Ice and snow in the Central Andes contain significant amounts of light-absorbing particles such as black carbon. The consequent accelerated melting of the cryosphere is not only a threat from a climate perspective but also for water resources and snow-dependent species and activities, worsened by the mega-drought affecting the region since the last decade. Given its proximity to the Andes, emissions from the Metropolitan Area of Santiago, Chile, are believed to be among the main contributors to deposition on glaciers. However, no evidence backs such an assertion, especially given the usually subsident and stable conditions in wintertime, when the snowpack is at its maximum extent. Based on high-resolution chemistry-transport modeling with WRF-CHIMERE, the present work shows that, for the month of July 2015, up to 40% of black carbon dry deposition on snow or ice covered areas in the Central Andes downwind from the Metropolitan area can be attributed to emissions from Santiago. Through the analysis of aerosol tracers we determine (i) that the areas of the Metropolitan Area where emissions matter most when it comes to export towards glaciers are located in Eastern Santiago near the foothills of the Andes, (ii) the crucial role of the network of Andean valleys that channels pollutants up to remote locations near glaciers, following gentle slopes. A direct corollary is that severe urban pollution, and deposition of impurities on the Andes, are anti-correlated phenomena. Finally, a two-variable meteorological index is developed that accounts for the dynamics of aerosol export towards the Andes, based on the zonal wind speed over the urban area, and the vertical diffusion coefficient in the valleys close to ice and snow covered terrain. Numerous large urban areas are found along the Andes so that the processes studied here can shed light on similar investigations for other glaciers-dependent Andean regions.

Ozone (O₃) is a harmful pollutant when present in the lowermost layer of the atmosphere. Therefore, the European Commission formulated directives to regulate O₃ concentrations in near-surface air. However, almost 50% of the 5068 air quality stations in Europe do not monitor O₃ concentrations. This study aims to provide a hybrid modeling system that fills these gaps in the hourly surface O₃ observations on a site scale with much higher accuracy than existing O₃ models. This hybrid model was developed using estimations from multiple linear regression-based eXtreme Gradient Boosting Machines (MLR-XGBM) and O₃ reanalysis from European regional air quality models (CAMS-EU). The binary classification of extremely high O₃ events and the 1- and 24-h forecasts of hourly O₃ were investigated as secondary aims. In this study thirteen stations in Northern Bavaria, out of which six do not monitor O₃, were chosen as test sites. Considering the computational complexity of machine learning algorithms (MLAs), we also applied two recent MLA interpretation methods, namely SHapley Additive exPlanations (SHAP) and Local interpretable model-agnostic explanations (LIME).With SHAP, we showed an increasing effect of temperature on O₃ concentrations which intensifies for temperatures exceeding 17 °C. According to LIME, O₃ concentration peaks are mainly governed by meteorological factors under dry and warm conditions on a regional scale, whereas local nitrogen oxide concentrations control base O₃ concentrations during cold and wet periods.While recently developed MLAs for the spatial estimation of hourly O₃ concentrations had a station-based root-mean-square error (RMSE) above 27 μg/m³, our proposed model significantly reduced the estimation errors by about 66% with an RMSE of 9.49 μg/m³. We also found that logistic regression (LR) and MLR-XGBM performed best in the site-scale classification and 24-h forecast of O₃ concentrations (with a station-averaged accuracy and RMSE of 0.95 and 19.34 μg/m³, respectively).

Quantum dots (QDs) are nanoparticles of inorganic semiconductors and have great promise in various applications. Many studies have indicated that mitochondria are the main organelles for the distribution and toxic effects of QDs. However, the underlying mechanism of QDs interacting with mitochondria and affecting their function is unknown. Here, we report the mechanism of toxic effects of 3-mercaptopropionic acid (MPA)-capped CdTe QDs on mitochondria. Human liver carcinoma (HepG2) cells were exposed to 25, 50 and 100 μmol/L of MPA-capped CdTe QDs. The results indicated that MPA-capped CdTe QDs inhibited HepG2 cell proliferation and increased the extracellular release of LDH in a concentration-dependent manner. Furthermore, MPA-capped CdTe QDs caused reactive oxygen species (ROS) generation and cell damage through intrinsic apoptotic pathway. MPA-capped CdTe QDs can also lead to the destruction of mitochondrial cristae, elevation of intracellular Ca²⁺ levels, decreased mitochondrial transmembrane potential and ATP production. Finally, we showed that MPA-capped CdTe QDs inhibited mitochondrial fission, mitochondrial inner membrane fusion and mitophagy. Taken together, MPA-capped CdTe QDs induced significant mitochondrial dysfunction, which may be caused by imbalanced mitochondrial fission/fusion and mitophagy inhibition. These findings provide insights into the regulatory mechanisms involved in MPA-capped CdTe QDs-induced mitochondrial dysfunction.

All European bats are protected by the EU and Associated Members legal regulations. Being insectivorous and top predators, they can be particularly exposed to persistent organic and inorganic pollutants. It is surprising how little is known about the impact of environmental pollutants on bats from physiological to populational levels. In this study we focused on contamination with trace metals of first-year bats from Kharkiv city, NE Ukraine. Tissues from the carcasses of two species, Nyctalus noctula (n = 20) and Eptesicus serotinus (n = 20), were used for metal analysis. The samples of external (wing membrane, fur) and internal (liver, lung, kidney, bones) tissues were analysed for contents of Pb, Cu, Zn, and Cd to see whether fur or wing membrane can be used as proxies for metal contamination of the vital internal tissues. In E. serotinus, significant positive correlations in Pb concentrations were found between all external and internal tissues. For Cd only, correlation between the fur and lung was found, for Cu between the fur and liver, and for Zn between the fur and kidney. In contrast, for N. noctula, only one such correlation was found – between Zn concentrations in the fur and kidney. The tissues differed significantly in concentrations of all studied metals, with no difference between the species. The results showed that the fur and wing membrane can be used as good proxies for Pb concentrations in internal organs of E. serotinus, but not necessarily for other metals or for N. noctula. The results for Pb are, however, encouraging enough to conclude that the topic is worth further studies, covering more species, a wider age range and more diverse environments.

The toxicity of nanoplastics to aquatic organisms has been widely studied in terms of biochemical indicators. However, there is little discussion about the underlying toxic mechanism of nanoplastics on microalgae. Therefore, the chronic effect of polystyrene (PS) nanoplastics (80 nm) on Chlorella pyrenoidosa was investigated, in terms of responses at the biochemical and molecular/omic level. It was surprising that both inhibitory and promoting effects of nanoplastcis on C. pyrenoidosa were found during chronic exposure. Before 13 days, the maximum growth inhibition rate was 7.55% during 10 mg/L PS nanoplastics treatment at 9 d. However, the inhibitory effect gradually weakened with the prolongation of exposure time. Interestingly, algal growth was promoted for 1–5 mg/L nanoplastics during 15–21 d exposure. Transcriptomic analysis explained that the inhibitory effect of nanoplastics could be attributed to suppressed gene expression of aminoacyl-tRNA synthetase that resulted in the reduced synthesis of related enzymes. The promotion phenomenon may be due to that C. pyrenoidosa defended against nanoplastics stress by promoting cell proliferation, regulating intracellular osmotic pressure, and accelerating the degradation of damaged proteins and organs. This study is conducive to provide theoretical basis for evaluating the actual hazard of nanoplastics to aquatic organisms.

Insufficient evidence exists regarding the visible physiological toxic endpoints of MPs exposures on zebrafish larvae due to their small sizes. Herein, the impacts of micro-polystyrene particles (μ-PS) and 100 nm polystyrene particles (n-PS) on the toxicity of cadmium (Cd) through altering neutrophil expressions were identified and quantified in the transgenic zebrafish (Danio rerio) larvae Tg(lyz:DsRed2), and the effects were size-dependent. When exposed together with μ-PS, the amount of neutrophils in Cd treated zebrafish larvae decreased by 25.56% through reducing Cd content in the larvae. By contrast, although n-PS exposure caused lower Cd content in the larvae, the expression of neutrophils under their combined exposure remained high. The mechanism of immune toxicity was analyzed based on the results of metabonomics. n-PS induced high oxidative stress in the larvae, which promoted taurine metabolism and unsaturated fatty biosynthesis in n-PS + Cd treatment. This observation was accordance with the significant inhibition of the activities of superoxide dismutase and catalase enzymes detected in their combined treatment. Moreover, n-PS promoted the metabolic pathways of catabolic processes, amino acid metabolism, purine metabolism, and steroid hormone biosynthesis in Cd treated zebrafish larvae. Nanoplasctis widely coexist with other pollutants in the environment at relatively low concentrations. We conclude that more bio-markers of immune impact should be explored to identify their toxicological mechanisms and mitigate the effects on the environment.

Copper (Cu) is a vital micronutrient required for numerous fundamental biological processes, but excessive Cu poses potential detrimental effects on public and ecosystem health. However, the molecular details linking endoplasmic reticulum (ER) stress and apoptosis in duck renal tubular epithelial cells have not been fully elucidated. In this study, duck renal tubular epithelial cells exposed to Cu sulfate (CuSO₄) (0, 100 and 200 μM) and a PERK inhibitor (GSK2606414, GSK, 1 μM) for 12 h were used to investigate the crosstalk between ER stress and apoptosis under Cu exposure. Cell and ER morphological and functional characteristics, intracellular calcium (Ca²⁺) levels, apoptotic rates, ER stress and apoptosis-related mRNA and protein levels were examined. The results showed that excessive Cu could cause ER expansion and swelling, increase the expression levels of ER stress-associated genes (PERK, eIF2α, ATF4 and CHOP) and proteins (p-PERK and CHOP), induce intracellular Ca²⁺ overload, upregulate the expression levels of apoptosis-associated genes (Bax, Bak1, Caspase9 and Caspase3) and the cleaved-Caspase3 protein, downregulate Bcl-xl and Bcl2 mRNA levels and trigger apoptosis. PERK inhibitor treatment could ameliorate the above changed factors caused by Cu. In conclusion, these findings indicate that excessive Cu could trigger ER stress via activation of the PERK/ATF4/CHOP signaling pathway and that ER stress might aggravate Cu-induced apoptosis in duck renal tubular epithelial cells.

Urban Heat Island (UHI) is posing a significant challenge due to growing urbanisations across the world. Green infrastructure (GI) is popularly used for mitigating the impact of UHI, but knowledge on their optimal use is yet evolving. The UHI effect for large cities have received substantial attention previously. However, the corresponding effect is mostly unknown for towns, where appreciable parts of the population live, in Europe and elsewhere. Therefore, we analysed the possible impact of three vegetation types on UHI under numerous scenarios: baseline/current GI cover (BGI); hypothetical scenario without GI cover (HGI-No); three alternative hypothetical scenarios considering maximum green roofs (HGR-Max), grasslands (HG-Max) and trees (HT-Max) using a dispersion model ADMS-Temperature and Humidity model (ADMS-TH), taking a UK town (Guildford) as a case study area. Differences in an ambient temperature between three different landforms (central urban area, an urban park, and suburban residential area) were also explored. Under all scenarios, the night-time (0200 h; local time) showed a higher temperature increase, up to 1.315 °C due to the lowest atmospheric temperature. The highest average temperature perturbation (change in ambient temperature) was 0.563 °C under HGI-No scenario, followed by HG-Max (0.400 °C), BGI (0.343 °C), HGR-Max (0.326 °C) and HT-Max (0.277 °C). Furthermore, the central urban area experienced a 0.371 °C and 0.401 °C higher ambient temperature compared with its nearby suburban residential area and urban park, respectively. The results allow to conclude that temperature perturbations in urban environments are highly dependent on the type of GI, anthropogenic heat sources (buildings and vehicles) and the percentage of land covered by GI. Among all other forms of GI, trees were the best-suited GI which can play a viable role in reducing the UHI. Green roofs can act as an additional mitigation measure for the reduction of UHI at city scale if large areas are covered.

Inhalation represents the most prevalent route of exposure with Thorium-232 compounds (Th-nitrate/Th-dioxide)/Th-containing dust in real occupational scenario. The present study investigated the mechanism of Th response in normal human alveolar epithelial cells (WI26), exposed to Th-nitrate or colloidal Th-dioxide (1–100 μg/ml, 24–72 h). Assessment in terms of changes in cell morphology, cell proliferation (cell count), plasma membrane integrity (lactate dehydrogenase leakage) and mitochondrial metabolic activity (MTT reduction) showed that Th-dioxide was quantitatively more deleterious than Th-nitrate to WI26 cells. TEM and immunofluorescence analysis suggested that Th-dioxide followed a clathrin/caveolin-mediated endocytosis, however, membrane perforation/non-endocytosis seemed to be the mode of Th internalization in cells exposed to Th-nitrate. Th-estimation by ICP-MS showed significantly higher uptake of Th in cells treated with Th-dioxide than with Th-nitrate at a given concentration. Both Th-dioxide and nitrate were found to increase the level of reactive oxygen species, which seemed to be responsible for lipid peroxidation, alteration in mitochondrial membrane potential and DNA-damage. Amongst HSPs, the protein levels of HSP70 and HSP90 were affected differentially by Th-nitrate/dioxide. Specific inhibitors of ATM (KU55933) or HSP90 (17AAG) were found to increase the Th- cytotoxicity suggesting prosurvival role of these signaling molecules in rescuing the cells from Th-toxicity.