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Special Issue "Old Challenges Meet Novel Tools: Prospects and Aims for Next-Generation Ecotoxicologists and Environmental Toxicologists"

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: 31 October 2019

Special Issue Editor

Guest Editor
Dr. Pedro M. Costa

UCIBIO - Research Unit on Applied Molecular Biosciences, Departamento de Ciências da Vida, Faculdade de Ciências e Tecnologia, Universidade Nova de Lisboa, 2829-516 Caparica, Portugal
Website | E-Mail
Interests: toxicology and environmental toxicology; aquatic biology; genotoxicology; marine toxins and biotechnology; toxicopathology; molecular toxicology

Special Issue Information

Dear Colleagues,

Environmental Toxicology and Ecotoxicology have come a long way since Clair Patterson’s and Rachel Carson’s “heads up”, back in the 1960s, sent shockwaves worldwide. After decades of struggle leaping the boundaries between science, public awareness and the court-of-law, the notion that the discharge of hazardous chemicals into the environment has major implications to wildlife, economy and human health is now firmly rooted. This leads to policy, guidelines and monitoring programs that now reach beyond the mere regional scope. However, the extraordinary pace of our advancing society is a continuous source of new challenges that environmental scientists must keep up with. Emerging pollutants, such as pharmaceuticals and new pesticides, nanomaterials and complex blends of all sorts of noxious chemicals and their metabolites, are just few examples. As we become aware that traditional toxicity testing and biomonitoring versus biomarker approaches are hardly able to objectively determine risk and causality in realistic scenarios (therefore complex), experts are revolutionizing the field by incorporating frontier concepts like ‘Exposome’, ‘Systems Biology’ and ‘Adverse Outcome Pathways’. Consequently, improved methods to determine and validate the presence of chemicals in the environment, high-content screening and bioinformatics are pushing environmental science into its next-generation. We call on specialists worldwide for contributions that integrate such state-of-the-art concepts and technology to respond to the ever-evolving challenges laid before ecotoxicologists and environmental toxicologists.

Dr. Pedro M. Costa
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 papers will be 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. International Journal of Environmental Research and Public Health is an international peer-reviewed open access semimonthly 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 1800 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

  • Emerging and traditional pollutants
  • Toxicant mixtures
  • Ecosystem and human health
  • Environmental Toxicology and Ecotoxicology
  • Adverse outcome pathways
  • Next-generation sequencing
  • Systems Toxicology
  • ‘Omics’
  • Bioinformatics
  • Integrated environmental risk assessment

Published Papers (4 papers)

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Research

Open AccessArticle
Oxidative Stress Effects of Soluble Sulfide on Human Hepatocyte Cell Line LO2
Int. J. Environ. Res. Public Health 2019, 16(9), 1662; https://doi.org/10.3390/ijerph16091662
Received: 1 April 2019 / Revised: 8 May 2019 / Accepted: 10 May 2019 / Published: 13 May 2019
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Abstract
Soluble sulfide is well known for its toxicity and corrosion for hundreds of years. However, recent studies have demonstrated that hydrogen sulfide (H2S)—a novel gasotransmitter—supports a critical role during neuromodulation, cell proliferation, and cardioprotection for organisms. In particular, soluble sulfide plays [...] Read more.
Soluble sulfide is well known for its toxicity and corrosion for hundreds of years. However, recent studies have demonstrated that hydrogen sulfide (H2S)—a novel gasotransmitter—supports a critical role during neuromodulation, cell proliferation, and cardioprotection for organisms. In particular, soluble sulfide plays multifaceted signaling functions in mammals during oxidative stress processes. However, the specific molecular regulation of soluble sulfide during oxidative stress remains unclear. In this study, Na2S was implemented as a soluble sulfide donor to expose LO2 cells. The 3-(4,5-dimethylthiazolyl-2),-2,5-diphenyltetrazolium bromide (MTT) assay, hydroxyl radical assay, superoxide dismutase (SOD) assay, and glutathione peroxidase (GSH-PX) assay were applied to analyze cytotoxicity, hydroxyl radical levels, SOD and GSH-Px activities, respectively. Soluble sulfide at a concentration 0.01–1.0 mM/L resulted in a marked and concentration-dependent reduction of LO2 cell viability. At low concentrations, sulfide solutions increased SOD activity and GSH-Px activity of LO2 after 24 h exposure, exhibiting a clear hormesis-effect and indicating the protective ability of soluble sulfide against oxidative stress. The decline in SOD and GSH-Px and the increase in hydroxyl radical (0.08–1.0 mM/L) suggested that oxidative damage could be a possible mechanism for sulfide-induced cytotoxicity. Full article
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Open AccessArticle
Age Differences in the Relationship between Secondhand Smoke Exposure and Risk of Metabolic Syndrome: A Meta-Analysis
Int. J. Environ. Res. Public Health 2019, 16(8), 1409; https://doi.org/10.3390/ijerph16081409
Received: 30 December 2018 / Revised: 1 April 2019 / Accepted: 17 April 2019 / Published: 19 April 2019
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Abstract
Secondhand smoke (SHS), a common environmental exposure factor, has become a serious public health problem. Metabolic syndrome is another worldwide clinical challenge. Our study tried to determine the age differences in the relationship between SHS and the risk of metabolic syndrome. Studies were [...] Read more.
Secondhand smoke (SHS), a common environmental exposure factor, has become a serious public health problem. Metabolic syndrome is another worldwide clinical challenge. Our study tried to determine the age differences in the relationship between SHS and the risk of metabolic syndrome. Studies were searched in PubMed and Web of Science from 11 November to 30 November 2018. Eighteen studies were finally included based on inclusion and exclusion criteria. The relationship between SHS and the risk indicators of metabolic syndrome was analyzed. The weighted mean difference (WMD) of fasting plasma glucose (FPG), insulin, body mass index (BMI), and waist circumference (WC), and the standard mean difference (SMD) of total cholesterol, triglycerides, and low- and high-density lipoprotein-cholesterol (LDL-C, HDL-C) were calculated in a meta-analysis. SHS was positively associated with the level of insulin and WC. According to the subgroup analysis based on age difference, SHS was positively associated with FPG in the upper age group, and positively associated with LDL-C and negatively associated with HDL-C in the lower age group. BMI showed a more obvious positive correlation in the adults group than in the children and the teenagers group. In conclusion, the association of metabolic syndrome with SHS varies with age. When exposed to SHS, older people may be more susceptible to glucose metabolic disorder, but younger people may be more susceptible to lipid metabolic disorder. Full article
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Open AccessArticle
Are Our Farm Workers in Danger? Genetic Damage in Farmers Exposed to Pesticides
Int. J. Environ. Res. Public Health 2019, 16(3), 358; https://doi.org/10.3390/ijerph16030358
Received: 23 November 2018 / Revised: 12 January 2019 / Accepted: 19 January 2019 / Published: 27 January 2019
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Abstract
Modern agriculture, practiced after the “green revolution” worldwide, aims to maximize production in order to provide food for the growing world population. Thus, farmers are required to modernize their practices through the mechanization of land use and, above all, the use of chemical [...] Read more.
Modern agriculture, practiced after the “green revolution” worldwide, aims to maximize production in order to provide food for the growing world population. Thus, farmers are required to modernize their practices through the mechanization of land use and, above all, the use of chemical pesticides to control agricultural pests. However, in addition to combating the target pest, chemical pesticides indirectly affect a wide range of species, including humans, leading to health damage. Among the main problems caused by the use of pesticides is the genotoxicity caused by chronic exposure. The present study aims to verify the occurrence of genetic damage in farmers who are occupationally exposed to agrochemicals compared to people of other professions that do not use toxic substances (control group). The research was conducted with 36 male participants (18 farmers and 18 control group, ages 24–71 for the farmer group and 22–61 for the control group). The comet assay and micronucleus test results revealed a higher rate of genetic damage in the group of farmers than in the control group. A questionnaire answered by the farmers showed that the Personal Protect Equipment (PPE) is used incorrectly or not used. In summary, our results indicate that farmers are exposed to occupational hazards. To mitigate this risk, we conducted awareness campaigns to notify the farmers of the risks and highlight the importance of using PPE correctly. Intensive efforts and training are thus required to build an awareness of safety practices and change the attitudes of farm workers in the hope of preventing harmful environmental and anthropogenic effects. Full article
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Open AccessArticle
The Increase of ROS Caused by the Interference of DEHP with JNK/p38/p53 Pathway as the Reason for Hepatotoxicity
Int. J. Environ. Res. Public Health 2019, 16(3), 356; https://doi.org/10.3390/ijerph16030356
Received: 26 December 2018 / Revised: 22 January 2019 / Accepted: 22 January 2019 / Published: 27 January 2019
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Abstract
As the most commonly used plasticizer, Di-(2-ethylhexyl)-phthalate (DEHP) exists everywhere in the environment due to the widespread use of polyvinyl chloride (PVC) in human life, and it is also a recognized environmental pollutant. Studies have proved the hepatotoxicity of DEHP, however the mechanism [...] Read more.
As the most commonly used plasticizer, Di-(2-ethylhexyl)-phthalate (DEHP) exists everywhere in the environment due to the widespread use of polyvinyl chloride (PVC) in human life, and it is also a recognized environmental pollutant. Studies have proved the hepatotoxicity of DEHP, however the mechanism has not been adequately explored, especially the role of the reactive oxygen species (ROS) in it. In the present study, 21 day-old ICR mice were administered DEHP with dose of 0, 125, 250, and 375 mg/kg/day for 28 days by intragastrical gavage. After contamination, histopathology displayed that liver tissue were damaged mildly with the effect of DEHP; a significant increase of the serum liver function index (including aspartate transaminase (AST) and alanine transaminase (ALT)) were observed. Additionally, the level of lipid peroxidation markedly rise, especially ROS and malondialdehyde (MDA), but the activation of superoxide dismutase (SOD) was obviously decreased in mice liver. In addition, DEHP promoted the phosphorylation of JNK and p38MAPK proteins in mice liver, as well as increased the expression of p53 protein and decreased the level of DNA methylation in the p53 gene promoter region. These results indicated that the hepatotoxicity of mice caused by DEHP may be through activating the JNK/p38MAPK/p53 signaling pathway and further promoting the generation of ROS to induce lipid peroxidation in liver, and the role of DNA methylation may be inevitable. Full article
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Int. J. Environ. Res. Public Health EISSN 1660-4601 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
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