PCB-induced neurodevelopmental toxicity in human infants and its potential mediation by endocrine dysfunction

Over the recent past, the global market of electrical and electronic equipment (EEE) has grown exponentially, while the lifespan of these products has become increasingly shorter. More of these products are ending up in rubbish dumps and recycling centers, posing a new challenge to policy makers. The purpose of this paper is to provide a review of the e-Waste problem and to put forward an estimation technique to calculate the growth of e-Waste.

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“…POPs negatively impact human and wildlife [38,39]. Other significant research on airborne as well as water-/ground based contamination exists.…”

Section: Discussionmentioning

confidence: 99%

Electronic Waste: A Growing Concern in Today′s Environment

Bhutta

Omar

Yang

2011

Economics Research International

144

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“…Researches have already demonstrated links between lead and polychlorinated biphenyl exposure and Intelligent and Biosensors 364 neurodevelopmental effects. It is now frightened that neurobehavioural and neurodevelopmental deterioration may take place in the next generations (Tang et al 1999, Winneke et al 2002, Stein et al 2002, Yang et al 2003. Reports which link autoimmune diseases to environmental factors have appeared in recent literatures (Molina & Ehrenfeld 2003, Dooley & Hogan 2003.…”

Section: Introductionmentioning

confidence: 99%

ALAD (δ-aminolevulinic Acid Dehydratase) as Biosensor for Pb Contamination

Konuk¹,

Korcan²

2010

Intelligent and Biosensors

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“…Initially, it was thought that the effect of PCB was exerted through inhibition of TH secretion from thyroid gland, or competitive inhibition of TH binding to TH-binding protein such as transthyretin in blood [39], both of which may induce hypothyroxinemia in plasma. However, although PCB treatment induces decrease in plasma TH in experimental animals, the PCB exposure level and the changes in plasma TH level are not correlated with one another in humans [40]. Even in the rat, although perinatal PCB exposure induces a decrease in the total T4 levels in plasma, the growth rate of PCBtreated animal is identical to that of control animal, indicating that the animal is generally euthyroid [41].…”

Section: Modulation Of Thyroid Hormone Action By Environmental Chemicalsmentioning

confidence: 98%

Regulation of Brain Development by Thyroid Hormone and its Modulation by Environmental Chemicals

Koibuchi

Iwasaki

2006

Endocr J

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THYROID hormone (TH; T3,3,5, T4,3,5,3', thyroxine) plays an important role in development and functional maintenance of the central nervous system [1]. TH deficiency during pre-and early postnatal period results in abnormal brain development known as cretinism in humans. However, the molecular mechanism of TH action in brain is not fully understood. In particular, brain development is severely affected by TH deficiency during a limited period, called the "critical period" of TH action, but the mechanism generating such a period is not known. Although TH treatment immediately after birth is sufficient to prevent brain damage induced by neonatal hypothyroidism (i.e., by thyroid dysgenesis), such treatment cannot fully rescue the abnormal brain development induced by hypothyroidism in utero (i.e., by maternal iodine deficiency). Thus, each brain region has a distinct critical period, during which neurons are particularly sensitive to TH.The effect of TH is mainly exerted through nuclear TH receptor (TR), a ligand-dependent transcription factor [2], although TH action at non-genomic site has also been proposed [3]. Thus, TH action in brain may also be exerted mainly through TH-TR interaction.To clarify the role of the TH-TR system in brain, one approach is to identify the target genes that are regulated by TH, while another is to understand the mechanism of brain-specific TR action, such as to identify the factors responsible for the generation of the critical period. For such purposes, we have been using the developing rodent cerebellum as a model system [4]. There are several advantages of using this model. First, although rodents are born much earlier than humans, the developmental pattern is not greatly different between the two species. Second, the rodent cerebellum largely develops postnatally, and TH deficiency during such a period markedly affects its development. Thus, postnatal rodent cerebellum is a good model to study TH action in developing brain, since TH status is easier to manipulate in postnatal animal than in fetus. In the present article, the molecular mechanism of TH action in developing brain is reviewed mainly by introducing our previous studies using rodent cerebellum model. Fig. 1 shows typical examples of the effect of perinatal hypothyroidism on brain development.This article also summarizes our recent studies on the effect of environmental pollutants on brain development. Exposure to certain pollutants may cause abnormal brain development similar to that seen in perinatal hypothyroidism [5]. In particular, brain damage by perinatal exposure of polychlorinated biphenyls (PCBs) has been considered to be induced in part through disruption of the TH system [6]. However, the mechanism of PCB action has not been well characterized. Recent findings have provided several clues to our further understanding of the possible molecular mechanism of PCB action.

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PCB-induced neurodevelopmental toxicity in human infants and its potential mediation by endocrine dysfunction

Cited by 119 publications

References 18 publications

Electronic Waste: A Growing Concern in Today′s Environment

Electronic Waste: A Growing Concern in Today′s Environment

ALAD (δ-aminolevulinic Acid Dehydratase) as Biosensor for Pb Contamination

Regulation of Brain Development by Thyroid Hormone and its Modulation by Environmental Chemicals

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PCB-induced neurodevelopmental toxicity in human infants and its potential mediation by endocrine dysfunction

Cited by 119 publications

References 18 publications

Electronic Waste: A Growing Concern in Today′s Environment

Electronic Waste: A Growing Concern in Today′s Environment

ALAD (&#948;-aminolevulinic Acid Dehydratase) as Biosensor for Pb Contamination

Regulation of Brain Development by Thyroid Hormone and its Modulation by Environmental Chemicals

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Product

Resources

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ALAD (δ-aminolevulinic Acid Dehydratase) as Biosensor for Pb Contamination