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Toxics
Special Issues
Adverse Health Effects of Persistent Environmental Toxicants
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Adverse Health Effects of Persistent Environmental Toxicants

A special issue of Toxics (ISSN 2305-6304).

Deadline for manuscript submissions: closed (20 April 2022) | Viewed by 11613

Special Issue Editor

Prof. Dr. Joshua R. Edwards

E-Mail Website
Guest Editor
Department of Pharmacology, Midwestern University, 555 31st Street, Science Hall Room 322-F, Downers Grove, IL 60513, USA
Interests: environmental toxicology; metal toxicology; renal toxicology; biomarkers; diabetogenic substances; obesogenic substances; neuro toxicology

Special Issue Information

Dear Colleagues,

The importance of the environment in human or animal health has long been known. Environmental toxicants such as metals, metalloids and PCBs, that persist in the environment for years tend to be especially harmful. To highlight this, 8 of the top 10 toxicants in the most recent (2019) Substance Priority List from the US Agency for Toxic Substances and Disease Registry are either moderately or highly persistent in the environment. Despite the apparent dangers of exposure, the mechanism(s) of action of many of these environmental substances remains unknown.

This special issue in Toxics will focus on persistent environmental toxicants known to cause significant adverse human or animal health effects. Studies that use a physiologically or environmentally relevant dose or exposure level of environmentally persistent toxicants are welcome for submission. Both in vivo and in vitro studies are encouraged.

Prof. Dr. Joshua R. Edwards
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

  • One Health
  • environmental toxicology
  • animal models
  • environmental health
  • pollutants

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Published Papers (4 papers)

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Research

9 pages, 1200 KiB  
Article
Toxic-Induced Nonthyroidal Illness Syndrome Induced by Acute Low-Dose Pesticides Exposure—Preliminary In Vivo Study
by Cristian Cobilinschi, Radu Țincu, Raluca Ungureanu, Ioana Dumitru, Alexandru Băetu, Sebastian Isac, Claudia Oana Cobilinschi, Ioana Marina Grințescu and Liliana Mirea
Toxics 2022, 10(9), 511; https://doi.org/10.3390/toxics10090511 - 29 Aug 2022
Cited by 2 | Viewed by 1903
Abstract
Background and Objectives: Conditions such as trauma, burns, sepsis, or acute intoxications have considerable consequences on the endocrine status, causing “sick euthyroid syndrome”. Organophosphate exposure may induce an increase in acetylcholine levels, thus altering the thyroid’s hormonal status. The present study aims to [...] Read more.
Background and Objectives: Conditions such as trauma, burns, sepsis, or acute intoxications have considerable consequences on the endocrine status, causing “sick euthyroid syndrome”. Organophosphate exposure may induce an increase in acetylcholine levels, thus altering the thyroid’s hormonal status. The present study aims to identify the effects of acetylcholinesterase inhibition on thyroid hormones. Material and methods: A prospective experimental study was conducted on twenty Wistar rats. Blood samples were drawn to set baseline values for thyroid-stimulating hormone (TSH), triiodothyronine (T3), and thyroxine (T4). Chlorpyrifos 0.1 mg/kg was administered by oral gavage to induce acetyl-cholinesterase inhibition. After exhibiting cholinergic symptoms, blood samples were collected to assess levels of cholinesterase and thyroid hormones using ELISA. Results: Butyrylcholinesterase levels confirmed major inhibition immediately after intoxication compared to the baseline, certifying the intoxication. A significant increase in T4 levels was noted (p = 0.01) both at 2 h and 48 h after administration of organophosphate in sample rats. Similarly, T3 almost doubled its value 2 h after poisoning (4.2 ng/mL versus 2.5 ng/mL at baseline). Surprisingly, TSH displayed acute elevation with an afterward slow descending trend at 48 h (p = 0.1), reaching baseline value. Conclusions: This study demonstrated that cholinesterase inhibition caused major alterations in thyroid hormone levels, which may be characterized by a transient hypothyroidism status with an impact on survival prognosis. Full article
(This article belongs to the Special Issue Adverse Health Effects of Persistent Environmental Toxicants)
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11 pages, 870 KiB  
Communication
Public Health Implications and Possible Sources of Lead (Pb) as a Contaminant of Poorly Regulated Kratom Products in the United States
by Walter Prozialeck, Alexandra Fowler and Joshua Edwards
Toxics 2022, 10(7), 398; https://doi.org/10.3390/toxics10070398 - 19 Jul 2022
Cited by 9 | Viewed by 3412
Abstract
Kratom (Mitragyna speciosa) is a tropical tree that is indigenous to Southeast Asia. Kratom leaf products have been used in traditional folk medicine for their unique combination of stimulant and opioid-like effects. Kratom is being increasingly used in the West for [...] Read more.
Kratom (Mitragyna speciosa) is a tropical tree that is indigenous to Southeast Asia. Kratom leaf products have been used in traditional folk medicine for their unique combination of stimulant and opioid-like effects. Kratom is being increasingly used in the West for its reputed benefits in the treatment of pain, depression, and opioid use disorder (OUD). Recent studies from the United States Food and Drug Administration (FDA, Silver Spring, MD, USA) and our laboratory have shown that many kratom products being sold in the United States are contaminated with potentially hazardous levels of lead (Pb). In this commentary, we discuss the public health implications of the presence of Pb in kratom products, particularly as they relate to the predicted levels of Pb exposure among kratom users. We also considered the specific toxic effects of Pb and how they might relate to the known physiologic and toxicologic effects of kratom. Finally, we consider the possible sources of Pb in kratom products and suggest several areas for research on this issue. Full article
(This article belongs to the Special Issue Adverse Health Effects of Persistent Environmental Toxicants)
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12 pages, 1798 KiB  
Article
Diabetogenic and Obesogenic Effects of Cadmium in Db/Db Mice and Rats at a Clinically Relevant Level of Exposure
by Jessica Nguyen, Arjun Patel, Andrew Gensburg, Rehman Bokhari, Peter Lamar and Joshua Edwards
Toxics 2022, 10(3), 107; https://doi.org/10.3390/toxics10030107 - 23 Feb 2022
Cited by 5 | Viewed by 2613
Abstract
Studies show an association between cadmium (Cd) exposure and prediabetes or type II diabetes mellitus. We have previously reported that Cd causes decreased levels of serum leptin in rats following 12 weeks of daily Cd dosing (0.6 mg/kg/b.w./day). Since leptin plays an important [...] Read more.
Studies show an association between cadmium (Cd) exposure and prediabetes or type II diabetes mellitus. We have previously reported that Cd causes decreased levels of serum leptin in rats following 12 weeks of daily Cd dosing (0.6 mg/kg/b.w./day). Since leptin plays an important role in metabolism, we examined the effects of Cd on rats and db/db mice, which are deficient in leptin receptor activity. We gave rats and mice daily subcutaneous injections of saline (control) or CdCl2 at a dose of 0.6 mg/kg of Cd for 2 weeks, followed by 2 weeks of no dosing. At the end of the 4-week study, exposure to Cd resulted in a more rapid increase in blood glucose levels following an oral glucose tolerance test in db/db vs. lean mice. During the two weeks of no Cd dosing, individual rat bodyweight gain was greater (p ≤ 0.05) in Cd-treated animals. At this time point, the combined epididymal and retroperitoneal fat pad weight was significantly greater (p ≤ 0.05) in the Cd-treated lean mice compared to saline-treated controls. Although this pilot study had relatively low N values (4 per treatment group for mice and 6 for rats) the results show that clinically relevant levels of Cd exposure resulted in diabetogenic as well as obesogenic effects. Full article
(This article belongs to the Special Issue Adverse Health Effects of Persistent Environmental Toxicants)
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12 pages, 1311 KiB  
Article
Zinc, Zinc Transporters, and Cadmium Cytotoxicity in a Cell Culture Model of Human Urothelium
by Soisungwan Satarug, Scott H. Garrett, Seema Somji, Mary Ann Sens and Donald A. Sens
Toxics 2021, 9(5), 94; https://doi.org/10.3390/toxics9050094 - 24 Apr 2021
Cited by 11 | Viewed by 2917
Abstract
We explored the potential role of zinc (Zn) and zinc transporters in protection against cytotoxicity of cadmium (Cd) in a cell culture model of human urothelium, named UROtsa. We used real-time qRT-PCR to quantify transcript levels of 19 Zn transporters of the Zrt-/Irt-like [...] Read more.
We explored the potential role of zinc (Zn) and zinc transporters in protection against cytotoxicity of cadmium (Cd) in a cell culture model of human urothelium, named UROtsa. We used real-time qRT-PCR to quantify transcript levels of 19 Zn transporters of the Zrt-/Irt-like protein (ZIP) and ZnT gene families that were expressed in UROtsa cells and were altered by Cd exposure. Cd as low as 0.1 µM induced expression of ZnT1, known to mediate efflux of Zn and Cd. Loss of cell viability by 57% was seen 24 h after exposure to 2.5 µM Cd. Exposure to 2.5 µM Cd together with 10–50 µM Zn prevented loss of cell viability by 66%. Pretreatment of the UROtsa cells with an inhibitor of glutathione biosynthesis (buthionine sulfoximine) diminished ZnT1 induction by Cd with a resultant increase in sensitivity to Cd cytotoxicity. Conversely, pretreatment of UROtsa cells with an inhibitor of DNA methylation, 5-aza-2’-deoxycytidine (aza-dC) did not change the extent of ZnT1 induction by Cd. The induced expression of ZnT1 that remained impervious in cells treated with aza-dC coincided with resistance to Cd cytotoxicity. Therefore, expression of ZnT1 efflux transporter and Cd toxicity in UROtsa cells could be modulated, in part, by DNA methylation and glutathione biosynthesis. Induced expression of ZnT1 may be a viable mechanistic approach to mitigating cytotoxicity of Cd. Full article
(This article belongs to the Special Issue Adverse Health Effects of Persistent Environmental Toxicants)
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