Early Life Exposure to Endocrine Disrupting Chemicals and Systemic Diseases

A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Toxicology".

Deadline for manuscript submissions: closed (31 January 2016) | Viewed by 22375

Special Issue Editor


E-Mail Website
Guest Editor
National Institute of Environmental Health Sciences, National Health Research Institutes, Miaoli 350, Taiwan
Interests: environmental children health with regards to exposure to POPs (i.e. dioxins, polychlorinated biphenyls); phthalates, and toxic metals (i.e. lead, arsenic) and the heath effects on endocrine system; neuro-cognitive function, and the related diseases like diabetes and cardiovascular disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Daily exposure to environmental endocrine disrupting chemicals (EDC) has been a public health concern. Early life exposure to EDC may exacerbate and prolong significant effects according to previous epidemiological studies, such as Yucheng’s research. Recent studies confirm the developmental origins of adult disease (Barker) hypothesis. For instance, atopic diseases might associate with increased hygiene and chemical priming. In addition to persistent organic pollutants, phthalate esters, nonylphenol, bisphenol A, flame retardants, and even certain metals, such as methyl-mercury, are widely used and found to cause effects on the immune, neuron, and endocrine systems. Examples include asthma, neurobehavioral problems, metabolic syndrome, and even malignant tumors. Although some of the effects have been reported, many await confirmation from human studies, especially from those involving susceptible fetuses. The aim is to assess the association of prenatal and postnatal exposure to EDCs with neurodevelopmental, endocrinal, reproductive, atopic, and cancerous statuses in currently available research studies.

Dr. Shu-Li Wang
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Toxics is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • prenatal exposure delayed effects
  • endocrine disrupting chemical
  • atopic disease
  • neurological effect
  • endocrine system
  • metabolic syndrome
  • cardiovascular disease
  • persistent organic pollutant
  • cancer

Published Papers (3 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

Jump to: Review

1599 KiB  
Article
Urinary Phthalate Metabolites and Biomarkers of Oxidative Stress in a Mexican-American Cohort: Variability in Early and Late Pregnancy
by Nina Holland, Karen Huen, Vy Tran, Kelly Street, Brian Nguyen, Asa Bradman and Brenda Eskenazi
Toxics 2016, 4(1), 7; https://doi.org/10.3390/toxics4010007 - 14 Mar 2016
Cited by 59 | Viewed by 7368
Abstract
People are exposed to phthalates through their wide use as plasticizers and in personal care products. Many phthalates are endocrine disruptors and have been associated with adverse health outcomes. However, knowledge gaps exist in understanding the molecular mechanisms associated with the effects of [...] Read more.
People are exposed to phthalates through their wide use as plasticizers and in personal care products. Many phthalates are endocrine disruptors and have been associated with adverse health outcomes. However, knowledge gaps exist in understanding the molecular mechanisms associated with the effects of exposure in early and late pregnancy. In this study, we examined the relationship of eleven urinary phthalate metabolites with isoprostane, an established marker of oxidative stress, among pregnant Mexican-American women from an agricultural cohort. Isoprostane levels were on average 20% higher at 26 weeks than at 13 weeks of pregnancy. Urinary phthalate metabolite concentrations suggested relatively consistent phthalate exposures over pregnancy. The relationship between phthalate metabolite concentrations and isoprostane levels was significant for the sum of di-2-ethylhexyl phthalate and the sum of high molecular weight metabolites with the exception of monobenzyl phthalate, which was not associated with oxidative stress at either time point. In contrast, low molecular weight metabolite concentrations were not associated with isoprostane at 13 weeks, but this relationship became stronger later in pregnancy (p-value = 0.009 for the sum of low molecular weight metabolites). Our findings suggest that prenatal exposure to phthalates may influence oxidative stress, which is consistent with their relationship with obesity and other adverse health outcomes. Full article
Show Figures

Graphical abstract

516 KiB  
Communication
Intergenerational Effect of Early Life Exposure to Permethrin: Changes in Global DNA Methylation and in Nurr1 Gene Expression
by Laura Bordoni, Cinzia Nasuti, Maria Mirto, Fabio Caradonna and Rosita Gabbianelli
Toxics 2015, 3(4), 451-461; https://doi.org/10.3390/toxics3040451 - 19 Nov 2015
Cited by 40 | Viewed by 5881
Abstract
Environmental exposure to pesticides during the early stages of development represents an important risk factor for the onset of neurodegenerative diseases in adult age. Neonatal exposure to Permethrin (PERM), a member of the family of synthetic pyrethroids, can induce a Parkinson-like disease and [...] Read more.
Environmental exposure to pesticides during the early stages of development represents an important risk factor for the onset of neurodegenerative diseases in adult age. Neonatal exposure to Permethrin (PERM), a member of the family of synthetic pyrethroids, can induce a Parkinson-like disease and cause some alterations in striatum of rats, involving both genetic and epigenetic pathways. Through gene expression analysis and global DNA methylation assessment in both PERM-treated parents and their untreated offspring, we investigated on the prospective intergenerational effect of this pesticide. Thirty-three percent of progeny presents the same Nurr1 alteration as rats exposed to permethrin in early life. A decrease in global genome-wide DNA methylation was measured in mothers exposed in early life to permethrin as well as in their offspring, whereas untreated rats have a hypermethylated genomic DNA. Further studies are however needed to elucidate the molecular mechanisms, but, despite this, an intergenerational PERM-induced damage on progenies has been identified for the first time. Full article
Show Figures

Graphical abstract

Review

Jump to: Research

1528 KiB  
Review
Developmental Bisphenol A Exposure Modulates Immune-Related Diseases
by Joella Xu, Guannan Huang and Tai L. Guo
Toxics 2016, 4(4), 23; https://doi.org/10.3390/toxics4040023 - 26 Sep 2016
Cited by 87 | Viewed by 8705
Abstract
Bisphenol A (BPA), used in polycarbonate plastics and epoxy resins, has a widespread exposure to humans. BPA is of concern for developmental exposure resulting in immunomodulation and disease development due to its ability to cross the placental barrier and presence in breast milk. [...] Read more.
Bisphenol A (BPA), used in polycarbonate plastics and epoxy resins, has a widespread exposure to humans. BPA is of concern for developmental exposure resulting in immunomodulation and disease development due to its ability to cross the placental barrier and presence in breast milk. BPA can use various mechanisms to modulate the immune system and affect diseases, including agonistic and antagonistic effects on many receptors (e.g., estrogen receptors), epigenetic modifications, acting on cell signaling pathways and, likely, the gut microbiome. Immune cell populations and function from the innate and adaptive immune system are altered by developmental BPA exposure, including decreased T regulatory (Treg) cells and upregulated pro- and anti-inflammatory cytokines and chemokines. Developmental BPA exposure can also contribute to the development of type 2 diabetes mellitus, allergy, asthma and mammary cancer disease by altering immune function. Multiple sclerosis and type 1 diabetes mellitus may also be exacerbated by BPA, although more research is needed. Additionally, BPA analogs, such as bisphenol S (BPS), have been increasing in use, and currently, little is known about their immune effects. Therefore, more studies should be conducted to determine if developmental exposure BPA and its analogs modulate immune responses and lead to immune-related diseases. Full article
Show Figures

Figure 1

Back to TopTop