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Example of diagrams obtained by using UCTS exploring the global centimetric ultrasound pulsatility in the two temporal lobes of a normal subject (A) and in a EHS self-reporting patient (B). Measurements are expressed in Pulsometric index (PI). Note that in A and B mean values of PI in each explored area recorded is from the cortex to the internal part of each temporal lobe; so on the left part of the two diagrams A and B for the right lobe from the left to the right; and on the right part of these diagrams for the left lobe from the right to the left. Note also that in A (normal subject) all values are over the normal median values whereas in B (EHS-self reporting patients) values in the capsulothalamic areas (the fifth and the second column for the right and left temporal lobe, respectively) are under the normal median values. 

Example of diagrams obtained by using UCTS exploring the global centimetric ultrasound pulsatility in the two temporal lobes of a normal subject (A) and in a EHS self-reporting patient (B). Measurements are expressed in Pulsometric index (PI). Note that in A and B mean values of PI in each explored area recorded is from the cortex to the internal part of each temporal lobe; so on the left part of the two diagrams A and B for the right lobe from the left to the right; and on the right part of these diagrams for the left lobe from the right to the left. Note also that in A (normal subject) all values are over the normal median values whereas in B (EHS-self reporting patients) values in the capsulothalamic areas (the fifth and the second column for the right and left temporal lobe, respectively) are under the normal median values. 

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Much of the controversy over the causes of electro-hypersensitivity (EHS) and multiple chemical sensitivity (MCS) lies in the absence of both recognized clinical criteria and objective biomarkers for widely accepted diagnosis. Since 2009, we have prospectively investigated, clinically and biologically, 1216 consecutive EHS and/or MCS-self reporting...

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... since brain mast cells have been shown to be critical regulators of the pathogenesis of CNS diseases including stroke, traumatic injury and neurodegenerative diseases (83, 90) (see also Section "EHS/MCS as a possible sentinel pathological disorder") we systematically looked for brain pathologic alterations in EHS and /or MCS patients. Routine cerebral MRI and/or scanner as well as carotid echography were critically considered to be normal in all evaluable cases. We thus measured the BBF-related pulsatil- ity 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). More precisely, by using pulsed ultra- sound computed tomosphygmography, we found that in comparison to normal subjects, cerebral pulsatility in EHS and /or MCS patients was decreased or even completely abolished in one or the two temporal lobes (Figure 2), sug- gesting that BBF might be specifically decreased or abol- ished in this brain area. We found that this abnormality, although being not specific, was so frequently observed in these patients that it may represent a typical brain alteration similar to that found in Alzheimer's disease and other neu- rodegenerative diseases (see Section "EHS/MCS as a possi- ble sentinel pathological disorder"). This finding therefore, strongly suggests that brain could be the main target of environmental EMFs and/or chemicals in EHS and/or MCS patients, and that both cerebral hypoperfusion and subse- quent histamine release whatever its neuronal or mast cell origin could be main contributing factors to BBB disruption. Furthermore, we found that cerebral blood pulsatility was quasi-constantly decreased in the capsulothalamic area of the temporal lobes, which includes the limbic system and the thalamus, and so correspond to particularly vulnerable areas to environmental stressors in the ...
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... addition, to these biochemical tests we used a non- invasive ultrasonic cerebral tomosphygmography method that we specifically set-up to investigate the blood flow in the patient temporal lobes and determined for each patient a pulsometric index (PI) that we measured cen- timeter by centimeter from the cortex to the diencephalic medial area (see Figure 1). This index varies between the territories studied. In this study, Pi determination for each cerebral territory in 727 EHS and/or MCS patients was compared to a retrospective series of 141 normal subjects which allowed to establish the normal median reference values of PI (see Figure 2). Finally since our study is still ongoing we did not reported any statistical analysis. This will follow in specific further ...

Citations

... Despite the attempts made to establish a definition and measurement protocol (Belpomme et al., 2015;Bergqvist et al., 1997;Eltiti et al., 2007;Hillert et al., 1999Hillert et al., , 2002, accepted diagnostic criteria for IEI-EMF, apart from the subjective reports of patients, are yet to be developed (Baliatsas et al., 2012a,b;Meg Tseng et al., 2011). Thus, the primary inclusion criterion of participants in IEI-EMF related research is self-reported sensitivity. ...
Article
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IEI-EMF refers to an environmental illness whose primary feature is the occurence of symptoms that are attributed to exposure to weak electromagnetic fields (EMFs). There is a growing evidence that this condition is characterized by marked individual differences thus a within-subject approach might add important information beyond the widely used nomothetic method. A mixed qualitative/quantitative idiographic protocol with a threefold diagnostic approach was tested with the participation of three individuals with severe IEI-EMF. In this qualitative paper, the environmental, psychosocial, and clinical aspects are presented and discussed (results of ecological momentary assessment are discussed in Part II of this study). For two participants, psychopathological factors appeared to be strongly related to the condition. Psychological assessment indicated a severe pre-psychotic state with paranoid tendencies, supplemented with a strong attentional focus on bodily sensations and health status. The psychological profile of the third individual showed no obvious pathology. Overall, the findings suggest that the condition might have uniformly been triggered by serious psychosocial stress for all participants. Substantial aetiological differences among participants with severe IEI-EMF were revealed. The substantial heterogeneity in the psychological and psychopathological profiles associated with IEI-EMF warrants the use of idiographic multimodal assessments in order to better understand the different ways of aetiology and to facilitate person-taylored treatments.
... As a result, exposure to thousands of radiofrequency signals in daily life, which is uncontrolled and involuntary, will have health consequences. [9,10] Radiofrequency waves and electromagnetic fields can have detrimental effects on homeostasis and automatic regulation (synchronization) and biological rhythm, and alter the content of biological information exchanged between cells. Changing the content of information destroys natural environmental guidelines and interferes with the information required for natural biological regulation. ...
Article
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Background: The objective of this study was to design and construct a CO2 incubator with nonmetallic walls and to investigate the viability of the cells and microwave irradiance inside this incubator. Methods: Because the walls of conventional incubators are made of metal, this causes scattering, reflection, and absorption of electromagnetic waves. We decided to build a nonmetallic wall incubator to examine cells under microwave radiation. Incubator walls were made using polyvinyl chloride and Plexiglas and then temperature, CO2 pressure, and humidity sensors were placed in it. Atmel® ATmega1284, a low-power CMOS 8-bit microcontroller, collects and analyzes the sensor information, and if the values are less or more than the specified limits, the command to cut off or connect the electric current to the heater or CO2 solenoid valve is sent. Using a fan inside the incubator chamber, temperature and CO2 are uniforms. The temperature of the points where the cell culture plates are placed was measured, and the temperature difference was compared. Ovarian cancer cells (A2780) were cultured in the hand-made and commercial incubators at different times, and cell viability was compared by the MTT method. Microwave radiation in the incubator was also investigated using a spectrum analyzer. The survival of cells after microwave irradiation in the incubator was measured and compared with control cells. Results: The data showed that there was no significant difference in temperature of different points in hand-made incubator and also there was no significant difference between the viability of cells cultured in the hand-made and commercial incubators. The survival of irradiated cells in the incubator was reduced compared to control cells, but this reduction was not significant. Conclusion: This incubator has the ability to maintain cells and study the effects of electromagnetic radiations on the desired cells, which becomes possible by using this device.
... The aforementioned studies, however, received criticism from a methodological point of view (Dieudonn e, 2020;Frei et al., 2010;Ledent et al., 2020;Schmiedchen et al., 2019). In the lack of biomarkers specific to IEI-EMF (Belpomme et al., 2015;Rubin et al., 2011), EMF provocation test is the only accepted paradigm for experimentally testing patients' self-diagnosis. As experimental manipulation and randomization take place, this method is theoretically able to shed light on causal relationships between exposure and symptoms (Rubin et al., 2010). ...
Article
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IEI-EMF refers to a self-reported sensitivity characterized by attribution of non-specific physical symptoms to exposure to weak EMFs. The majority of empirical results do not support the existence of a causal relationship between EMF and IEI-EMF. However, this conclusion was drawn from environmental and experimental studies that are not without methodological limitations. In the current study, as part of a complex biopsychosocial approach, an ecological momentary assessment (EMA) protocol was applied for the investigation of the temporal relationship between actual radio frequency (RF) EMF exposure and IEI-EMF, at the individual level. Continuous measurement of autonomic variables by holter electrocardiogram (ECG) monitors and the ambient RF EMF by personal dosimeters, as well as repeated (8/day) paper-and-pencil assessments of momentary internal states (symptoms, mood, perceived EMF intensity) and situational factors was conducted for 21 days with the participation of three individuals with severe IEI-EMF. Temporal relationships were examined by time series analyses. For two participants, the results did not support the association between the suspected EMF frequency range(s) and symptom reports. Nevertheless, the results revealed a reverse association with respect to another frequency range (GSM900 downlink), which contradicts the IEI-EMF condition. Autonomic activation related findings were inconsistent. For the third participant, the claimed association was partly supported, both for symptom reports and autonomic reactions (UMTS downlink, total RF; RMS values). The findings of this study suggest that IEI-EMF does not have a unitary aetiology. For certain individuals, a biophysical background cannot be excluded, whereas no such underlying factor appears to be at work for others. EMA is a useful method for the investigation of the aetiology of IEI-EMF.
... This table is based with some additions on a publication by Belpomme et al. [18] on symptoms in the first 100 patients in their case series. It is noteworthy that for this presented person almost all symptoms declined during sick leave, most notably the most serious health problems. ...
... There are no reliable biomarkers for EHS. In a case series by Belpomme et al. [18] a number of biomarkers were described. The 24 h urine 6-hydroxymelatonin sulfate (6-OHMS)/creatinin ratio was found to be decreased (<0.8) in all investigated cases which might be of interest. ...
Article
A previously healthy worker developed symptoms assigned to electromagnetic hypersensitivity (EHS) after moving to an office with exposure to high levels of anthropogenic electromagnetic fields (EMFs). These symptoms consisted of e.g. headache, arthralgia, tinnitus, dizziness, memory loss, fatique, insomnia, transitory cardiovascular abnormalities, and skin lesions. Most of the symptoms were alleviated after 2 weeks sick leave. The highest radiofrequency (RF) field level at the working place was 1.72 V/m (7,852 μW/m2). Maximum value for extremely low frequency electromagnetic field (ELF-EMF) from electric power at 50 Hz was measured to 285 nT (mean 241 nT). For electric train ELF-EMF at 16.7 Hz was measured to 383 nT (mean 76 nT). Exposure to EMFs at the working place could be the cause for developing EHS related symptoms. The association was strengthened by the symptom reduction outside the working place.
... This approach is expensive, very likely to yield false positives, and may even be deemed unethical (for the lack of a strong rational for collecting biological samples in human subjects). The studies of the Belpomme group illustrate these difficulties very well [3,4]. The root cause of that situation is that EHS people's attribution conflict with decades of biophysical research, providing no practical direction for searching for biomarkers of EHS. ...
... There is also a clear gender effect in EHS as measured by Belpomme and Irigaray, who built a database of more than 2,000 people declaring themselves to be electrohypersensitive (EHS) and/or claiming to suffer from multiple chemical sensitivities (MCS). 36, 43 An earlier analysis I made on this work 19 shows that the gender ratio for EHS syndrome is similar to the gender effect for phobias: the gender ratio for EHS syndrome has been measured around 1.9, i.e., in close agreement with the gender ratios for any type of phobias, or for simple phobias as measured by several scientific studies ( Table 1, ...
Article
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Electrohypersensitivity syndrome is a set of symptoms attributed to exposure to artificial electromagnetic radiation. However, mechanisms that would explain such effect of radiation on human remain unknown to date. Conversely, EHS could be well explainable by existing biological and psychological mechanisms known for being at work in phobias. In this paper, we present our cognitive approach to EHS and advocate for the development of cognitive behavioral techniques as a potential treatment.
... Jalava et al. [200] found that fine particulate matter in urban air are triggers for inflammatory and cytotoxic effects. Moreover, Belpomme, Campagnac and Irigaray [201] observed that MCS and Electro-Hypersensitivity (EHS) patients exhibited higher levels of histamine, inflammatory processes affecting thalamus and limbic system, and oxidative stress compared to controls (for a consensus report on specific markers in electrohypersensitivity, see [202]). The authors considered these as reliable and objective etiopathogenic biomarkers for diagnosis, suggesting a common pathological mechanism in the two disorders [see De Luca et al. [34] for an interesting review on dependable biological markers of MCS and Hoover at al. [203] regarding the relationship between reliability of some immunological tests and MCS]. ...
... The presence of elevated levels of nitric oxide (NO) and peroxynitrite (PN), two indices of oxidative stress, have been claimed to be an etiopathogenic marker in persons with this condition. Belpomme et al. [201,202] found in their MCS and EHS patients an increased amount of serum nytrotirosin, a marker of PN, suggesting the presence of oxidative stress. Similarly, Hirvonen et al. [198] observed an increased concentration of NO in their nasal lavage samples of persons exposed to mold-related microbes. ...
Article
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Multiple Chemical Sensitivity (MCS), a condition also known as Chemical Sensitivity (CS), Chemical Intolerance (CI), Idiopathic Environmental Illness (IEI) and Toxicant Induced Loss of Tolerance (TILT), is an acquired multifactorial syndrome characterized by a recurrent set of debilitating symptoms. The symptoms of this controversial disorder are reported to be induced by environmental chemicals at doses far below those usually harmful to most persons. They involve a large spectrum of organ systems and typically disappear when the environmental chemicals are removed. However, no clear link has emerged among self-reported MCS symptoms and widely accepted objective measures of physiological dysfunction, and no clear dose-response relationship between exposure and symptom reactions has been observed. In addition, the underlying etiology and pathogenic processes of the disorder remain unknown and disputed, although biologic and psychologic hypotheses abound. It is currently debated whether MCS should be considered a clinical entity at all. Nevertheless, in the last few decades MCS has received considerable scientific and governmental attention in light of the many persons reporting this illness. In this review, we provide a general overview of the history, definition, demographics, prevalence, and etiologic challenges in defining and understanding MCS.
... Additional file 1: Table S1 lists selected MC mediators involved in neuroinflammation (after Theoharides et al. [56][57][58][59]. Many investigators have documented neuroinflammation and inflammatory mediators in CI [53,[60][61][62]. ...
Article
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Background This paper explores the relationship between chemical intolerance (CI) and mast cell activation syndrome (MCAS). Worldwide observations provide evidence for a two-stage disease process called toxicant-induced loss of tolerance (TILT) as a mechanism for CI. TILT is initiated by a major exposure event or a series of lower-level exposures. Subsequently, affected individuals report that common chemical inhalants, foods, and drugs (i.e., various xenobiotics) trigger multi-system symptoms. Purpose To determine whether MCAS provides a plausible biological mechanism for CI/TILT. Methods Using the validated Quick Environmental Exposure and Sensitivity Inventory (QEESI), we compared patients diagnosed with MCAS (n = 147) to individuals who reported chemical intolerances (CI/TILT) following various exposures (n = 345) and to healthy controls (n = 76). Using ANOVA, we compared QEESI scores across groups. Clinical scores for the MCAS patient group were used to predict CI status using logistic regression. Results More than half (59%) of the MCAS group met criteria for CI. A logistic regression model illustrates that as the likelihood of patients having MCAS increased, their likelihood of having CI/TILT similarly increased, to a near-perfect correspondence at the high ends of the QEESI and clinical MCAS scores. Symptom and intolerance patterns were nearly identical for the CI and MCAS groups. Discussion We present data suggesting that xenobiotic activation of mast cells may underlie CI/TILT. The strikingly similar symptom and intolerance patterns for MCAS and TILT suggest that xenobiotics disrupt mast cells, leading to either or both of these challenging conditions. Faced with patients suffering from complex illness affecting multiple organ systems and fluctuating inflammatory, allergic, and dystrophic symptoms, clinicians can now ask themselves two questions: (1) Could MCAS be at the root of these problems? (2) Could environmental exposures be driving MC activation and mediator release? Increasing our understanding of the connection between TILT and MCs has the potential to expose a new link between environmental exposures and illness, offering new opportunities for improving individual and public health. Conclusion The close correspondence between QEESI scores and symptom patterns for MCAS and TILT patients supports xenobiotic-driven mast cell activation and mediator release (i.e., MCAS) as a plausible unifying biological mechanism for CI/TILT, with profound implications for medicine, public health, and regulatory toxicology.
... An assay of the serum S100B protein is recommended to evaluate the permeability of the blood-brain barrier that may be altered by MCS triggers [87]. A neuron-specific enolase (NSE) assay in serum is suggested to evaluate current or even previous mercury-related neurological signs and symptoms [88,89]. ...
... Metabolism perturbations due to or provoked by environmental exposures are currently under evaluation and the preliminary data suggest abnormalities in the detoxification metabolism (i.e., glutathione transferase, catalase, superoxide dismutase), energetic metabolism (i.e., intracellular adenosine triphosphate (ATP) in erythrocytes and platelets) and inflammatory response (pro-inflammatory serum cytokines) [43,87,105,[109][110][111][112][113][114]. These promising biomarkers evaluated on serum, whole blood and peripheral blood mononuclear cells (PBMCs) are detected with methods validated only in experimental conditions and are not applicable to daily clinical practice. ...
Article
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Multiple chemical sensitivity (MCS) is a multisystem, recurrent, environmental disorder that flares in response to different exposures (i.e., pesticides, solvents, toxic metals and molds) under the threshold limit value (TLV) calculated for age and gender in the general population. MCS is a syndrome characterized by cutaneous, allergic, gastrointestinal, rheumatological, endocrinological, cardiological and neurological signs and symptoms. We performed a systematic review of the literature to summarize the current clinical and therapeutic evidence and then oriented an eDelphi consensus. Four main research domains were identified (diagnosis, treatment, hospitalization and emergency) and discussed by 10 experts and an MCS patient. Thus, the first Italian MCS consensus had the double aim: (a) to improve MCS knowledge among healthcare workers and patients by standardizing the clinical and therapeutic management to MCS patients; and (b) to improve and shed light on MCS misconceptions not supported by evidence-based medicine (EBM).
... These results suggest a toxico-genetic effect of SMF exposure related to an imbalance in SOD2 activity associated with the AA16 genotype (45). Interestingly, hypersensitivity to electromagnetic field, also called EHS, is a common co-morbidity of MCS (9,46) in which oxidative stress plays a major role (47). ...
Article
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Chronically increased oxidative stress has been reported in patients with multiple chemical sensitivity (MCS). Recently, a single nucleotide polymorphism of the gene coding for mitochondrial superoxide dismutase (SOD2), namely the missense substitution A16V (C47>T) resulting in alteration of SOD2 enzyme activity, has been reported to be associated with MCS. However, the influence of SOD2 A16V genetic background on redox status of patients with MCS has not yet been investigated. Here, the results of a retrospective analysis aimed to evaluate the role of the SOD2 A16V polymorphism in the alterations of antioxidant defense markers as well as fatty acid (FA) composition of erythrocyte membranes in 67 patients with MCS matched with 55 healthy controls is reported. The mutated SOD2 V16 variant was observed more frequently in the MCS group compared with the control group, and this difference was statistically significant. The most common genotype in both groups was the heterozygous SOD2 AV16 variant, whereas the mutated SOD2 VV16 variant was more frequently observed in the MCS group, although the difference was not significant. The MCS cohort showed significantly depleted levels of plasma total antioxidant activity, ubiquinol, erythrocyte reduced glutathione and membrane polyunsaturated FA levels, coupled with significant increases in glutathione peroxidase activity, likely accounting for sustained detoxification from lipoperoxides. Notably, the highest levels of oxidative stress were found in patients with MCS bearing the genotype SOD2 AA16, whereas intermediate levels were found in patients bearing the heterozygous AV16 genotype. Healthy subjects bearing the SOD2 AA16 genotype also showed increased oxidative stress compared with carriers of other SOD2 genotypes. Despite the need for further confirmations in larger cohorts, due to MCS population genetic heterogeneity, these preliminary findings suggest that SOD2 defective activity makes certain patients with MCS more susceptible to developing oxidative stress following a chronic daily exposure to pro-oxidant insults.