L’International Journal of Environmental Research and Public Health consacre un numéro en Open Access sur la recherche de risques environnementaux de l’autisme.

1. Geier D, Kern J, King P, Sykes L, Geier M. Hair Toxic Metal Concentrations and Autism Spectrum Disorder Severity in Young Children. International Journal of Environmental Research and Public Health ;2012 ;9(12):4486-4497.

Previous studies have found a higher body-burden of toxic metals, particularly mercury (Hg), among subjects diagnosed with an autism spectrum disorder (ASD) in comparison to neurotypical controls. Moreover, Hg body-burden was associated with ASD severity. This cross-sectional study examined the potential correlation between hair toxic metal concentrations and ASD severity in a prospective cohort of participants diagnosed with moderate to severe ASD. The Institutional Review Board at the University of Texas Southwestern Medical Center at Dallas (Dallas, TX) approved the present study. Qualifying study participants (n = 18) were evaluated for ASD severity using the Childhood Autism Rating Scale (CARS) and quantitatively for arsenic, Hg, cadmium, lead, chromium, cobalt, nickel, aluminum, tin, uranium, and manganese using hair toxic element testing by Doctor’s Data (a CLIA-approved laboratory). CARS scoring and hair toxic element testing were blinded to one another. Increasing hair Hg concentrations significantly correlated with increased ASD severity. In contrast, no significant correlations were observed between any other of the hair toxic metals examined and ASD severity. This study helps to provide additional mechanistic support for Hg in the etiology of ASD severity, and is supported by an increasing number of recent critical reviews that provide biological plausibility for the role of Hg exposure in the pathogenesis of ASDs.

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2. Lung F-W, Chiang T-L, Lin S-J, Shu B-C. Incinerator Pollution and Child Development in the Taiwan Birth Cohort Study. International Journal of Environmental Research and Public Health ;2013 ;10(6):2241-2257.

This study aimed to investigate the direct and indirect effects of environmental pollutants on child development and parental concerns. It focused on the pathway relationships among the following factors : living within three kilometers of an incinerator, breastfeeding, place of residence, parental concerns about development, and parent-perceived child development. The Taiwan Birth Cohort Study (TBCS) dataset includes randomized community data on 21,248 children at six, 18, and 36 months of age. The Parental Concern Checklist and the Taiwan Birth Cohort Study-Developmental Instrument were used to measure parental concern and parent-perceived child development. Living within three kilometers of an incinerator increased the risk of children showing delayed development in the gross motor domain at six and 36 months. Although breastfeeding is a protective factor against uneven/delayed developmental disability (U/DDD), children living near an incinerator who were breastfed had an increased risk of U/DDD compared with those who did not live near incinerators. The presence of a local incinerator affected parent-perceived child development directly and indirectly through the mediating factor of breastfeeding. Further follow-up of these children to investigate the long-term effects of specific toxins on their development and later diagnostic categorization is necessary.

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3. Lyall K, Baker A, Hertz-Picciotto I, Walker C. Infertility and Its Treatments in Association with Autism Spectrum Disorders : A Review and Results from the CHARGE Study. International Journal of Environmental Research and Public Health ;2013 ;10(8):3715-3734.

Previous findings on relationships between infertility, infertility therapies, and autism spectrum disorders (ASD) have been inconsistent. The goals of this study are first, to briefly review this evidence and second, to examine infertility and its treatments in association with having a child with ASD in newly analyzed data. In review, we identified 14 studies published as of May 2013 investigating infertility and/or its treatments and ASD. Overall, prior results showed little support for a strong association, though some increases in risk with specific treatments were found ; many limitations were noted. In new analyses of the CHildhood Autism Risk from Genetics and the Environment (CHARGE) population-based study, cases with autism spectrum disorder (ASD, n = 513) and controls confirmed to have typical development (n = 388) were compared with regard to frequencies of infertility diagnoses and treatments overall and by type. Infertility diagnoses and treatments were also grouped to explore potential underlying pathways. Logistic regression was used to obtain crude and adjusted odds ratios overall and, in secondary analyses, stratified by maternal age (≥35 years) and diagnostic subgroups. No differences in infertility, infertility treatments, or hypothesized underlying pathways were found between cases and controls in crude or adjusted analyses. Numbers were small for rarer therapies and in subgroup analyses ; thus the potential for modest associations in specific subsets cannot be ruled out. However, converging evidence from this and other studies suggests that assisted reproductive technology is not a strong independent risk factor for ASD. Recommendations for future studies of this topic are provided.

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4. McGinnis W, Audhya T, Edelson S. Proposed Toxic and Hypoxic Impairment of a Brainstem Locus in Autism. International Journal of Environmental Research and Public Health ;2013 ;10(12):6955-7000.

Electrophysiological findings implicate site-specific impairment of the nucleus tractus solitarius (NTS) in autism. This invites hypothetical consideration of a large role for this small brainstem structure as the basis for seemingly disjointed behavioral and somatic features of autism. The NTS is the brain’s point of entry for visceral afference, its relay for vagal reflexes, and its integration center for autonomic control of circulatory, immunological, gastrointestinal, and laryngeal function. The NTS facilitates normal cerebrovascular perfusion, and is the seminal point for an ascending noradrenergic system that modulates many complex behaviors. Microvascular configuration predisposes the NTS to focal hypoxia. A subregion—the “pNTS”—permits exposure to all blood-borne neurotoxins, including those that do not readily transit the blood-brain barrier. Impairment of acetylcholinesterase (mercury and cadmium cations, nitrates/nitrites, organophosphates, monosodium glutamate), competition for hemoglobin (carbon monoxide, nitrates/nitrites), and higher blood viscosity (net systemic oxidative stress) are suggested to potentiate microcirculatory insufficiency of the NTS, and thus autism.

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5. Quaak I, Brouns M, Van de Bor M. The Dynamics of Autism Spectrum Disorders : How Neurotoxic Compounds and Neurotransmitters Interact. International Journal of Environmental Research and Public Health ;2013 ;10(8):3384-3408.

In recent years concern has risen about the increasing prevalence of Autism Spectrum Disorders (ASD). Accumulating evidence shows that exposure to neurotoxic compounds is related to ASD. Neurotransmitters might play a key role, as research has indicated a connection between neurotoxic compounds, neurotransmitters and ASD. In the current review a literature overview with respect to neurotoxic exposure and the effects on neurotransmitter systems is presented. The aim was to identify mechanisms and related factors which together might result in ASD. The literature reported in the current review supports the hypothesis that exposure to neurotoxic compounds can lead to alterations in the GABAergic, glutamatergic, serotonergic and dopaminergic system which have been related to ASD in previous work. However, in several studies findings were reported that are not supportive of this hypothesis. Other factors also might be related, possibly altering the mechanisms at work, such as time and length of exposure as well as dose of the compound. Future research should focus on identifying the pathway through which these factors interact with exposure to neurotoxic compounds making use of human studies.

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6. Siniscalco D, Cirillo A, Bradstreet J, Antonucci N. Epigenetic Findings in Autism : New Perspectives for Therapy. International Journal of Environmental Research and Public Health ;2013 ;10(9):4261-4273.

Autism and autism spectrum disorders (ASDs) are complex neurodevelopmental disorders characterized by dysfunctions in social interactions, communications, restricted interests, and repetitive stereotypic behaviors. Despite extensive genetic and biological research, significant controversy surrounds our understanding of the specific mechanisms of their pathogenesis. However, accumulating evidence points to the involvement of epigenetic modifications as foundational in creating ASD pathophysiology. Epigenetic modifications or the alteration of DNA transcription via variations in DNA methylation and histone modifications but without alterations in the DNA sequence, affect gene regulation. These alterations in gene expression, obtained through DNA methylation and/or histone modifications, result from transcriptional regulatory influences of environmental factors, such as nutritional deficiencies, various toxicants, immunological effects, and pharmaceuticals. As such these effects are epigenetic regulators which determine the final biochemistry and physiology of the individual. In contrast to psychopharmacological interventions, bettering our understanding of how these gene-environmental interactions create autistic symptoms should facilitate the development of therapeutic targeting of gene expression for ASD biomedical care.

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7. Yasuda H, Tsutsui T. Assessment of Infantile Mineral Imbalances in Autism Spectrum Disorders (ASDs). International Journal of Environmental Research and Public Health ;2013 ;10(11):6027-6043.

The interactions between genes and the environment are now regarded as the most probable explanation for autism. In this review, we summarize the results of a metallomics study in which scalp hair concentrations of 26 trace elements were examined for 1,967 autistic children (1,553 males and 414 females aged 0–15 years-old), and discuss recent advances in our understanding of epigenetic roles of infantile mineral imbalances in the pathogenesis of autism. In the 1,967 subjects, 584 (29.7%) and 347 (17.6%) were found deficient in zinc and magnesium, respectively, and the incidence rate of zinc deficiency was estimated at 43.5% in male and 52.5% in female infantile subjects aged 0–3 years-old. In contrast, 339 (17.2%), 168 (8.5%) and 94 (4.8%) individuals were found to suffer from high burdens of aluminum, cadmium and lead, respectively, and 2.8% or less from mercury and arsenic. High toxic metal burdens were more frequently observed in the infants aged 0–3 years-old, whose incidence rates were 20.6%, 12.1%, 7.5%, 3.2% and 2.3% for aluminum, cadmium, lead, arsenic and mercury, respectively. These findings suggest that infantile zinc- and magnesium-deficiency and/or toxic metal burdens may be critical and induce epigenetic alterations in the genes and genetic regulation mechanisms of neurodevelopment in the autistic children, and demonstrate that a time factor “infantile window” is also critical for neurodevelopment and probably for therapy. Thus, early metallomics analysis may lead to early screening/estimation and treatment/prevention for the autistic neurodevelopment disorders.

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