110-126), Wroclaw, Poland. Singapore: World Scientific.

6. Ketchenm, E. E., Porter, W. E., & Bolton, N. E. (1978). The biological effects of magnetic fields on man. J. Am. Ind. Hyg. Assoc., 39, 1-11.

 7. Smith, C.W., & Best, S. (1989). Electromagnetic man. New York: St. Martins Press.

8. Choy, R. V. S., Monro, J. A., & Smith, C. W. (1986). Electrical senitivities in allergy patients. Clin. Ecol., 4, 93-102.

9. Shirakawa, S., Rea, W. J., Ishikawa, S., & Johnson, A.R. (Year?). Evaluation of the autonomic nervous system response by pupillographical study in the chemically sensitive patient. What is this? Where was it published?

                           10. Microwave News, (1986, Sept./Oct.). (pp. 5, 14)
11. Ad ey, R.W., Bawin, F. M., & Lawrence, A.F. (1982). Effects of weak amplitude-modulated fields in calcium efflux from awake cat cerebral cortex. J. Bioelectromagnetics Soc., 3, 295-308.
                           12. Bullock, T. H. (1977). Electromagnetic sensing in fish. Neurosci. Res. Program Bull., 15, 17-22.
13. Subrohmangam, S., Narayan, O. V. S., Porkodis, M., & Murugan, S. (1985). Effect of ELF magnetic micropulsations on physiology of Albino rats. Int. J. Bio Meteor., 29, 184-185.

14. Easterly, C. E. (1982). Cardiovascular risk from exposure to static magnetic fields. J. Am. Ind. Hyg. Assoc., 43, 533-539.

                          15. Randegger, E. (1988). Electromagnetic pollution. Environ., 7, 22-26,

                           16. Silverman, C. (1980). Epidemiological studies of microwave effects. Proc. I.E.E.E., 68, 78-84.

                           17. Petersen, R. C. (1980). Bioeffects of microwaves: A review of current knowledge. J. Occup. Med., 25, 103-111.

18. Birenbaum, L., Kaplan, L.T., Metaly, W., et. al. (1969). Effect of microwave on the rabbit eye.. J. Microwave Pwr., 4, 232-243.
                          19. Michaelson, S. M. (1980). Microwave biological overview. Proc. I.E.E.E., 68, 60-69.

                          20. Carpenter, R. L., & Van Ummersen, C.A. (1968). The effects of 2.4 Ghz radiation. J. Microwave Pwr., 3, 3-19.

                          21. Clealry, S. (1980). Microwave cataractogenesis. Proc. I.E.E.E., 68, 49-55.

22. McCally, R. L., Farrell, R. A., Burgeron, C. B., et. al. (1986). Neuronizing radiation damage in the eye. Johns Hopkins Apl. Tech. Dig., 7, 73-91.

23. Paz, J.D., Milliken, R., Ingram, W.T.,Arthur, F., and Atkin, A. (1987). Potential ocular damage from microwave exposure during electrosurgery: Dosimetric survey. J. Occup. Med., 29, 580-583.

24. Zimmerman, I. (1985). Dry and wet skin resistance: Cow's lumbosacral regions under 750 KV lines. Int. J. Bio. Meteor., 29, 184.

                            25. Banks, R.S. (1988). Electric and magnetic fields: A new health issue. Health and Environ., 2, 1-3.
 
 

Table 1

Phase II - Single-blind Challenge of 100 Patients

 

No. of

Patients

 
No. of Active Challenges
 
No. of Blank Challenges
 
Positive Reactions to Active Challenges
 
Positive Reactions to Blanks
 
50
 
1050
 
250
 
750
 
150
 
25
 
525
 
125
 
0
 
0
 
25
 
525
 
125
 
325
 
0


 
 

Table 2

Phase III - 25 Patients Previously Positive

Rechallenged and 25 Controls Tested Double-Blind

 

No. of Persons

 

No. of Active Challenges

 

No. of Blank Challenges

 

Positive Reactions to Challenges

 

Positive Reactions to Blanks

 

16 patients

(out of 25 reacting positively)

 
336
 
80
 
179
 
6
 

25 controls

(none of them reacting positively)

 
525
 
125
 
0
 
0
 


 
 

Table 3

Percentage of 16 Patients with Positive Reaction to Different Frequencies

 
Frequency (Hz)
 
Patients with Positive Reaction (%)
 
Frequency (Hz)
 

Patients with Positive Reaction (%)

 
0.1
 
31
 
1K
 
56
 
0.5
 
44
 
5K
 
38
 
1.0
 
75
 
10K
 
69
 
2.5
 
75
 
20K
 
56
 
5.0
 
69
 
35K
 
31
 
10.0
 
69
 
50K
 
50
 
20.0
 
69
 
75K
 
50
 
40.0
 
50
 
100K
 
38
 
50.0
 
50
 
1M
 
50
 
60.0
 
63
 
5M
 
31
 
100.0
 
56
 
 
 
 
 


 
 

Table 4

Comparison of Symptoms and Signs Induced by Frequencies

 
Hz
 
# Patients
w/pos reaction
 
Neurological
 
Musculoskeletal
 
Cardiovascular
 
Respiratory
 
Gastrointestinal
 
Eyes
 
Skin
 
# of Pts
 
%
 
# of Pts
 
%
 
# of Pts
 
%
 
# of Pts
 
%
 
# of Pts
 
%
 
# of Pts
 
%
 
# of Pts
 
%
 

0.1

 
5
 
3
 
60
 
0
 
0
 
0
 
0
 
0
 
0
 
1
 
20
 
0
 
0
 
0
 
0
 

0.5

 
7
 
4
 
57
 
0
 
0
 
0
 
0
 
0
 
0
 
0
 
0
 
0
 
0
 
0
 
0
 

1

 
12
 
4
 
33
 
3
 
25
 
0
 
0
 
1
 
8
 
1
 
8
 
0
 
0
 
0
 
0
 

2.5

 
12
 
5
 
42
 
2
 
17
 
0
 
0
 
1
 
8
 
1
 
8
 
0
 
0
 
0
 
0
 

5

 
11
 
5
 
46
 
0
 
0
 
1
 
9
 
2
 
18
 
1
 
9
 
0
 
0
 
0
 
0
 

10

 
11
 
7
 
64
 
1
 
9
 
0
 
0
 
2
 
18
 
0
 
0
 
0
 
0
 
0
 
0
 

20

 
11
 
4
 
36
 
0
 
0
 
1
 
9
 
1
 
9
 
1
 
9
 
0
 
0
 
0
 
0
 

40

 
8
 
4
 
50
 
0
 
0
 
0
 
0
 
2
 
25
 
0
 
0
 
0
 
0
 
1
 
13
 

50

 
8
 
5
 
63
 
0
 
0
 
2
 
25
 
1
 
13
 
0
 
0
 
0
 
0
 
0
 
0
 

60

 
10
 
5
 
50
 
0
 
0
 
1
 
10
 
3
 
30
 
0
 
0
 
0
 
0
 
0
 
0
 

100

 
9
 
4
 
44
 
0
 
0
 
1
 
11
 
2
 
22
 
1
 
11
 
0
 
0
 
0
 
0
 

1K

 
9
 
6
 
67
 
0
 
0
 
1
 
11
 
0
 
0
 
0
 
0
 
1
 
11
 
0
 
0
 

5K

 
6
 
2
 
33
 
1
 
17
 
0
 
0
 
1
 
17
 
0
 
0
 
0
 
0
 
0
 
0
 

10K

 
11
 
4
 
36
 
1
 
9
 
0
 
0
 
0
 
0
 
0
 
0
 
0
 
0
 
0
 
0
 

20K

 
9
 
5
 
56
 
0
 
0
 
2
 
22
 
0
 
0
 
0
 
0
 
0
 
0
 
1
 
11
 

35K

 
5
 
2
 
40
 
0
 
0
 
0
 
0
 
1
 
20
 
0
 
0
 
0
 
0
 
1
 
20
 

50K

 
8
 
2
 
25
 
0
 
0
 
1
 
13
 
2
 
25
 
0
 
0
 
0
 
0
 
1
 
13
 

75K

 
8
 
1
 
13
 
0
 
0
 
1
 
13
 
3
 
38
 
0
 
0
 
1
 
13
 
0
 
0
 

100K

 
6
 
2
 
33
 
2
 
33
 
0
 
0
 
2
 
33
 
0
 
0
 
0
 
0
 
0
 
0
 

1M

 
8
 
4
 
50
 
1
 
13
 
0
 
0
 
0
 
0
 
0
 
0
 
0
 
0
 
0
 
0
 

5M

 
5
 
2
 
40
 
1
 
20
 
0
 
0
 
0
 
0
 
0
 
0
 
0
 
0
 
0
 
0
 
 

Table 5

Phase IV-Sixteen Patients Rechallenged to One Active Frequency on Two Separate Episoded and in Addition to Five Blank Challenges on Each Episode-Double-blind

 

First Episode of Challenge

 
 
 
 
 

No. of

Patients

 
Total No. of Frequencies
 
Total No. of Blanks
 

No. of Patients Reacting to Active Challenge

 

No. of Patients Reacting to Blanks

 
16
 
16
 
80
 
16
 
0
 
 
 
 
 
 
 
 
 
 
 

Second Episode of Challenge

 
 
 
 
 

No. 4 of Patients

 
Total No. of Frequencies
 
Total No. of Blanks
 

No. of Patients Reacting to Active Challenge

 

No. of Patients Reacting to Blanks

 
16
 
16
 
80
 
16
 
0
 


 
 

Table 6

Parameters of 25 Normal Controls' Pupillary Light Reflex-Iriscorder-EHC-Dallas

(Right and Left Eyes Combined)

 

Parameter

 
 
 

x ▒ SD

 
 
 
% Variation
 

Al

 
5.70
 
=
 
3.58
 
10.0
 

Cr

 
0.46
 
=
 
0.048
 
10.4
 

T2

 
190.74
 
=
 
18.36
 
9.6
 

VC

 
49.67
 
=
 
5.86
 
11.8
 

AC

 
503.20
 
=
 
75.80
 
15.1
 

T5

 
1520.04
 
=
 
286.86
 
18.7
 

VD

 
13.65
 
=
 
2.44
 
17.9