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Health Risk and Toxicity Mechanism of Nanoparticles or Ultrafine Particles...
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Health Risk and Toxicity Mechanism of Nanoparticles or Ultrafine Particles Inhalation

A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Exposome Analysis and Risk Assessment".

Deadline for manuscript submissions: closed (10 June 2023) | Viewed by 8370

Special Issue Editors

Prof. Dr. Jinglong Tang

E-Mail Website
Guest Editor
School of Public Health, Qingdao University, Qingdao, China
Interests: inhalation toxicology; nanotoxicology; environmental toxicology
Prof. Dr. Rong Zhang

E-Mail Website
Guest Editor
Department of Toxicology, School of Public Health, Hebei Medical University, Shijiazhuang, China
Interests: environmental health; toxicology; epidemiology; particulate matter

Special Issue Information

Dear Colleagues,

The application of nanomaterials is experiencing unprecedented expansion in the 21st century. Nanoparticle pollution is becoming an emerging pollution issue, and it is difficult to manage and control. Besides engineered nanoparticle emission from waste matter or byproducts that occur during the manufacture or use of nanomaterials, natural nanoparticles, also called ultrafine particulate matter, are other sources of nanopollution. Both forms of nanosized particles can expedite the emergence of potential risks to industrial workers, consumers, and the environment. Long-term inhalation exposure to these nanoparticles or ultrafine particles may cause serious damage to the respiratory tract and increase the incidence rate of pulmonary diseases, cardiovascular diseases, and premature death. There is an increasing demand to consider environmental implications of nanoparticles or ultrafine particles and to monitor the outcome of nanoparticles after inhalation exposure. Therefore, the health risk and toxicity mechanism of nanoparticles or ultrafine particle inhalation is an essential topic to understand the toxic effect of these nanoparticles on human health.

We are pleased to invite you to submit to this Special Issue on “Health Risk and Toxicity Mechanism of Nanoparticles or Ultrafine Particles Inhalation”, with the aim of improving knowledge on this topic and enriching public understanding of the health effect of nanoparticle inhalation.

For this Special Issue, original research articles, reviews, and short communications are welcome. Research areas may include (but are not limited to) public health, environmental chemistry, and toxicology. We also encourage manuscripts that propose new concepts and techniques to evaluate the health effect of nanoparticles.

Prof. Dr. Jinglong Tang
Prof. Dr. Rong Zhang
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

  • nanotoxicology
  • particulate matter
  • risk assessment
  • inhalation toxicology
  • toxicological mechanism

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Published Papers (5 papers)

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Research

19 pages, 6675 KiB  
Article
Exploration of the Pathogenesis of Chronic Obstructive Pulmonary Disease Caused by Smoking—Based on Bioinformatics Analysis and In Vitro Experimental Evidence
by Yingchi Zhang, Yuxin Sheng, Yanrong Gao, Yujia Lin, Bin Cheng, Hongmei Li, Ling Zhang and Haiming Xu
Toxics 2023, 11(12), 995; https://doi.org/10.3390/toxics11120995 - 7 Dec 2023
Cited by 2 | Viewed by 1329
Abstract
This study was aimed at investigating the pathogenesis of chronic obstructive pulmonary disease (COPD) caused by smoking—based on bioinformatics analysis and in vitro experimental evidence. The GEO, GEO2R, TargetScan, miRDB, miRWalk, DAVID, and STRING databases were used for bioinformatics analysis. The mRNA expression [...] Read more.
This study was aimed at investigating the pathogenesis of chronic obstructive pulmonary disease (COPD) caused by smoking—based on bioinformatics analysis and in vitro experimental evidence. The GEO, GEO2R, TargetScan, miRDB, miRWalk, DAVID, and STRING databases were used for bioinformatics analysis. The mRNA expression and the protein levels were determined by real-time PCR and ELISA. After taking the intersection of the diversified results of the databases, four differentially expressed miRNAs (hsa-miR-146a, hsa-miR-708, hsa-miR-150, and hsa-miR-454) were screened out. Subsequently, a total of 57 target genes of the selected miRNAs were obtained. The results of DAVID analysis showed that the selected miRNAs participated in COPD pathogenesis through long-term potentiation, the TGF-β signaling pathway, the PI3K-Akt signaling pathway, etc. The results of STRING prediction showed that TP53, EP300, and MAPK1 were the key nodes of the PPI network. The results of the confirmatory experiment showed that, compared with the control group, the mRNA expression of ZEB1, MAPK1, EP300, and SP1 were up-regulated, while the expression of MYB was down-regulated and the protein levels of ZEB1, MAPK1, and EP300 were increased. Taken together, miRNAs (hsa-miR-146a, hsa-miR-708, hsa-miR-150, and hsa-miR-454) and their regulated target genes and downstream protein molecules (ZEB1, EP300, and MAPK1) may be closely related to the pathological process of COPD. Full article
(This article belongs to the Special Issue Health Risk and Toxicity Mechanism of Nanoparticles or Ultrafine Particles Inhalation)
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15 pages, 27986 KiB  
Article
Pulmonary Toxicity Assessment after a Single Intratracheal Inhalation of Chlorhexidine Aerosol in Mice
by Jianzhong Zhang, Xinmin Jiang, Xin Li, He Sun, Mingyue Wang, Wanjun Zhang, Haonan Li, Hongmei Wang, Min Zhuang, Lin Zhang, Lin Lu and Jinglong Tang
Toxics 2023, 11(11), 910; https://doi.org/10.3390/toxics11110910 - 7 Nov 2023
Cited by 1 | Viewed by 1865
Abstract
Guanidine disinfectants are important chemical agents with a broad spectrum of activity that are effective against most microorganisms. Chlorhexidine, one of the most used guanidine disinfectants, is added to shampoo and mouthwash and applied in medical device sterilization. During the use of chlorhexidine, [...] Read more.
Guanidine disinfectants are important chemical agents with a broad spectrum of activity that are effective against most microorganisms. Chlorhexidine, one of the most used guanidine disinfectants, is added to shampoo and mouthwash and applied in medical device sterilization. During the use of chlorhexidine, aerosols with micron particle size may be formed, which may cause inhalation toxicity. To assess the toxicity of inhaled chlorhexidine aerosol, mice underwent the intratracheal instillation of different concentrations of chlorhexidine (0, 0.125%, 0.25%, 0.5%, and 1%) using a MicroSprayer Aerosolizer. The mice were exposed for eight weeks and then sacrificed to obtain lung tissue for subsequent experiments. Histopathology staining revealed damaged lung tissues and increased collagen exudation. At the same time, pulmonary function tests showed that chlorhexidine exposure could cause restrictive ventilatory dysfunction, consistent with pulmonary fibrosis. The results of transcriptome analyses suggest that chlorhexidine may trigger an inflammatory response and promote the activation of pathways related to extracellular matrix deposition. Further, we identified that chlorhexidine exposure might enhance mucus secretion by up-regulating Muc5b and Muc5ac genes, thereby inducing fibrosis-like injury. These findings underscore the need for standardized use of disinfectants and the assessment of their inhalation toxicity. Full article
(This article belongs to the Special Issue Health Risk and Toxicity Mechanism of Nanoparticles or Ultrafine Particles Inhalation)
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18 pages, 19677 KiB  
Article
Preliminary Study on the Effect and Molecular Mechanism of Tetrandrine in Alleviating Pulmonary Inflammation and Fibrosis Induced by Silicon Dioxide
by Yi Wang, Bin Cheng, Yu-Jia Lin, Rui Wang, Jie Xuan and Hai-Ming Xu
Toxics 2023, 11(9), 765; https://doi.org/10.3390/toxics11090765 - 9 Sep 2023
Cited by 2 | Viewed by 1386
Abstract
This study aims to explore the molecular mechanism of tetrandrine (Tet) in alleviating pulmonary inflammation and fibrosis induced by silica (SiO2) from the perspective of autophagy. C57BL/6J mice were selected as experimental animals, and SiO2 was exposed by intranasal instillation. [...] Read more.
This study aims to explore the molecular mechanism of tetrandrine (Tet) in alleviating pulmonary inflammation and fibrosis induced by silica (SiO2) from the perspective of autophagy. C57BL/6J mice were selected as experimental animals, and SiO2 was exposed by intranasal instillation. Tet was intervened by oral gavage. The mice were euthanized on the 7th and 42nd day of SiO2 exposure, and lung tissues were collected for histopathological, molecular biological, immunological, and transmission electron microscopy analysis. The results showed that SiO2 exposure could lead to significant lung inflammation and fibrosis, while Tet could significantly reduce SiO2 exposure-induced lung inflammation and fibrosis. Molecular mechanism research indicated that, compared with SiO2 expose group, Tet intervention could significantly reduce the expression levels of inflammatory cytokines and fibrosis markers (TNF-α, IL-1β, MCP-1, TGF-β1, HYP, Col-I, and Fn), and regulate the expression of key molecules ATG7, microtubule-associated protein 1 light chain 3B (LC3B), and P62 in the autophagy pathway to improve the blocking of autophagic flux, promote the recovery of autophagic lysosomal system function, and inhibit apoptosis. In summary, Tet can alleviate silica-induced lung inflammation and fibrosis, which may be achieved by regulating the expression of key molecules in the autophagy process and associated apoptotic pathway. Full article
(This article belongs to the Special Issue Health Risk and Toxicity Mechanism of Nanoparticles or Ultrafine Particles Inhalation)
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15 pages, 9002 KiB  
Article
CXCL17 Attenuates Diesel Exhaust Emissions Exposure-Induced Lung Damage by Regulating Macrophage Function
by Yize Yin, Chaohui Mu, Jiahui Wang, Yixuan Wang, Wenmin Hu, Wenjing Zhu, Xinjuan Yu, Wanming Hao, Yuxin Zheng, Qinghai Li and Wei Han
Toxics 2023, 11(8), 646; https://doi.org/10.3390/toxics11080646 - 26 Jul 2023
Cited by 2 | Viewed by 1501
Abstract
Exposure to diesel exhaust emissions (DEE) is strongly linked to innate immune injury and lung injury, but the role of macrophage chemoattractant CXCL17 in the lung damage caused by DEE exposure remains unclear. In this study, whole-body plethysmography (WBP), inflammatory cell differential count, [...] Read more.
Exposure to diesel exhaust emissions (DEE) is strongly linked to innate immune injury and lung injury, but the role of macrophage chemoattractant CXCL17 in the lung damage caused by DEE exposure remains unclear. In this study, whole-body plethysmography (WBP), inflammatory cell differential count, and histopathological analysis were performed to assess respiratory parameters, airway inflammation, and airway injury in C57BL/6 male mice exposed to DEE for 3 months. qRT-PCR, IHC (immunohistochemistry), and ELISA were performed to measure the CXCL17 expression in airway epithelium or BALF (bronchoalveolar lavage fluid) following DEE/Diesel exhaust particle (DEP) exposure. Respiratory parameters, airway inflammation, and airway injury were assessed in CXCL17-overexpressing mice through adeno-associated virus vector Type 5 (AAV5) infection. Additionally, an in vitro THP-1 and HBE co-culture system was constructed. Transwell assay was carried out to evaluate the effect of rh-CXCL17 (recombinant human protein-CXCL17) on THP-1 cell migration. Flow cytometry and qRT-PCR were conducted to assess the impacts of rh-CXCL17 on apoptosis and inflammation/remodeling of HBE cells. We found that the mice exposed to DEE showed abnormal respiratory parameters, accompanied by airway injury and remodeling (ciliary injury in airway epithelium, airway smooth muscle hyperplasia, and increased collagen deposition). Carbon content in airway macrophages (CCAM), but not the number of macrophages in BALF, increased significantly. CXCL17 expression significantly decreased in mice airways and HBE after DEE/DEP exposure. AAV5-CXCL17 enhanced macrophage recruitment and clearance of DEE in the lungs of mice, and it improved respiratory parameters, airway injury, and airway remodeling. In the THP-1/HBE co-culture system, rh-CXCL17 increased THP-1 cell migration while attenuating HBE cell apoptosis and inflammation/remodeling. Therefore, CXCL17 might attenuate DEE-induced lung damage by recruiting and activating pulmonary macrophages, which is expected to be a novel therapeutic target for DEE-associated lung diseases. Full article
(This article belongs to the Special Issue Health Risk and Toxicity Mechanism of Nanoparticles or Ultrafine Particles Inhalation)
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16 pages, 4694 KiB  
Article
Comprehensive Analysis of lncRNA–mRNA Expression Profiles in Depression-like Responses of Mice Related to Polystyrene Nanoparticle Exposure
by Qingping Liu, Wentao Hu, Yaling Zhang, Jie Ning, Yaxian Pang, Huaifang Hu, Meiyu Chen, Mengqi Wu, Mengruo Wang, Peihao Yang, Lei Bao, Yujie Niu and Rong Zhang
Toxics 2023, 11(7), 600; https://doi.org/10.3390/toxics11070600 - 10 Jul 2023
Cited by 1 | Viewed by 1586
Abstract
Plastics in the environment can break down into nanoplastics (NPs), which pose a potential threat to public health. Studies have shown that the nervous system constitutes a significant target for nanoplastics. However, the potential mechanism behind nanoplastics’ neurotoxicity remains unknown. This study aimed [...] Read more.
Plastics in the environment can break down into nanoplastics (NPs), which pose a potential threat to public health. Studies have shown that the nervous system constitutes a significant target for nanoplastics. However, the potential mechanism behind nanoplastics’ neurotoxicity remains unknown. This study aimed to investigate the role of lncRNA in the depressive-like responses induced by exposure to 25 nm polystyrene nanoplastics (PS NPs). Forty mice were divided into four groups administered doses of 0, 10, 25, and 50 mg/kg via gavage for 6 months. After conducting behavioral tests, RNA sequencing was used to detect changes in mRNAs, miRNAs, and lncRNAs in the prefrontal cortex of the mice in the 0 and 50 mg/kg PS NPs groups. The results revealed that mice exposed to chronic PS NPs developed depressive-like responses in a dose-dependent manner. It was demonstrated that 987 mRNAs, 29 miRNAs, and 116 lncRNAs were significantly different between the two groups. Then, a competing endogenous RNA (ceRNA) network containing 6 lncRNAs, 18 miRNAs, and 750 mRNAs was constructed. Enrichment results suggested that PS NPs may contribute to the onset of depression-like responses through the activation of axon guidance, neurotrophin-signaling pathways, and dopaminergic synapses. This study provided evidence of the molecular relationship between PS NPs and depression-like responses. Full article
(This article belongs to the Special Issue Health Risk and Toxicity Mechanism of Nanoparticles or Ultrafine Particles Inhalation)
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