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

Deadline for manuscript submissions: closed (30 August 2023) | Viewed by 10603

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Special Issue Editors

Dr. Zhangjian Chen

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Guest Editor

School of Public Health, Peking University, Beijing, China
Interests: nanotoxicology; toxicity of titanium dioxide nanoparticles; occupational health; environmental health; genotoxicity of nanomaterials
Special Issues, Collections and Topics in MDPI journals

Prof. Dr. Guang Jia

E-Mail Website
Guest Editor

School of Public Health, Peking University, Beijing, China
Interests: mechanism and prevention of occupational and environmental pollutants (including nano-toxicology research, health risk assessment of heavy metals, biological monitoring and biomarker research, and multi-omics technology combined application)
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The impact of occupational and environmental pollutants on human health has received widespread attention. Pollutants that can occur in both the workplace and the environment require special attention due to their large impact range, and the question of whether traditional pollutants such as heavy metals, or new pollutants such as nanomaterials, can cause serious impacts on occupational workers or the environment. Research on the potential toxic effects and mechanisms of environmental and occupational pollutants can provide a scientific basis for related prevention work.

The purpose of this Special Issue is to publish research on the potential toxicity and mechanisms of occupational and environmental pollutants on humans or the environment. We encourage the use of new methods such as multi-omics techniques, or research on new pollutants such as nanomaterials. Research using biomarkers to conduct biological monitoring to assess the impact of exposure to environmental or occupational pollutants on human health is also included in the scope. Reviews summarizing relevant recent advances are also welcome.

Dr. Zhangjian Chen
Prof. Dr. Guang Jia
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. 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

titanium dioxide nanoparticles
nanotoxicity
toxic effects
environmental impact
human health

Published Papers (7 papers)

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Research

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15 pages, 5168 KiB

Open AccessArticle

The Associations between Exposure to Multiple Heavy Metals and Total Immunoglobulin E in U.S. Adults

by Xin Song, Xiaowen Ding, Piye Niu, Tian Chen and Tenglong Yan

Toxics 2024, 12(2), 116; https://doi.org/10.3390/toxics12020116 - 30 Jan 2024

Viewed by 955

Abstract

Immunoglobulin E (IgE) is a type of immunoglobulin, and elevated serum total IgE is often present in allergic diseases. Exposure to environmental heavy metals has been markedly linked to allergic diseases, leading to elevated total IgE levels. However, studies concerning the effects of multiple metal exposures on total IgE levels are limited. Therefore, the current study seeks to explore the correlation between heavy-metal co-exposure and total IgE levels based on the National Health and Nutrition Examination Survey (NHANES, 2005–2006). Participants possessed complete data on total IgE levels, 11 urinary metal concentrations and other covariates. The correlations between 11 metals and total IgE levels were analyzed using multiple linear regression, and total IgE levels were a continuous variable. Total IgE levels exceeding 150 kU/L were considered sensitized. Binary logistic regression analyses were employed to assess the correlation between metal exposure and the occurrence of an allergic state. Then, the association between co-exposure to the 11 metals and total IgE levels or the occurrence of sensitization status was further analyzed by Bayesian kernel machine regression (BKMR), a multi-contaminant model. There were 1429 adults with complete data included. Based on the median concentration, molybdenum (Mo) had the highest concentration (46.60 μg/L), followed by cesium (Cs), barium (Ba), lead (Pb), and mercury (Hg). And the median (interquartile range) for total IgE levels was 43.7 (17.3, 126.0) kU/L. Multiple linear regression results showed that Pb was significantly and positively associated with total IgE levels (β = 0.165; 95% CI: 0.046, 0.284). Binary logistic regression showed a significant positive correlation between urinary Pb (OR: 1.258; 95% CI: 1.052, 1.510) and tungsten (W) (OR: 1.251; 95% CI: 1.082, 1.447). Importantly, the BKMR model found a positive correlation between combined-metal exposure and total IgE levels and the occurrence of sensitization status. The mixed heavy-metal exposure was associated with increased total IgE levels, and this association may be driven primarily by the exposure of Pb and W. This study provides new insights into the relationship between heavy-metal exposure and allergic diseases. More research is needed to confirm these findings. Full article

(This article belongs to the Special Issue Toxicity and Mechanisms of Occupational and Environmental Pollutants)

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13 pages, 2191 KiB

Open AccessArticle

Thioredoxin 1 and Thioredoxin Reductase 1 Redox System Is Dysregulated in Neutrophils of Subjects with Autism: In Vitro Effects of Environmental Toxicant, Methylmercury

by Samiyah Alshehri, Sheikh F. Ahmad, Norah A. Albekairi, Sana S. Alqarni, Naif O. Al-Harbi, Laila Y. Al-Ayadhi, Sabry M. Attia, Ali S. Alfardan, Saleh A. Bakheet and Ahmed Nadeem

Toxics 2023, 11(9), 739; https://doi.org/10.3390/toxics11090739 - 29 Aug 2023

Cited by 3 | Viewed by 1061

Abstract

Autism spectrum disorder (ASD) is a complex developmental disorder in children that results in abnormal communicative and verbal behaviors. Exposure to heavy metals plays a significant role in the pathogenesis or progression of ASD. Mercury compounds pose significant risk for the development of ASD as children are more exposed to environmental toxicants. Increased concentration of mercury compounds has been detected in different body fluids/tissues in ASD children, which suggests an association between mercury exposure and ASD. Thioredoxin1 (Trx1) and thioredoxin reductase1 (TrxR1) redox system plays a crucial role in detoxification of oxidants generated in different immune cells. However, the effect of methylmercury and the Nrf2 activator sulforaphane on the Trx1/TrxR1 antioxidant system in neutrophils of ASD subjects has not been studied previously. Therefore, this study examined the effect of methylmercury on Trx1/TrxR1 expression, TrxR activity, nitrotyrosine, and ROS in neutrophils of ASD and TDC subjects. Our study shows that Trx1/TrxR1 protein expression is dysregulated in ASD subjects as compared to the TDC group. Further, methylmercury treatment significantly inhibits the activity of TrxR in both ASD and TDC groups. Inhibition of TrxR by mercury is associated with upregulation of the Trx1 protein in TDC neutrophils but not in ASD neutrophils. Furthermore, ASD neutrophils have exaggerated ROS production after exposure to methylmercury, which is much greater in magnitude than TDC neutrophils. Sulforaphane reversed methylmercury-induced effects on neutrophils through Nrf2-mediated induction of the Trx1/TrxR1 system. These observations suggest that exposure to the environmental toxicant methylmercury may elevate systemic oxidative inflammation due to a dysregulated Trx1/TrxR1 redox system in the neutrophils of ASD subjects, which may play a role in the progression of ASD. Full article

(This article belongs to the Special Issue Toxicity and Mechanisms of Occupational and Environmental Pollutants)

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11 pages, 1724 KiB

Open AccessArticle

Independent and Combined Associations of Blood Manganese, Cadmium and Lead Exposures with the Systemic Immune-Inflammation Index in Adults

by Qiya Zhong, Wenxin Zhou, Jiaqi Lin, Wen Sun, Yao Qin, Xiang Li and Huadong Xu

Toxics 2023, 11(8), 659; https://doi.org/10.3390/toxics11080659 - 01 Aug 2023

Cited by 2 | Viewed by 1271

Abstract

Manganese (Mn), cadmium (Cd) and lead (Pb) have toxic effects on the immune system. However, their independent and combined effects on immune-inflammation responses are unclear. In recent years, the systemic immune-inflammation index (SII) has been developed as an integrated and novel inflammatory indicator. A retrospective cross-sectional study of 2174 adults ≥20 years old from the National Health and Nutrition Examination Survey (NHANES) 2015–2016 was conducted. Generalized linear models were used to evaluate the independent and combined associations of SII with blood Mn, Cd and Pb levels. As continuous variables, both blood Cd and Mn showed dose-dependent relationships with the SII before and after adjusting for all potential confounding factors. Metal concentrations were then converted into categorical variables. Compared with the adults in the lowest Cd or Mn tertile, those in the highest tertile had higher risks of elevated SII. Furthermore, co-exposure to Mn and Cd also showed a positive relationship with the SII after adjusting for all confounding factors. However, the single effect of Pb exposure and the joint effect of Pb and other metal exposures on the SII were not observed. This study provides important epidemiological evidence of the associations of SII with single and co-exposure effects of blood Mn, Cd, and Pb. Full article

(This article belongs to the Special Issue Toxicity and Mechanisms of Occupational and Environmental Pollutants)

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13 pages, 5419 KiB

Open AccessFeature PaperArticle

Long Non-Coding RNA Expression Profile Alteration Induced by Titanium Dioxide Nanoparticles in HepG2 Cells

by Jiaqi Shi, Yi Zhang, Ying Ma, Zhangjian Chen and Guang Jia

Toxics 2022, 10(12), 724; https://doi.org/10.3390/toxics10120724 - 25 Nov 2022

Cited by 1 | Viewed by 1227

Abstract

The liver is considered the major target organ affected by oral exposure to titanium dioxide nanoparticles (TiO₂ NPs), but the mechanism of hepatotoxicity is not fully understood. This study investigated the effect of TiO₂ NPs on the expression profile of long non-coding RNA (lncRNA) in hepatocytes and tried to understand the potential mechanism of hepatotoxicity through bioinformatics analysis. The human hepatocellular carcinoma cells (HepG2) were treated with TiO₂ NPs at doses of 0–200 μg/mL for 48 h and then RNA sequencing was implemented. The differential lncRNAs between the control and TiO₂ NPs-treated groups were screened, then the lncRNA–mRNA network and enrichment pathways were analyzed via multivariate statistics. As a result, 46,759 lncRNAs were identified and 129 differential lncRNAs were screened out. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showed that the targeted mRNAs of those differential lncRNAs were enriched in the Hedgehog signaling pathway, Vasopressin-regulated water reabsorption, and Glutamatergic synapse. Moreover, two lncRNA–mRNA networks, including lncRNA NONHSAT256380.1-JRK and lncRNA NONHSAT173563.1-SMIM22, were verified by mRNA detection. This study demonstrated that an alteration in the lncRNA expression profile could be induced by TiO₂ NPs and epigenetics may play an important role in the mechanism of hepatotoxicity. Full article

(This article belongs to the Special Issue Toxicity and Mechanisms of Occupational and Environmental Pollutants)

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Review

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16 pages, 858 KiB

Open AccessReview

Association between Air Pollution and Lipid Profiles

by Yi Zhang, Jiaqi Shi, Ying Ma, Nairui Yu, Pai Zheng, Zhangjian Chen, Tiancheng Wang and Guang Jia

Toxics 2023, 11(11), 894; https://doi.org/10.3390/toxics11110894 - 31 Oct 2023

Cited by 2 | Viewed by 1815

Abstract

Dyslipidemia is a critical factor in the development of atherosclerosis and consequent cardiovascular disease. Numerous pieces of evidence demonstrate the association between air pollution and abnormal blood lipids. Although the results of epidemiological studies on the link between air pollution and blood lipids are unsettled due to different research methods and conditions, most of them corroborate the harmful effects of air pollution on blood lipids. Mechanism studies have revealed that air pollution may affect blood lipids via oxidative stress, inflammation, insulin resistance, mitochondrial dysfunction, and hypothalamic hormone and epigenetic changes. Moreover, there is a risk of metabolic diseases associated with air pollution, including fatty liver disease, diabetes mellitus, and obesity, which are often accompanied by dyslipidemia. Therefore, it is biologically plausible that air pollution affects blood lipids. The overall evidence supports that air pollution has a deleterious effect on blood lipid health. However, further research into susceptibility, indoor air pollution, and gaseous pollutants is required, and the issue of assessing the effects of mixtures of air pollutants remains an obstacle for the future. Full article

(This article belongs to the Special Issue Toxicity and Mechanisms of Occupational and Environmental Pollutants)

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29 pages, 4605 KiB

Open AccessReview

Genotoxicity Evaluation of Titanium Dioxide Nanoparticles In Vivo and In Vitro: A Meta-Analysis

by Yue Cao, Jinyao Chen, Qian Bian, Junyu Ning, Ling Yong, Tong Ou, Yan Song and Sheng Wei

Toxics 2023, 11(11), 882; https://doi.org/10.3390/toxics11110882 - 27 Oct 2023

Viewed by 1334

Abstract

Background: Recent studies have raised concerns about genotoxic effects associated with titanium dioxide nanoparticles (TiO₂ NPs), which are commonly used. This meta-analysis aims to investigate the potential genotoxicity of TiO₂ NPs and explore influencing factors. Methods: This study systematically searched Chinese and English literature. The literature underwent quality evaluation, including reliability evaluation using the toxicological data reliability assessment method and relevance evaluation using routine evaluation forms. Meta-analysis and subgroup analyses were performed using R software, with the standardized mean difference (SMD) as the combined effect value. Results: A total of 26 studies met the inclusion criteria and passed the quality assessment. Meta-analysis results indicated that the SMD for each genotoxic endpoint was greater than 0. This finding implies a significant association between TiO₂ NP treatment and DNA damage and chromosome damage both in vivo and in vitro and gene mutation in vitro. Subgroup analysis revealed that short-term exposure to TiO₂ NPs increased DNA damage. Rats and cancer cells exhibited heightened susceptibility to DNA damage triggered by TiO₂ NPs (p < 0.05). Conclusions: TiO₂ NPs could induce genotoxicity, including DNA damage, chromosomal damage, and in vitro gene mutations. The mechanism of DNA damage response plays a key role in the genotoxicity induced by TiO₂ NPs. Full article

(This article belongs to the Special Issue Toxicity and Mechanisms of Occupational and Environmental Pollutants)

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16 pages, 6608 KiB

Open AccessFeature PaperReview

Effect of Nanomaterials on Gut Microbiota

by Ying Ma, Jiahe Zhang, Nairui Yu, Jiaqi Shi, Yi Zhang, Zhangjian Chen and Guang Jia

Toxics 2023, 11(4), 384; https://doi.org/10.3390/toxics11040384 - 17 Apr 2023

Cited by 4 | Viewed by 2022

Abstract

Nanomaterials are widely employed in everyday life, including food and engineering. Food additives on a nanoscale can enter the body via the digestive tract. The human gut microbiota is a dynamically balanced ecosystem composed of a multitude of microorganisms that play a crucial role in maintaining the proper physiological function of the digestive tract and the body’s endocrine coordination. While the antibacterial capabilities of nanomaterials have received much interest in recent years, their impacts on gut microbiota ought to be cautioned about and explored. Nanomaterials exhibit good antibacterial capabilities in vitro. Animal studies have revealed that oral exposure to nanomaterials inhibits probiotic reproduction, stimulates the inflammatory response of the gut immune system, increases opportunistic infections, and changes the composition and structure of the gut microbiota. This article provides an overview of the impacts of nanomaterials, particularly titanium dioxide nanoparticles (TiO₂ NPs), on the gut microbiota. It advances nanomaterial safety research and offers a scientific foundation for the prevention, control, and treatment of illnesses associated with gut microbiota abnormalities. Full article

(This article belongs to the Special Issue Toxicity and Mechanisms of Occupational and Environmental Pollutants)

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