Abstract Heavy metals are naturally occurring components of the Earth’s crust and persistent environmental pollutants. Human exposure to heavy metals occurs via various pathways, including inhalation of air/dust particles, ingesting contaminated water or soil, or through the food chain. Their bioaccumulation may lead to diverse toxic effects affecting different body tissues and organ systems. The toxicity of heavy metals depends on the properties of the given metal, dose, route, duration of exposure (acute or chronic), and extent of bioaccumulation. The detrimental impacts of heavy metals on human health are largely linked to their capacity to interfere with antioxidant defense mechanisms, primarily through their interaction with intracellular glutathione (GSH) or sulfhydryl groups (R-SH) of antioxidant enzymes such as superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), glutathione reductase (GR), and other enzyme systems. Although arsenic (As) is believed to bind directly to critical thiols, alternative hydrogen peroxide production processes have also been postulated. Heavy metals are known to interfere with signaling pathways and affect a variety of cellular processes, including cell growth, proliferation, survival, metabolism, and apoptosis. For example, cadmium can affect the BLC-2 family of proteins involved in mitochondrial death via the overexpression of antiapoptotic Bcl-2 and the suppression of proapoptotic (BAX, BAK) mechanisms, thus increasing the resistance of various cells to undergo malignant transformation. Nuclear factor erythroid 2-related factor 2 (Nrf2) is an important regulator of antioxidant enzymes, the level of oxidative stress, and cellular resistance to oxidants and has been shown to act as a double-edged sword in response to arsenic-induced oxidative stress. Another mechanism of significant health threats and heavy metal (e.g., Pb) toxicity involves the substitution of essential metals (e.g., calcium (Ca), copper (Cu), and iron (Fe)) with structurally similar heavy metals (e.g., cadmium (Cd) and lead (Pb)) in the metal-binding sites of proteins. Displaced essential redox metals (copper, iron, manganese) from their natural metal-binding sites can catalyze the decomposition of hydrogen peroxide via the Fenton reaction and generate damaging ROS such as hydroxyl radicals, causing damage to lipids, proteins, and DNA. Conversely, some heavy metals, such as cadmium, can suppress the synthesis of nitric oxide radical (NO · ), manifested by altered vasorelaxation and, consequently, blood pressure regulation. Pb-induced oxidative stress has been shown to be indirectly responsible for the depletion of nitric oxide due to its interaction with superoxide radical (O 2 ·− ), resulting in the formation of a potent biological oxidant, peroxynitrite (ONOO − ). This review comprehensively discusses the mechanisms of heavy metal toxicity and their health effects. Aluminum (Al), cadmium (Cd), arsenic (As), mercury (Hg), lead (Pb), and chromium (Cr) and their roles in the development of gastrointestinal, pulmonary, kidney, reproductive, neurodegenerative (Alzheimer’s and Parkinson’s diseases), cardiovascular, and cancer (e.g. renal, lung, skin, stomach) diseases are discussed. A short account is devoted to the detoxification of heavy metals by chelation via the use of ethylenediaminetetraacetic acid ( EDTA), dimercaprol (BAL), 2,3-dimercaptosuccinic acid (DMSA), 2,3-dimercapto-1-propane sulfonic acid (DMPS), and penicillamine chelators. 

Heavy metals: toxicity and human health effects

High levels of toxic elements have harmful effects on all aspects of the environment (water, air, plants, etc.). Trace elements, many of which are heavy metals, can compromise soil quality, cause toxicity to plants, and ultimately contaminate the food chain. This book summarizes the effects of trace elements in the environment. Section 1 discusses the influence of trace elements on soil and the ecosystem and Section 2 examines the influence of trace elements on water. The book also discusses microplastics, which accumulate trace elements and pollute the oceans, harming both aquatic and human life. 

pdf/trace-metals-in-the-environment-33r21ct2tb.pdf

Trace Metals in the Environment

Long-term exposure to urban dust containing potentially toxic elements (PTEs) poses detrimental impacts on human health. However, studies estimating human health risks in urban dusts from a global perspective are scarce. We evaluated data for twelve PTEs in urban dusts across 59 countries from 463 published articles, including their concentrations, input sources, and probabilistic risks to human health. We found that 34.1 and 60.3% of those investigated urban dusts have been heavily contaminated with As and Cd, respectively. The input of PTEs was significantly correlated with economic structure due to emissions of industrial activities and traffic emissions being the major sources. Based on the Monte Carlo simulation, we found that the mean hazard index below the safe threshold (1.0) could still cause non-negligible risks to human health. Arsenic and Cr were the major PTEs threatening human health, and relatively high risk levels were observed in cities in China, Korea, Chile, Malaysia, and Australia. Importantly, our analysis suggested that PTEs threaten the health of approximately 92 million adults and 280 million children worldwide. Overall, our study provides important foundational understanding and guidance for policy decision-making to reduce the potential risks associated with PTE exposure and to promote sustainable development of urban economies. 

Sources and human health risks associated with potentially toxic elements (PTEs) in urban dust: A global perspective

The ligand attribute of biomolecules to form coordination bonds with metal ions led to the discovery of a novel class of materials called biomolecule-associated metal-organic frameworks (Bio-MOFs). These biomolecules coordinate in multiple ways and provide versatile applications. Far-spread bio-ligands include nucleobases, amino acids, peptides, cyclodextrins, saccharides, porphyrins/metalloporphyrin, proteins, etc. Low-toxicity, self-assembly, stability, designable and selectable porous size, the existence of rigid and flexible forms, bio-compatibility, and synergistic interactions between metal ions have led Bio-MOFs to be commercialized in industries such as sensors, food, pharma, and eco-sensing. The rapid growth and commercialization are stunted by absolute bio-compatibility issues, bulk morphology that makes it rigid to alter shape/porosity, longer reaction times, and inadequate research. This review elucidates the structural vitality, biocompatibility issues, and vital sensing applications, including challenges for incorporating bio-ligands into MOF. Critical innovations in Bio-MOFs' applicative spectrum, including sustainable food packaging, biosensing, insulin and phosphoprotein detection, gas sensing, CO2 capture, pesticide carriers, toxicant adsorptions, etc., have been elucidated. Emphasis is placed on biosensing and biomedical applications with biomimetic catalysis and sensitive sensor designing. 

Trajectory in biological metal-organic frameworks: Biosensing and sustainable strategies-perspectives and challenges.

An adverse outcome pathway (AOP) framework can be applied as an efficient tool for the rapid screening of environmental chemicals. For the development of an AOP, a database mining approach can support an expert derivation approach by gathering a wider range of evidence than in a literature review. In this study, data from various databases were integrated and analyzed to supplement the AOP leading to pulmonary fibrosis by analyzing additional evidence using a data mining approach and establishing an application domain for chemicals. First, we collected chemicals, genes, and phenotypes that were studied and related to pulmonary fibrosis through the Comparative Toxicogenomics Database (CTD). CGPD-tetramers constructed by linking each related chemical, gene, phenotype, and disease can provide the basic components for the assembly of putative AOPs. Next, an AOP network was established by connecting eight existing AOPs for pulmonary fibrosis developed by expert derivation from the AOP Wiki. Finally, the pulmonary fibrosis AOP network was proposed by integrating the AOP network from AOP Wiki and the CGPD-tetramers from the CTD. To prioritize potential chemical stressors in the AOP network, 61 chemicals were ranked using the relevance of the chemical to the AOP and chemical exposure information from the CompTox Chemicals Dashboard. The approach proposed in this study can guide the utilization of available evidence from various databases as well as the literature in constructing AOP networks related to specific diseases.

Integrative Data Mining Approach: Case Study with Adverse Outcome Pathway Network Leading to Pulmonary Fibrosis.

Heavy metals are defined as metals with relatively high density and atomic weight, and their various applications have raised serious concerns about the environmental impacts and potential human health effects. Chromium is an important heavy metal that is involved in biological metabolism, but Cr exposure can induce a severe impact on occupational workers or public health. In this study, we explore the toxic effects of Cr exposure through three exposure routes: dermal contact, inhalation, and ingestion. We propose the underlying toxicity mechanisms of Cr exposure based on transcriptomic data and various bioinformatic tools. Our study provides a comprehensive understanding of the toxicity mechanisms of different Cr exposure routes by diverse bioinformatics analyses.

/pdf/adverse-human-health-effects-of-chromium-by-exposure-route-a-16ml6o23.pdf

Adverse Human Health Effects of Chromium by Exposure Route: A Comprehensive Review Based on Toxicogenomic Approach

Formaldehyde is a colorless, pungent, highly reactive, and toxic environmental pollutant used in various industries and products. Inhaled formaldehyde is a human and animal carcinogen that causes genotoxicity, such as reactive oxygen species formation and DNA damage. This study aimed to identify the toxic effects of inhaled formaldehyde through an integrated toxicogenomic approach utilizing database information. Microarray datasets (GSE7002 and GSE23179) were collected from the Gene Expression Omnibus database, and differentially expressed genes were identified. The network analyses led to the construction of the respiratory system-related biological network associated with formaldehyde exposure, and six upregulated hub genes (AREG, CXCL2, HMOX1, PLAUR, PTGS2, and TIMP1) were identified. The expression levels of these genes were verified via qRT-PCR in 3D reconstructed human airway tissues exposed to aerosolized formaldehyde. Furthermore, NRARP was newly found as a potential gene associated with the respiratory and carcinogenic effects of formaldehyde by comparison with human in vivo and in vitro formaldehyde-exposure data. This study improves the understanding of the toxic mechanism of formaldehyde and suggests a more applicable analytic pipeline for predicting the toxic effects of inhaled toxicants. 

/pdf/network-based-integrated-analysis-for-toxic-effects-of-high-3sz49uns.pdf

Network-based integrated analysis for toxic effects of high-concentration formaldehyde inhalation exposure through the toxicogenomic approach

Network-based toxicogenomic approach to explore oral benzo(a)pyrene exposure effect on respiratory system

PURPOSE: A motion picture service method using a mobile terminal is provided so that motion pictures photographed by the mobile terminal can be received, edited, stored and output by a motion picture service server upon the user's request. CONSTITUTION: A network access unit(11) receives motion pictures from a mobile terminal through a mobile communication network(20). A user authentication unit(12) receives user information from the network access unit(11) and authenticates a user. A motion picture receiving unit(13) receives the motion pictures from the network access unit(11). A motion picture storing unit(14) receives the motion pictures from the motion picture receiving unit(13), and stores them in a database(16). A motion picture search unit(17) receives motion picture search conditions from the network access unit(11), searches contents in the database(16) and transmits them to the mobile terminal. A motion picture editing unit(15) receives motion picture edition conditions from the network access unit(11), edits the motion pictures stored in the database(16), and transmits them to the mobile terminal. When the mobile terminal accesses a motion picture service server through the mobile communication network, photographs the motion pictures, and transmits them to the motion picture service server, the motion picture service server stores, edits and outputs the motion pictures.

Motion picture service method using mobile terminal

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Adverse Human Health Effects of Chromium by Exposure Route: A Comprehensive Review Based on Toxicogenomic Approach

Network-based integrated analysis for toxic effects of high-concentration formaldehyde inhalation exposure through the toxicogenomic approach

Network-based toxicogenomic approach to explore oral benzo(a)pyrene exposure effect on respiratory system

Motion picture service method using mobile terminal