Elsevier

Pathophysiology

Volume 20, Issue 3, June 2013, Pages 191-209
Pathophysiology

Autism and EMF? Plausibility of a pathophysiological link – Part I

https://doi.org/10.1016/j.pathophys.2013.08.001Get rights and content

Abstract

Although autism spectrum conditions (ASCs) are defined behaviorally, they also involve multileveled disturbances of underlying biology that find striking parallels in the physiological impacts of electromagnetic frequency and radiofrequency exposures (EMF/RFR). Part I of this paper will review the critical contributions pathophysiology may make to the etiology, pathogenesis and ongoing generation of core features of ASCs. We will review pathophysiological damage to core cellular processes that are associated both with ASCs and with biological effects of EMF/RFR exposures that contribute to chronically disrupted homeostasis. Many studies of people with ASCs have identified oxidative stress and evidence of free radical damage, cellular stress proteins, and deficiencies of antioxidants such as glutathione. Elevated intracellular calcium in ASCs may be due to genetics or may be downstream of inflammation or environmental exposures. Cell membrane lipids may be peroxidized, mitochondria may be dysfunctional, and various kinds of immune system disturbances are common. Brain oxidative stress and inflammation as well as measures consistent with blood–brain barrier and brain perfusion compromise have been documented. Part II of this paper will review how behaviors in ASCs may emerge from alterations of electrophysiological oscillatory synchronization, how EMF/RFR could contribute to these by de-tuning the organism, and policy implications of these vulnerabilities. Changes in brain and autonomic nervous system electrophysiological function and sensory processing predominate, seizures are common, and sleep disruption is close to universal. All of these phenomena also occur with EMF/RFR exposure that can add to system overload (‘allostatic load’) in ASCs by increasing risk, and worsening challenging biological problems and symptoms; conversely, reducing exposure might ameliorate symptoms of ASCs by reducing obstruction of physiological repair. Various vital but vulnerable mechanisms such as calcium channels may be disrupted by environmental agents, various genes associated with autism or the interaction of both. With dramatic increases in reported ASCs that are coincident in time with the deployment of wireless technologies, we need aggressive investigation of potential ASC – EMF/RFR links. The evidence is sufficient to warrant new public exposure standards benchmarked to low-intensity (non-thermal) exposure levels now known to be biologically disruptive, and strong, interim precautionary practices are advocated.

Introduction

The premise of this review is that although scant attention has been paid to possible links between electromagnetic fields and radiofrequency radiation exposures (EMF/RFR) and Autism Spectrum Conditions (ASCs), such links probably exist. The rationale for this premise is that the physiological impacts of EMF/RFR and a host of increasingly well-documented pathophysiological phenomena in ASCs have remarkable similarities, spanning from cellular and oxidative stress to malfunctioning membranes, channels and barriers to genotoxicity, mitochondrial dysfunction, immune abnormalities, inflammatory issues, neuropathological disruption and electrophysiological dysregulation – in short, multi-scale contributors to de-tuning the organism. Additional support may be found in the parallels between the rise in reported cases of ASCs and the remarkable increases in EMF/RFR exposures over the past few decades

Reviewing these similarities does not prove that these parallels imply causality. Moreover, the physiological processes affected by EMF/RFR are also impacted by other environmental factors, and are known to be present in myriad other chronic illnesses. A set of in-depth reviews on the science and public health policy implications of EMF/RFR has been published in a special issue of Pathophysiology 16 (2,3) 2009. This two-volume special issue of Pathophysiology offers a broad perspective on the nature of health impacts of man-made EMFs, documenting biological effects and health impacts of EMFs including genotoxicity, neurotoxicity, reproductive and developmental effects, physiological stress, blood–brain barrier effects, immune system effects, various cancers including breast cancer, glioma and acoustic neuroma, Alzheimer's disease; and the science as a guide to public health policy implications for EMF diseases [1]. Many of these reviews have been updated in the BioInitiative 2012 Report [2], with 1800 new papers added. Further reinforcement is published in seminal research reviews including the two-volume Non-Thermal effects and Mechanisms of Interaction between Electromagnetic Fields and Living Matter, Giuliani L and Soffritti, M (Eds.), ICEMS, Ramazzini Institute, Bologna, Italy (2010) [3]; the World Health Organization INTERPHONE Final Report (2010) [4]; and the WHO International Agency for Research on Cancer RFR Monograph [5] designating RFR as a Group 2B Possible Human Carcinogen. The National Academy of Sciences Committee on Identification of Research Needs Relating to Potential Biological or Adverse Health Effects of Wireless Communication Devices (2008) [6] called for health research on wireless effects on children and adolescents and pregnant women; wireless personal computers and base station antennas; multiple element base station antennas under highest radiated power conditions; hand-held cell phones; and better dosimetric absorbed power calculations using realistic anatomic models for both men, women and children of different height and ages. Yet EMF/RFR does not need to be a unique contributor to ASCs to add significantly to system overload (‘allostatic load’) and dysfunction [7]. Even so these pathophysiological overlaps do suggest that the potential for an EMF/RFR-ASC connection should be taken seriously, and that their biological fragility may make many with ASCs more likely to experience adverse EMF/RFR impacts. This is a sufficient basis to recommend that precautionary measures should be implemented, that further research should be prioritized, and that policy level interventions based on existing and emerging data should be designed and pursued. Moreover, pursuing this link could help us understand ASCs better and find more ways to improve the lives of people with ASCs and of so many others.

This paper is divided into two parts. Part I (http://dx.doi.org/10.1016/j.pathophys.2013.08.001) describes the pathophysiology and dynamism of common behavioral manifestations in autism, and pathophysiological damage to core cellular processes that is associated both with ASCs and with impacts of EMF/RFR. Part II (http://dx.doi.org/10.1016/j.pathophys.2013.08.002) reviews how behaviors in ASCs may emerge from alterations of electrophysiological oscillatory synchronization and how EMF/RFR could contribute to these by de-tuning the organism. Part II also discusses public health implications, and proposes recommendations for harm prevention and health promotion.

Section snippets

How are biology and behavior related?

Appreciating the plausibility of a link between ASCs and EMF/RFR requires considering the relationship between ASC's behavioral and biological features. ASCs were first labeled as ‘autism’ in 1943 by Leo Kanner, a child psychiatrist who extracted several key behavioral features, related to communication and social interaction challenges and a tendency toward restricted interests and repetitive behaviors [8]. There has been some modification of the characterization of these behavioral features,

Parallels in pathophysiology

This section will review parallels in pathophysiology between ASCs and impacts of EMF/RFR. It will begin with a review of mechanisms of direct impact and damage at the level of molecules, cells, tissues and genes. It will then move on to consider how these levels of damage lead to degradation of the integrity of functional systems including mitochondrial bioenergetics, melatonin metabolism, immune function and nervous system physiology. The review of parallels concludes with electromagnetic

References (298)

  • S.E. Rotschafer et al.

    Minocycline treatment reverses ultrasonic vocalization production deficit in a mouse model of Fragile X Syndrome

    Brain Res.

    (2012)
  • I. Soulieres et al.

    Enhanced mental image mapping in autism

    Neuropsychologia

    (2011)
  • C. Lintas et al.

    Genome-wide expression studies in autism spectrum disorder, Rett syndrome, and Down syndrome

    Neurobiol. Dis.

    (2012)
  • A. Kanthasamy et al.

    Emerging neurotoxic mechanisms in environmental factors-induced neurodegeneration

    Neurotoxicology

    (2012)
  • R.A. Roberts et al.

    Toxicological and pathophysiological roles of reactive oxygen and nitrogen species

    Toxicology

    (2010)
  • A. Frustaci et al.

    Oxidative stress-related biomarkers in autism: systematic review and meta-analyses

    Free Radic. Biol. Med.

    (2012)
  • G.A. Mostafa et al.

    Oxidative stress in Egyptian children with autism: relation to autoimmunity

    J. Neuroimmunol.

    (2010)
  • A. Chauhan et al.

    Oxidative stress in autism

    Pathophysiology

    (2006)
  • M. Blank
  • International Commission for Electromagnetic Safety (ICEMS)

    Non-thermal effects and mechanisms of interaction between electromagnetic fields and living matter

    Eur. J. Oncol. Libr.

    (2010)
  • Interphone Study Group

    Brain tumour risk in relation to mobile telephone use: results of the INTERPHONE international case–control study

    Int. J. Epidemiol.

    (2010)
  • N.R.C. Committee on Identification of Research Needs Relating to Potential Biological or Adverse Health Effects of Wireless Communications Devices

    Identification of Research Needs Relating to Potential Biological or Adverse Health Effects of Wireless Communication

    (2008)
  • M.R. Herbert et al.
  • L. Kanner

    Autistic disturbances of affective contact

    Nerv. Child

    (1943)
  • American Psychiatric Association, Diagnostic and Statistical Manual of Mental Disorders DSM-IV-TR Fourth Edition (Text...
  • American Psychiatric Association, Diagnostic and Statistical Manual of Mental Disorders DSM-v, American Psychiatric...
  • M.R. Herbert

    Autism: a brain disorder or a disorder that affects the brain?

    Clin. Neuropsychiatry

    (2005)
  • I. Rapin et al.

    Neurobiology of autism

    Ann. Neurol.

    (1998)
  • F. Polleux et al.

    Toward a developmental neurobiology of autism

    Ment. Retard. Dev. Disabil. Res. Rev.

    (2004)
  • X. Ming et al.

    Metabolic perturbance in autism spectrum disorders: a metabolomics study

    J. Proteome Res.

    (2012)
  • S. Tsaluchidu et al.

    Fatty acids and oxidative stress in psychiatric disorders

    BMC Psychiatry

    (2008)
  • A. Gonzalez et al.

    The mind–body-microbial continuum

    Dialogues Clin. Neurosci.

    (2011)
  • R.N. Nikolov et al.

    Gastrointestinal symptoms in a sample of children with pervasive developmental disorders

    J. Autism Dev. Disord.

    (2009)
  • M. Kaartinen et al.

    Autonomic arousal to direct gaze correlates with social impairments among children with ASD

    J. Autism Dev. Disord.

    (2012)
  • C. Daluwatte et al.

    Atypical pupillary light reflex and heart rate variability in children with autism spectrum disorder

    J. Autism Dev. Disord.

    (2013)
  • R. Tuchman et al.

    Epilepsy and autism: neurodevelopmental perspective

    Curr. Neurol. Neurosci. Rep.

    (2011)
  • R. Canitano

    Epilepsy in autism spectrum disorders

    Eur. Child Adolesc. Psychiatry

    (2007)
  • B.A. Malow

    Sleep disorders, epilepsy, and autism

    Ment. Retard. Dev. Disabil. Res. Rev.

    (2004)
  • J.Q. Kang et al.

    A common susceptibility factor of both autism and epilepsy: functional deficiency of GABA(A) receptors

    J. Autism Dev. Disord.

    (2013)
  • I.S. Kohane et al.

    The co-morbidity burden of children and young adults with autism spectrum disorders

    PLoS ONE

    (2012)
  • T.A. Trikalinos et al.

    A heterogeneity-based genome search meta-analysis for autism-spectrum disorders

    Mol. Psychiatry

    (2006)
  • H. Ring et al.

    Clinical heterogeneity among people with high functioning autism spectrum conditions: evidence favouring a continuous severity gradient

    Behav. Brain Funct.

    (2008)
  • K.A. Pelphrey et al.

    Research review: constraining heterogeneity: the social brain and its development in autism spectrum disorder

    J. Child Psychol. Psychiatry

    (2011)
  • D. Mandell

    The heterogeneity in clinical presentation among individuals on the autism spectrum is a remarkably puzzling facet of this set of disorders

    Autism

    (2011)
  • D. Hall et al.

    Sharing heterogeneous data: the national database for autism research

    Neuroinformatics

    (2012)
  • A.J. Whitehouse et al.

    Maternal vitamin D levels and the autism phenotype among offspring

    J. Autism Dev. Disord.

    (2013)
  • R.J. Schmidt et al.

    Prenatal vitamins, one-carbon metabolism gene variants, and risk for autism

    Epidemiology

    (2011)
  • P.J. Landrigan

    What causes autism? Exploring the environmental contribution

    Curr. Opin. Pediatr.

    (2010)
  • E.M. Roberts et al.

    Maternal residence near agricultural pesticide applications and autism spectrum disorders among children in the California Central Valley

    Environ. Health Perspect.

    (2007 Oct)
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