Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
3.4
4.6
Journals
Toxics
Special Issues
Toxicity and Human Health Assessment of Air Pollutants
share announcement

Toxicity and Human Health Assessment of Air Pollutants

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

Deadline for manuscript submissions: 30 September 2024 | Viewed by 6627

Special Issue Editors

Dr. Ting Wang

E-Mail Website
Guest Editor
College of Environmental Science and Engineering, Nankai University, Tianjin, China
Interests: environmental health; air pollution; particulate matter; risk assessment; exposure science; toxic effect and mechanism
Dr. Tingting Ku

E-Mail Website
Guest Editor
School of Environment and Resource Sciences, Shanxi University, Taiyuan, China
Interests: environmental health; air pollution; nanoparticles; exposure and toxicity identification; molecular mechanism
Dr. Jia Xu

E-Mail Website
Guest Editor
Chinese Research Academy of Environmental Sciences, Beijing, China
Interests: exposure modeling; particulate matter; oxidative potential; environmental health

Special Issue Information

Dear Colleagues,

Air pollution has been shown to be responsible for the morbidity and mortality of a variety of major diseases. The World Health Organization (WHO) estimates that almost all of the global population breathe air that exceeds WHO guidelines and contains high levels of pollutants. To date, however, the key constituents of air pollution which impact health and the potential mechanisms remain largely unstudied. In addition, comprehensive assessments of evidence from in vitro and in vivo studies, high-quality cohort studies, and high-resolution model simulations of health impacts are still substantially sparse. Hence, assessing the health risks, identifying the toxic effects, and elucidating the underlying mechanisms are of great importance. In the Special Issue “Toxicity and Human Health Assessment of Air Pollutants”, we aim to present a collection of original articles or reviews on the following topics:

  1. Exposure assessment in the locality, region, and microenvironments impacted by ambient air pollution.
  2. Identification of the key constituents of air pollution which impact health.
  3. Evaluation of the toxic mechanisms and signal pathways of air pollutants.
  4. Assessing and modeling the effect of air pollution on health risk.
  5. Development of novel methodologies for assessing the toxicity and health effects of air pollutants.

Dr. Ting Wang
Dr. Tingting Ku
Dr. Jia Xu
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 pollution
  • pollution characteristics
  • effect consistent
  • in vitro toxicity
  • in vivo toxicity
  • toxic mechanism
  • cohort study
  • exposure assessment.

Published Papers (7 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

17 pages, 1668 KiB  
Article
Lipid Dysregulation Induced by Gasoline and Diesel Exhaust Exposure and the Interaction with Age
by Yutong Gao, Xinzhuo Zhang, Xinting Li, Jinsheng Zhang, Zongyan Lv, Dongping Guo, Hongjun Mao and Ting Wang
Toxics 2024, 12(4), 303; https://doi.org/10.3390/toxics12040303 - 19 Apr 2024
Viewed by 419
Abstract
Limited knowledge exists regarding gasoline and diesel exhaust effects on lipid metabolism. This study collected gasoline and diesel exhaust under actual driving conditions and conducted inhalation exposure on male young and middle-aged C57BL/6J mice for 4 h/day for 5 days to simulate commuting [...] Read more.
Limited knowledge exists regarding gasoline and diesel exhaust effects on lipid metabolism. This study collected gasoline and diesel exhaust under actual driving conditions and conducted inhalation exposure on male young and middle-aged C57BL/6J mice for 4 h/day for 5 days to simulate commuting exposure intensity. Additionally, PM2.5 from actual roadways, representing gasoline and diesel vehicles, was generated for exposure to human umbilical vein endothelial cells (HUVECs) and normal liver cells (LO2) for 24, 48, and 72 h to further investigate exhaust particle toxicity. Results showed that diesel exhaust reduced total cholesterol and low-density lipoprotein cholesterol levels in young mice, indicating disrupted lipid metabolism. Aspartate aminotransferase and alanine aminotransferase levels increased by 53.7% and 21.7%, respectively, suggesting potential liver injury. Diesel exhaust exposure decreased superoxide dismutase and increased glutathione peroxidase levels. Cell viability decreased, and reactive oxygen species levels increased in HUVECs and LO2 following exposure to exhaust particles, with dose- and time-dependent effects. Diesel exhaust particles exhibited more severe inhibition of cell proliferation and oxidative damage compared to gasoline exhaust particles. These findings provide novel evidence of the risk of disrupted lipid metabolism due to gasoline and diesel exhaust, emphasizing the toxicity of diesel exhaust. Full article
(This article belongs to the Special Issue Toxicity and Human Health Assessment of Air Pollutants)
►▼ Show Figures

Graphical abstract

15 pages, 1609 KiB  
Article
Investigation of the Association between Air Pollution and Non-Alcoholic Fatty Liver Disease in the European Population: A Mendelian Randomization Study
by Jing Yang, Yaqi Zhang, Yin Yuan, Zhongyang Xie and Lanjuan Li
Toxics 2024, 12(3), 228; https://doi.org/10.3390/toxics12030228 - 21 Mar 2024
Viewed by 1004
Abstract
Non-alcoholic fatty liver disease (NAFLD) is currently the most prevalent chronic liver disease worldwide. At the same time, the relationship between air pollution and the likelihood of developing NAFLD has been a subject of debate due to conflicting findings in previous observational research. [...] Read more.
Non-alcoholic fatty liver disease (NAFLD) is currently the most prevalent chronic liver disease worldwide. At the same time, the relationship between air pollution and the likelihood of developing NAFLD has been a subject of debate due to conflicting findings in previous observational research. Our objective was to examine the potential correlation between air pollutant levels and the risk of NAFLD in the European population by employing a two-sample Mendelian randomization (MR) analysis. The UK Biobank Consortium provided the summary statistics for various air pollution indicators (PM2.5, PM2.5 absorbance, PM2.5–10, PM10, NO2, and NOx). Additionally, information on NAFLD was obtained from three studies, including one derivation set and two validation sets. Heterogeneity, pleiotropy, and sensitivity analyses were performed under different MR frameworks, and instrumental variables associated with confounders (such as education, smoking, alcohol, and BMI) were detected by tools. In the derivation set, causal relationships between PM2.5, NO2, and NAFLD were observed in univariable Mendelian randomization (UVMR) (Odds Ratio (OR) = 1.99, 95% confidence interval (95% CI) = [1.22–3.22], p = 0.005; OR = 2.08, 95% CI = [1.27–3.40], p = 0.004, respectively). After adjustment for air pollutants or alcohol intake frequency in multivariable Mendelian randomization (MVMR), the above genetic correlations disappeared. In validation sets, the null associations remained in UVMR. Our findings from MR analysis using genetic data did not provide evidence for a causal association between air pollution and NAFLD in the European population. The associations observed in epidemiological studies could be partly attributed to confounders. Full article
(This article belongs to the Special Issue Toxicity and Human Health Assessment of Air Pollutants)
►▼ Show Figures

Figure 1

19 pages, 13348 KiB  
Article
The Impact of Atmospheric Cadmium Exposure on Colon Cancer and the Invasiveness of Intestinal Stents in the Cancerous Colon
by Shuai Zhang, Ruikang Li, Jing Xu, Yan Liu and Yanjie Zhang
Toxics 2024, 12(3), 215; https://doi.org/10.3390/toxics12030215 - 14 Mar 2024
Viewed by 849
Abstract
Background: Inhalation exposure to carcinogenic metals such as cadmium (Cd) is a significant global health concern linked to various cancers. However, the precise carcinogenic mechanism underlying inhalation exposure remains elusive. Methods: In this study, CT26 mouse colon cancer (CC) cells were implanted into [...] Read more.
Background: Inhalation exposure to carcinogenic metals such as cadmium (Cd) is a significant global health concern linked to various cancers. However, the precise carcinogenic mechanism underlying inhalation exposure remains elusive. Methods: In this study, CT26 mouse colon cancer (CC) cells were implanted into BALB/c mice to establish CC mouse models. Some of the CC mice were implanted with intestinal stents. The mice were exposed to atomized oxygen and nitrogen (O2/N2) gas containing Cd. Results: Atmospheric Cd intensified inflammation in CC cells and heightened Nicotinamide Adenine Dinucleotide Phosphate (NADPH) Oxidase 1 (NOX1) activity, which is an indirect measurement of increased reactive oxygen species (ROS) production. This escalated ROS production triggered abnormal Wnt protein secretion, activated the Wnt/β-catenin signaling pathway, and stimulated CC cell proliferation. No discernible body weight effect was seen in the CC mice, possibly due to the later-stage tumor weight gain, which masked the changes in body weight. Cd facilitated colon tumor restructuring and cell migration at the later stage. The implantation of intestinal stents inhibited the expression of Superoxide Dismutase 1 (SOD1) in the colon tumors of the CC mice, with no evident effects on the expression levels of NOX1, SOD2, and Catalase (CAT) enzymes. Elevated ROS levels, indirectly reflected by enzyme activity, did not substantially impact the Wnt/β-catenin signaling pathway and even contributed to slowing its imbalance. Stent implantation eased the inflammation occurring in colon tumors by reducing CC cell proliferation but it induced discomfort in the mice, leading to a reduction in food intake and weight. Conclusions: Cd partially fosters CC tumorigenesis via the ROS-mediated Wnt/β-catenin signaling pathway. The effect of Cd on the invasive effect of intestinal stents in the cancerous colon is not significant. Full article
(This article belongs to the Special Issue Toxicity and Human Health Assessment of Air Pollutants)
►▼ Show Figures

Figure 1

14 pages, 7199 KiB  
Article
Comparison of Population-Weighted Exposure Estimates of Air Pollutants Based on Multiple Geostatistical Models in Beijing, China
by Yinghan Wu, Jia Xu, Ziqi Liu, Bin Han, Wen Yang and Zhipeng Bai
Toxics 2024, 12(3), 197; https://doi.org/10.3390/toxics12030197 - 01 Mar 2024
Viewed by 837
Abstract
Various geostatistical models have been used in epidemiological research to evaluate ambient air pollutant exposures at a fine spatial scale. Few studies have investigated the performance of different exposure models on population-weighted exposure estimates and the resulting potential misclassification across various modeling approaches. [...] Read more.
Various geostatistical models have been used in epidemiological research to evaluate ambient air pollutant exposures at a fine spatial scale. Few studies have investigated the performance of different exposure models on population-weighted exposure estimates and the resulting potential misclassification across various modeling approaches. This study developed spatial models for NO2 and PM2.5 and conducted exposure assessment in Beijing, China. It explored three spatial modeling approaches: variable dimension reduction, machine learning, and conventional linear regression. It compared their model performance by cross-validation (CV) and population-weighted exposure estimates. Specifically, partial least square (PLS) regression, random forests (RF), and supervised linear regression (SLR) models were developed based on an ordinary kriging (OK) framework for NO2 and PM2.5 in Beijing, China. The mean squared error-based R2 (R2mse) and root mean squared error (RMSE) in leave-one site-out cross-validation (LOOCV) were used to evaluate model performance. These models were used to predict the ambient exposure levels in the urban area and to estimate the misclassification of population-weighted exposure estimates in quartiles between them. The results showed that the PLS-OK models for NO2 and PM2.5, with the LOOCV R2mse of 0.82 and 0.81, respectively, outperformed the other models. The population-weighted exposure to NO2 estimated by the PLS-OK and RF-OK models exhibited the lowest misclassification in quartiles. For PM2.5, the estimates of potential misclassification were comparable across the three models. It indicated that the exposure misclassification made by choosing different modeling approaches should be carefully considered, and the resulting bias needs to be evaluated in epidemiological studies. Full article
(This article belongs to the Special Issue Toxicity and Human Health Assessment of Air Pollutants)
►▼ Show Figures

Figure 1

13 pages, 1964 KiB  
Article
In Vitro Profiling of Toxicity Effects of Different Environmental Factors on Skin Cells
by Minghui Fu, Yingxin Yang, Xiaolan Zhang, Bingli Lei, Tian Chen and Yuanqi Chen
Toxics 2024, 12(2), 108; https://doi.org/10.3390/toxics12020108 - 27 Jan 2024
Cited by 1 | Viewed by 1159
Abstract
The skin is constantly exposed to a variety of environmental threats. Therefore, the influence of environmental factors on skin damage has always been a matter of concern. This study aimed to investigate the cytotoxic effects of different environmental factors, including cooking oil fumes [...] Read more.
The skin is constantly exposed to a variety of environmental threats. Therefore, the influence of environmental factors on skin damage has always been a matter of concern. This study aimed to investigate the cytotoxic effects of different environmental factors, including cooking oil fumes (COFs), haze (PM2.5), and cigarette smoke (CS), on epidermal HaCaT cells and dermal fibroblast (FB) cells. Cell viability, intracellular reactive oxygen species (ROS) generation, inflammatory cytokine levels, and collagen mRNA expression were used as toxicity endpoints. Additionally, the effects of ozone (O3) on cell viability and release of inflammatory cytokines in 3D epidermal cells were also examined. The results showed that the organic extracts of CS, COFs, and PM2.5 significantly inhibited the viability of HaCaT and FB cells at higher exposure concentrations. These extracts also increased intracellular ROS levels in FB cells. Furthermore, they significantly promoted the release of inflammatory cytokines, such as IL-1α and TNF-α, in HaCaT cells and down-regulated the mRNA expression of collagen I, III, IV, and VII in FB cells. Comparatively, SC organic extracts exhibited stronger cytotoxicity to skin cells compared to PM2.5 and COFs. Additionally, O3 at all test concentrations significantly inhibited the viability of 3D epidermal cells in a concentration-dependent manner and markedly increased the levels of TNF-α and IL-1α in 3D epidermal cells. These findings emphasize the potential cytotoxicity of COFs, PM2.5, CS, and O3 to skin cells, which may lead to skin damage; therefore, we should pay attention to these environmental factors and take appropriate measures to protect the skin from their harmful effects. Full article
(This article belongs to the Special Issue Toxicity and Human Health Assessment of Air Pollutants)
►▼ Show Figures

Figure 1

Review

Jump to: Research

25 pages, 721 KiB  
Review
Developmental Toxicity of Fine Particulate Matter: Multifaceted Exploration from Epidemiological and Laboratory Perspectives
by Ruifeng Yan, Danni Ma, Yutong Liu, Rui Wang, Lifan Fan, Qiqi Yan, Chen Chen, Wenhao Wang, Zhihua Ren, Tingting Ku, Xia Ning and Nan Sang
Toxics 2024, 12(4), 274; https://doi.org/10.3390/toxics12040274 - 06 Apr 2024
Viewed by 596
Abstract
Particulate matter of size ≤ 2.5 μm (PM2.5) is a critical environmental threat that considerably contributes to the global disease burden. However, accompanied by the rapid research progress in this field, the existing research on developmental toxicity is still constrained by [...] Read more.
Particulate matter of size ≤ 2.5 μm (PM2.5) is a critical environmental threat that considerably contributes to the global disease burden. However, accompanied by the rapid research progress in this field, the existing research on developmental toxicity is still constrained by limited data sources, varying quality, and insufficient in-depth mechanistic analysis. This review includes the currently available epidemiological and laboratory evidence and comprehensively characterizes the adverse effects of PM2.5 on developing individuals in different regions and various pollution sources. In addition, this review explores the effect of PM2.5 exposure to individuals of different ethnicities, genders, and socioeconomic levels on adverse birth outcomes and cardiopulmonary and neurological development. Furthermore, the molecular mechanisms involved in the adverse health effects of PM2.5 primarily encompass transcriptional and translational regulation, oxidative stress, inflammatory response, and epigenetic modulation. The primary findings and novel perspectives regarding the association between public health and PM2.5 were examined, highlighting the need for future studies to explore its sources, composition, and sex-specific effects. Additionally, further research is required to delve deeper into the more intricate underlying mechanisms to effectively prevent or mitigate the harmful effects of air pollution on human health. Full article
(This article belongs to the Special Issue Toxicity and Human Health Assessment of Air Pollutants)
►▼ Show Figures

Figure 1

14 pages, 1515 KiB  
Review
Ambient Air Pollution and Vision Disorder: A Systematic Review and Meta-Analysis
by Zhuo Han, Chao Zhao, Yuhua Li, Meng Xiao, Yuewei Yang, Yizhuo Zhao, Chunyu Liu, Juan Liu and Penghui Li
Toxics 2024, 12(3), 209; https://doi.org/10.3390/toxics12030209 - 10 Mar 2024
Viewed by 1000
Abstract
The effects of air pollution on physical health are well recognized, with many studies revealing air pollution’s effects on vision disorder, yet no relationship has been established. Therefore, a meta-analysis was carried out in this study to investigate the connection between vision disorder [...] Read more.
The effects of air pollution on physical health are well recognized, with many studies revealing air pollution’s effects on vision disorder, yet no relationship has been established. Therefore, a meta-analysis was carried out in this study to investigate the connection between vision disorder and ambient particles (diameter ≤ 2.5 µm (PM2.5), diameter ≤ 10 µm (PM10)) and gaseous pollutants (nitrogen dioxide (NO2), sulfur dioxide (SO2), carbon monoxide (CO), Ozone (O3)). Twelve relevant studies published by 26 February 2024 were identified in three databases. A pooled odds ratios (ORs) of 95% confidence intervals (CIs) were obtained using random-effects meta-analysis models. Meta-analysis results revealed that for every 10 µg/m3 increase in PM2.5 and NO2 exposure, a substantially higher incidence of vision disorder was observed (OR = 1.10; 95% CI: 1.01, 1.19; OR = 1.08, 95% CI: 1.00, 1.16). No significant correlation existed between exposure to PM10, SO2 and CO and vision disorder. However, O3 exposure was negatively associated with vision disorder. In addition, subgroup analyses revealed that PM2.5 exposure was significantly correlated with the risk of glaucoma and age-related macular degeneration and that children and adolescents were more susceptible to NO2 and PM2.5 than adults. Overall, exposure to air pollutants, especially PM2.5 and NO2, may increase the incidence of vision disorder. Full article
(This article belongs to the Special Issue Toxicity and Human Health Assessment of Air Pollutants)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-7
Back to TopTop