Deployment of the 5G is unlike earlier generations of wireless technology. The base stations for the 5G will be very densely located, in close proximity to people dwellings and working places. Furthermore, once 5G will employ millimeter-waves there will be a need to deploy mini-base stations inside apartments and places of work because the millimeter-waves do not penetrate walls of buildings.
The increased density of base stations and the future location of these inside buildings causes anxiety among the electro-hyper-sensitive persons (EHS).
There are two approaches to study EHS, by either (i) the psychological provocation studies or by (ii) biochemical studies looking for physiological markers for diagnosis of EHS.
EHS research is dominated by psychology provocation studies and I have elaborated on it earlier.
Biochemical studies looking for physiological markers of EHS are performed by a single team in France. It appears that EHS sufferers and anti-EMF activists consider these French studies as valid evidence that can be used for the clinical diagnosis of EHS
French researchers, using biochemical approach, claim finding of several markers of EHS associated with EMF exposures. Unfortunately, French studies have major design problems that invalidate their final conclusions.
The first experimental study by the French team was published in 2015:
Belpomme D, Campagnac Ch, Irgaray P. Reliable disease biomarkers characterizing and identifying electrohypersensitivity and multiple chemical sensitivity as two etiopathogenic aspects of a unique pathological disorder. Rev Environ Health, 2015, 30(4): 251-271.
The authors indicated that the collection of physiological samples and interviews with the self-diagnosed EHS patients begun in 2009. The cohort consisted of 1216 persons of whom 727 were analyzed in this study. Remaining, unanalyzed, patients were excluded by some not precisely described criteria, including some pathologies discovered after the enrollment in the study.
According to the authors the cohort consisted of persons from, not specified, different European countries as well as from the USA, Canada, Australia, Russia, China, Middle East and Africa. Considering this geographical dispersion, the authors did not explain how the various biological samples were collected and analyzed and how was assured that the decay of the biological samples did not happen.
There is lack of explanation whether the cohort members themselves approached scientists or whether they were, in some way, pre-selected by the research team. This is of importance because the authors claim that the females are more susceptible to develop EHS because the analyzed cohort consisted of 495 women and only 232 men. The claim of higher susceptibility of women might be questionable because the higher number of participating women might be just a selection bias, because women more easily contact physicians with health problems than the men.
The working hypothesis of the French team was:
“Our working hypothesis was that under the influence of environmental factors such as EMFs and/or chemicals, some neuro-inflammation and oxidative stress might occur in the brain, with blood-brain barrier (BBB) disruption as a consequence.”
The health status of the patients was analyzed using battery of physiological tests for which there is complete lack of information that would assure reliable quality of sample collection and analysis, especially in the context of the geographical spread of the cohort.
The biochemical tests analyzed the following end-points, fitting well the working hypothesis presented above:
- High-sensitivity C reactive protein (hs-CRP),
- Vitamin D2-D3,
- Histamine,
- IgE,
- Protein S100B,
- Nitrotyrosine (NTT),
- Heat shock protein 70 (HSP70),
- Heat shock protein 27 (HSP27),
- Anti-O-myelin autoantibodies,
- Hydroxy-melatonin sulfate (6-OHMS), and
- 6-OHMS/creatinine.
In addition to the biochemical tests, the authors analyzed blood flow in the temporal lobes and determined the pulsometric index (PI) using a non-invasive method of ultrasonic tomosphygmography.
Selection of patients for the study was done in face-to-face interview using, as the researchers described, a “validated pre-established questionnaire”. However, the questionnaire as well as its validation method were not presented in the article.
Based on the clinical findings, the following inclusion criteria were used by the French team (with my, DL, comments):
- Absence of known pathology accounting for the observed clinical symptoms; (DL – this may cause selection bias. Some ailments might predispose patients to be more or less responsive to EMF exposures)
- Reproducibility of symptom occurrence under the influence of EMFs and/or multiple chemicals whatever their incriminated source; (DL – claim of reproducibility of the symptoms whenever the exposure happens is based solely on the opinion provided by the volunteer. No testing in the presence of EMF exposures were performed. As presented in the study it is subjective and unreliable claim)
- Regression or disappearance of symptoms in the case of EMF and/or multiple chemical avoidance; (DL – also claim of regression and of disappearance of symptoms is based solely on the opinion of the volunteer. No testing in the presence of EMF. As presented in the study it is subjective and unreliable claim)
- Chronic evolution; (DL – also claim of chronic evolution of symptoms in the presence of exposure is based solely on the opinion of volunteer. As presented in the study it is subjective and unreliable claim)
- Symptoms such as headache, superficial and/or deep sensibility abnormalities, skin lesions, sympathetic nerve dysfunction, reduced cognitive ability including loss of immediate memory and attention and/or concentration deficiencies, insomnia, chronic fatigue and depressive tendency, all main clinical symptoms reported as non-specific symptoms in the scientific literature, but which when grouped together may evoke clinically the diagnosis of EHS (data not shown); DL- because data was not shown, this claim is unreliable)
- No serious pre-existing pathology such as atherosclerosis, diabetes, cancer; and/or neurodegenerative or psychiatric diseases which have been associated with EHS and/or MCS in the past or at the inclusion time but would render difficult the interpretation of clinical symptoms and biomarker data; (DL – possibility of selection bias. Some pathologies might predispose person for EHS. Volunteers with pathologies should be used in studies but analyzed separately from other EHS volunteers)
- For each patient written informed consent. Study of this large cohort of patients was not a case-control study neither a randomized study so there was no specific control group; (Lack of control group leads to lack of baseline of the effects observed in EHS persons and makes the size of the observed effects impossible to asses)
The changes in expression of the examined biochemical markers were not found in majority of the patients but only in relatively small percentages of patients self-diagnosed as EHS, MCS or EHS+MCS.
For example, the claim that:
“Since histamine was found to be increased in the peripheral blood of nearly 40% of the patients, this molecule appears to be a key pathogenic mediator, whatever the environmental stressors”
…seems to be farfetched as only 40% of patients experienced it in blood stream. The authors speculate that histamine might be also released elsewhere in response to EMF exposure, without getting into blood stream, but they do not have any evidence to support this claim.
In fact, none of the examined biochemically stress factors was prevalent in EHS persons:
- hs-CRP increased in 15% of EHS
- D2-D3 declined in 23.2% of EHS
- Histamine increased in 40% of EHS
- IgE increased in 22% of EHS
- Protein S100B increased in 15.5% of EHS
- Nitrotyrosin (NTT) increased in 29% of EHS
- Hsp27, Hsp70 detected in 7-19%of EHS
- Antibody to O-myelin detected in 17-29% of EHS
- Melatonin to creatinine ratio declined in EHS but variation was too large to provide specific number
- Pulsatility declined in 50.5% of EHS, but data not shown (!)
The authors did not specify whether there was any overlap among the self-diagnosed EHS persons expressing different markers and whether there was any EHS person that expressed all or even many of the markers.
There was no experimental evidence that any of the examine biochemical markers was EMF-induced.
The authors concluded that EHS and MCS were both associated with the same abnormalities, as seen from the analyses of biochemical factors in this study. Thus, the French team suggested that both pathologies, EHS and MCS, share a common pathophysiological mechanism.
It might be so but not necessarily. It might be also, that the groups of self-diagnosed EHS patients and self-diagnosed MCS patients are cross-contaminated due to incorrect self-diagnoses of some of the patients.
The claim of the common pathophysiological mechanism for EHS and MCS is not proven and needs a better supportive evidence.
Later on, the French team has proposed a pathophysiological model for the development of EHS. However, without the evidence linking in any way symptoms of self-diagnosed EHS persons with the EMF exposures, this model of mechanism is unreliable. Here are the proposed mechanism steps with my (DL) comments:
- Under the influence of EMFs a cerebral hypoperfusion/hypoxia-related neuro-inflammation may occur; (DL – the authors did not demonstrate that EMF exposures cause or lead to cerebral hypoperfusion or neuro-inflammation. This link is claimed only because of the self-diagnosis of EHS persons. If self-diagnosis is incorrect the whole mechanism collapses…)
- Due to the release of histamine and other mediators BBB disruption and permeability increase may be induced through resulting oxidative and/or nitrosative stress; (DL – the authors did not show impact on BBB. Only 40% of self-diagnosed EHS had increased blood histamine that might affect permeability of BBB. The other 60% did not have increased histamine levels. Possibility that they might have local release of histamine is only speculation, not supported by the data)
- Circulating inflammatory cells could then enter the brain to initiate a vicious circle which may considerably amplify the neuro-inflammation process; (DL – no evidence, just speculation)
- Because of oxidative and nitrosative stress and subsequent decreased melatonin bioavailability and autoimmune response, physiological defence mechanisms are weakened making EHS and/or MCS patients potentially at risk of chronic neurodegenerative diseases and cancer; (DL – no evidence, just speculation)
The authors very misleadingly state in the end of the article:
“Present research vainly focus on the causal role of EMFs and chemicals as possible triggers of EHS and MCS, respectively and not enough on the actually unmet health care needs at a socioeconomic and public health setting for persons with environmental sensitivity, as it is particularly the case for EHS and/or MCS persons.”
The authors did not examine effects of EMF at all.
They only speculated that they examined EMF effects because the involvement of EMF was not tested but the authors relied solely on the claims of self-diagnosed EHS persons.
The majority of the article is just filled out with elaborate speculations “what would be if it would be”.
In the last part of the article, the authors rightly state that:
“Whatever the causal origin of EHS and/or MCS, there is compelling evidence that EHS and/or MCS self-reporting patients constitute an unsolved, large and growing health problem worldwide.”
Indeed. However their study did not advance the knowledge about the possible cause of EHS.
Lastly, it is necessary to mention that several tables in the article had errors and that corrigendum to this 2015 article was published in 2016.
The second experimental study from the French team was published in 2018 in already non-existent (predatory) journal, published by the www.omicsonline.org : JBR Journal of Clinical Diagnosis and Research:
Irigaray P, Lebar P, Belpomme D. How ultrasonic cerebral tomosphygmography can contribute to the diagnosis of electrohypersensitivity. J. Clin Diagn Res 2018, 6:1
In this study, the authors presented data suggesting that they found diagnostic criteria for distinguishing EHS persons from non-EHS persons. However, this claim is not proven by the presented data.
Firstly, the Table 1 (see copy) lists 23 symptoms that were evaluated in EHS and non-EHS persons. The data is presented solely as percentage of persons having symptoms. For majority of symptoms in non-EHS persons (14 out of 23) the percentage is =0%. For each symptom was also calculated p value but the validity of it is not possible to asses.
It is not possible to determine reliability of the p values because symptoms are presented as single percentage numbers. For example, for symptom ‘headache’ the value for EHS persons is 88% and for non-EHS controls it is 0% and the p value is listed as p<0.0001.
Does it mean that non-EHS persons do not have headaches?
The reliability of the Table 1 is not possible to determine based on the provided data.
There is also the following, not supported by the evidence, statement:
In a previous study we showed that EHS and/or MCS bearing patients may present with a significant decrease in mean PI in several tissue areas of temporal lobes, suggesting these abnormalities may correspond to some decrease in brain blood flow (BBF) and/or neuronal dysfunction.
The reference, mentioned as “in previous study”, is referring to the study published by this team in 2015, and mentioned above. Unfortunately, the statement is misleading because the 2015 study did not show data for changes in the blood flow:
We thus measured the BBF-related pulsatility in the patient hemispheres by using echodoppler of the middle cerebral artery, and found that resistance index and systolic and diastolic velocity indexes were associated with cerebral hypoperfusion in one or the two hemisphere in 50.5% of the cases, whatever the patient group considered (data not shown).
In the Material and Method section the authors listed the inclusion criteria for enrollment of EHS persons for the study. However, again as in the 2015 study, it is not possible to evaluate the reliability of these inclusion criteria because of the lack of data. For example, there is stated about “reproducibility and regression” as follows:
Reproducibility of symptoms each time the patient claims to be exposed to EMFs; Regression or disappearance of clinical symptoms claimed by the patient to be associated with EMF avoidance;
However, the authors did not expose persons to EMF.
The authors relied solely on the self-statements of the self-diagnosed EHS persons, claiming that they recognize exposures to EMF and the symptoms subside when avoiding exposures.
This is in clear contradiction with the results of the psychological provocation studies.
If confirmed, it would mean that the French team has found several hundreds of persons who indeed feel EMF exposures…
…but the French team did not present any evidence of reliability of the recognition of EMF exposure by the self-diagnosed EHS persons.
Examining the pulsatility index of brain front lobes has led the French team to claim that persons experiencing EHS have lower pulsatility index, what means decreased blood flow in some areas of the brain. The French team stated:
“Table 4 indicates about 90% of the EHS or EHS/MCS patients present with decreased mean PI values in the capsulothalamic and adjacent areas in one or the two temporal lobes, suggesting these abnormalities may be biologically relevant. Note however that similar abnormalities were found in about 10%-20% of the concomitant healthy controls, meaning that among these apparently normal subjects so far investigated, a small percentage of them may in fact be not biologically normal.”
However, it is not known whether all of the self-diagnosed EHS persons indeed suffer of the EHS. Thus, the claim that anyone having decline in pulsatility index is suffering of EHS is farfetched and not supported by the presented evidence.
The third experimental study from the French team was published in 2018:
Irigaray P, Caccamo D, Belpomme D. 2018. Oxidative stress in electrohypersensitivity self-reporting patients: Results of a prospective in vivo investigation with comprehensive molecular analysis. Int J Mol Med 42(4):1885-1898.
In this study as the inclusion criteria were used pulsatility index and 4 markers of oxidative stress: plasma histamine, serum protein S100B, serum Hsp70 and serum Hsp27. The main criteria were self-reported EHS combined with the decline in pulsativity index and presence of at least one of the four inflammation-associated markers listed above.
This means that, yet again, the reliability of the self-diagnosed EHS was not tested but researchers relayed solely on the claim of the self-diagnosed person.
French team did not determine whether EMF played any role in the occurrence of the tested, purportedly, EHS markers.
The article presents a very long list of how oxidative stress influences normal physiology. However, there is no information that the oxidative stress experienced by the self-diagnosed EHS persons was caused by the EMF exposures. The same applies to pulsativity index – it is not known what caused the decline in the pulsativity index.
Claimed role of EMF was not examined at all and was not proven.
Considering the above lack of evidence of link between self-diagnosed EHS and physiological markers examined by the French team, it is surprising that the French team has arrived at the conclusion where new name was coined for the EHS. It includes, in the name of the syndrome, term “electromagnetic fields” but speaks of “regardless of its causal origin”:
“Finally, it may be concluded that regardless of its causal origin, EMFIS [electromagnetic fields intolerance syndrome] may be biologically characterized as a novel pathological disorder, and thus may be diagnosed in medical practice on the basis of clinical symptoms, and more objectively by measuring: Inflammation‑associated biomarkers, including histamine, protein S100B and the cellular stress chaperone proteins Hsp70 and Hsp27 (3); oxidative stress biomarkers, including TBARs, MDA, GSS and NTT in plasma; and antioxidative defense biomarkers, including SOD in RBCs, and GSH and GPx in plasma.”
This claim of EMF link is not supported by the evidence presented by the French team in neither of the three published studies.
Summa summarum, the French team, purpotedly studying EHS using biochemical and physiological markers, has the same problem as the psychological provocation studies:
- Selection of the study subjects relies solely on the opinion presented by the self-diagnosed EHS person. The scientists do not know whether the self-diagnoses are correct or not. The scientists do not know the possible “contamination”, of the EHS volunteers group, by the incorrectly self-diagnosed EHS persons.
- No attempt to determine whether expression of any of the examined physiological markers is dependent, in any way, of the EMF exposures.
- The scientists do not know whether any of the observed changes in pulsativity index or oxidative stress markers were caused by EMF exposures or is an outcome of non-EMF-related, yet unknown causing factor.
- The authors did not provide information whether any of the self-diagnosed EHS persons expressed more that one of the examined markers.
THERE IS NO EVIDENCE, IN STUDIES PUBLISHED BY THE FRENCH TEAM OF DOMINIQUE BELPOMME THAT THE EXAMINED PATIENTS HAD THEIR SYMPTOMS CAUSED BY EXPOSURES TO EMF.
