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Metabolic and Genetic Screening of Electromagnetic Hypersensitive Subjects as a Feasible Tool for Diagnostics and Intervention

Posted on March 13, 2020 at 8:25 AM

 


Chiara De Luca, Jeffrey Chung Sheun Thai, [...], and Liudmila Korkina

 

Additional article information

 

Abstract

Growing numbers of “electromagnetic hypersensitive” (EHS) people worldwide self-report severely disabling, multiorgan, non-specific symptoms when exposed to low-dose electromagnetic radiations, often associated with symptoms of multiple chemical sensitivity (MCS) and/or other environmental “sensitivity-related illnesses” (SRI). This cluster of chronic inflammatory disorders still lacks validated pathogenetic mechanism, diagnostic biomarkers, and management guidelines. We hypothesized that SRI, not being merely psychogenic, may share organic determinants of impaired detoxification of common physic-chemical stressors. Based on our previous MCS studies, we tested a panel of 12 metabolic blood redox-related parameters and of selected drug-metabolizing-enzyme gene polymorphisms, on 153 EHS, 147 MCS, and 132 control Italians, confirming MCS altered (P < 0.05–0.0001) glutathione-(GSH), GSH-peroxidase/S-transferase, and catalase erythrocyte activities. We first described comparable—though milder—metabolic pro-oxidant/proinflammatory alterations in EHS with distinctively increased plasma coenzyme-Q10 oxidation ratio. Severe depletion of erythrocyte membrane polyunsaturated fatty acids with increased ω6/ω3 ratio was confirmed in MCS, but not in EHS. We also identified significantly (P = 0.003) altered distribution-versus-control of the CYP2C19∗1/∗2 SNP variants in EHS, and a 9.7-fold increased risk (OR: 95% C.I. = 1.3–74.5) of developing EHS for the haplotype (null)GSTT1 + (null)GSTM1 variants. Altogether, results on MCS and EHS strengthen our proposal to adopt this blood metabolic/genetic biomarkers' panel as suitable diagnostic tool for SRI.

 

1. Introduction

The term electromagnetic hypersensitivity or electrosensitivity (EHS) referred to a clinical condition characterized by a complex array of symptoms typically occurring following exposure to electromagnetic fields (EMFs) even below recommended reference levels and is followed by remission through the complete isolation [1, 2]. The most frequently claimed trigger factors include video display units, radio, televisions, electrical installations, extremely low-frequency ranges of electromagnetic fields or radio-frequencies—including the so-called dirty electricity due to poor isolation of electric wires and telephonic lines, wireless devices, and wi-fi—fluorescent lamps and low-energy lights, appliances with motors, photocopiers, microwave transmitters, and high tension power lines (reviewed in [3, 4]). EHS is characterized by a broad range of nonspecific multiple-organ symptoms implying both acute and chronic inflammatory processes, involving mainly skin and nervous, respiratory, cardiovascular, musculoskeletal, and gastrointestinal systems, in most cases self-reported in absence of organic pathological signs except skin manifestations (reviewed in [2, 5]).

 

Many efforts have been made to determine if a causal relationship between exposure to EMFs and claimed health symptoms does exist and to identify biologically plausible mechanisms underlying this syndrome (for review, see [2, 6, 7]). Despite the growing wealth of evidences gathered both in vitro and in vivo on animal models, data from human case-control and double-blind trials attempting to correlate EMFs exposure and claimed symptoms, resulted so far controversial [8–10]. Nowadays, wide gaps still exist in understanding EHS, which most often remains neglected by the medical community or confined within the frame of mere psychogenic etiology [11, 12]. In the persistent lack of a proven pathogenetic mechanism for electromagnetic hypersensitivity and of clinical consensus on the few proposed diagnostic and therapeutic approaches hypothesized, no guideline for safe and efficient validated treatments has been made available until now to the patients worldwide [13, 14].

 

Nevertheless, the number of subjects self-reporting EHS is progressively increasing, especially in European countries [15–17], with symptoms that are often strongly disabling both professionally and socially, motivating patients to leave home and job to find rescue in “electromagnetic pollution-free” environmental settings. Because of the huge socioeconomic impact anticipated for EHS syndrome worldwide, the World Health Organization has devoted considerable attention to EHS, acknowledging this condition and recommending that people self-reporting sensitivities receive a comprehensive health evaluation [18].

 

Clinical similarities and frequent comorbidity between EHS and the other medically unexplained multisystem conditions of environmental origin, like multiple chemical sensitivity (MCS), fibromyalgia (FM), chronic fatigue syndrome (CFS), sick building syndrome, Persian Gulf War veteran syndrome, and amalgam disease, to which EHS is often associated [19, 20], have induced many authors to hypothesize that these so-called idiopathic environmental intolerances (IEI), more extensively also defined as sensitivity-related illnesses (SRI) [21], may share common genetic and/or metabolic molecular determinants connected with an impaired capability to detoxify xenobiotics (for review, see [19, 22]). Our group has evidenced for the first time a set of altered metabolic blood parameters—comprising selected redox-active and detoxifying enzymes, low-molecular weight antioxidants and oxidation markers, membrane polyunsaturated fatty acid, and proinflammatory cytokine patterns—specifically and selectively compatible with the MCS condition [23]. Recently, we contributed to the still open issue of possible genetic polymorphic patterns associated with MCS proneness, proposing a pattern of genotypic alterations of the cytochrome P450 isoenzymes CYP2C9, CYP2C19, and CYP2D6, as candidate risk factors for this specific condition, also being potentially able to discriminate different environmental-borne hypersensitivities (MCS, FM, and CFS), depending on specific combinations of their mutated alleles [24].

 

In this study, the working hypothesis was that EHS, as previously proposed for MCS and other environmental SRI [19, 22], may as well be based on aberrant responses to physic or chemical xenobiotic stressors through airborne or other routes of exposure, due to inherited or/and acquired dysfunction of the chemical defensive system, that is the interrelated network of phase I and II xenobiotic-metabolizing and antioxidant enzymes [19]. Based on the results of our past clinical studies on MCS, FM, and CFS, we sought to assess if similar profiles of metabolic or genetic dysfunctions could be found in those subjects self-reporting EHS phenotype. To this purpose, we measured possible alterations of a previously identified panel of twelve blood redox and lipid parameters and frequencies of selected genetic mutated variants of a set of drug-metabolizing enzymes and transcription factors with first-line roles in the detoxification of physical and chemical xenobiotics, in a group of 153 patients self-reporting EHS symptoms, co-morbid in most cases with different degrees of MCS symptoms. Results were compared to those obtained on 147 MCS patients without EHS symptoms and on a healthy control group of 132 age- and sex-matched subjects, all groups enrolled within the Italian population. ....... https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4000647/#!po=74.0385

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