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Toxics
Special Issues
Molecular Mechanisms of Toxicity from Air Pollutant Exposure
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Molecular Mechanisms of Toxicity from Air Pollutant Exposure

A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Air Pollution and Health".

Deadline for manuscript submissions: closed (10 April 2024) | Viewed by 3367

Special Issue Editors

Prof. Dr. Yongjie Wei

E-Mail Website
Guest Editor
State Key Laboratory of Environmental Criteria and Risk Assessment, Chinese Research Academy of Environmental Sciences, Beijing 100012, China
Interests: atmospheric chemistry; environmental health; toxicology; epidemiology; molecular biology; environmental criteria; environmental damage identification; environmental ethics
Dr. Zhi-Gang Li

E-Mail Website
Guest Editor
State Key Laboratory of Environmental Criteria and Risk Assessment, Chinese Research Academy of Environmental Sciences, Beijing 100012, China
Interests: environmental health; environmental toxicology; molecular biology; regulatory mechanism; environmental epidemiology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Air pollutants, including PM2.5, O3, NO2, SO2, etc., play an important role in causing many adverse health effects. Extensive epidemiological investigations have revealed that exposure to PM2.5 increases the risk of cardiovascular disease and respiratory disease. O3 exposure has the potential to interfere with the secretion of hormones, including insulin, glucocorticoids, etc. Exposure to NO2 also elevates an individual’s risk of inflammation and other health conditions, such as birth defects. Volatile organic compounds (VOCs) constitute crucial components of air pollutants. However, there are few studies on the adverse health effect induced by VOCs. Additionally, indoor environments host various types of air pollutants, meaning that the health effects of indoor air pollution are a matter of concern. While toxicological studies have pointed out some reference pathogeneses for these adverse health outcomes, referring to inflammation, oxidative stress, imbalance of the autonomic nervous system, epigenetic modification, etc., there are many necessary topics regarding the specific molecular mechanisms and regulatory pathways of air pollutant-induced adverse health outcomes that remain to be explored.

This Special Issue will focus on highlighting timely research studies addressing the effects of air pollutant toxicity on health. Authors are invited and welcome to submit original research papers, reviews, and short communications. 

Topics may include, but are not limited to, the following:

  1. The molecular mechanisms of air pollutant-induced adverse health effects.
  2. The molecular mechanisms of epigenetic modifications in air pollutant-induced adverse health effects.
  1. The molecular mechanisms of hormone secretion disorders in air pollutant-induced adverse health.
  2. The health effects of indoor air pollution and the molecular mechanisms responsible.

Prof. Dr. Yongjie Wei
Dr. Zhi-Gang Li
Guest Editors

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

  • air pollutants
  • molecular mechanisms
  • toxicity
  • volatile organic compounds
  • indoor air pollution
  • epigenetic modification
  • inflammation
  • oxidative stress

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Published Papers (2 papers)

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Research

9 pages, 1130 KiB  
Article
The Impact of the Reduction in Environmental Pollution during COVID-19 Lockdown on Healthy Individuals
by Christian Romero-Mesones, Miquel de Homdedeu, David Soler-Segovia, Carlos Gómez-Ollés, David Espejo-Castellanos, Inigo Ojanguren, Berta Saez-Gimenez, María-Jesús Cruz and Xavier Munoz
Toxics 2024, 12(7), 492; https://doi.org/10.3390/toxics12070492 - 4 Jul 2024
Viewed by 1430
Abstract
The lockdown imposed to combat the COVID-19 pandemic produced a historic fall in air pollution in cities like Barcelona. This exceptional situation offered a unique context in which to examine the effects of air pollutants on human health. The present study aims to [...] Read more.
The lockdown imposed to combat the COVID-19 pandemic produced a historic fall in air pollution in cities like Barcelona. This exceptional situation offered a unique context in which to examine the effects of air pollutants on human health. The present study aims to determine and compare the oxidative stress biomarkers Th1/Th2 and inflammatory-related cytokines in healthy individuals first during lockdown and then six months after the easing of the restrictions on mobility. A prospective study of a representative sample of 58 healthy, non-smoking adults was carried out. During lockdown and six months post-easing of restrictions, blood samples were drawn to measure the percentage of eosinophils, levels of Th1/Th2 and inflammatory-related cytokines assessed by a multiplex assay (BioRad Laboratories S.A., Marnes-la-Coquette, France), and levels of 8-isoprostane, glutathione peroxidase activity, and myeloperoxidase (Cayman Chemical Co., Ann Arbor, MI, USA), to assess their value as biomarkers of oxidative stress. Six months after easing mobility restrictions, increases in the levels of 8-isoprostane (p < 0.0001), IL-1β (p = 0.0013), IL-1ra (p = 0.0110), IL-4 (p < 0.0001), IL-13 (p < 0.0001), G-CSF (p = 0.0007), and CCL3 (p < 0.0001) were recorded, along with reductions in glutathione peroxidase (p < 0.0001), IFN-γ (p = 0.0145), TNFα (p < 0.0001), IP-10 (p < 0.0001), IL-2 (p < 0.0001), IL-7 (p < 0.0001), basic FGF (p < 0.0001), CCL4 (p < 0.0001), and CCL5 (p < 0.0001). No significant differences were observed in the rest of the biomarkers analyzed. The reduction in environmental pollution during the COVID-19 lockdown significantly lowered the levels of oxidative stress, systemic inflammation, and Th2-related cytokines in healthy people. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Toxicity from Air Pollutant Exposure)
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20 pages, 3854 KiB  
Article
PM2.5 Extracts Induce INFγ-Independent Activation of CIITA, MHCII, and Increases Inflammation in Human Bronchial Epithelium
by Héctor Jirau-Colón and Braulio D. Jiménez-Vélez
Toxics 2024, 12(4), 292; https://doi.org/10.3390/toxics12040292 - 16 Apr 2024
Viewed by 1412
Abstract
The capacity of particulate matter (PM) to enhance and stimulate the expression of pro-inflammatory mediators has been previously demonstrated in non-antigen-presenting cells (human bronchial epithelia). Nonetheless, many proposed mechanisms for this are extrapolated from known canonical molecular pathways. This work evaluates a possible [...] Read more.
The capacity of particulate matter (PM) to enhance and stimulate the expression of pro-inflammatory mediators has been previously demonstrated in non-antigen-presenting cells (human bronchial epithelia). Nonetheless, many proposed mechanisms for this are extrapolated from known canonical molecular pathways. This work evaluates a possible mechanism for inflammatory exacerbation after exposure to PM2.5 (from Puerto Rico) and CuSO4, using human bronchial epithelial cells (BEAS-2B) as a model. The induction of CIITA, MHCII genes, and various pro-inflammatory mediators was investigated. Among these, the phosphorylation of STAT1 Y701 was significantly induced after 4 h of PM2.5 exposure, concurrent with a slight increase in CIITA and HLA-DRα mRNA levels. INFγ mRNA levels remained low amidst exposure time, while IL-6 levels significantly increased at earlier times. IL-8 remained low, as expected from attenuation by IL-6 in the known INFγ-independent inflammation pathway. The effects of CuSO4 showed an increase in HLA-DRα expression after 8 h, an increase in STAT1 at 1 h, and RF1 at 8 h We hypothesize and show evidence that an inflammatory response due to PM2.5 extract exposure in human bronchial epithelia can be induced early via an alternate non-canonical pathway in the absence of INFγ. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Toxicity from Air Pollutant Exposure)
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