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Toxics
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Feature Papers

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

Deadline for manuscript submissions: closed (15 October 2013) | Viewed by 44447

Special Issue Editor

Prof. Dr. David Bellinger

E-Mail Website
Guest Editor
Boston Children's Hospital, Harvard Medical School, Harvard University, 300 Longwood Ave, Boston, MA 02115, USA
Interests: children; epidemiology; metals; brain

Special Issue Information

Dear Colleagues,

With this inaugural issue, Toxics begins its life as a peer-reviewed, open access journal focusing on all aspects of toxic chemicals. We are interested in publishing papers that present a wide range of perspectives on toxicants and naturally occurring toxins, including exposure, biomarkers, kinetics, biological effects, fate and transport, treatment, and remediation. Toxics differs from many other journals in the absence of a page or word limit on contributions, permitting authors to present their work in as much detail as they wish. Toxics will publish original research papers, conventional reviews, meta-analyses, short communications, theoretical papers, case reports, commentaries and policy perspectives, and book reviews (Book reviews will be solicited and should not be submitted without invitation). Toxins and toxicants concern individuals from a wide range of disciplines, and Toxics is interested in receiving papers that represent the full range of approaches applied to their study, including in vitro studies, studies that use experimental animal or non-animal models, studies of humans or other biological populations, and mathematical modeling. We are excited to get underway and look forward to working with authors in the scientific and medical communities and providing them with a novel venue for sharing their work.

Dr. David Bellinger
Editor-in-Chief

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

  • toxicants, toxins
  • exposure
  • biomarkers
  • kinetics
  • biological effects
  • fate and transport
  • treatment
  • remediation

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Further information on MDPI's Special Issue polices can be found here.

Published Papers (5 papers)

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Research

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785 KiB  
Article
Chronic Exposure to Particulate Nickel Induces Neoplastic Transformation in Human Lung Epithelial Cells
by Amie L. Holmes, Therry The, Kelsey Thompson, Michael Mason, Sanjeev Kandpal, Tongzhang Zheng and John Pierce Wise, Sr.
Toxics 2013, 1(1), 46-59; https://doi.org/10.3390/toxics1010046 - 25 Nov 2013
Cited by 2 | Viewed by 6713
Abstract
Nickel is a well-known human lung carcinogen with the particulate form being the most potent; however, the carcinogenic mechanism remains largely unknown. Few studies have investigated the genotoxicity and carcinogenicity of nickel in its target cell, human bronchial epithelial cells. Thus, the goal [...] Read more.
Nickel is a well-known human lung carcinogen with the particulate form being the most potent; however, the carcinogenic mechanism remains largely unknown. Few studies have investigated the genotoxicity and carcinogenicity of nickel in its target cell, human bronchial epithelial cells. Thus, the goal of this study was to investigate the effects of particulate nickel in human lung epithelial cells. We found that nickel subsulfide induced concentration- and time-dependent increases in both cytotoxicity and genotoxicity in human lung epithelial cells (BEP2D). Chronic exposure to nickel subsulfide readily induced cellular transformation, inducing 2.55, 2.9 and 2.35 foci per dish after exposure to 1, 2.5 and 5 μg/cm2 nickel subsulfide, respectively. Sixty-one, 100 and 70 percent of the foci isolated from 1, 2.5, and 5 μg/cm2 nickel subsulfide treatments formed colonies in soft agar and the degree of soft agar colony growth increased in a concentration-dependent manner. Thus, chronic exposure to particulate nickel induces genotoxicity and cellular transformation in human lung epithelial cells. Full article
(This article belongs to the Special Issue Feature Papers)
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498 KiB  
Article
Genotoxicity of Silver Nanoparticles in Lung Cells of Sprague Dawley Rats after 12 Weeks of Inhalation Exposure
by Hyun Sun Cho, Jae Hyuck Sung, Kyung Seuk Song, Jin Sik Kim, Jun Ho Ji, Ji Hyun Lee, Hyeon Ryol Ryu, Kangho Ahn and Il Je Yu
Toxics 2013, 1(1), 36-45; https://doi.org/10.3390/toxics1010036 - 19 Nov 2013
Cited by 16 | Viewed by 6638
Abstract
Due to the widespread use of silver nanoparticles in consumer products, the toxicity of silver nanoparticles has also been studied in relation to their application. However, most genotoxicity studies of silver nanoparticles have been performed in vitro. Therefore, this study evaluated the [...] Read more.
Due to the widespread use of silver nanoparticles in consumer products, the toxicity of silver nanoparticles has also been studied in relation to their application. However, most genotoxicity studies of silver nanoparticles have been performed in vitro. Therefore, this study evaluated the DNA damage to lung cells caused by repeated inhalation of silver nanoparticles. Male Sprague Dawley rats were exposed to silver nanoparticles for 12 weeks in a whole-body inhalation chamber. The animals were divided into one control group and three dose groups that were exposed to silver nanoparticles (14–15 nm diameter) at concentrations of 0.66 × 106 particles/cm3 (49 μg/m3, low dose), 1.41 × 106 particles/cm3 (117 μg/m3, middle dose), and 3.24 × 106 particles /cm3 (381 μg/m3, high dose), respectively, for six hours/day over 12 weeks. The rats were sacrificed after the 12-week exposure period and the DNA damage assessed using a Comet assay of cells obtained from the right lungs. The olive tail moment values were 2.93 ± 0.19, 3.81 ± 0.23, 3.40 ± 0.22, and 5.16 ± 0.32 for the control, low-, middle-, and high-dose groups, respectively. Although no dose-dependent results were observed, a significant increase in the level of DNA damage was noted for the high-dose group. Full article
(This article belongs to the Special Issue Feature Papers)
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Review

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616 KiB  
Review
Chemical Atherogenesis: Role of Endogenous and Exogenous Poisons in Disease Development
by Matthew K. Ross, Anberitha T. Matthews and Lee C. Mangum
Toxics 2014, 2(1), 17-34; https://doi.org/10.3390/toxics2010017 - 22 Jan 2014
Cited by 15 | Viewed by 10273
Abstract
Chemical atherogenesis is an emerging field that describes how environmental pollutants and endogenous toxins perturb critical pathways that regulate lipid metabolism and inflammation, thus injuring cells found within the vessel wall. Despite growing awareness of the role of environmental pollutants in the development [...] Read more.
Chemical atherogenesis is an emerging field that describes how environmental pollutants and endogenous toxins perturb critical pathways that regulate lipid metabolism and inflammation, thus injuring cells found within the vessel wall. Despite growing awareness of the role of environmental pollutants in the development of cardiovascular disease, the field of chemical atherogenesis can broadly include both exogenous and endogenous poisons and the study of molecular, biochemical, and cellular pathways that become dysregulated during atherosclerosis. This integrated approach is logical because exogenous and endogenous toxins often share the same mechanism of toxicity. Chemical atherogenesis is a truly integrative discipline because it incorporates concepts from several different fields, including biochemistry, chemical biology, pharmacology, and toxicology. This review will provide an overview of this emerging research area, focusing on cellular and animal models of disease. Full article
(This article belongs to the Special Issue Feature Papers)
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584 KiB  
Review
Ecotoxicology: The Challenges for the 21st Century
by Marco Vighi and Sara Villa
Toxics 2013, 1(1), 18-35; https://doi.org/10.3390/toxics1010018 - 18 Nov 2013
Cited by 26 | Viewed by 11977
Abstract
The usual procedures for ecological risk assessment (ERA) have been based for decades on simplified approaches in order to provide basic information on the huge amount of chemicals introduced into the environment. These approaches allowed the development of international regulatory tools capable of [...] Read more.
The usual procedures for ecological risk assessment (ERA) have been based for decades on simplified approaches in order to provide basic information on the huge amount of chemicals introduced into the environment. These approaches allowed the development of international regulatory tools capable of substantially reducing the adverse effects on ecosystems in developed countries. Nevertheless, these approaches suffer from a lack of ecological realism and are poorly suitable for understanding the actual consequences for ecosystem health. The need for more ecologically-based approaches is now recognized by the scientific community and has been highlighted by a recent document of the European Commission. In this paper, a synthesis is presented of the most important issues and the need for research to improve the ecological realism of exposure and effect assessment and the tools that should be developed to reach this objective. In particular, the major challenges are the following: the effects of variable exposure patterns; the vulnerability of ecosystems; the indirect ecological effects; the responses to multiple stress factors; the improvement of ecological modeling. The possibilities for using new scientific achievements in regulatory ERA are also discussed. Full article
(This article belongs to the Special Issue Feature Papers)
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429 KiB  
Review
Inorganic Arsenic Exposure and Children’s Neurodevelopment: A Review of the Evidence
by David C. Bellinger
Toxics 2013, 1(1), 2-17; https://doi.org/10.3390/toxics1010002 - 15 Oct 2013
Cited by 12 | Viewed by 8258
Abstract
Experimental studies suggest a myriad of mechanisms by which inorganic arsenic can interfere with central nervous system development, and, indeed, epidemiological studies published in the last dozen years suggest that exposure to arsenic impairs children’s cognitive development. Most of the studies have been [...] Read more.
Experimental studies suggest a myriad of mechanisms by which inorganic arsenic can interfere with central nervous system development, and, indeed, epidemiological studies published in the last dozen years suggest that exposure to arsenic impairs children’s cognitive development. Most of the studies have been conducted in developing countries (e.g., Bangladesh, India, Mexico), where exposure to arsenic is thought to be considerably higher than it is in developed countries. This review summarizes the results of these studies, focusing in particular on issues pertinent to risk assessment, including the existence of critical windows of vulnerability, characteristics of the dose-effect relationships (e.g., the lowest adverse effect level, the functional form), the most sensitive neurodevelopmental endpoints, and potential effect modifiers such as host characteristics (e.g., methylation efficiency, sex) and co-exposures to other neurotoxicants (e.g., lead, manganese). At present, the epidemiological data do not permit firm conclusions to be drawn regarding these issues. Several factors that complicate an effort to compare the results of studies are identified, including use of a variety of indices of external and internal exposure, and inconsistency in the measurement of important potential confounders for neurodevelopmental outcomes. Full article
(This article belongs to the Special Issue Feature Papers)
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