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Toxics, Volume 8, Issue 3 (September 2020) – 8 articles

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Open AccessArticle
Sustained Effects on Lung Function in Community Members Following Exposure to Hazardous PM2.5 Levels from Wildfire Smoke
Toxics 2020, 8(3), 53; https://doi.org/10.3390/toxics8030053 (registering DOI) - 05 Aug 2020
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Abstract
Extreme wildfire events are becoming more common and while the immediate risks of particulate exposures to susceptible populations (i.e., elderly, asthmatics) are appreciated, the long-term health effects are not known. In 2017, the Seeley Lake (SL), MT area experienced unprecedented levels of wildfire [...] Read more.
Extreme wildfire events are becoming more common and while the immediate risks of particulate exposures to susceptible populations (i.e., elderly, asthmatics) are appreciated, the long-term health effects are not known. In 2017, the Seeley Lake (SL), MT area experienced unprecedented levels of wildfire smoke from July 31 to September 18, with a daily average of 220.9 μg/m3. The aim of this study was to conduct health assessments in the community and evaluate potential adverse health effects. The study resulted in the recruitment of a cohort (n = 95, average age: 63 years), for a rapid response screening activity following the wildland fire event, and two follow-up visits in 2018 and 2019. Analysis of spirometry data found a significant decrease in lung function (FEV1/FVC ratio: forced expiratory volume in first second/forced vital capacity) and a more than doubling of participants that fell below the lower limit of normal (10.2% in 2017 to 45.9% in 2018) one year following the wildfire event, and remained decreased two years (33.9%) post exposure. In addition, observed FEV1 was significantly lower than predicted values. These findings suggest that wildfire smoke can have long-lasting effects on human health. As wildfires continue to increase both here and globally, understanding the health implications is vital to understanding the respiratory impacts of these events as well as developing public health strategies to mitigate the effects. Full article
(This article belongs to the Special Issue Molecular Basis of Air-Pollution-Induced Disease Risk)
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Open AccessArticle
Ambient Exposure to Agricultural Pesticides during Pregnancy and Risk of Cerebral Palsy: A Population-Based Study in California
Toxics 2020, 8(3), 52; https://doi.org/10.3390/toxics8030052 - 31 Jul 2020
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Abstract
Cerebral palsy (CP) is the most common neuro-motor disability in young children. Disruptions of maternal hormone function during pregnancy have been linked to CP risk. We investigated whether prenatal exposure to pesticide compounds with endocrine-disrupting action affect CP risk. We conducted a case-control [...] Read more.
Cerebral palsy (CP) is the most common neuro-motor disability in young children. Disruptions of maternal hormone function during pregnancy have been linked to CP risk. We investigated whether prenatal exposure to pesticide compounds with endocrine-disrupting action affect CP risk. We conducted a case-control study of 3905 CP cases and 39,377 controls born between 1998 and 2010 in California to mothers who lived in proximity (within 2 km) to any agricultural pesticide application recorded in the California Pesticide Use Reporting (PUR) system. We focused on 23 pesticides considered endocrine disruptors that are frequently used, and we found that exposure to any of the 23 pesticides in the first trimester was associated with elevated CP risks in female offspring (OR = 1.19; 95% CI: 1.05–1.35) but not males (OR = 0.99; 95% CI: 0.89–1.09) compared to the unexposed offspring. Positive associations were estimated for 15 pesticides suspected to affect the estrogen and 7 pesticides suspected to affect the thyroid hormone system. Our study suggests that first trimester exposure to pesticides that are suspected endocrine disruptors are associated with CP risk in female offspring. Pesticide exposures in early pregnancy may have sex-specific influences on the neuro-motor development of the fetus by interfering with endocrine systems. Full article
Open AccessArticle
Astrocytes Are More Vulnerable than Neurons to Silicon Dioxide Nanoparticle Toxicity in Vitro
Toxics 2020, 8(3), 51; https://doi.org/10.3390/toxics8030051 - 29 Jul 2020
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Abstract
Some studies have shown that silicon dioxide nanoparticles (SiO2-NPs) can reach different regions of the brain and cause toxicity; however, the consequences of SiO2-NPs exposure on the diverse brain cell lineages is limited. We aimed to investigate the neurotoxic [...] Read more.
Some studies have shown that silicon dioxide nanoparticles (SiO2-NPs) can reach different regions of the brain and cause toxicity; however, the consequences of SiO2-NPs exposure on the diverse brain cell lineages is limited. We aimed to investigate the neurotoxic effects of SiO2-NP (0–100 µg/mL) on rat astrocyte-rich cultures or neuron-rich cultures using scanning electron microscopy, Attenuated Total Reflection-Fourier Transform Infrared spectroscopy (ATR-FTIR), FTIR microspectroscopy mapping (IQ mapping), and cell viability tests. SiO2-NPs were amorphous particles and aggregated in saline and culture media. Both astrocytes and neurons treated with SiO2-NPs showed alterations in cell morphology and changes in the IR spectral regions corresponding to nucleic acids, proteins, and lipids. The analysis by the second derivative revealed a significant decrease in the signal of the amide I (α-helix, parallel β-strand, and random coil) at the concentration of 10 µg/mL in astrocytes but not in neurons. IQ mapping confirmed changes in nucleic acids, proteins, and lipids in astrocytes; cell death was higher in astrocytes than in neurons (10–100 µg/mL). We conclude that astrocytes were more vulnerable than neurons to SiO2-NPs toxicity. Therefore, the evaluation of human exposure to SiO2-NPs and possible neurotoxic effects must be followed up. Full article
(This article belongs to the collection Environmental and Health Risks of Nanotechnology)
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Open AccessArticle
Increased Mitochondrial Fragmentation Mediated by Dynamin-Related Protein 1 Contributes to Hexavalent Chromium-Induced Mitochondrial Respiratory Chain Complex I-Dependent Cytotoxicity
Toxics 2020, 8(3), 50; https://doi.org/10.3390/toxics8030050 - 29 Jul 2020
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Abstract
Hexavalent chromium (Cr(VI)) pollution is a severe public health problem in the world. Although it is believed that mitochondrial fragmentation is a common phenomenon in apoptosis, whether excessive fission is crucial for apoptosis remains controversial. We previously confirmed that Cr(VI) mainly targeted mitochondrial [...] Read more.
Hexavalent chromium (Cr(VI)) pollution is a severe public health problem in the world. Although it is believed that mitochondrial fragmentation is a common phenomenon in apoptosis, whether excessive fission is crucial for apoptosis remains controversial. We previously confirmed that Cr(VI) mainly targeted mitochondrial respiratory chain complex I (MRCC I) to induce reactive oxygen species (ROS)-mediated apoptosis, but the related mechanism was unclear. In this study, we found Cr(VI) targeted MRCC I to induce ROS accumulation and triggered mitochondria-related cytotoxicity. Cr(VI)-induced cytotoxicity was alleviated by pretreatment of Glutamate/malate (Glu/Mal; MRCC I substrates), and was aggravated by cotreatment of rotenone (ROT; MRCC I inhibitor). Cr(VI) induced excessive mitochondrial fragmentation and mitochondrial dynamin-related protein 1 (Drp1) translocation, the application of Drp1-siRNA alleviated Cr(VI)-induced apoptosis. The cytotoxicity in the Drp1-si plus Cr(VI) treatment group was alleviated by the application of Glu/Mal, and was aggravated by the application of ROT. Drp1 siRNA promoted the inhibition of Glu/Mal on Cr(VI)-induced cytotoxicity, and alleviated the aggravation of ROT on Cr(VI)-induced cytotoxicity. Taken together, Cr(VI)-induced Drp1 modulation was dependent on MRCC I inhibition-mediated ROS production, and Drp1-mediated mitochondrial fragmentation contributed to Cr(VI)-induced MRCC I-dependent cytotoxicity, which provided the experimental basis for further elucidating Cr(VI)-induced cytotoxicity. Full article
(This article belongs to the Special Issue Toxic Metals, Chronic Diseases and Related Cancers)
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Open AccessArticle
Mechanism of Vascular Toxicity in Rats Subjected to Treatment with a Tyrosine Kinase Inhibitor
Toxics 2020, 8(3), 49; https://doi.org/10.3390/toxics8030049 - 20 Jul 2020
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Abstract
Sunitinib (Su) is a tyrosine kinase inhibitor with antiangiogenic and antineoplastic effects that is recommended therapy for renal cell carcinoma, gastrointestinal stromal tumors, and pancreatic neuroendocrine tumors. Arterial hypertension is one of the adverse effects observed in the treatment with Su. The aim [...] Read more.
Sunitinib (Su) is a tyrosine kinase inhibitor with antiangiogenic and antineoplastic effects that is recommended therapy for renal cell carcinoma, gastrointestinal stromal tumors, and pancreatic neuroendocrine tumors. Arterial hypertension is one of the adverse effects observed in the treatment with Su. The aim of this work was to deepen our understanding of the underlying mechanisms involved in the development of this side effect. Studies on endothelial function, vascular remodeling and nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase) system were carried out in thoracic aortas from rats treated with Su for three weeks. Animals subjected to Su treatment presented with increased blood pressure and reduced endothelium-dependent vasodilation, the latter being reverted by NADPH oxidase blockade. Furthermore, vascular remodeling and stronger Masson trichrome staining, together with enhanced immunofluorescence signal for collagen 1 alpha 1 (Col1α1), were observed in aortas from treated animals. These results were accompanied by a significant elevation in superoxide anion production and the activity/protein/gene expression of NADPH oxidase isoforms (NOX1, NOX2, and NOX4), which was also prevented by NOX inhibition. Furthermore, a decrease in nitric oxide (NO) levels and endothelial nitric oxide synthase (eNOS) activation was observed in aortas from Su-treated animals. All these results indicate that endothelial dysfunction secondary to changes in vascular remodeling and oxidative stress might be responsible for the typical arterial hypertension that develops following treatment with Su. Full article
(This article belongs to the Section Toxicology and Public Health)
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Open AccessCase Report
Recycling Waste Electrical and Electronic Equipment (WEEE) and the Management of Its Toxic Substances in Taiwan—A Case Study
Toxics 2020, 8(3), 48; https://doi.org/10.3390/toxics8030048 - 07 Jul 2020
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Abstract
In the past two decades, the waste electrical and electronic equipment (WEEE) management has become an important environmental issue internationally because it contained hazardous substances like heavy metals and brominated flame retardants. Moreover, some valuable substances were used in the electrical and electronic [...] Read more.
In the past two decades, the waste electrical and electronic equipment (WEEE) management has become an important environmental issue internationally because it contained hazardous substances like heavy metals and brominated flame retardants. Moreover, some valuable substances were used in the electrical and electronic products, thus representing a circular industry for recycling of WEEE. Therefore, the Taiwan government formulated a legal WEEE recycling system since 1998 in response to the international trends of sustainable waste management and extended producer responsibility (EPR). This article adopted the national statistics in Taiwan regarding the online reporting amounts of collected WEEE since it has been officially designated as one of the mandatory recyclable wastes. Furthermore, the regulatory measures were addressed to update the status and subsidiary fee rates of WEEE recycling in Taiwan. In addition, this article also put emphasis on the regulations governing the toxic chemical substances contained in the WEEE. It showed that the average annual recycling amounts of home electronic appliances, information technology products and lighting in Taiwan during the 2017–2018 were around 117,000, 18,000 and 4500 metric tons, respectively. It was also indicated that the current WEEE recycling market in Taiwan has become saturated, reflecting the regulatory promulgation and promotional measures successfully. In response to the Stockholm Convention on persistent organic pollutants (POPs) and the Minamata Convention on Mercury, the Taiwan government declared some brominated flame retardants and heavy metals (i.e., mercury and cadmium) as a “toxic chemical substance” under the Toxic and Concerned Chemical Substance Control Act (TCCSCA), which shall be prohibited to use in the preparation of electrical and electronic equipment (EEE) since 1 January 2016. Through the central governing authority, local governments, and private recyclers in Taiwan, the successful WEEE recycling system not only reduce the pressure on sanitary disposal systems, but also prevent the chemical hazards from solid waste incineration systems. More significantly, the WEEE recycling in Taiwan echoed the United Nations (UN) Agenda 2030 for sustainable development goals. Full article
(This article belongs to the Special Issue Electronic-Waste: Management and Challenges)
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Open AccessArticle
Mercury Exposure and Associations with Hyperlipidemia and Elevated Liver Enzymes: A Nationwide Cross-Sectional Survey
Toxics 2020, 8(3), 47; https://doi.org/10.3390/toxics8030047 - 01 Jul 2020
Viewed by 347
Abstract
Mercury (Hg) has obesogenic properties. However, the associated health outcomes of population-level mercury exposure were unclear. This study investigated the relationships between blood mercury levels and obesity-related outcomes such as hyperlipidemia and elevated liver enzymes. Using the second cycle of the Korean National [...] Read more.
Mercury (Hg) has obesogenic properties. However, the associated health outcomes of population-level mercury exposure were unclear. This study investigated the relationships between blood mercury levels and obesity-related outcomes such as hyperlipidemia and elevated liver enzymes. Using the second cycle of the Korean National Environmental Health Survey (n = 6454), we performed logistic regression to examine the effects of Hg on hyperlipidemia and elevated liver enzymes. The blood mercury levels were significantly higher in the hyperlipidemia group (n = 3699, male: 4.03 μg/L, female: 2.83 μg/L) compared to the non-hyperlipidemia group (n = 2755, male: 3.48 μg/L, female: 2.69 μg/L), and high blood mercury levels were associated with an 11% higher risk of hyperlipidemia. The elevated liver enzymes group had higher mean blood mercury levels (n = 1189, male: 4.38 μg/L, female: 3.25 μg/L) than the normal group (n = 5265, male: 3.64 μg/L, female: 2.70 μg/L), and elevated blood mercury was associated with a 35% higher risk of elevated liver enzymes. Moreover, the effect was constant after adjusting for personal medications. These results indicate that mercury exposure is significantly associated with hyperlipidemia and elevated liver enzymes. Full article
(This article belongs to the Special Issue Toxic Metals, Chronic Diseases and Related Cancers)
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Open AccessArticle
Pulmonary Toxicity and Inflammatory Response of E-Cigarette Vape Cartridges Containing Medium-Chain Triglycerides Oil and Vitamin E Acetate: Implications in the Pathogenesis of EVALI
Toxics 2020, 8(3), 46; https://doi.org/10.3390/toxics8030046 - 28 Jun 2020
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Abstract
Recently, there has been an outbreak associated with the use of e-cigarette or vaping products, associated lung injury (EVALI). The primary components of vaping products, vitamin E acetate (VEA) and medium-chain triglycerides (MCT), may be responsible for acute lung toxicity. Currently, little information [...] Read more.
Recently, there has been an outbreak associated with the use of e-cigarette or vaping products, associated lung injury (EVALI). The primary components of vaping products, vitamin E acetate (VEA) and medium-chain triglycerides (MCT), may be responsible for acute lung toxicity. Currently, little information is available on the physiological and biological effects of exposure to these products. We hypothesized that these e-cig vape cartridges and their constituents (VEA and MCT) induce pulmonary toxicity, mediated by oxidative damage and inflammatory responses, leading to acute lung injury. We studied the potential mechanisms of e-cig vape cartridge aerosol induced inflammatory response by evaluating the generation of reactive oxygen species by MCT, VEA, and cartridges and their effects on the inflammatory state of pulmonary epithelium and immune cells both in vitro and in vivo. Cells exposed to these aerosols generated reactive oxygen species, caused cytotoxicity, induced epithelial barrier dysfunction, and elicited an inflammatory response. Using a murine model, the parameters of acute toxicity to aerosol inhalation were assessed. Infiltration of neutrophils and lymphocytes was accompanied by significant increases in IL-6, eotaxin, and G-CSF in the bronchoalveolar lavage fluid (BALF). In mouse plasma, eicosanoid inflammatory mediators, leukotrienes, were significantly increased. Plasma from e-cig users also showed increased levels of hydroxyeicosatetraenoic acid (HETEs) and various eicosanoids. Exposure to e-cig vape cartridge aerosols showed the most significant effects and toxicity compared to MCT and VEA. In addition, we determined SARS-CoV-2 related proteins and found no impact associated with aerosol exposures from these tested cartridges. Overall, this study demonstrates acute exposure to specific e-cig vape cartridges induces in vitro cytotoxicity, barrier dysfunction, and inflammation and in vivo mouse exposure induces acute inflammation with elevated proinflammatory markers in the pathogenesis of EVALI. Full article
(This article belongs to the Special Issue Current Knowledge of E-cigarettes and Heated Tobacco Products)
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