Occupational and Environmental Exposures, Diseases and Epidemiology: From Basic Research to Human Health

A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Human Toxicology and Epidemiology".

Deadline for manuscript submissions: 20 December 2024 | Viewed by 1013

Special Issue Editors


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Guest Editor
KU Leuven, Department of Public Health and Primary Care, Centre for Environment and Health, Leuven, Belgium
Interests: inhalation and dermal exposure assessment; biomonitoring; chemical sensitizers; experimental in vivo models; skin/lung interaction

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Guest Editor
Research Unit of Pulmonology, University Hospital Vall d’Hebron, Barcelona, Spain
Interests: occupational and environmental respiratory diseases; experimental in vivo models; allergy

Special Issue Information

Dear Colleagues,

Frequent exposure to chemical, biological and physical agents can lead to adverse health outcomes and a decreased live expectancy. Depending on age, exposure can occur in the general environment (indoors and outdoors), at  school, or at the workplace, leading to the risk of a shortened lifespan. This can arise from air and water pollution, climate change, endocrine disruptors, heavy metals, and phthalates in the general environment to very specific occupational exposure to chemicals. For this Special Issue, ‘Occupational and Environmental Exposures, Diseases and Epidemiology: From Basic Research to Human Health’, we would like to invite you to submit your novel research on:

  • Novel environmental and occupational risks and the health effects.
  • Novel mechanisms of early adverse health effects.
  • The association or contribution of occupational exposure and health outcomes, with environmental exposure and health outcomes.
  • Development of improved risk assessment methods, with estimations of improved life quality.
  • Exposure during pregnancy and at other vulnerable moments in life (from cradle to grave).
  • Early identification of exposure and disease via novel biomonitoring methods (e.g., metabolomics or proteomics) and markers.
  • The current knowledge and meta-analysis of data.

From large-scale cohort studies to personalized medicine, what are the next steps?

Dr. Jeroen Vanoirbeek
Dr. María Jesús Cruz Carmona
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

  • early identification
  • exposure
  • inhalation
  • dermal
  • ingestion
  • occupational
  • environmental
  • cohort research
  • in vivo research
  • disease mechanisms

Published Papers (2 papers)

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Research

14 pages, 2146 KiB  
Article
Immunological Effects of Diesel Particles in a Murine Model of Healthy Mice
by David Soler-Segovia, Miquel de Homdedeu, Silvia Sánchez-Díez, Christian Romero-Mesones, David Espejo, Fopke Marain, Jeroen Vanoirbeek, Xavier Munoz and María-Jesús Cruz
Toxics 2024, 12(8), 530; https://doi.org/10.3390/toxics12080530 - 23 Jul 2024
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Abstract
Introduction: Exposure to environmental pollutants such as diesel exhaust particles (DEP) increases the risk of respiratory disease exacerbation. However, the possible effects of these particles on the general population remain poorly understood. The present study aimed to assess the immunomodulatory and inflammatory effects [...] Read more.
Introduction: Exposure to environmental pollutants such as diesel exhaust particles (DEP) increases the risk of respiratory disease exacerbation. However, the possible effects of these particles on the general population remain poorly understood. The present study aimed to assess the immunomodulatory and inflammatory effects of the inhalation of DEP in a model of healthy mice undergoing short-, mid- and long-term exposure. Materials and Methods: BALB/c ByJ mice were randomly divided into five experimental groups. The control group received three intranasal instillations of saline over 8 days while the other four groups received intranasal instillations of 150 µg of DEP 3 days per week for 8, 17, 26, and 53 days. Lung function assessment and flow cytometry were performed. Results: In lung tissue, intranasal exposure to DEP decreased total monocytes (p < 0.015 in all groups). At 26 days, a reduction in inflammatory monocytes and an increase in resident monocytes were observed, p = 0.001 and 0.0001, respectively. Eosinophils and neutrophils decreased at 26 days (p = 0.017 and p = 0.041, respectively). The intranasal challenges of DEP increased the total population of dendritic cells (DC) at 26 and 53 days (p = 0.017 and p = 0.022, respectively) and decreased the total and alveolar populations of macrophages (p < 0.003 for all groups compared to control), while interstitial macrophage populations increased over the time period (p = 0.0001 for all groups compared to control). Conclusions: Continuous DEP exposure triggers immune mechanisms that predispose healthy individuals to a pro-inflammatory and hyper-reactive microenvironment. This mouse model provides evidence of the capacity of DEP to increase DC, interstitial macrophages, and resident monocytes. Full article
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12 pages, 968 KiB  
Article
Personal Exposure to Sulfuric Acid in the Electroplating Industry: Development and Validation of a Predictive Model
by Austin B. Wang, Kai-Jen Chuang, Ven-Shing Wang and Ta-Yuan Chang
Toxics 2024, 12(7), 489; https://doi.org/10.3390/toxics12070489 - 3 Jul 2024
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Abstract
This study aimed to measure personal exposure to sulfuric acid in the electroplating industry to establish a predictive model and test its validation. We collected indoor air parameters and related information from four electroplating plants. Silica gel sorbents were used to collect air [...] Read more.
This study aimed to measure personal exposure to sulfuric acid in the electroplating industry to establish a predictive model and test its validation. We collected indoor air parameters and related information from four electroplating plants. Silica gel sorbents were used to collect air samples using high-performance ion chromatography. We collected air samples from three plants (i.e., Plant B, Plant C, and Plant D) and applied multiple linear regressions to build a predictive model. Eight samples collected from the fourth plant (i.e., Plant A) were used to validate the model. A total of 41 samples were collected with a mean of 25.0 ± 9.8 μg/m3 (range 12.1–51.7 μg/m3) in this study, including Plant A (8 samples, 17.5 ± 2.8 μg/m3, 13.0–22.0 μg/m3), Plant B (11 samples, 36.5 ± 9.7 μg/m3, 23.1–51.7 μg/m3), Plant C (11 samples, 16.4 ± 1.7 μg/m3, 12.1–17.8 μg/m3), and Plant D (11 samples, 27.4 ± 1.7 μg/m3, 24.1–29.9 μg/m3). Plant B was significantly higher in sulfuric acid than the other plants. Workers from the electroplating process plants were exposed to sulfuric acid at 29.0 ± 11.5 μg/m3. The predictive model for personal exposure to sulfuric acid fit the data well (r2 = 0.853; adjusted r2 = 0.837) and had an accuracy of 5.52 μg/m3 (bias ± precision; 4.98 ± 2.38 μg/m3), validated by the personal sampling of the fourth plant. This study observed that sulfuric acid exposure was lower than the permissible exposure level of 1000 μg/m3 in Taiwan and the United States, and only two samples were lower than the European Union standard of 50 μg/m3. The developed model can be applied in epidemiological studies to predict personal exposure to sulfuric acid in plants using electroplating. Full article
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