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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 (30 September 2020) | Viewed by 27279

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Dr. Daniele La Russa

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Department of Pharmacy, Health and Nutritional Sciences, University of Calabria, 87036 Rende, Italy
Interests: oxidative stress; biological antioxidant potential; kidney damage; cardiovascular diseases; nutraceutical treatment; brain ischemia

Special Issue Information

Dear colleagues,

The negative effects on health from exposure to environmental pollution have been a worldwide concern for the last half a century. Both traditional pollutants (metals) and emerging contaminants (endocrine disrupting chemicals, brominated and perfluorinate compounds, pharmaceuticals, and personal care products) represent a serious threat to aquatic and terrestrial organisms, including humans.

Epidemiological studies have estimated that several human diseases are due to chronic exposure to pollution in air/water/food, but mechanisms underlying this correlation are complex and often poorly characterized. Experimental evidence has indicated that an important mechanism of pollution-induced health effects involves an inflammation-related cascade and an oxidative status imbalance. Oxidation damage has been implicated in many degenerative and nondegenerative diseases, including cardiovascular, kidney and pulmonary diseases, diabetes, and Alzheimer’s disease.

This Special Issue aims to cover the most recent research findings on oxidative status alteration and pollution exposure to elucidate the role of traditional and emerging contaminants as the cause and perpetuating factor of oxidative status. Clinical, preclinical, and translational studies are welcome, as well as pertinent reviews with a critical synthesis of relevant published data. The issue also encourages submissions of investigations of oxidative stress as a therapeutic target in a variety of topics.

Dr. Daniele La Russa
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. 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

Environmental contamination
Human risk assessment
Oxidative stress
Antioxidant defense
Inflammation

Published Papers (6 papers)

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Research

Jump to: Review

10 pages, 7073 KiB

Open AccessFeature PaperArticle

Quantification of the Aluminum Content Leached into Foods Baked Using Aluminum Foil

by Paola Fermo, Gabriele Soddu, Alessandro Miani and Valeria Comite

Int. J. Environ. Res. Public Health 2020, 17(22), 8357; https://doi.org/10.3390/ijerph17228357 - 12 Nov 2020

Cited by 8 | Viewed by 4502

Abstract

In this study, determinations of the aluminum content in meat and fish performed after having cooked these foods using commercially available aluminum foil have been performed. The release of this chemical element was evaluated by cooking beef, chicken, and fish wrapped with commercial aluminum foil using seasoning or without seasoning in order to evaluate the effect on Al leaching into the food. The characterization of the food samples was carried out using two different analytical methods: inductively coupled plasma optical emission spectrometry (ICP-OES), for the quantification of aluminum, and scanning electron microscopy coupled with energy dispersion spectroscopy (SEM-EDS) to evaluate any structural changes occurring inside the aluminum foil after the cooking procedure. It has been demonstrated that the leaching that occurs when the foods are cooked by wrapping them in Al foil is not negligible and that the consumption of these foods, together with the consumption of other foodstuffs, such as, for example, some vegetables that may naturally contain aluminum, can lead to consuming a weekly dose not far from the TWI (tolerable weekly intake). Full article

(This article belongs to the Special Issue Environmental Pollution and Oxidative Status)

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28 pages, 8069 KiB

Open AccessArticle

Pyrethroid-Induced Organ Toxicity and Anti-Oxidant-Supplemented Amelioration of Toxicity and Organ Damage: The Protective Roles of Ascorbic Acid and α-Tocopherol

by Mohsen S. Al-Omar, Mamuna Naz, Salman A. A. Mohammed, Momina Mansha, Mohd N. Ansari, Najeeb U. Rehman, Mehnaz Kamal, Hamdoon A. Mohammed, Mohammad Yusuf, Abubaker M. Hamad, Naseem Akhtar and Riaz A. Khan

Int. J. Environ. Res. Public Health 2020, 17(17), 6177; https://doi.org/10.3390/ijerph17176177 - 25 Aug 2020

Cited by 11 | Viewed by 3231

Abstract

The pyrethroid toxicants, fatal at high doses, are found as remnants of crop pesticides and ingredients of commercially available insecticides. The toxic effects of high-content insecticidal pyrethroid formulations are available in 0.05 g, 1.17 g, and 0.04 g pyrethroid-instilled products, namely burning coils, pyrethroid-soaked mats, and liquid formulations of pyrethroids that release pyrethroid vapor/smoke upon heating. They provided 5.46 g/kg, 21.15 g/kg, and 4.24 g/kg of toxicants to the experimental animals over a total of 3 weeks/5 h per os (p.o.) administration, producing necrosis, hyperemia, and fatty changes in the liver; fiber separation in cardiac muscles; atrophy, lymphatic infiltration, blood vessel congestion, and hyperemia in the heart tissues of the experimental animals. The glomerular tuft necrosis, cytoplasmic degeneration of renal tubular cells, necrotic tubules, congestion, and dilatation of blood vessels were observed in the kidney tissue of intoxicated animals. Air-space enlargement, interstitial inflammation, lymphocyte infiltration aggregates, connective tissue infiltration by inflammatory cells, and hyperemia were found in the lung tissues. The pyrethroid toxicants also produced nervous tissue degeneration and decreased neurons in the brain, which were observed through histopathological examinations of the brain, lungs, heart, kidneys, and liver. The protective effects of ascorbic acid (AA/vitamin C) and α-tocopherol (E307/vitamin E) at 100 mg/kg oral doses administered daily for the entire period of the toxicant exposure of three weeks to the experimental mice, aged between 3–4 months and weighing ≈30 g, ameliorated the tissue damage, as observed through the histopathological examinations. The ascorbic acid caused recovery of the liver, kidney, brain, and heart tissue damage, while α-tocopherol was effective at ameliorating the damage in the kidneys and lung tissue compared with the control groups. The high levels of tissue damage recovery suggested a prophylactic effect of the concurrent use of ascorbic acid and α-tocopherol for the subjects under the exposure of pyrethroids. Full article

(This article belongs to the Special Issue Environmental Pollution and Oxidative Status)

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22 pages, 2781 KiB

Open AccessArticle

Synergistic Effect of WTC-Particulate Matter and Lysophosphatidic Acid Exposure and the Role of RAGE: In-Vitro and Translational Assessment

by Rachel Lam, Syed H. Haider, George Crowley, Erin J. Caraher, Dean F. Ostrofsky, Angela Talusan, Sophia Kwon, David J. Prezant, Yuyan Wang, Mengling Liu and Anna Nolan

Int. J. Environ. Res. Public Health 2020, 17(12), 4318; https://doi.org/10.3390/ijerph17124318 - 17 Jun 2020

Cited by 5 | Viewed by 2819

Abstract

World Trade Center particulate matter (WTC-PM)-exposed firefighters with metabolic syndrome (MetSyn) have a higher risk of WTC lung injury (WTC-LI). Since macrophages are crucial innate pulmonary mediators, we investigated WTC-PM/lysophosphatidic acid (LPA) co-exposure in macrophages. LPA, a low-density lipoprotein metabolite, is a ligand of the advanced glycation end-products receptor (AGER or RAGE). LPA and RAGE are biomarkers of WTC-LI. Human and murine macrophages were exposed to WTC-PM, and/or LPA, and compared to controls. Supernatants were assessed for cytokines/chemokines; cell lysate immunoblots were assessed for signaling intermediates after 24 h. To explore the translatability of our in-vitro findings, we assessed serum cytokines/chemokines and metabolites of symptomatic, never-smoking WTC-exposed firefighters. Agglomerative hierarchical clustering identified phenotypes of WTC-PM-induced inflammation. WTC-PM induced GM-CSF, IL-8, IL-10, and MCP-1 in THP-1-derived macrophages and induced IL-1α, IL-10, TNF-α, and NF-κB in RAW264.7 murine macrophage-like cells. Co-exposure induced synergistic elaboration of IL-10 and MCP-1 in THP-1-derived macrophages. Similarly, co-exposure synergistically induced IL-10 in murine macrophages. Synergistic effects were seen in the context of a downregulation of NF-κB, p-Akt, -STAT3, and -STAT5b. RAGE expression after co-exposure increased in murine macrophages compared to controls. In our integrated analysis, the human cytokine/chemokine biomarker profile of WTC-LI was associated with discriminatory metabolites (fatty acids, sphingolipids, and amino acids). LPA synergistically elaborated WTC-PM’s inflammatory effects in vitro and was partly RAGE-mediated. Further research will focus on the intersection of MetSyn/PM exposure. Full article

(This article belongs to the Special Issue Environmental Pollution and Oxidative Status)

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13 pages, 1227 KiB

Open AccessArticle

In Vitro Evaluation of Iron-Induced Salivary Lipid Oxidation Associated with Exposure to Iron Nanoparticles: Application Possibilities and Limitations for Food and Exposure Sciences

by Susan Mirlohi

Int. J. Environ. Res. Public Health 2020, 17(10), 3622; https://doi.org/10.3390/ijerph17103622 - 21 May 2020

Cited by 4 | Viewed by 2019

Abstract

Zerovalent iron nanotechnologies are widely used for groundwater remediation and increasingly considered for advance oxidation treatment in drinking water applications. Iron nanoparticles have been detected in drinking water systems and considered for food fortification; therefore, the potential for human exposure through ingestion can be a concern. This study aimed to assess whether ingestion of iron nanoparticles from drinking water could be detected through flavor perception using In Vitro salivary lipid oxidation as an indicator for metallic flavor perception. Ten female subjects, aged 29–59 years, donated saliva samples for use in the In Vitro experiments. Test samples consisted of 1:1 mixture of saliva and bottled drinking water (control) and three treatment solutions, spiked with ferrous sulfate, stabilized zerovalent iron nanoparticles (nZVI), and an aggregated/microsized suspension of mixed zerovalent iron and microsized suspension of iron and iron oxide metal powder, (mZVI). Upon mixing, samples were subjected to 15 min incubation at 37 °C to resemble oral conditions. Salivary lipid oxidation (SLO) was measured in all samples as micromoles of thiobarbituric acid reactive substances (TBARS)/mg Fe. Exposure to iron in all three forms induced significant amount of SLO in all treatment samples as compared to the control (p < 0.0001). The mean SLO levels were the highest in the ferrous treatment, followed by nZVI and mZVI treatments; the differences in the mean SLO levels were significant (p < 0.05). The findings indicate that oral exposure to stabilized ZVI nanoparticles may induce sensory properties different from that of ferrous salt, likely predictive of diminished detection of metallic flavor by humans. Full article

(This article belongs to the Special Issue Environmental Pollution and Oxidative Status)

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13 pages, 2485 KiB

Open AccessFeature PaperArticle

Particulate Matter Decreases Intestinal Barrier-Associated Proteins Levels in 3D Human Intestinal Model

by Brittany Woodby, Maria Lucia Schiavone, Erika Pambianchi, Angela Mastaloudis, Shelly N. Hester, Steven M. Wood, Alessandra Pecorelli and Giuseppe Valacchi

Int. J. Environ. Res. Public Health 2020, 17(9), 3234; https://doi.org/10.3390/ijerph17093234 - 06 May 2020

Cited by 18 | Viewed by 2820

Abstract

(1) Background: The gastrointestinal tract (GI) tract is one of the main organs exposed to particulate matter (PM) directly through ingestion of contaminated food or indirectly through inhalation. Previous studies have investigated the effects of chronic PM exposure on intestinal epithelia in vitro using Caco−2 cells and in vivo using mice. In this study, we hypothesized that chronic PM exposure would increase epithelial permeability and decrease barrier function due to altered redox homeostasis, which alters levels and/or localization of barrier-associated proteins in human three-dimensional (3D) intestinal tissues. (2) Methods: Transepithelial electrical resistance (TEER) in tissues exposed to 50, 100, 150, 250, and 500 µg/cm² of PM for 1 week and 2 weeks was analyzed. Levels and localization of tight junction proteins zonula occludens protein 1 (ZO−1) and claudin−1 and desmosome-associated desmocollin were analyzed using immunofluorescence. As a marker of oxidative stress, levels of 4-hydroxy-nonenal (4HNE) adducts were measured. (3) Results: No differences in TEER measurements were observed between exposed and un-exposed tissues. However, increased levels of 4HNE adducts in exposed tissues were observed. Additionally, decreased levels of ZO−1, claudin−1, and desmocollin were demonstrated. (4) Conclusion: These data suggest that chronic PM exposure results in an increase of oxidative stress; modified levels of barrier-associated proteins could possibly link to GI tract inflammatory conditions. Full article

(This article belongs to the Special Issue Environmental Pollution and Oxidative Status)

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Review

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45 pages, 5305 KiB

Open AccessEditor’s ChoiceReview

PFAS Environmental Pollution and Antioxidant Responses: An Overview of the Impact on Human Field

by Marco Bonato, Francesca Corrà, Marta Bellio, Laura Guidolin, Laura Tallandini, Paola Irato and Gianfranco Santovito

Int. J. Environ. Res. Public Health 2020, 17(21), 8020; https://doi.org/10.3390/ijerph17218020 - 30 Oct 2020

Cited by 63 | Viewed by 11189

Abstract

Due to their unique properties, perfluorinated substances (PFAS) are widely used in multiple industrial and commercial applications, but they are toxic for animals, humans included. This review presents some available data on the PFAS environmental distribution in the world, and in particular in Europe and in the Veneto region of Italy, where it has become a serious problem for human health. The consumption of contaminated food and drinking water is considered one of the major source of exposure for humans. Worldwide epidemiological studies report the negative effects that PFAS have on human health, due to environmental pollution, including infertility, steroid hormone perturbation, thyroid, liver and kidney disorders, and metabolic disfunctions. In vitro and in vivo researches correlated PFAS exposure to oxidative stress effects (in mammals as well as in other vertebrates of human interest), produced by a PFAS-induced increase of reactive oxygen species formation. The cellular antioxidant defense system is activated by PFAS, but it is only partially able to avoid the oxidative damage to biomolecules. Full article

(This article belongs to the Special Issue Environmental Pollution and Oxidative Status)

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