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Endocrine Disruptor, Exposure and Potential Health Impact

A special issue of International Journal of Environmental Research and Public Health (ISSN 1660-4601). This special issue belongs to the section "Environmental Health".

Deadline for manuscript submissions: closed (20 February 2020) | Viewed by 10421

Special Issue Editor


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Guest Editor
Department of Public Health, University of Tennessee, Knoxville, TN 37996, USA
Interests: endocrine disruptors; early life exposure; reproductive toxicology; gut microbiota and susceptibility to pathogen infection

Special Issue Information

Dear Colleagues,

There is a growing public concern regarding the potential health impact of endocrine disrupting chemicals (EDCs) exposure from the environment. First coined in the early 1990s, EDCs are characterized as a group of exogenous chemicals that target various components of the endocrine system. The existence of EDCs in our daily life is ubiquitous, and the sources of EDC exposure are diverse. EDC disrupts the homeostasis of an endogenous system through multiple mechanisms, acting as a mimic or antagonist on classic nuclear receptors and membrane associated receptors. They may also interfere with the synthesis and function of critical enzymes in a specific endocrine system. Initial research efforts on EDCs were primarily focused on reproductively-relevant health risks. The scope of recent research has further expanded to delve into the consequence of transgenerational exposure, epigenetic effects, neurological and behavioral changes, and the potential link of EDC exposure to metabolic disorders.

This Special Issue seeks original research papers on various aspects of EDCs, from their detection in various environment/biological matrices to the adverse consequences of their exposure. In particular, we encourage the submission of research that focuses on issues related to EDC exposure on the development of critical systems, including but not limited to endocrine, neurological, reproductive, metabolic, and immune systems. We also encourage the submission of original research works on the impact of low-level EDC exposure, exposure to EDC mixtures, early life exposure, the identification of novel EDCs, and multigenerational studies that are designed to understand the underlying mechanisms and long term health risk of EDC exposure from the environment. We also welcome epidemiological studies that demonstrate the link between EDC exposure and its potential health risks.

Assoc. Prof. Dr. Jiangang Chen
Guest Editor

Manuscript Submission Information

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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. International Journal of Environmental Research and Public Health 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 2500 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

  • Endocrine disruptor
  • Hormonal system
  • Endocrine system
  • Health outcomes
  • Low-level exposure
  • Toxicity

Published Papers (3 papers)

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Research

14 pages, 2955 KiB  
Article
Environmental Pollution as a Risk Factor in Testicular Tumour Development: Focus on the Interaction between Bisphenol A and the Associated Immune Response
by Karen Elizabeth Nava-Castro, Ricardo Ramírez-Nieto, Lucía Angélica Méndez-García, Manuel Iván Girón-Pérez, Mariana Segovia-Mendoza, Migdalia Sarahy Navidad-Murrieta and Jorge Morales Montor
Int. J. Environ. Res. Public Health 2019, 16(21), 4113; https://doi.org/10.3390/ijerph16214113 - 25 Oct 2019
Cited by 7 | Viewed by 2799
Abstract
Bisphenol A (BPA) is an endocrine disruptor to which animals and humans are highly exposed. Many reports have established a relationship between BPA exposure and breast cancer incidence, especially during critical periods of development. However, its effects on the immune response in testicular [...] Read more.
Bisphenol A (BPA) is an endocrine disruptor to which animals and humans are highly exposed. Many reports have established a relationship between BPA exposure and breast cancer incidence, especially during critical periods of development. However, its effects on the immune response in testicular tumour growth have not yet been described. Thus, we wanted to analyse the effect of perinatal BPA exposure in pregnant female mice and the immune response modulation and tumour growth in an intratesticular cancer model in offspring male mice. Pregnant female mice were exposed to a dose of 250 mg/kg/day/body weight of BPA in their drinking water. In adulthood, male offspring underwent intrascrotal inoculation with 4T1 cancer cells. On day 21 after inoculation, mice were euthanised, and serum was obtained to measure BPA levels using HPLC coupled to mass spectrometry. The percentages of immune cell populations in peripheral lymph nodes (PLN), the spleen and tumours were evaluated by flow cytometry. In addition, the tumour expression of IL-10, TNF-α and TGF-β was analysed by RT-PCR. Of note, we found detectable circulating levels of BPA in the offspring of mothers exposed to it while pregnant. Remarkably, BPA treatment promoted tumour growth by about 75% compared to mice coming from female mice that did not receive the compound. Perinatal exposure to BPA modulated the percentages of different immune cells in the spleen and PLN. In addition, the expression of inflammatory-related cytokines (IL-10 and TNF-α) in the tumours was significantly enhanced compared to control and vehicle groups. In conclusion, the perinatal BPA administration in pregnant female mice modulated different cellular and molecular immune components that resulted in outstanding testicular tumour size in male offspring. Full article
(This article belongs to the Special Issue Endocrine Disruptor, Exposure and Potential Health Impact)
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13 pages, 332 KiB  
Article
Thyroid Hormones in Conventional and Organic Farmers in Thailand
by Pornpimol Kongtip, Noppanun Nankongnab, Nichcha Kallayanatham, Ritthirong Pundee, Nattagorn Choochouy, Jutharak Yimsabai and Susan Woskie
Int. J. Environ. Res. Public Health 2019, 16(15), 2704; https://doi.org/10.3390/ijerph16152704 - 29 Jul 2019
Cited by 26 | Viewed by 3749
Abstract
Pesticides can act as endocrine disruptors by different mechanisms including inhibition of iodine absorption, increases in thyroid hormone clearance, decreased cellular uptake of thyroid hormones, or changes in expression of thyroid hormone regulated genes. This study examined how exposure to pesticides impacts thyroid [...] Read more.
Pesticides can act as endocrine disruptors by different mechanisms including inhibition of iodine absorption, increases in thyroid hormone clearance, decreased cellular uptake of thyroid hormones, or changes in expression of thyroid hormone regulated genes. This study examined how exposure to pesticides impacts thyroid hormone levels, thyroid stimulating hormone (TSH), triiodothyronine (T3), thyroxine (T4), free T3 (FT3), and free T4 (FT4) by comparing conventional (n = 195) and organic farmers (n = 222), and by evaluating which types of pesticides might be associated with changes in thyroid hormone levels. Questionnaires were used to collect information about farmer characteristics, self-reported stress, agricultural activities, and history of pesticide use. Conventional farmers were asked to report the type and quantity of pesticides used each day. The TSH, FT3, T3, and T4 levels of conventional farmers were 1.6, 1.2, 1.3, and 1.1 times higher than those of organic farmers, respectively, after adjusting for covariates. Several specific herbicides had a significant relationship between the amount applied and an increase in thyroid hormone levels, after covariate adjustment. They included: paraquat (TSH, FT3 and T3); acetochlor (FT4); atrazine (TSH, FT3 and T3); glyphosate (T4); diuron (TSH) and the “other” herbicides including alachlor, propanil, and butachlor (FT4 and T3). The most commonly used herbicide among conventional farmers was glyphosate, followed by paraquat, 2,4-dichlorophenoxyacetic acid (2,4-D). These findings suggest that exposure to pesticides could impact the development of metabolic diseases and other health outcomes by altering the endocrine system (the thyroid hormone levels) through the hypothalamic–pituitary–thyroid (HPT) axis. This work is a part of a longitudinal study which will evaluate the sub-chronic effects of repeated exposure to different types of pesticides on thyroid hormone levels. Full article
(This article belongs to the Special Issue Endocrine Disruptor, Exposure and Potential Health Impact)
12 pages, 1026 KiB  
Article
Transcriptional Analysis of Chlorella pyrenoidosa Exposed to Bisphenol A
by Leyi Duan, Qi Chen and Shunshan Duan
Int. J. Environ. Res. Public Health 2019, 16(8), 1374; https://doi.org/10.3390/ijerph16081374 - 16 Apr 2019
Cited by 27 | Viewed by 3453
Abstract
Bisphenol A (BPA) is the raw material of 71% of polycarbonate-based resins and 27% of epoxy-based resins which are used for coating metal-based food and beverage cans. Meanwhile, it is taken into account as a typical environmental pollutant. Hormesis may occur in algae [...] Read more.
Bisphenol A (BPA) is the raw material of 71% of polycarbonate-based resins and 27% of epoxy-based resins which are used for coating metal-based food and beverage cans. Meanwhile, it is taken into account as a typical environmental pollutant. Hormesis may occur in algae exposed to BPA. In this study, the effects of BPA on Chlorella pyrenoidosa were assessed based on growth inhibition and transcriptome analysis. We have focused on two exposure scenarios as follows: (1) exposure to a low stimulation concentration (0.1 mg.L−1, 19.35% promotion in cell density on the 3rd day); (2) exposure to a high inhibition concentration (10 mg.L−1, 64.71% inhibition in cell density on the 3rd day). Transcriptome analysis showed enrichment in nucleotide transport, single-organism transport, cellular respiration. Among them, adenosine triphosphate (ATP) synthase and Nicotinamide adenine dinucleotide (NADH) dehydrogenase were upregulated under 0.1 mg.L−1 BPA treatment. These changes enhanced the physiological and energy metabolic pathways of C. pyrenoidosa, thereby stimulating cell proliferation. At exposure to the high BPA, severe inhibited changes in the expression levels of several pathways were observed, which were related to tricarboxylic acid (TCA) cycle, glycolysis, fatty acid metabolism, oxidative phosphorylation, and photosynthesis. Therefore, BPA could negatively affect growth inhibition through the multiple energy metabolism processes. These results may result in a deeper insight into BPA-induced biphasic responses in algae, and provide vital information to assess the potential ecological risks of exposure to BPA in an aquatic ecosystem. Full article
(This article belongs to the Special Issue Endocrine Disruptor, Exposure and Potential Health Impact)
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