The unified missing link, oxidative stress  as a result  of altered  water structure at gas -liquid interfaces leading to apparent electromagnetic memory  and accounting for very diverse instances of radio frequency induced plant and animal bio-damage such as Tree Die- back, Cancers and even Stroke, by Dr Chris Barnes , Bangor Scientific and Educational Consultants. E  -mail doctor.barnes@univ.bangor.ac.uk

Dr Barnes Homepage http://www.drchrisbarnes.co.uk

 

 

 Abstract

Safety concerns  of  RF radiation are briefly raised and discussed. Some literature suggests that RF could be either a carcinogen or a cancer promoter.    The need to take the quantum mechanical aspects of radio propagation into account together with the compounding effects of atmospheric pollution and other carcinogens is once again highlighted.  An observation that not only cancer and tree damage may be caused by RF, but also there is the possibility of it being implicated in increased stroke risk in 15-44 year olds.  A new model based on the perturbation of  the balance of  natural biological free radical reaction processes by RF at gas-liquid interfaces is developed.  The model accounts elegantly for a significant  number of effects of RF including  changes in calcium channel behaviour, dominance of association with cancers of the blood and lymphatic systems, damage to trees and plants and even the seemingly new and high prevalence of stroke in the younger age groups who are more likely to be engaging with mobile and WIFI RF technologies.   The model is strongly supported by existing experimental evidence in a number of related physical and life science fields.   RF even at very low levels may prove to be an additional lifestyle risk factor rather like smoking or alcohol.  Due to the long half-lives of altered water structure in the presence of micro and nano-gas bubbles medium term exposure, such as sleeping in elevated levels of RF, may be as or more dangerous than occasional exposure to very high levels.                  

 

Introduction

There is growing concern about the safety of radio frequency technologies as they now totally pervade our daily living. Some studies suggest that electromagnetic fields and/or RF Radiation could be either carcinogenic, see WHO report 2011 [1] or at least cancer promoters, see Rom and Markovitz (2007) [2].    Although very numerous, studies both epidemiological and experimental often produce conflicting results.  Given the very enormous range of possible exposure levels, frequencies and modulation schemes this is perhaps unsurprising.  Further there are a great number of differing hypotheses as to the possible interaction of r.f. energy with tissue and no unifying theory.

 

I have also previously explained that, given the nature of radio antennas and radio propagation, particularly if a full quantum science based explanation of electromagnetic energy with matter is taken into account, a simple radial analysis decay method for epidemiology is flawed.   Taking the quantum model into account allows a Bayesian re-evaluation making far more sense of studies of cancer association such as those of Dolk and Cherry for the effects of TV transmitters, for example. Further improvement is made when the compounding effects of atmospheric pollution are considered, see Barnes [3]. 

 

There is also to be found stark evidence of how damaging r.f. radiation can be to vegetation and trees, see for example Haggerty (2004) [4].

 

The findings follow a recent study in the journal Annals of Neurology, show that hospitalizations for ischemic stroke have gone up by 37 percent from 1995 to 2008 among people between ages 15 and 44.  The use of mobile phone and wifi systems also peaks within this age group yet no one has shown any real association with stroke or provided a mechanism.  It is hoped this publication might set the record straight. 

 

Cancer, strokes and plant cell death at first sight would appear to be three very diverse and different phenomena. However, the question to be posed is do they have a common denominator?  Cancers of the blood and lymphatic systems appear to be most strongly associated with electromagnetic radiation in the existing literature.  Both are systems which involve the transport of fluid.  Strokes are also associated with the transport of fluid. A stroke occurs when an area of the brain is deprived of its blood supply for long enough to cause vital brain tissue to die. There are two types of stroke. The most common type is called ischaemic stroke, which happens when a clot blocks the blood supply to the brain. The second type, called haemorrhagic stroke, is caused by bleeding in the brain. Plants also transport fluids. Oxidative stress seems to fit the bill as a common cause of bio-damage in these three diverse scenarios. 

 

Any model which can fully explain what is happening must be able to reconcile a causative association between RF energy and a modulation of oxidative stress at a cellular or sub- cellular level and to be able to explain how its introduction may involve a bio-fluid or transport by a bio-fluid.   The purpose of this paper is to develop this theme further.

 

 

Unifying model and hypothesis on how RF radiation provides oxidative stress. 

Free radical production is essential for a number of biological processes. The number density of such radicals, their lifetimes, their reactions and catalysis and the quenching processes involved are critical to the normal function of organisms both plants and animals.  Disturbance of the mechanism may lead to oxidative stress which is associated with inflammation and carcinogenesis in animal cells and with growth rate changes in plant cells.        

 

All biological systems contain varying amounts of water.   Further, plants and animals have crucial systems involving gas exchange and gas-liquid interfaces.  The hypothesis is that is r.f. energy can perturb gas-liquid interfaces in simple water and provide free radical species not only could this be a reason for apparent water memory effects but crucially and furthermore when the water finds itself as part of the bio-fluids of a complete biological system it could perturb the delicate radical balance   referred to above thus  causing oxidative stress in the whole or parts of the said biological system.   Further if the model can account for other experimentally    observed effects of EMF and EMR such as altered calcium channel behaviour it becomes even more convincing.

 

Previous attempts to explain altered calcium channel behaviour have been inconsistent because very high field strengths are needed to cause rectification at cellular membranes.   Water memory effects based on free radical induced chemical change and dissolved gases would be expected to have long half -lives and their products could circulate through, for instance, blood, lymph and plant sap.  Thus, via this potential mechanism r.f., could affect parts of the body or bio-system   beyond normal RF skin penetration depth or even geometric quantum multiples thereof. 

 

 The ultimate test of the model is if it able to predict and confirm known associations of  RF ( EMR) and/or EMF with very particular or specific types of cancer  at the same time being able to account for other newly observed phenomena such as a very increased  ischemic stroke rate in 15-44 year old individuals and species unspecific tree -die back in the region of mobile phone base station antennas.    

 

A possible criticism that could be levelled at this present hypothesis is that as RF is non-ionising radiation it is simply not energetic enough to break chemical bonds.   Professor Gerald Scott, an authority on polymer chemistry and free radicals, comments: "To distinguish between ionising and non-ionising radiation on the grounds that only ions cause biological damage is both simplistic and misleading. UV radiation is damaging because it produces neutral free radicals that are a major cause of disease in biological organisms. Furthermore there does not seem to be one chemist among the contributors who might understand the mechanisms of free radical formation, which as we have discussed previously frequently involves low energy excitation of atoms (particularly in transition metal complexes such as haematin) from a ground to an excited state that is quite different from breaking a carbon-carbon bond by high energy irradiation but can be equally damaging to cells."

 

Further, there is other independent research evidence of the degassing of bio-liquids in low electromagnetic fields, see Shatalov ( ‎2011)[5].

 

Finally,  a famous UK Scientist Martin Chaplin BSc PhD CChem FRSC  has reached the same or similar conclusions on water to those of Colic and Morse, see http://www.lsbu.ac.uk/water/sitemap.html [6].

 

I wish  to make it clear that this present  model should not be regarded as the only mechanism by which RF (EMR) and/or EMF can couple into a biological system.  Nothing in the model I present here excludes the simultaneous possibility of  energy coupling by other known physical means such as for example dielectric absorption directly with tissue at bulk, cellular, macromolecular and sub-molecular levels  or coupling at the skin surface  by      thermo-acoustic and/or electro-strictitve pulse interaction at the skin surface leading to eventual micro molecular mechanic-transduction via cellular DNA tensegrity matrices, see Barnes http://www.drchrisbarnes.co.uk/RFAS.htm[7].  Most likely, in reality these processes will compete side by side with the dominant process being determined by factors such as r.f. excitation frequency, wave polarisation and modulation format.  

 

 

Evidence for the model and developing the model in detail (cancer and stroke).

The notion of rf perturbing water is by no means new.  The main work in the field is by .Colic and Morse (1998)[8]. Up to then, the mechanism of the magnetic “water memory” effect, though, was largely unknown. In their work, they presented evidence that the primary “receptor” of the electromagnetic radiation was the gas/liquid interface. Gas can be either already present in water or produced by the effects of electromagnetic fields. Perturbed gas/liquid interfaces require hours to equilibrate. Certain RF and magnetic signals could also produce reactive oxygen and hydrogen species (superoxide, hydrogen peroxide, hydrogen, atomic hydrogen). The perturbed gas/liquid interface modifies the hydrogen bonding networks in water and also the hydration of ions and interfaces. Careful outgassing removed all of the effects of the electromagnetic fields, including the magnetic memory effect. The amplitude of the applied field influenced the observed effects. Different amplitudes of RF radiation perturbed the interfacial water in different ways and consequently affected the behaviour of colloids and ions in specific manners. For instance, the bulk and template precipitation of calcium carbonate, zeta potentials of suspended colloids, rate of dissolution of colloidal silica, and attachment of colloidal silica to metal surfaces were modified in specific ways with the low amplitude or high amplitude RF treatments. The solubility/diffusivity of gas species was also modified in a different manner, and finally they concluded this was probably at the core of the specificity of the RF amplitude effects.

 

 Further in their 1999 paper ‘The elusive mechanism of the magnetic ‘memory’ of water’ they explain it has been claimed that preliminary water treatment with magnetic or electromagnetic (EM) fields can help de-scale metal surfaces, improve cement hydration, change ζ potential of colloids, make plants irrigated with such water grow faster, enhance efflux of calcium through bio membranes or influence the structure of model liposomes. My comment and observation is very clearly that the  former is not unlike a claimed effect of r.f. radiation .  The effects persist minutes or hours after the water treatment. It is well known that relaxation phenomena in water occur on a picosecond to second timescale. The nature of these ‘mysterious’ and questionable phenomena uniquely known as the ‘magnetic memory of water’ has recently been scrutinized. Based on their work a model for the observed phenomena was proposed based that the gas liquid interface is perturbed by the action of magnetic and electromagnetic fields. They noted that as in the case of the sonochemical gas liquid interface treatment, some free radicals and/or reactive oxygen species are observed after the treatment (ozone, superoxide, hydroxyl radicals, singlet oxygen, atomic hydrogen, hydrogen peroxide, hypochlorous acid, etc.). The perturbations of the gas liquid interface relax more slowly (minutes to hours). They further noted the  presence of gases, such as carbon dioxide or noble gases which promote clathrate-like structures of water, significantly enhanced the observed effects. Some reactive oxygen species such as hydrogen peroxide are also stable for hours or days in the absence of heavy metals. The ‘magnetic memory of water’, they proposed, is the combination of perturbations of the gas liquid interface and the production of reactive oxygen species

 

Strong support also comes from the experimental work of Vallee et al (2005) [9] who in a light scattering study of the effects of low frequency electromagnetic fields on water show that electromagnetic fields disturb the ionic double layer that leads to bubble stabilisation.  Further support comes from the work of Roy, Rao and  Kanzius (2008) [10] who show that RF fields at 13.56 MHz  can radiation catalyse  the dissociation of salt solutions into combustible mixtures of hydrogen and oxygen.

 

The notion that RF fields might behave rather like sono-chemical    fields is also important because it gives a basis for reconciliation with the present author’s alternative pulse pressure based tensegrity-matrix model where demodulation and bio-effects of RF in tissue may occur as a result of thermo-acoustic and/or electrostrictitve pulse interaction at the skin surface and micro molecular mechanic-transduction via cellular DNA tensegrity matrices.

 

Having established that RF fields can form a family of free radicals in gas water and gas salt solution mixtures one can next explore the relevance of the same or similar radicals in biology.

 

 

Very usefully Floyd (1990) [11] has commented on both the role of free radicals in carcinogenesis and brain ischemia. He has stated that even though oxygen is necessary for aerobic life, it can also participate in potentially toxic reactions involving oxygen free radicals and transition metals such as Fe that damage membranes, proteins, and nucleic acids. Oxygen free radical reactions and oxidative damage are in most cases held in check by antioxidant defense mechanisms, but where an excessive amount of oxygen free radicals are produced or defense mechanisms are impaired, oxidative damage may occur and this appears to be important in contributing to several pathological conditions including aging, carcinogenesis, and stroke. Several newer methods, such as in vivo spin-trapping, have become available to monitor oxygen free radical flux and quantitate oxidative damage. Using a combination of these newer methods collectively focused on one model, recent results show that oxidative damage plays a key role in brain injury that occurs in stroke. Subtle changes, such as oxidative damage-induced loss of glutamine synthetase activity, may be a key event in stroke-induced brain injury. Oxygen free radicals may play a key role in carcinogenesis by mediating formation of base adducts, such as 8-hydroxyguanine, which can now be quantitated to very low levels.

 

RF can contribute through the gas-liquid interface hypothesis to exactly the excess oxygen radicals to which Floyd refers.

 

Dreher and Junod (1996) [12] further  emphasise this conclusion, for in aerobic life, oxidative stress arises from both endogenous and exogenous sources. Despite antioxidant defence mechanisms, cell damage from oxygen free radicals (OFR) is ubiquitous. OFR-related lesions that do not cause cell death can stimulate the development of cancer.  Mutagenesis through oxidative DNA damage is widely hypothesised to be a frequent event in the normal human cell. A large body of evidence suggests important roles of OFR in the expansion of tumour clones and the acquisition of malignant properties. In view of these facts, OFR may be considered as an important class of carcinogens. Therefore, the ineffectiveness of preventive antioxidant treatments, as documented in several recent clinical trials, is surprising. However, the difficulties of antioxidant intervention are explained by the complexity of both free radical chemistry and cancer development.

 

Thus, reducing the avoidable endogenous and exogenous causes of oxidative stress is, for the present, the safest option. The present author suggests, if this means changing RF technologies or relocating out transmitting antennas than perhaps for the benefit of human kind and other life forms this may be worthwhile?

 

So if RF produces, at water-gas  interfaces and biofluid-gas interfaces, radicals especially   oxygen radicals, peroxides and hydroxyl radicals  it should be instructive to examine what such radicals do to biological systems particularly those pertinent to the present enquiry when arising from other non- RF sources.

 

Pryor (1997) [13] has suggested for instance that radicals arising as a result of cigarette smoke can cause both cancer initiation and promotion.  Aqueous cigarette tar (ACT) extracts and by a model of these solutions, aged solutions of catechol. ACT solutions as well as aged solutions of catechol contain a quinone-hydroquinone-semiquinone system that can reduce oxygen to produce superoxide and hence hydrogen peroxide and the hydroxyl radical. Both the cigarette tar radical and the catechol-derived radical can penetrate viable cells, bind to DNA, and cause nicks.  These are the self-same radicals that can be generated by RF at gas-liquid interfaces.  

 

It is further instructive to note that hydroxyl radical generation has been associated with the respiratory ingestion of certain ultrafine atmospheric pollution type nanoparticles, see Dick et al (2003) [14].    The present author has shown nano-particles to act in both collaboration with RF for plant and tree damage and has also shown how the Dolk (II) results can be properly reconciled for the association  of cancer with TV transmitter emissions only if  atmospheric pollution is taken into account.

 

Adey (1993) [15] has concluded that a clear emergent conclusion is that many observed interactions of RF are not based on tissue heating. Further that modulation of cell surface chemical events by weak EM fields indicates a major amplification of initial weak triggers associated with binding of hormones, antibodies, and neurotransmitters to their specific binding sites. Finally that calcium ions play a key role in this amplification.  Several other studies have shown associations between the application of RF energy and changes in calcium ion transport .  It is thus pertinent to enquire if this is a separate mechanism or could it be related to RF free radical production.  Another peculiar and possibly related effect is microwave hearing. There has been debate concerning whether demodulation occurs in the brain or the cochlea?

 

Ikeda et al (1993)[16] have shown that superoxide anion increases calcium influx across the  membrane of the guinea pig cochlear outer hair cell.  This not only provides a possible mechanism linking radicals and calcium transport but also provides support for the notion of the cochlear being the site of microwave induced hearing.

 

 

Stroke

The relationship between calcium influx and free radicals is also dealt with by Kristian and Siesjo (1998) [17] in particular in the case of ischemic cell death.   They conclude it is clear that a coupling exists between influx of calcium into cells and their production of reactive oxygen species, such as ·O2−, H2O2, and ·OH. Their  results  underscored the role of calcium in ischemic cell death. They demonstrated a coupling has been demonstrated among glutamate release, calcium influx, and enhanced production of reactive metabolites such as ·O2−, ·OH, and nitric oxide. It has become equally clear that the combination of ·O2− and nitric oxide can yield peroxynitrate, a metabolite with potentially devastating effects. The mitochondria have again come into the focus of interest. This is because certain conditions, notably mitochondrial calcium accumulation and oxidative stress, can trigger the assembly (opening) of a high-conductance pore in the inner mitochondrial membrane.

 

Halliwell (1994) [18] comments similarly. It is of course by now well known that radicals are species containing one or more unpaired electrons. The oxygen radical superoxide (O 2 - ) and the non-radical oxidants hydrogen peroxide (H2O2) and hypochlorous acid (HOCl) are produced during normal metabolism and perform several useful functions. Excessive production of O 2 - and H2O2 can result in tissue damage, which often involves generation of highly reactive hydroxy 1 radical (· OH) and other oxidants in the presence of “catalytic” iron or copper ions. A major form of antioxidant defence is the storage and transport of iron or copper ions in forms that will not catalyze formation of reactive radicals. Tissue injury, e. g., by ischaemia or trauma, can cause increased iron availability and accelerate free radical reactions. This may be especially important in the brain, since areas of this organ are rich in iron and cerebrospinal fluid cannot bind released iron ions. Oxidative stress upon nervous tissue can produce damage by several interacting mechanisms, including rises in intracellular free Ca2+ and, possibly, release of excitatory amino acids.

 

The link with pulsed wireless emissions which I affirm here has been tested experimentally by Nittby et al (2008) [19] who have commented  on increased blood–brain barrier permeability in mammalian brain 7 days after exposure to the radiation from a GSM-900 mobile phone.

 

Yurekli et al (2006) [20]  have observed oxidative stress in rats exposed to GSM radiation. Meral et al (2007) reached a similar conclusion for Guinea Pig brain. Ilhan et al (2004) have shown that GSM   oxidative stress in rat brain can be reversed by the herbal antioxidant Ginko Bilboa.

 

 

The radicals which Kristian and Seisjo  and the rest of theses authors discuss are exactly those which can be created by RF energy at the liquid –gas interface. 

 

It thus becomes possible to see how RF might have a role to play in Stroke as well as in carcinogenesis.   This ties in extremely well with my initially cited observation of recent significantly increased stroke numbers in the 15-44 age groups. 

 

 

Extension of my model to plant and tree damage

Active oxygen species are generated as an essential part of plant metabolism. The light-dependent generation of active oxygen species is termed photo-oxidative stress. Foyer et al (1994) explain that this can occur in two ways: (1) the donation of energy or electrons directly to oxygen as a result of photosynthetic activity; (2) exposure of tissues to ultraviolet irradiation. The light-dependent destruction of catalase compounds the problem. Although generally detrimental to metabolism, superoxide and hydrogen peroxide may serve useful functions if rigorously controlled and compartmentalised. During photosynthesis the formation of active oxygen species is minimised by a number of complex and refined regulatory mechanisms. When produced, active oxygen species are eliminated rapidly by efficient anti-oxidative systems. The chloroplast is able to use the production and destruction of hydrogen peroxide to regulate the thermal dissipation of excess excitation energy. This is an intrinsic feature of the regulation of photosynthetic electron transport. Photo-inhibition and photo-oxidation only usually occur when plants are exposed to stress. Active oxygen species are part of the alarm-signalling processes in plants. These serve to modify metabolism and gene expression so that the plant can respond to adverse environmental conditions, invading organisms and ultraviolet irradiation. The capacity of the anti-oxidative defence system is often increased at such times but if the response is not sufficient, radical production will exceed scavenging and ultimately lead to the disruption of metabolism. Oxidative damage arises in high light principally when the latter is in synergy with additional stress factors such as chilling temperatures or pollution.

 

Environmental stress can modify the photo-oxidative processes in various ways ranging from direct involvement in light-induced free radical formation to the inhibition of metabolism that renders previously optimal light levels excessive. It is in just such situations that the capacity for the production of active oxygen species can exceed that for scavenging by the anti-oxidative defence systems.

 

I thus  propose that with regard to plants, RF energy   in its ability to provide additional active oxygen species and other free radicals at the sap –gas interface may simply be seen as yet an additional environmental stress. Indeed besides death and die back, plants have been observed to respond in a number of different ways to RF energy, see for example but not exclusively, Vian et al (2007) [21] and this is perfectly consistent with the above.      

 

The advent of plant genetic transformation, however, may have placed within our grasp the possibility of engineering greater stress tolerance in plants by enhancement of the anti-oxidative defence system.  This may become more and more essential as the use of RF technologies expands.

 

Becana et al (1998) [22] have noted that free catalytic iron as opposed to protein bound iron accumulates in many stressed plant tissues. 

 

It is my further hypothesis that   the presence of this free iron may further assist absorption of RF energy into plants and together with the action of adsorbed and absorbed roadside nano-particles facilitates the behaviour of plant leaves as radio antennas and  further contributes to  and speeds their demise.     The concentration of this free iron probably also explains the parasitic re-radiation effect which I have recently observed experimentally for certain dead and dying trees and vegetation (Barnes 2013) [ 23].

 

     Monica and Cremonini (2009) [24]   have shown that some plants have the ability to concentrate and translocate nanoparticles whereas others don’t. This may account for some of the conflicting accounts for in the literature. 

        

                                                                                              

Conclusions, Discussion and Further work

 

I   have created and justified a unified hypothesis which accounts for the effects of and the association with RF energy and electromagnetic fields in a number of apparently unrelated biological scenarios which are

1.                                                                                                                                                                                  Cancer association – especially cancers of the blood and lymphatic systems

2.                                                                                                                                                                                  Ischemic stroke 

3.                                                                                                                                                                                   Tree and vegetation death and die-back 

 

In the belief that  RF energy perturbs water or aqueous solution –gas interfaces and releases free radicals such as oxygen and hydroxyl and chemical species such as peroxides and superoxides is supported by personal experimentation an those of others.  This helps explain so called elusive water ‘magnetic memory’ and also   since water is a prime component of the relevant biological fluids namely blood, lymph and sap the same radicals are expected to be released by RF or electromagnetic fields in biology leading to a disruption of natural radical processes and hence oxidative stress.

 

Of all the cancers which others have previously   associated with RF, probably the most documented is Acute Myeloid Leukaemia. Zhou et al (2010) [25] has shown a strong association between oxidative stress and the incidence of disease relapse was observed, which has potential prognosis implications. These results indicate that oxidative stress is a crucial feature of AML and probably affects the development and relapse of AML.

 

Wang et al (2006) [26] reaches a similar conclusion regarding oxidative stress for NHL ( Non Hodgkin Lymphoma)  the other main cancer associated with RF.

 

The common dominator, radicals are already known to be implicated via oxidative stress in carcinogenic processes both initiation and promotion and in ischemic stroke and in plant stress and death.    I have shown RF and its link in perturbing the   water /gas interface  (so called magnetic memory)  structure to be the second and linking dominator.

 

Since radicals are implicated in both cancer initiation and promotion this may well account as to why some studies have concluded RF to be a carcinogen and others merely a promoter. 

 

Thus for cancer RF becomes merely an additional risk factor rather as say smoking and asbestos both also associated with free radicals.   Undoubtedly certain types of frequency and modulation are more effective at disturbing the gas –liquid interface.  There is more peak energy in amplitude pulsed modulation systems for example. 

 

It would seem atmospheric pollution works hand in hand with RF in producing yet more radicals and oxidative stress in all three diverse bio-situations.          

 

This work gives also, perhaps, the first ever meaningful insight and explanation of increasing ischemic stroke rates in younger people.    

 

The links uncovered here are ultimately perhaps not that unsurprising, see for instance Mena et al (2009)   who comment that reactive oxygen species (ROS) are the more abundant free radicals in nature and have been related with a number of tissue/organ injuries induced by xenobiotics, ischemia, activation of leucocytes, UV exposition, etc. Oxidative stress is caused by an imbalance between ROS production and a biological system's ability to readily detoxify these reactive intermediates or easily repair the resulting damage. Thus, oxidative stress is accepted as a critical pathophysiological mechanism in different frequent human pathologies, including cancer. In fact ROS can cause protein, lipid, and DNA damage, and malignant tumors often show increased levels of DNA base oxidation and mutations.

 

Different lifestyle- and environmental-related factors (including, e.g., tobacco smoking, diet, alcohol, ionizing radiations, biocides, pesticides, viral infections) and other health-related factors (e.g. obesity or the aging process) may be pro-carcinogenic. In all these cases oxidative stress acts as a critical patho-physiological mechanism. Nevertheless it is important to remark that, in agreement with present knowledge, oxidative/nitrosative/metabolic stress, inflammation, senescence, and cancer are linked concepts that must be discussed in a coordinated manner.

 

Further confirmation experimentally that oxidative stress as a result of RF is not just a mammalian feature but also found in plants is provided by  Tkalec et al (2007) [27]

 

Finally, Toyokuni et al (1995) [28] remark that DNA of cancers such as renal cell carcinoma and mammary invasive ductal carcinoma, is  persistently exposed to more oxidative stress than that of adjacent normal tissue.  With regard to the latter, I have already recently identified breast cancer as one of the strongest   ‘RF’ cancers by means of my UK and Worldwide geographic mapping analyses (Barnes 2013) [29,30] .  For RF we can simply substitute RF induced oxidative stress.  Further I agree whole heartedly with   the Toyokuni et al  suggestion  that the concept of ‘persistent oxidative stress in cancer’ may open up a new research area, explaining part of the characteristic tumour biology of cancer such as activated transcription factors and proto-oncogenes, genomic instability, chemotherapy-resistance, invasion and metastasis.

 

Based on this, the present author expects   one would perhaps expect more cancers in geographic locations and buildings where RF fields are persistently above average.  Problems might also   be expected,  for example, if a person works and sleeps significantly differing levels of electromagnetic fields.  This may be more relevant than brief exposures to high fields for instance. The author is now urgently investigating this notion. 

 

References

 

1.      http://www.iarc.fr/en/media-centre/pr/2011/pdfs/pr208_E.pdf

2.      https://books.google.co.uk/books?id=H4Sv9XY296oC&pg=PA1288&lpg=PA1288&dq=rf+energy+a+cancer+promoter&source=bl&ots=xB1TnVT9GI&sig=k8AhMKz8S0K9XsUSzwcGPzzhE84&hl=en&sa=X&ei=mZOcVKSiL4mWaubFgdgM&ved=0CDYQ6AEwAw#v=onepage&q=rf%20energy%20a%20cancer%20promoter&f=false

1.      http://drchrisbarnes.co.uk/Cancer%20Epidemiology.html

2.      http://www.hindawi.com/journals/ijfr/2010/836278/

3.      http://arxiv.org/ftp/arxiv/papers/1105/1105.5689.pdf

4.      http://www.lsbu.ac.uk/water/sitemap.html

5.       http://www.drchrisbarnes.co.uk/RFAS.htm

6.      M. Colic, D. Morse, J. Colloid Interface Sci., 1998, 200, 265-272. 18.

7.       http://www.hal.inserm.fr/file/index/docid/29266/filename/JCP_CEM_water_photoluminescence.pdf

8.      R Roy, M L Rao and J Kanzius 2008 Materials Research Innovations 12 3.

9.      Floyd 1990  http://www.ncbi.nlm.nih.gov/pubmed/2189775

10.   http://www.ncbi.nlm.nih.gov/pubmed/8695238

11.  http://www.ncbi.nlm.nih.gov/pubmed/9255574

12.  http://ehp.niehs.nih.gov/wp-content/uploads/117/1/ehp.11370.pdf  ( Dick reference in here)

 

13.  Adey 1993 http://www.ncbi.nlm.nih.gov/pubmed/8388394

 

14.  Ikeda, K., Sunose, H. and Takasaka, T. (1993) Effects of free radicals on the intracellular calcium concentration in the isolated outer hair cell of the guinea pig cochlea. Acta Otolaryngol (Stockh), 113, 137-41.  Back to cited text no. 28    

 

15.  http://www.ncbi.nlm.nih.gov/pubmed/9506616

 

16.  http://www.auraresearch.com/hall2.htm

 

17.  http://www.ccst.us/projects/smart/documents/082009_Nittby_Increased_Permeability.pdf

 

18.  http://informahealthcare.com/doi/abs/10.1080/15368370600875042

 

19.  Vian et al (2006) http://onlinelibrary.wiley.com/doi/10.1111/j.1399-3054.2006.00740.x/full

 

20.  http://www.jstor.org/discover/10.2307/42948312?sid=21105513946563&uid=70&uid=2&uid=3738032&uid=2129&uid=4

 

21.  http://www.drchrisbarnes.co.uk/TD03.htm

 

22.  Monica RC, Cremonini R. Nanoparticles and higher plants. Caryologia. 2009;62:161–165.

 

23.  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2865279/

 

24.  http://www.ncbi.nlm.nih.gov/pubmed/16543247

 

25.  http://www.sciencedirect.com/science/article/pii/S0048969707008017

 

26.  http://www.finom.fi/oxistresscancer.pdf

 

27.  http://www.drchrisbarnes.co.uk/Meta.html

28.  http://www.drchrisbarnes.co.uk/World.htm

29.   

 

 

30.   

 

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