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A special issue of International Journal of Environmental Research and Public Health (ISSN 1660-4601). This special issue belongs to the section "Toxicology and Public Health".

Deadline for manuscript submissions: closed (31 October 2019) | Viewed by 45559

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Dr. Cristina M. L. Carvalho

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Research Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, Universidade de Lisboa, Av. Prof. Gama Pinto, 1649-003 Lisboa, Portugal
Interests: molecular mechanisms of toxicity; thioredoxin and glutaredoxin systems; cancer; mercury and methylmercury toxicity; environmental and human risk assessment; biomarkers & food safety
Special Issues, Collections and Topics in MDPI journals

Dr. Vasco Branco

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1. Research Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, Universidade de Lisboa, 1649-003 Lisboa, Portugal
2. Centro de Investigação Interdisciplinar Egas Moniz (CiiEM), Instituto Universitário Egas Moniz (IUEM), Quinta da Granja, Monte de Caparica, 2829-511 Caparica, Portugal
Interests: mercury toxicity; selenium and selenoproteins; redox active systems; mechanisms of toxicity
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Metals differ from other toxic substances, because, as elements, they are neither created nor destroyed by humans; they exist in the environment and sometimes exert toxicity independent of environmental pollution, although anthropogenic contribution tends to concentrate metals in the biosphere and contributes to human exposure through water and food ingestion. Epidemiological evaluations of subpopulations at higher risk such as pregnant women, children, and occupationally exposed workers are among the concerns of worldwide organizations.

Knowledge of molecular mechanisms of metals toxicity has been improving, especially in recent years, yet there are gaps, and studies contributing to clarify them are very welcome.

The aim of this Special Issue is to review metals’ (including metalloids) toxicity, to identify and characterize hazards in order to protect human populations from the risks associated with exposure. Emphasis will be given to metals that alone, as part of complexes, or conjugated with molecules produce significant toxicity to humans. These include mercury, cadmium, arsenic, lead, and chromium, but also essential metals with potential for toxicity and metal-based therapeutic agents requiring a risk-benefit analysis.

Contributions, in the form of review, research papers and case studies, should be related to the following topics:

Metals Toxicity (Neurotoxicity, Carcinogenicity, Immunotoxicity, etc.)
Metals Fate in the Environment and Consequences for Toxicity
The Chemical Mechanisms of Metal Toxicity
Factors Impacting Metal Toxicity
Biomarkers of Metal Exposure, Effect and Susceptibility
Molecular Responses to Metal Exposure
Metal-Binding Proteins and Metal Transporters
Chelation and Treatment of Metals Intoxication

Dr. Cristina M. L. Carvalho
Dr. Vasco Branco
Guest Editors

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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. International Journal of Environmental Research and Public Health is an international peer-reviewed open access monthly journal published by MDPI.

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Keywords

Human exposure to metals
Metals' mechanisms of toxicity
Toxic effects of metals
Biomarkers
Risk Assessment
Therapeutics

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Published Papers (9 papers)

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Research

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18 pages, 1720 KiB

Open AccessArticle

Toxicity Evaluation of Quantum Dots (ZnS and CdS) Singly and Combined in Zebrafish (Danio rerio)

by Beatriz Matos, Marta Martins, Antonio Cid Samamed, David Sousa, Isabel Ferreira and Mário S. Diniz

Int. J. Environ. Res. Public Health 2020, 17(1), 232; https://doi.org/10.3390/ijerph17010232 - 28 Dec 2019

Cited by 28 | Viewed by 4588

Abstract

The exponential growth of nanotechnology has led to the production of large quantities of nanomaterials for numerous industrial, technological, agricultural, environmental, food and many other applications. However, this huge production has raised growing concerns about the adverse effects that the release of these nanomaterials may have on the environment and on living organisms. Regarding the effects of QDs on aquatic organisms, existing data is scarce and often contradictory. Thus, more information is needed to understand the mechanisms associated with the potential toxicity of these nanomaterials in the aquatic environment. The toxicity of QDs (ZnS and CdS) was evaluated in the freshwater fish Danio rerio. The fishes were exposed for seven days to different concentrations of QDs (10, 100 and 1000 µg/L) individually and combined. Oxidative stress enzymes (catalase, superoxide dismutase and glutathione S-transferase), lipid peroxidation, HSP70 and total ubiquitin were assessed. In general, results suggest low to moderate toxicity as shown by the increase in catalase activity and lipid peroxidation levels. The QDs (ZnS and CdS) appear to cause more adverse effects singly than when tested combined. However, LPO results suggest that exposure to CdS singly caused more oxidative stress in zebrafish than ZnS or when the two QDs were tested combined. Levels of Zn and Cd measured in fish tissues indicate that both elements were bioaccumulated by fish and the concentrations increased in tissues according to the concentrations tested. The increase in HSP70 measured in fish exposed to 100 µg ZnS-QDs/L may be associated with high levels of Zn determined in fish tissues. No significant changes were detected for total ubiquitin. More experiments should be performed to fully understand the effects of QDs exposure to aquatic biota. Full article

(This article belongs to the Special Issue Metal Exposure and Health Risk Assessment)

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24 pages, 3673 KiB

Open AccessArticle

Human Health Risk Assessment and Potentially Harmful Element Contents in the Fruits Cultivated in the Southern Poland

by Agnieszka Gruszecka-Kosowska

Int. J. Environ. Res. Public Health 2019, 16(24), 5096; https://doi.org/10.3390/ijerph16245096 - 13 Dec 2019

Cited by 11 | Viewed by 2911

Abstract

The presence of potentially harmful elements (PHEs) in popularly consumed fruits in Poland was determined by inductively coupled plasma mass spectrometry. The As, Cd, Co, Cr, Cu, Hg, Ni, Pb, Se, Sb, Tl, and Zn contents were investigated in 21 fruit species grouped as berry, pome, stone, and shell fruits. The PHE contents belonged to the following ranges (mg/kg wet weight): Cd < limit of detection (LOD)–0.116, Co < LOD–0.062, Cu < LOD–15.5, Ni < LOD–2.23, Pb < LOD–2.07, Sb < LOD–0.240, Tl < LOD–0.110, and Zn 0.37–37.7. Their concentrations exceeded the maximum allowable concentration (MAC) set by European Union regulation for Pb only. Bioconcentration coefficient (BC) values, calculated in accordance to the PHE contents in exchangeable and acid soluble forms in soil after first step of the Community Bureau of Reference (BCR) sequential extraction procedure, revealed that berry fruits had potential for accumulation of Cu, Ni, Sb, and Tl; stone fruits—Cu, Sb, and Tl; pome fruits—Cu, Ni, and Sb, and shell fruit (walnut)—Cu. Human health risk assessment associated with the intake of PHEs in fruits was evaluated in terms of daily intake rates (DIR), and carcinogenic and non-carcinogenic risk by cancer risk (CR) and hazard quotient (HQ), respectively. For Pb margin of exposure (MOE) approach was used for health risk evaluation. Daily intake rates for all PHEs were below the provisional maximum tolerable daily intake (PMTDI) values. The mean total non-carcinogenic risk values were the following: berry fruits HQ = 0.47, pome fruits HQ = 0.36, stone fruits HQ = 0.42, and shell fruits (walnut) HQ = 0.22, indicating no health hazards. The carcinogenic risk for As in walnut only under an adult intake scenario (CR = 1.98 × 10⁻⁶) was found to be above the acceptable risk level. The mean Pb health risk, according to Polish statistical intake rates, was acceptable low as the MOE value was equal to 15.7 for adults. In reference to the intake rates recommended by United States Environmental Protection Agency (USEPA), MOE values for Pb indicated acceptable low risk both for adults (MOE = 14.0) and children (MOE = 1.64). In general, the finding of this research revealed no health risk arising from PHE consumption with fruits for the population of Poland. Full article

(This article belongs to the Special Issue Metal Exposure and Health Risk Assessment)

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11 pages, 1372 KiB

Open AccessArticle

In Vitro Assessment of the Efficacy of a Macrocyclic Chelator in Reversing Methylmercury Toxicity

by Paula Nobre, Maria de Fátima Cabral, Judite Costa, Margarida Castro-Caldas, Cristina Carvalho and Vasco Branco

Int. J. Environ. Res. Public Health 2019, 16(23), 4817; https://doi.org/10.3390/ijerph16234817 - 30 Nov 2019

Cited by 2 | Viewed by 2626

Abstract

Methylmercury (MeHg) is a highly neurotoxic compound to which human populations are exposed via fish consumption. Once in cells, MeHg actively binds thiols and selenols, interfering with the activity of redox enzymes such as thioredoxin (Trx) and the selenoenzyme thioredoxin reductase (TrxR) which integrate the thioredoxin system. In fact, it has been shown that inhibition of this system by MeHg is a critical step in the unfolding of cell death. Current clinical approaches to mitigate the toxicity of MeHg rely on the use of chelators, such as meso-2,3-dimercaptosuccinic acid (DMSA) which largely replaced British anti-Lewisite or 2,3-dimercapto-1-propanol (BAL) as the prime choice. However, therapeutic efficacy is limited and therefore new therapeutic options are necessary. In this work, we evaluated the efficacy of a macrocyclic chelator, 1-thia-4,7,10,13-tetraazacyclopentadecane ([15]aneN₄S), in preventing MeHg toxicity, namely by looking at the effects over relevant molecular targets, i.e., the thioredoxin system, using both purified enzyme solutions and cell experiments with human neuroblastoma cells (SH-SY5Y). Results showed that [15]aneN₄S had a similar efficacy to DMSA and BAL in reversing the inhibition of MeHg over purified TrxR and Trx by looking at both the 5,5′-dithiobis(2-nitrobenzoic acid) (DTNB) reduction assay and insulin reduction capability. In experiments with cells, none of the chelating agents could reverse the inhibition of TrxR by MeHg, which corroborates the high affinity of MeHg to the selenol in TrxR active site. [15]aneN₄S and BAL, unlike DMSA, could prevent inhibition of Trx, which allows the maintenance of downstream functions, although BAL showed higher toxicity to cells. Overall these findings highlight the potential of using [15]aneN₄S in the treatment of MeHg poisoning and encourage further studies, namely in vivo. Full article

(This article belongs to the Special Issue Metal Exposure and Health Risk Assessment)

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12 pages, 2193 KiB

Open AccessArticle

Influence of Iron on Cytotoxicity and Gene Expression Profiles Induced by Arsenic in HepG2 Cells

by Yonghua Wang, Yuxuan Liu, Su Liu and Bing Wu

Int. J. Environ. Res. Public Health 2019, 16(22), 4484; https://doi.org/10.3390/ijerph16224484 - 14 Nov 2019

Cited by 5 | Viewed by 2589

Abstract

The toxicity of arsenic (As) could be influenced by many environmental factors and elements. Iron (Fe) is one of the elements that could be involved in As-induced toxicity. In this study, the interactive effects of Fe and As in HepG2 cells were analyzed based on cytotoxicity and transcriptomic analyses. The results showed that Fe could decrease cell viability and increase mitochondrial depolarization induced by As exposure. Oxidative stress and damage have been proven to be one of the main mechanisms of As toxicity. Our results showed that Fe increased the generation of reactive oxygen species (ROS) and lipid peroxidation product malondialdehyde (MDA) induced by As exposure. Microarray analysis further verified that Fe increased the alteration of gene expression and biological processes related to oxidative stress, cell proliferation, and the apoptotic signaling pathway caused by As exposure. Both results of cytotoxicity and transcriptomic analyses suggest that an increase of Fe in the human body could increase the As-induced toxicity, which should be considered during the health risk assessment of As. Full article

(This article belongs to the Special Issue Metal Exposure and Health Risk Assessment)

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12 pages, 1115 KiB

Open AccessArticle

Association of Typical Toxic Heavy Metals with Schizophrenia

by Jiahui Ma, Lailai Yan, Tongjun Guo, Siyu Yang, Chen Guo, Yaqiong Liu, Qing Xie and Jingyu Wang

Int. J. Environ. Res. Public Health 2019, 16(21), 4200; https://doi.org/10.3390/ijerph16214200 - 30 Oct 2019

Cited by 17 | Viewed by 4421

Abstract

Toxic heavy metals (THMs) are contaminants commonly found in the environment. Although a large number of studies have demonstrated their damage to the biological functions of the human being, their potential associations with the risk of developing schizophrenia remain controversial. In this study, we investigated the associations between four THMs (chromium (Cr), cadmium (Cd), lead (Pb) and arsenic (As)) in serum and the risk of schizophrenia. In total, 95 patients with schizophrenia (cases) and 95 normal subjects (controls) were recruited from Hebei Province, China. The serum concentrations of the 4 THMs were analyzed by inductively coupled plasma mass spectrometry (ICP-MS). A higher concentration of Pb was found significantly associated with an elevated risk of schizophrenia (OR = 3.146; 95%CI: 1.238–7.994, p = 0.016), while significant association for the other three THMs were not observed. Besides, significant correlations were found between the metabolic biomarkers and the concentrations of Pb and As, respectively. In order to further characterize the association between these THMs and schizophrenia with greater statistical power, we conducted meta-analysis by including 538 cases and 1040 controls from the current study and 5 available datasets published from 2002 to 2018. Using a random-effect model, Cr was significantly associated with schizophrenia (SMD = 0.3246; 95%CI: 0.0166–0.6326, p < 0.01). Overall, this study suggested that higher levels of Pb and Cr may be one of the factors associated with an elevated risk of schizophrenia. Full article

(This article belongs to the Special Issue Metal Exposure and Health Risk Assessment)

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17 pages, 3078 KiB

Open AccessArticle

The Neuroprotective Role of Coenzyme Q10 Against Lead Acetate-Induced Neurotoxicity Is Mediated by Antioxidant, Anti-Inflammatory and Anti-Apoptotic Activities

by Al Omar S. Yousef, Alkhuriji A. Fahad, Ahmed E. Abdel Moneim, Dina M. Metwally, Manal F. El-khadragy and Rami B. Kassab

Int. J. Environ. Res. Public Health 2019, 16(16), 2895; https://doi.org/10.3390/ijerph16162895 - 13 Aug 2019

Cited by 85 | Viewed by 6302

Abstract

Heavy metal exposure, in lead (Pb) particularly, is associated with severe neuronal impairment though oxidative stress mediated by reactive oxygen species, and antioxidants may be used to abolish these adverse effects. This study investigated the potential neuroprotective role of coenzyme Q10 (CoQ₁₀) against lead acetate (PbAc)-induced neurotoxicity. Twenty-eight male Wistar albino rats were divided into four equal groups (n = 7) and treated as follows: the control group was injected with physiological saline (0.9% NaCl); the CoQ₁₀ group was injected with CoQ₁₀ (10 mg/kg); PbAc group was injected with PbAc (20 mg/kg); PbAc + CoQ₁₀ group was injected first with PbAc, and after 1 h with CoQ₁₀. All groups were injected intraperitoneally for seven days. PbAc significantly increased cortical lipid peroxidation, nitrate/nitrite levels, and inducible nitric oxide synthase expression, and decreased glutathione content, superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase activity and mRNA expression, as well as nuclear factor erythroid 2–related factor 2 (Nrf2) and homoxygenase-1 (HO-1) expression. PbAc also promoted the secretion of interleukin-1ß and tumor necrosis factor-α, inhibited interleukin-10 production, triggered the activation of pro-apoptotic proteins, and suppressed anti-apoptotic proteins. Additionally, PbAc increased the cortical levels of serotonin, dopamine, norepinephrine, GABA, and glutamate, and decreased the level of ATP. However, treatment with CoQ₁₀ rescued cortical neurons from PbAc-induced neurotoxicity by restoring the balance between oxidants and antioxidants, activating the Nrf2/HO-1 pathway, suppressing inflammation, inhibiting the apoptotic cascade, and modulating cortical neurotransmission and energy metabolism. Altogether, our findings indicate that CoQ₁₀ has beneficial effects against PbAc-induced neuronal damage through its antioxidant, anti-inflammatory, anti-apoptotic, and neuromodulatory activities. Full article

(This article belongs to the Special Issue Metal Exposure and Health Risk Assessment)

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24 pages, 590 KiB

Open AccessArticle

Neurotoxicity, Behavior, and Lethal Effects of Cadmium, Microplastics, and Their Mixtures on Pomatoschistus microps Juveniles from Two Wild Populations Exposed under Laboratory Conditions―Implications to Environmental and Human Risk Assessment

by Tiago Miranda, Luis R. Vieira and Lúcia Guilhermino

Int. J. Environ. Res. Public Health 2019, 16(16), 2857; https://doi.org/10.3390/ijerph16162857 - 10 Aug 2019

Cited by 91 | Viewed by 5834

Abstract

Microplastics (MPs) were found to modulate the toxicity of other pollutants but the knowledge on the topic is still limited. The goals of this study were to investigate the short-term toxicity of cadmium (Cd) to wild Pomatochistus microps juveniles, the potential modulation of acute Cd toxicity by 1–5 µm polyethylene MPs in this species, and possible differences of sensitivity to Cd and MPs-Cd mixtures between juveniles from two distinct wild populations. Juveniles were collected in the estuaries of Minho (M-est) and Lima (L-est) Rivers (NW Portugal). One 96 h bioassay with M-est juveniles and another one with L-est juveniles were carried out in laboratory conditions. Each bioassay had 12 treatments: control, 5 Cd concentrations, 1 MPs concentration, and 5 MPs-Cd mixtures. No significant differences in Cd-induced mortality between juveniles from distinct estuaries or between juveniles exposed to Cd alone and those exposed to MPs-Cd mixtures were found. The total 96h LC₁₀ and LC₅₀ of Cd alone were 2 mg/L (95% CI: 0–4 mg/L) and 8 mg/L (95% CI: 2–17 mg/L), respectively. Cd alone significantly decreased the post-exposure predatory performance (PEPP) of M-est (≥6 mg/L) and L-est juveniles (≥3 mg/L), and acetylcholinesterase (AChE) activity of M-est juveniles (13 mg/L). MPs alone (0.14 mg/L) significantly reduced the PEPP and AChE activity of L-est juveniles but not of M-est juveniles. MPs-Cd mixtures (3–13 mg/L of Cd + 0.14 mg/L of MPs) significantly inhibited the PEPP of juveniles from both estuaries and AChE of L-est estuary juveniles but not of M-est juveniles. Evidences of toxicological interactions, namely antagonism, between MPs and Cd were found. Overall, the results indicate that MPs modulated the sub-lethal toxic effects of Cd in wild P. microps juveniles, especially neurotoxicity. Moreover, the environmental conditions of the natural habitats to which juveniles were exposed during pre-developmental phases influence the sub-lethal toxicity of Cd, MPs, and their mixtures. The implications to environmental and human risk assessment are discussed and further research is needed. Full article

(This article belongs to the Special Issue Metal Exposure and Health Risk Assessment)

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10 pages, 1149 KiB

Open AccessArticle

Heavy Metals in California Women Living in a Gold Mining-Impacted Community

by Julie Von Behren, Ruiling Liu, Jane Sellen, Christine N. Duffy, Ryszard Gajek, Key-Young Choe, Josephine DeGuzman, M. Katy Janes, Joanne Hild and Peggy Reynolds

Int. J. Environ. Res. Public Health 2019, 16(13), 2252; https://doi.org/10.3390/ijerph16132252 - 26 Jun 2019

Cited by 5 | Viewed by 6585

Abstract

Gold mining activities occurred throughout the foothills of the Sierra Nevada Mountains in California, leaving behind persistent toxic contaminants in the soil, dust, and water that include arsenic and cadmium. Despite a high level of concern among local residents about potential exposure and high breast cancer rates, no biomonitoring data has been collected to evaluate the levels of heavy metals. We conducted a study to characterize the urinary levels of heavy metals among women in this region by working with the community in Nevada County. Sixty women provided urine samples and completed a questionnaire. We examined levels of arsenic, cadmium, and other metals in relation to the length of residency in the area, age, dietary factors, recreational activities, and smoking. We compared urinary metal levels in participants to levels in the United States National Health and Nutrition Examination Survey (NHANES). Overall, study participants had higher urinary levels of arsenic than women in the national sample. Cadmium levels were similar to the national average, although they were elevated in women ≥35 years who had lived in the region for 10 years or more. Arsenic levels were higher among women who smoked, ate fish, ate home-grown produce, and who reported frequent hiking or trail running, although these differences were not statistically significant. This study established a successful community–research partnership, which facilitated community dialogue about possible human health consequences of living in a mining-impacted area. Full article

(This article belongs to the Special Issue Metal Exposure and Health Risk Assessment)

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Review

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16 pages, 333 KiB

Open AccessReview

New Insights on the Role of Manganese in Alzheimer’s Disease and Parkinson’s Disease

by Airton Cunha Martins, Jr., Patricia Morcillo, Omamuyovwi Meashack Ijomone, Vivek Venkataramani, Fiona Edith Harrison, Eunsook Lee, Aaron Blaine Bowman and Michael Aschner

Int. J. Environ. Res. Public Health 2019, 16(19), 3546; https://doi.org/10.3390/ijerph16193546 - 22 Sep 2019

Cited by 74 | Viewed by 8972

Abstract

Manganese (Mn) is an essential trace element that is naturally found in the environment and is necessary as a cofactor for many enzymes and is important in several physiological processes that support development, growth, and neuronal function. However, overexposure to Mn may induce neurotoxicity and may contribute to the development of Alzheimer’s disease (AD) and Parkinson’s disease (PD). The present review aims to provide new insights into the involvement of Mn in the etiology of AD and PD. Here, we discuss the critical role of Mn in the etiology of these disorders and provide a summary of the proposed mechanisms underlying Mn-induced neurodegeneration. In addition, we review some new therapy options for AD and PD related to Mn overload. Full article

(This article belongs to the Special Issue Metal Exposure and Health Risk Assessment)

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