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Health Effects of Exposure to Environmental Pollutants—2nd Edition

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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 April 2026) | Viewed by 13242

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Special Issue Editors

Prof. Dr. Guang Jia

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Guest Editor

Department of Occupational & Environmental Health Sciences, School of Public Health, Peking University, Beijing 100871, 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, as well as multi-omics technology combined application)
Special Issues, Collections and Topics in MDPI journals

Dr. Zhangjian Chen

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Guest Editor

1. Department of Occupational and Environmental Health Sciences, School of Public Health, Peking University, Beijing 100191, China
2. Beijing Key Laboratory of Toxicological Research and Risk Assessment for Food Safety, School of Public Health, Peking University, Beijing 100191, China
Interests: nanotoxicology; occupational health; environmental health; heavy metal toxicology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The study of the effects of environmental pollutants on human health has received widespread attention, including whether traditional pollutants such as particulate matter and heavy metals, or new pollutants such as nanoparticles and microplastics, can have a serious impact on the environment and human health. Research into the potential toxic effects and mechanisms of environmental 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 environmental pollutants affecting humans or the environment. We encourage the use of novel 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 environmental or occupational pollutants on human exposure or health is welcomed, as well as reviews summarizing relevant recent advances.

In Volume I, we published papers exploring the impacts of various environmental exposures (including air pollutants, heavy metals, nanoparticles, etc.) on human and animal health, covering aspects like neuro damage, cell cytotoxicity, health-related associations, and genetic damage, advancing our understanding of environmental–health relationships. We focus on environmental exposure and its effects on biological systems; original research articles, communications, and reviews in this area are welcome to be submitted.

Prof. Dr. Guang Jia
Dr. Zhangjian Chen
Guest Editors

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Keywords

toxic effects
toxic mechanism
biomarkers
multi-omics techniques
nanotoxicity
heavy metals

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Published Papers (11 papers)

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Research

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15 pages, 4523 KB

Open AccessFeature PaperArticle

Co-Exposure to Food-Grade and Nano-TiO₂ with High-Fat Diet Induces Multi-Organ Injury in Liver, Intestine, Brain, and Testicles

by Ying Ma, Nairui Yu, Yi Zhang, Jiaqi Shi, Xinyan Zhou, Xiaojin Li, Li Guan, Guang Jia and Zhangjian Chen

Toxics 2026, 14(4), 350; https://doi.org/10.3390/toxics14040350 - 21 Apr 2026

Viewed by 660

Abstract

Titanium dioxide nanoparticles (TiO₂ NPs), widely used as food additives, frequently coexist with high-fat diets (HD) in modern dietary patterns, yet their combined in vivo toxicity remains poorly understood. This study investigated the multi-organ effects of co-exposure to TiO₂ NPs or food-grade E171 and HD in male C57BL/6J mice. Mice were randomly assigned to six groups and fed regular or high-fat diets containing 1 wt% TiO₂ NPs or E171 for 13 weeks. Histopathology, serum biochemistry, organ coefficients, and open-field behavioral tests were used to assess tissue injury and functional alterations. Co-exposure to TiO₂ NPs and HD markedly exacerbated tissue damage across multiple organs. In the liver, more severe ballooning degeneration, necrosis, and inflammatory infiltration were observed, accompanied by altered liver enzymes and reduced organ coefficients. Intestinal injury was characterized by crypt distortion and increased inflammation, particularly in the HD + TiO₂ group. Testicular tissues showed disorganized seminiferous tubules, loss of spermatogenic cells, and interstitial hyperplasia. In the brain, hippocampal neurons exhibited pyknosis and disarray, with decreased brain coefficients and impaired exploratory behavior. E171 induced similar but milder effects. These findings indicate that HD enhances TiO₂ NPs induced multi-organ toxicity, highlighting the health risks of realistic co-exposure to dietary nanoparticles and high-fat foods. Full article

(This article belongs to the Special Issue Health Effects of Exposure to Environmental Pollutants—2nd Edition)

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19 pages, 1418 KB

Open AccessArticle

Tissue-Specific Mercury Bioaccumulation and Probabilistic Human Health Risk in Freshwater Fish from the Arda River Reservoir Cascade (Bulgaria)

by Violina R. Angelova, Ljudmila N. Nikolova, Stanimir G. Bonev and Georgi K. Georgiev

Toxics 2026, 14(4), 291; https://doi.org/10.3390/toxics14040291 - 28 Mar 2026

Viewed by 588

Abstract

Mercury (Hg) bioaccumulation in freshwater fish represents a major pathway of human exposure, particularly in cascade reservoir systems where hydrological retention and legacy contamination can enhance methylmercury (MeHg) formation and trophic transfer. This study quantified total mercury (THg) concentrations in seven tissues of seven fish species from the Arda River cascade (Bulgaria). Multi-tissue measurements were integrated with morphometric predictors, multivariate statistical analyses, and combined deterministic and probabilistic human-health risk assessments. Muscle and liver contained the highest THg concentrations, whereas gills and gonads exhibited the lowest levels. Predatory species and larger individuals accumulated significantly more Hg, reflecting trophic magnification and size-dependent exposure. A longitudinal gradient across the cascade reservoirs suggests hydrological retention effects influencing mercury distribution. Species- and tissue-specific size–Hg relationships further indicate heterogeneous bioaccumulation dynamics among taxa. Risk assessment indicated acceptable exposure for adults and pregnant women at average consumption (140 g·week⁻¹), but elevated exposure for children consuming high-Hg predators. Monte Carlo simulations (N = 30,000) revealed upper-tail risks, while Safe Weekly Intake thresholds provided species-specific consumption limits. These findings highlight the value of integrating multi-tissue monitoring with probabilistic risk modelling to support evidence-based fish-consumption advisories in contaminated freshwater systems. Full article

(This article belongs to the Special Issue Health Effects of Exposure to Environmental Pollutants—2nd Edition)

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21 pages, 9243 KB

Open AccessArticle

Welding Fumes in a Chinese Shipyard: Exposure Characteristics and Occupational Health Risk Assessment

by Yulu Hu, Jingbo Zhang, Xiangpei Lyu, Chunhui Ni and Huanqiang Wang

Toxics 2026, 14(3), 259; https://doi.org/10.3390/toxics14030259 - 16 Mar 2026

Viewed by 894

Abstract

Welding fumes in the shipbuilding industry severely threaten workers’ health. This study systematically investigated welding fume exposure in a Chinese shipyard, analyzing mass concentration, particle size distribution, and harmful metal content using data from 2015. Differences were observed across welding sites and processes. Confined spaces and gas metal arc welding (GMAW) were associated with significantly higher exposure levels. Welding fumes were dominated by particles smaller than 1.00 μm, a distribution influenced by welding site, distance from the welding spot, and process. Iron (Fe) and manganese (Mn) were the predominant metal components, with concentrations significantly higher in respirable dust than in total dust. Risk assessment indicated minimal non-cancer hazards for Fe, zinc, and copper. However, Mn posed the predominant risk (Hazard Quotient >> 1), while nickel (Ni) and chromium (Cr) also exceeded safety thresholds at most points. Consequently, confined spaces and GMAW should be prioritized as key control targets in shipyards, as respirable dust rich in metal-bearing particles poses greater health risks. Therefore, China urgently requires the establishment of specific occupational exposure limits for respirable welding fumes. Additionally, personal sampling is more focused and efficient than area sampling for precise occupational health risk assessment due to the greater mobility of welding operations. Full article

(This article belongs to the Special Issue Health Effects of Exposure to Environmental Pollutants—2nd Edition)

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13 pages, 10215 KB

Open AccessEditor’s ChoiceArticle

Chromium(VI) Modulates Macrophage Polarization and Metabolic Reprogramming to Impair Immune Function

by Cheng Li, Ruihang Zhang, Yuhan Zhang, Hongxi Yu, Yu Zheng, Yifei Du, Shiyi Hong, Lihua Hu, Chaoyang Wang, Guang Jia and Guiping Hu

Toxics 2026, 14(2), 160; https://doi.org/10.3390/toxics14020160 - 8 Feb 2026

Viewed by 707

Abstract

Hexavalent chromium (Cr(VI)) is a recognized environmental and occupational hazard with significant implications for immune function. However, the cell-intrinsic mechanisms by which Cr(VI) coordinately reshapes macrophage polarization together with immunometabolic and mitochondrial alterations remain incompletely characterized. This study investigated how Cr(VI) exposure influences macrophage morphology, polarization, energy metabolism, and mitochondrial integrity using an in vitro model. Macrophages exposed to Cr(VI) exhibited morphological changes, including pseudopod growth and fusiform shapes, alongside a shift toward M1-type polarization. Key M1 associated biomarkers, including TNF-α, CD36, and CD80, increased 24 h after Cr(VI) exposure, whereas the M2 associated VEGFb decreased. Cr(VI) exposure also impaired energy metabolism, reducing ATP production and shifting metabolism towards glycolysis, despite increased glucose uptake. Mitochondrial damage, membrane potential collapse, and elevated oxidative stress further highlighted the immunotoxic effects of Cr(VI). Cr(VI) exposure may drive a metabolic shift in macrophages toward less efficient energy production pathways, such as glycolysis. These findings provide critical insights into Cr(VI)-induced macrophage dysfunction and emphasize the environmental risks associated with Cr(VI) pollution, underscoring the need for further mechanistic research and mitigation strategies to safeguard public health. Full article

(This article belongs to the Special Issue Health Effects of Exposure to Environmental Pollutants—2nd Edition)

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28 pages, 1924 KB

Open AccessArticle

Contamination and Health Risk Assessment of Potentially Toxic Elements in Household Dust Across the Haze Season in Upper Northern Thailand

by Kawinwut Somsunun, Teetawat Santijitpakdee, Kanyapak Kohsuwan, Natwasan Jeytawan, Sukrit Kirtsaeng, Dan Norbäck and Tippawan Prapamontol

Toxics 2025, 13(12), 1008; https://doi.org/10.3390/toxics13121008 - 21 Nov 2025

Viewed by 1305

Abstract

Indoor exposure to potentially toxic elements (PTEs) presents a global health concern, yet comprehensive seasonal assessments in Thailand remain limited, particularly during air pollution episodes. We assessed 15 PTEs in household dust collected across eight provinces of upper northern Thailand (UNT) during the haze and non-haze seasons to evaluate contamination levels, identify sources, and assess health risks. Five elements (Cr, Mo, Ni, Pb, and Zn) showed significantly higher concentrations during the haze season (p < 0.05), accompanied by corresponding increases in contamination indices and more diverse pollution sources being identified compared to the non-haze season, with Sb showing the highest enrichment degree (EF = 117.8). Source identification revealed potential enrichment from mixed anthropogenic sources, natural soil, industrial activities, agricultural inputs, and biomass burning. Health risk assessment showed that children faced unacceptable non-carcinogenic risks (HI = 2.51), increasing to 2.79 during the haze season, exceeding safe thresholds. Both adults and children experienced unacceptable carcinogenic risks from chromium exposure, particularly through inhalation during haze episodes. Total lifetime cancer risks increased from 1.20 × 10⁻⁴ to 1.74 × 10⁻⁴ for children and from 4.02 × 10⁻⁴ to 6.06 × 10⁻⁴ for adults during the haze season. These findings underscore the critical need for integrated pollution control strategies addressing biomass burning emissions to reduce indoor dust contamination and protect public health in biomass-burning-impacted regions. Full article

(This article belongs to the Special Issue Health Effects of Exposure to Environmental Pollutants—2nd Edition)

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24 pages, 3163 KB

Open AccessArticle

Social Inequalities in Exposure to Air Pollution in the EPIC Cohorts of Turin and Varese

by Mattia Costantino, Francesco Sera, Carlotta Sacerdote, Sabina Sieri, Valeria Pala, Fulvio Ricceri and Chiara Di Girolamo

Toxics 2025, 13(9), 724; https://doi.org/10.3390/toxics13090724 - 28 Aug 2025

Cited by 1 | Viewed by 1145

Abstract

In Europe, evidence on the relationship between socioeconomic position (SEP) and air pollution exposure is mixed. We assessed the association between individual SEP (education and occupation) and air pollution in the Turin and Varese European Prospective Investigation into Cancer and Nutrition cohorts. This cross-sectional study included participants enrolled between 1992–1998, categorised by three educational (high, medium, and low) and three occupational (high-, medium-, and low-skilled) levels. Air pollution exposure (2008–2011) at residential addresses was estimated using Land Use Regression models. Nitrogen dioxide (NO₂) and nitrogen oxide (NOx) data were available for both cohorts; particulate matter (PM_2.5, PM₁₀) only for Turin. Linear regression models (adjusted for sex, age, and marital status) estimated associations between SEP and annual mean pollutant concentrations (µg/m³), stratified by cohort. In Varese, lower education was associated with lower NOx exposure. In Turin, medium and low education were also linked to lower NOx exposure, though without a clear gradient. In both cohorts, individuals in medium- and low-skilled occupations had lower nitrogen exposure than those in high-skilled jobs. Associations between SEP and PM exposure in Turin were weak to null. In conclusion, lower SEP was associated with slightly lower nitrogen exposure; no clear link was found with PM. Full article

(This article belongs to the Special Issue Health Effects of Exposure to Environmental Pollutants—2nd Edition)

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12 pages, 736 KB

Open AccessArticle

Visual Search Test for Residents Chronically Exposed to Methylmercury in the Minamata Area

by Shigeru Takaoka and Kenta Matsunaga

Toxics 2025, 13(8), 657; https://doi.org/10.3390/toxics13080657 - 31 Jul 2025

Viewed by 1573

Abstract

In individuals exposed to relatively mild methylmercury, even if they appeared to be independent in activities of daily living (ADL), slower judgment and motor responses in daily activities were observed, suggesting potential cognitive impairment. To quantitatively assess this impairment, we measured reaction time (RT) in a visual search test, as a visual cognitive ability test. The study participants included 24 residents from contaminated areas with sensory impairments in the limbs but no visual field defects (E group), as well as 12 individuals from non-contaminated areas (Group C). The 24 participants from contaminated areas were further divided into two groups: 12 without hand motor coordination disorders (Group E-HA) and 12 with such disorders (Group E+HA). Participants were instructed to search for the target letter “Z” on a computer screen, and the visual stimuli consisted of two, six, or ten alphabet letters. An equal number of trials contained “Z” and did not contain “Z,” for a total of thirty trials, which were conducted twice. RT was significantly longer in Group E+HA, followed by Group E-HA, and then Group C. However, in the second test, RT decreased in all cases, with a greater reduction in the exposed groups compared to the control group. These results suggest that methylmercury exposure may cause cognitive impairment, yet it also possesses plasticity. Full article

(This article belongs to the Special Issue Health Effects of Exposure to Environmental Pollutants—2nd Edition)

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15 pages, 1978 KB

Open AccessArticle

Exposure to Metal Mixtures and Metabolic Syndrome in Residents Living near an Abandoned Lead–Zinc Mine: A Cross-Sectional Study

by Min Zhao, Qi Xu, Lingqiao Qin, Tufeng He, Yifan Zhang, Runlin Chen, Lijun Tao, Ting Chen and Qiuan Zhong

Toxics 2025, 13(7), 565; https://doi.org/10.3390/toxics13070565 - 3 Jul 2025

Viewed by 1562

Abstract

Information regarding the impact of polymetallic exposure on metabolic syndrome (MetS) among residents living near abandoned Pb-Zn mines is limited. Our objective was to investigate the impact of co-exposure to metal mixtures on the prevalence of MetS among residents. ICP-MS was used to measure the levels of 24 metals in the urine of 1744 participants, including 723 participants living near abandoned Pb-Zn mines, labeled as exposed area, and 1021 participants from other towns, labeled as reference area in the same city. Multivariable generalized linear regression, adaptive LASSO penalized regression, and BKMR were used to assess the associations between metals and MetS. The levels of eleven metals were higher, while those of nine metals were lower in the exposed area than those in the reference area. Mg, Cd, Ti, TI, Zn, Rb, and Pb were selected as important MetS predictors using LASSO regression. In exposed area, urinary Zn and TI were positively associated with MetS, whereas Mg was negatively associated with MetS. In the reference area, urinary Zn was positively associated with MetS, whereas Mg and Ti were negatively associated with MetS. The BKMR model indicates a statistically significant positive overall effect of the seven metal mixtures on MetS in the exposed area. Polymetallic exposure was positively associated with MetS risk in the abandoned Pb-Zn mining areas, suggesting that excessive Zn and TI may be associated with a higher MetS risk among residents living near abandoned Pb-Zn mines. Full article

(This article belongs to the Special Issue Health Effects of Exposure to Environmental Pollutants—2nd Edition)

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13 pages, 3193 KB

Open AccessArticle

HMGB1 as a Key Mediator in Malignant Mesothelioma and a Potential Target for Asbestos-Related Cancer Therapy

by Yi-Fang Zhong, Chan Ding, Chun-Ji Yao, Jia-Chun Wang, Min-Qian Feng, Xiao-Xue Gong, Lin Yu, Hua-Dong Xu and Hai-Ling Xia

Toxics 2025, 13(6), 448; https://doi.org/10.3390/toxics13060448 - 28 May 2025

Viewed by 1708

Abstract

Malignant mesothelioma (MM) is a highly aggressive cancer strongly associated with asbestos exposure, and accumulating evidence suggests that high mobility group box 1 (HMGB1) plays a central role in its pathogenesis. Our in vitro and in vivo experiments revealed that HMGB1 was highly expressed in MM. Both genetic and pharmacological inhibition of HMGB1 markedly suppressed MM cell viability, migration, and invasion, while inducing G1-phase cell cycle arrest and enhancing apoptosis. Interestingly, the inhibition of Toll-like receptor 4 (TLR4), achieved through both siRNA and TAK-242 treatment, not only suppressed tumor-promoting signals but also reduced HMGB1 expression, suggesting a self-amplifying HMGB1-TLR4 loop. Mechanistically, in vitro experiments indicated that suppression of HMGB1 and TLR4 was associated with decreased activation of NF-κB, AKT, and ERK pathways, which are involved in regulating MM cell survival and motility. In xenograft models, treatment with ethyl pyruvate (EP) and TAK-242 significantly suppressed tumor growth and HMGB1 expression, reinforcing their therapeutic potential. Given HMGB1’s influence on both tumor cell behavior and the immune microenvironment, targeting the HMGB1-TLR4 axis may not only provide a novel therapeutic strategy for MM but also offer insights into the mechanisms underlying asbestos-induced tumorigenesis, potentially guiding future prevention and intervention strategies in asbestos-exposed populations. Full article

(This article belongs to the Special Issue Health Effects of Exposure to Environmental Pollutants—2nd Edition)

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Review

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18 pages, 3769 KB

Open AccessReview

Genetic Polymorphisms as Modifiers of Health Risks from Exposure to Toxic Elements: A Traditional Literature Review

by Mariangela Palazzo, Andrea Borghini, Elisa Bustaffa, Silvia Baldacci, Francesca Gorini and Fabrizio Minichilli

Toxics 2026, 14(5), 375; https://doi.org/10.3390/toxics14050375 - 27 Apr 2026

Viewed by 951

Abstract

A growing body of epidemiological and toxicological evidence indicates that exposure to toxic elements (TEs), including As, Cd, Cr(VI), Pb, and Hg, is associated with a wide range of adverse health outcomes, including cancer, neurological and cardiovascular diseases. Given their widespread presence and toxicity, understanding the factors underlying inter-individual differences in susceptibility is essential, as not all exposed individuals develop the same health effects. Genetic variability, particularly single-nucleotide polymorphisms (SNPs), is increasingly recognized as a key determinant of individual responses to TE exposure. Variants in genes involved in metal transport, detoxification, and DNA repair, including DMT1, GSTP1, MT2A, hOGG1, and XRCC1, may influence internal dose and biological effects and have been proposed as potential susceptibility markers. However, current evidence remains inconsistent due to small sample sizes, heterogeneous exposure assessments, and limited considerations of ethnic diversity and gene–environment interactions. Future research should prioritize large and well-characterized populations integrating detailed exposure and lifestyle data. This review focuses on genetic susceptibility and gene–environment interactions in TE exposure, with particular emphasis on SNPs as key modulators of individual risk. It summarizes major toxic metals, reviews epidemiological evidence of the associated health risks, and highlights the role of genetic background in modulating TE-induced toxicity. Full article

(This article belongs to the Special Issue Health Effects of Exposure to Environmental Pollutants—2nd Edition)

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30 pages, 1296 KB

Open AccessReview

Spatial Patterns of Breast Cancer Risk Associated with Industrial and Environmental Pollutants: A Scoping Review

by Darashagam Nahal, Abigail Hoffpauir, Kush Kinariwala, Priscilla Tetteh, Francesca Orenge, Anjali Patel, Ashreen Ghalib and Kari Northeim

Toxics 2026, 14(2), 139; https://doi.org/10.3390/toxics14020139 - 30 Jan 2026

Viewed by 1060

Abstract

This scoping review examined published evidence linking environmental and industrial exposures to breast cancer, synthesizing studies conducted between 2015 and 2025. Using the Arksey and O’Malley framework, 51 peer-reviewed studies were identified and analyzed across five domains: study design, evidence quality, pollutant associations, geographic emphasis, and research gaps. Most studies used retrospective designs, primarily case–control, ecological, cross-sectional, and cohort approaches, which identified associations but could not establish causation. Evidence of quality varied due to heterogeneous environmental modeling methods, exposure to misclassification concerns, and unmeasured confounding, even though 86 percent of studies had sample sizes larger than 1000 cases. Pesticides, polycyclic aromatic hydrocarbons (PAHs), and polychlorinated biphenyls (PCBs) were consistently associated with breast cancer, and nitrogen oxides (NOx), particulate matter (PM), and endocrine-disrupting chemicals (EDCs) also showed frequent significant associations. Research was geographically concentrated in North America and Europe, and few studies examined industrial hotspots or low-income regions. Gaps included the need for stronger epidemiological designs, multipollutant models, standardized exposure metrics, and clearer integration of significant environmental findings into public health protections. Overall, while evidence of pollution-related breast cancer risk continued to accumulate, the precautionary principle remained largely unimplemented. Advancing environmental policy, improving exposure transparency, and incorporating hotspot-based approaches are critical for reducing pollutant burdens and strengthening cancer prevention. Full article

(This article belongs to the Special Issue Health Effects of Exposure to Environmental Pollutants—2nd Edition)

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