Exposure to endocrine disrupting chemicals and neurodevelopmental alterations

Pinson, Anneline; Bourguignon, Jean-Pierre; Parent, Anne-Simone

doi:10.1111/andr.12211

Cited by 54 publications

(37 citation statements)

References 170 publications

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“…Our review found “sufficient evidence of toxicity” based on diminished intelligence associated with increased exposure to PBDEs, and “limited evidence of toxicity” based on increases in ADHD and attention-related behaviors with increased exposure to PBDEs. We identified nine reviews of this topic published between 2003 and 2016 ( Berghuis et al 2015 ; Brandt 2012 ; Chao et al 2014 ; De Cock et al 2012 ; Kim et al 2014 ; Muir 2003 ; Pinson et al 2016 ; Roth and Wilks 2014 ; Vrijheid et al 2016 ), none of which conducted a meta-analysis or consistently applied all nine components of a systematic literature review as described in the Literature Review Appraisal Toolkit (LRAT), a tool derived from a number of standard practice appraisals of the methodological quality of the literature reviews conducted in the medical sciences (see http://policyfromscience.com/lrat/ ) ( Ades et al 2012 ; Garg et al 2008 ; Higgins and Green 2011 ; Moher et al 2009 ; Mulrow 1987 ; Oxman et al 1994 ; Schulz et al 2010 ; Shea et al 2007 ). Broadly, our results that PBDEs are associated with adverse neurodevelopment (either directly or indirectly, e.g, as a thyroid hormone disruptor), were generally consistent with the findings of all but one of the nine reviews ( Roth and Wilks 2014 ).…”

Section: Discussionmentioning

confidence: 99%

Developmental PBDE Exposure and IQ/ADHD in Childhood: A Systematic Review and Meta-analysis

Lam

Lanphear

Bellinger

et al. 2017

Environ Health Perspect

194

121

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Background:In the United States, one in six children are affected by neurodevelopmental disorders, and polybrominated diphenyl ethers (PBDEs) in flame-retardant chemicals are measured ubiquitously in children.Objective:We conducted a systematic a systematic review regarding developmental exposure to PBDEs and intelligence or Attention Deficit/Hyperactivity Disorder (ADHD) and attention-related behavioral conditions in humans.Methods:We searched articles published up to 26 September 2016, and included original studies that quantified exposures to PBDEs incurred any time in proximity to conception or during in utero, perinatal, or childhood time periods. We evaluated the risk of bias of individual studies and the overall quality and strength of the evidence according to the Navigation Guide systematic review methodology. We established criteria in advance to identify studies that could be combined using random effects meta-analyses (DerSimonian-Laird method).Results:Fifteen studies met the inclusion criteria; 10 studies met the criteria for intelligence and nine for attention-related problems. We rated studies generally with “low” to “probably low” risk of bias and rated the overall body of evidence as “moderate” quality with “sufficient” evidence for an association between Intelligence Quotient (IQ) and PBDEs. Our meta-analysis of four studies estimated a 10-fold increase (in other words, times 10) in PBDE exposure associated with a decrement of 3.70 IQ points (95% confidence interval: 0.83, 6.56). We concluded the body of evidence was of “moderate” quality for ADHD with “limited” evidence for an association with PBDEs, based on the heterogeneity of association estimates reported by a small number of studies and the fact that chance, bias, and confounding could not be ruled out with reasonable confidence.Conclusion:We concluded there was sufficient evidence supporting an association between developmental PBDE exposure and reduced IQ. Preventing developmental exposure to PBDEs could help prevent loss of human intelligence. https://doi.org/10.1289/EHP1632

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Section: Discussionmentioning

confidence: 99%

Developmental PBDE Exposure and IQ/ADHD in Childhood: A Systematic Review and Meta-analysis

Lam

Lanphear

Bellinger

et al. 2017

Environ Health Perspect

194

121

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“…Bu işlem engellenir ise, nörogelişimsel bozukluklar ortaya çıkabilmektedir. 22 Memeli beyin gelişimi, tam olgunlaşmaya eriş-meden önce çeşitli içsel gelişim süreçlerini ve aşa-malarını içermektedir. Beyin gelişme süreci (BGS) olarak adlandırılan bu dönem, aksonal ve dendritik büyüme, sinaptogenez, glial çoğalma, miyelinasyonun olgunlaşması ve nöral bağların kurulması gibi birçok kritik gelişimsel değişikliğin görüldüğü ve zararlı kimyasal maddelere maruziyet açısından hassas bir süreçtir.…”

Section: Beyi̇n Geli̇şi̇mi̇ Ve Bi̇li̇şsel Fonksi̇yonlar üZeri̇ne Etki̇leri̇unclassified

The Neuroendocrine and Neurodevelopmental Effects of Endocrine Disrupting Chemicals

Yirün¹,

Erkekoğlu²,

Koçer-Gümüşel³

2018

Turkiye Klinikleri J Neur

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Ö ÖZ ZE ET T Yaşamın değişik dönemlerinde endokrin bozucu kimyasal madde (EBK)'lere maruziyet, organizmada santral sinir sistemi dahil olmak üzere pek çok sistem üzerinde istenmeyen etkilere yol açabilmektedir. Özellikle anne karnındaki maruziyet ile çocukluk dönemindeki maruziyetin etkilerinin çok daha önemli olabileceği ve ciddi sonuçlara yol açabileceği üzerinde durulmaktadır. Son yıllarda, EBK'lere temas ile bilişsel eksiklikler, yavaş nörogelişim, agresyon ve depresyon insidansında artış, hiperaktivite ve dikkat sorunlarını ilişkilendiren çalışmalar bulunmaktadır. Santral sinir sistemi tüm nörotransmitter, nöropeptit ve nörohormon sistemleri ile denge durumunda işlemek-tedir. EBK'ler mevcut duygudurum dengesini bozarak duygusal, sosyal, davranışsal değişimlere veya nörodejeneratif hasarlara, öğrenme ve hafıza bozukluklarına neden olabilmektedirler. Maruziyetin sonuçları maruz kalınan doza, maruziyet zamanına ve maruz kalınan maddenin karakteristik özel-liklerine göre değişim göstermektedir. Nöronal hasarlar özellikle sinir sisteminin gelişme dönem-lerinde meydana gelen maruziyetlerde daha belirgin olmaktadır. Belirtiler (öğrenme güçlüğü, otizm, dikkat eksikliği, hiperaktivite, nörodejeneratif hastalıklar) çoğunlukla birden fazla mekanizmanın birlikte etkilenmesiyle ortaya çıkmakta ve özellikle karışım hâlinde EBK'lere maruziyet sonucunda daha belirgin etkiler oluşabileceği öngörülebilmektedir. Bu çalışmada, çevrede çok yaygın olarak bulunan ve endokrin bozucu etkileri bilinen bisfenol A ve ftalatların nöroendokrin sistem ve nöro-gelişim üzerindeki toksik etkilerinin incelenmesi amaçlanmıştır.A An na ah h t ta ar r K Ke e l li i m me e l le er r: : Bisfenol A; nörodavranış; nöroendokrin bozucu; nörogelişim; ftalatlar; cinsel dimorfizm A AB BS S T TR RA AC CT T Endocrine disrupting chemicals (EDCs) can cause undesirable effects on many systems, including the central nervous system, in exposed organisms at different periods of life. It can be emphasized that the effects of maternal and childhood exposure may be more important and may lead to serious consequences. In recent years, EDC exposure has been associated with cognitive deficits, slow neurodevelopment, increased incidence of aggression and depression, hyperactivity and attention problems. The central nervous system operates in balance with all neurotransmitters, neuropeptide and neurohormone systems. EDCs may cause emotional, social and behavioral changes or neurodegenerative damage, learning and memory disorders by disturbing the current state of mood balance. The results of EDC exposure vary according to dose, time of exposure and the characteristics of the substance. Neuronal damage is more pronounced in exposures that occur during the developmental stages of the nervous system. Symptoms (learning disability, autism, attention deficit, hyperactivity, neurodegenerative diseases) are often the consequences of multiple mechanisms being affected together, and it can be suggested that symptoms may be more significant, particularly as a result of exposure ...

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“…Since the beginning of the 2000s, studies started to focus on prenatal to postnatal exposure to environmental agents as non-genetic risk factors. Early development is a recognized window of susceptibility to external cues, which can have detrimental effects, potentially modulating the neuropathological events that lead to the onset of the disorder (21). To infer associations between Table 1: Data regarding characteristics of the ASD-and control population datasets used in this study.…”

Section: Introductionmentioning

confidence: 99%

A role for gene-environment interactions in Autism Spectrum Disorder is suggested by variants in genes regulating exposure to environmental factors

Santos

Rasga

Marques

et al. 2019

Preprint

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Introduction: Autism Spectrum Disorder (ASD) is a clinically heterogeneous neurodevelopmental disorder defined by deficits in social communication and interaction and repetitive and stereotyped interests and behaviors. ASD heritability estimates of 50-83% support a strong role of genetics in its onset, with large sequencing studies reporting a high burden of rare potentially pathogenic copy number variants (CNVs) and single nucleotide variants (SNVs) in affected subjects. Recent data strongly suggests that prenatal to postnatal exposure to ubiquitous environmental factors (e.g. environmental toxins, medications and nutritional factors) contribute to ASD risk. Detoxification processes and physiological permeability barriers (i.e. blood-brain barrier, placenta and respiratory cilia) are crucial in regulating exposure and response to external agents during early development. Thus, the objectives of this study were: 1) to find genes involved in detoxification and regulation of barriers permeability with a high load of relevant CNVs and SNVs in ASD subjects; 2) to explore interactions between the identified genes and environmental factors relevant for the disorder. Material and Methods: Through literature and databases review we searched for genes involved in detoxification and regulation of barriers permeability processes. Genetic data collected from large datasets of subjects with ASD (Autism Genome Project (AGP), Simmons Simplex Collection (SSC), and Autism Sequencing Consortium (ASC)) was used to identify potentially pathogenic variants targeting detoxification and barrier genes. Data from control subjects without neuropsychiatric disorder history was used for comparison purposes. The Comparative Toxicogenomics Database (CTD) was interrogated to identify putatively relevant gene-environment interactions reported in humans throughout the literature. Results:We compiled a list of 519 genes involved in detoxification and regulation of permeability barriers. The analysis of AGP and SSC data resulted in the identification of 7 genes more-frequently targeted by CNVs in ASD subjects from both datasets, after Bonferroni correction for multiple testing (AGP: P<3.5211x10 -4 ; SSC: P< 4.587x10 -4 ). Moreover, 8 genes were exclusively targeted by CNVs from ASD subjects. Regarding SNVs analyses using the ASC dataset, we found 40 genes targeted by potentially pathogenic loss-of-function and/or missense SNVs exclusive to 6 or more cases. The CTD was interrogated for interactions between 55 identified genes and 54 terms for unique chemicals associated with the disorder. A total of 212 gene-environment interaction pairs, between 51/55 (92.7%) genes and 38/54 (70.4%) chemicals, putatively relevant for ASD, were discovered. ABCB1, ABCG2, CYP2C19, GSTM1, CYP2D6, and SLC3A2 were the genes that interacted with more chemicals, while valproic acid, benzo(a)pyrene (b(a)p), bisphenol A, particulate matter and perfluorooctane sulfonic acid (PFOS) were the top chemicals. Discussion: The identified genes code for functionally diverse proteins...

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Exposure to endocrine disrupting chemicals and neurodevelopmental alterations

Cited by 54 publications

References 170 publications

Developmental PBDE Exposure and IQ/ADHD in Childhood: A Systematic Review and Meta-analysis

Developmental PBDE Exposure and IQ/ADHD in Childhood: A Systematic Review and Meta-analysis

The Neuroendocrine and Neurodevelopmental Effects of Endocrine Disrupting Chemicals

A role for gene-environment interactions in Autism Spectrum Disorder is suggested by variants in genes regulating exposure to environmental factors

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