Potential suppression of fertility due to mobile phone radiation remains a focus of researchers. We conducted meta-analyses on the effects of mobile phone radiation on sperm quality using recent evidence and propose some perspectives on this issue. Using the MEDLINE/PubMed, Embase, WOS, CENTRAL, and ClinicalTrials.gov databases, we retrieved and screened studies published before December 2020 on the effects of mobile phone use/mobile phone RF-EMR on sperm quality. Thirty-nine studies were included. Data quality and general information of the studies were evaluated and recorded. Sperm quality data (density, motility, viability, morphology, and DFI) were compiled for further analyses, and we conducted subgroup, sensitivity, and publication bias analyses. The pooled results of human cross-sectional studies did not support an association of mobile phone use and a decline in sperm quality. Different study areas contributed to the heterogeneity of the studies. In East Europe and West Asia, mobile phone use was correlated with a decline in sperm density and motility. Mobile phone RF-EMR exposure could decrease the motility and viability of mature human sperm in vitro. The pooled results of animal studies showed that mobile phone RF-EMR exposure could suppress sperm motility and viability. Furthermore, it reduced sperm density in mice, in rats older than 10 weeks, and in rats restrained during exposure. Differences regarding age, modeling method, exposure device, and exposure time contributed to the heterogeneity of animal studies. Previous studies have extensively investigated and demonstrated the adverse effects of mobile phone radiation on sperm. In the future, new standardized criteria should be applied to evaluate potential effects of mobile phone RF-EMR dosages. Further sperm-related parameters at the functional and molecular levels as well as changes in biological characteristics of germ cells should be evaluated. Moreover, the impact of mobile phone RF-EMR on individual organs should also be examined.

Polychlorinated biphenyls (PCBs) are one of the most refractory organic environmental pollutants that ubiquitous existence in nature. Due to the polymorphism of their metabolic pathway and corresponding downstream metabolites, PCBs’ toxicities are complicated and need extended investigation. In the present study, we discovered a novel regulatory mechanism of PCB quinone metabolite-driven programmed cell death (PCD), namely, necroptosis. We first confirmed that PCB quinone induces cancerous HeLa and MDA-MB-231 cells necroptosis via the phosphorylation of mixed lineage kinase domain-like MLKL (p-MLKL). Then, we found that PCB quinone-stimulated p-MLKL enhances exosome biogenesis and secretion. Exosome interacts with p-MLKL and releases p-MLKL to the outside of the cell, and ultimately alleviating PCB quinone-induced necroptosis. The inhibition of exosome secretion by GW4869 significantly elevated necroptotic level, indicating the establishment of a short negative feedback loop of MLKL-exosome secretion upon PCB quinone challenge. Since exosome-mediated signaling showed great implications in various human diseases, this work may provide a new mechanism for PCBs-associated toxicity.

The sedimentary history of polycyclic aromatic hydrocarbons (PAHs) and organochlorine pesticides (OCPs) over the past 140 years in a lake sediment core from Huixian karst wetland was reconstructed. The total PAHs and OCPs concentrations ranged from 40.0 to 210 ng g⁻¹ and 0.98 to 31.4 ng g⁻¹, respectively. The vertical distribution of PAHs and OCPs in different stages was great consistent with the history of regional socio-economic development and the usage of OCPs. As the indicators of socio-economic development, gross domestic product (GDP), population, energy consumption, highway mileage, and private vehicles correlated with the PAHs concentrations, indicating the impact of human activities on PAHs levels. The PAHs and OCPs concentrations were also affected by environmental changes in the wetland, as reconstructed by total organic carbon (TOC), sand, silt, clay, quartz, and calcite in sediments. Redundancy analysis (RDA) results showed TOC was the dominant factor to explain the concentrations of PAHs and OCPs with the explanation of 86.7% and 43.5%, respectively. In addition, TOC content had significantly positive correlation with PAHs (0.96, p < 0.01) and OCPs (0.78, p < 0.01). In particular, the significantly positive correlation (p < 0.05) between calcite and PAHs and OCPs inferred that karstification might play an important role in the migration of PAHs and OCPs in the karst area. Therefore, the lake in Huixian wetland tended to be a sink more than a source of PAHs and OCPs influenced by the increasing TOC content and karstification under climate warming.

or sugar-derived compounds were used as environmentally friendly additives for the depolymerization of Kraft lignin waste and organosolv lignin prepared from Miscanthus giganteus. The yields of the aromatic monomers obtained from Kraft lignin increased from 5.1 to 49.2% with the addition of mannitol, while those obtained from organosolv lignin increased from 44.4 to 83.0% with the addition of sucrose. This improved lignin depolymerization was also confirmed by gel permeation chromatography and nuclear magnetic resonance spectroscopy. The above results clearly indicate the beneficial effects of carbohydrate derivatives on the lignin depolymersization process, more specifically, suggesting that the presence of carbohydrates improve the lignin depolymerization of lignocellulose, as observed for the raw lignocellulose feed.

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.

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.

The annual mean PM₂.₅ mass concentration has decreased because of the stringent emission controls implemented in Beijing, China in recent years, whereas the nitrate NO3– mass fraction in PM₂.₅ increases gradually. Low-visibility events occur frequently even though PM₂.₅ pollution has been mitigated significantly, with the daily mean PM₂.₅ mass concentration mostly less than 75 μg/m³. In this study, the non-linear relationship was analyzed between atmospheric visibility and PM₂.₅ based on chemical composition from a two-year field observation. Our results showed that NO3– became the main constituent of PM₂.₅, especially during the haze pollution episodes. A localized parameterization scheme was proposed between the atmospheric extinction coefficient (σext) and major chemical constituents of PM₂.₅ by multiple linear regression (MLR). The contribution of NO3– to σext increased with increasing air pollution, and NO3– became the most important contributor for PM₂.₅ above 75 μg/m³. The visibility decreased with increasing NO3– mass fraction for the same PM₂.₅ mass concentration when PM₂.₅ was above 20 μg/m³. The hygroscopicity of PM₂.₅ increased with increasing mass fraction of hygroscopic NO3–. These results stressed the importance of reducing particulate NO3– and its precursors (for instance, NH₃) through effective emission control measures as well as the tightening of PM₂.₅ standards to further improve air quality and visibility in Beijing.

Organomineral assemblages are building units of soil micro-aggregates and exert their essential roles in immobilizing toxic elements. Currently, our knowledge of the adsorption and partitioning behaviors of coexisting Cd–As onto organomineral composites is limited. Herein, we carefully studied Cd–As cosorption onto ferrihydrite organomineral composites made with either living or non-living organics, i.e., bacteria (Delftia sp.) or humic acid (HA), using batch adsorption and various spectroscopies. Batch results show that As(V) only enhances Cd(II) sorption on pure Fh at pH < 6 but cannot promote Cd(II) sorption to Fh–organo composites. However, Cd(II) noticeably promotes As(V) sorption at pH>~5–6. Synchrotron micro X-ray fluorescence indicates that Cd(II) adsorbs predominately to the bacterial fraction (Cd versus P, r = 0.924), whereas As(V) binds mainly to the Fh fraction (As versus Fe, r = 0.844) of the Fh–bacteria composite. On Fh–HA composite, however, Cd(II) and As(V) are both primarily sorbed by the Fh fraction (Cd/As versus P, r > 0.8), based on the scanning transmission electron microscopy-energy disperse spectroscopy analyses. Elemental distribution characterization also manifests the co-localization of Cd(II) and As(V) within the organomineral composite, particular in Fh–HA composite (Cd versus As, r = 0.8), which is further identified as the Fh–As–Cd ternary complex based on the observations (higher frequencies at ~753–761 cm⁻¹) of attenuated total reflection Fourier-transform infrared spectroscopy. Moreover, this ternary interaction is more pronounced in Fh–HA than in Fh–bacteria. In summary, our results suggest that Cd–As coadsorption behaviors on Fh–organo composites are different from those on pure minerals, and the presence of bacteria/HA can significantly affect metal (loid)s speciation, distribution, and ternary interaction. Therefore organomineral composites are a more suitable analog than pure mineral phases to predict the mobility and fate of Cd–As in natural environments.

Cadmium (Cd) is a heavy metal toxicant as a common pollutant derived from many agricultural and industrial sources. The absorption of Cd takes place primarily through Cd-contaminated food and water and, to a significant extent, via inhalation of Cd-contaminated air and cigarette smoking. Epidemiological data suggest that occupational or environmental exposure to Cd increases the health risk for osteoporosis and spontaneous fracture such as itai-itai disease. However, the direct effects and underlying mechanism(s) of Cd exposure on bone damage are largely unknown. We used primary bone marrow-derived mesenchymal stromal cells (BMMSCs) and found that Cd significantly induced BMMSC cellular senescence through over-activation of NF-κB signaling pathway. Increased cell senescence was determined by production of senescence-associated secretory phenotype (SASP), cell cycle arrest and upregulation of p21/p53/p16ᴵᴺᴷ⁴ᵃ protein expression. Additionally, Cd impaired osteogenic differentiation and increased adipogenesis of BMMSCs, and significantly induced cellular senescence-associated defects such as mitochondrial dysfunction and DNA damage. Sprague-Dawley (SD) rats were chronically exposed to Cd to verify that Cd significantly increased adipocyte number, and decreased mineralization tissues of bone marrow in vivo. Interestingly, we observed that Cd exposure remarkably retarded bone repair and regeneration after operation of skull defect. Notably, pretreatment of melatonin is able to partially prevent Cd-induced some senescence-associated defects of BMMSCs including mitochondrial dysfunction and DNA damage. Although Cd activated mammalian target of rapamycin (mTOR) pathway, rapamycin only partially ameliorated Cd-induced cell apoptosis rather than cellular senescence phenotypes of BMMSCs. In addition, a selective NF-κB inhibitor moderately alleviated Cd-caused the senescence-related defects of the BMMSCs. The study shed light on the action and mechanism of Cd on osteoporosis and bone ageing, and may provide a novel option to ameliorate the harmful effects of Cd exposure.

Insecticide resistance is one of the major obstacles for controlling agricultural pests. There have been a lot of studies on insecticides stimulating the development of insect resistance. Herbicides account for the largest sector in the agrochemical market and are often co-applied with insecticides to control insect pests and weeds in the same cropland ecosystem. However, whether and how herbicides exposure will affect insecticide resistance in insect pests is largely unexplored. Here we reported that after exposure to herbicide butachlor, the lepidopteran Spodoptera litura larvae reduced susceptibility to the insecticide chlorpyrifos. Docking simulation studies suggested that general odorant-binding protein 2 (GOBP2) could bind to butachlor with high binding affinity, and silencing SlGOBP2 by RNA interference (RNAi) decreased larval tolerance to chlorpyrifos. Butachlor exposure induced ecdysone biosynthesis, whose function on increasing chlorpyrifos tolerance was supported in synergism experiments and confirmed by silencing the key gene (SlCYP307A1) for ecdysone synthesis. Butachlor exposure also activated the expression of detoxification enzyme genes. Silencing the genes with the highest herbicide-induced expression among the three detoxification enzyme genes led to increased larval susceptibility to chlorpyrifos. Collectively, we proposed a new mechanism that olfactory recognition of herbicides by GOBP2 triggers insect hormone biosynthesis and leads to high metabolic tolerance against insecticides. These findings provide valuable information for the dissection of mechanisms of herbicide-induced resistance to insecticides and also supplements the development of reduced-risk strategies for pest control.