Whether toxicity of silver nanoparticles (AgNPs) to organisms originates from the nanoparticles themselves or from the dissolved Ag-ions is still debated, with the majority of studies claiming that extracellular release of Ag-ions is the main cause of toxicity. The objective of this study was to determine the contributions of both particles and dissolved ions to toxic responses, and to better understand the underlying mechanisms of toxicity. In addition, the pathways of AgNPs exposure to plants might play an important role and therefore are explicitly studied as well. We systematically assessed the phytotoxicity, internalization, biodistribution, and antioxidant responses in lettuce (Lactuca sativa) following root or foliar exposure to AgNPs and ionic Ag at various concentrations. For each endpoint the relative contribution of the particle-specific versus the ionic form was quantified. The results reveal particle-specific toxicity and uptake of AgNPs in lettuce as the relative contribution of particulate Ag accounted for more than 65% to the overall toxicity and the Ag accumulation in whole plant tissues. In addition, particle toxicity is shown to originate from the accumulation of Ag in plants by blocking nutrient transport, while ion toxicity is likely due to the induction of excess ROS production. Root exposure induced higher toxicity than foliar exposure at comparable exposure levels. Ag was found to be taken up and subsequently translocated from the exposed parts of plants to other portions regardless of the exposure pathway. These findings suggest particle related toxicity, and demonstrate that the accumulation and translocation of silver nanoparticles need to be considered in assessment of environmental risks and of food safety following consumption of plants exposed to AgNPs by humans.

Terminating harmful algal blooms by using algicidal agents is a strong disturbance event in marine environment, which has powerful structural influences on microbial ecosystems. But, the response of microbial ecosystem to algicidal agent is largely unknown. Here, we conducted Phaeocystis globosa microcosms to investigate the dynamics, assembly processes, and co-occurrence patterns of microbial communities in response to algicidal process induced by a highly efficient algicidal agent, prodigiosin, by using 16S rRNA gene amplicon sequencing. The α-diversity of microbial community showed no obvious changes during the algicidal process in P. globosa microcosm treated with prodigiosin (group PD). Rhodobacteraceae increased significantly (P < 0.05) during algicidal process in PD, and this was mainly due to the lysis of P. globosa cells. Compared to the control group, the temporal turnover rates of common and rare taxa in PD were significantly higher because of the lysis of P. globosa induced by prodigiosin. Neutral processes mainly drove the assembly of microbial communities in all microcosms, even though the algicidal process induced by prodigiosin had no effect on the assembly processes. In addition, the time-decay relationship and co-occurrence network analysis indicate that rare taxa play important roles in maintaining microbial community stability in response to the algicidal process, rather than prodigiosin. These findings suggest that prodigiosin cannot affect the dynamics of microbial communities directly; however, future investigations into the function of microbial communities in response to prodigiosin remain imperative.

Field observations have suggested that particulate nitrate can promote the aging of black carbon (BC), yet the mechanisms of the aging process and its impacts on BC’s light absorption are undetermined. Here we performed laboratory simulation of internal mixing of flame-generated BC aggregates with ammonium nitrate. Variations in particle size, mass, coating thickness, effective density, dynamic shape factor, and optical properties were determined online by a suite of instruments. With the development of coatings, the particle size initially decreased until reaching a coating thickness of ∼10 nm and then started increasing, accompanied by an increase in effective density and a decrease in dynamic shape factor, reflecting the transformation of BC particles from highly fractal to near-spherical morphology. This is partially attributable to the restructuring of BC cores to more compact forms. Exposing coated particles to elevated relative humidity (RH) led to additional BC morphology changes, even after drying. Particle light absorption and scattering were also amplified with ammonium nitrate coating, increasing with coating thickness and RH. For BC particles with a 17.8 nm coating, absorption and scattering were increased by 1.5- and 7.9-fold when cycled through 70% RH (5-70-5% RH), respectively. The irreversible restructuring of the BC core caused by condensation of ammonium nitrate and water altered both absorption and scattering, with a magnitude comparable to or even exceeding the effects of increased coating. Results show that ammonium nitrate is among the most efficient coating materials with respect to modifying BC morphology and optical properties compared with other inorganic and organic species investigated previously. Accordingly, mitigation of nitrate aerosols is necessary for the benefits of both air pollution control and reducing the impacts of BC on visibility impairment and radiative forcing on climate change. Our results also pointed out that the effect of BC core restructuring needs to be considered when evaluating BC’s light absorption enhancement.

Communities in low-income and middle-income countries (LMIC) are disproportionally affected by industrial pollution compared to more developed nations. This study evaluates the dispersal and associated health risk of contaminant-laden soil and dust at a copper (Cu) smelter in Tsumeb, Namibia. It is Africa’s only smelter capable of treating complex Cu ores that contain high arsenic (As) contents (<1%). The analyses focused on the primary trace elements associated with ore processing at the smelter: As, Cu, and lead (Pb). Portable X-Ray fluorescence spectrometry (pXRF) of trace elements in soils (n = 83) and surface dust wipes (n = 80) showed that elemental contamination was spatially associated with proximity to smelter operations. Soil concentrations were below US EPA soil guidelines. Dust wipe values were elevated relative to sites distal from the facility and similar to those at other international smelter locations (As = 1012 μg/m² (95% CI 687–1337); Cu = 1838 μg/m² (95% CI 1191–2485); Pb = 1624 μg/m² (95% CI 862–2385)). Source apportionment for Pb contamination was assessed using Pb isotopic compositions (PbIC) of dust wipes (n = 22). These data revealed that the PbIC of 73% (n = 16/22) of these wipes corresponded to the PbIC of smelter slag and tailings, indicating contribution from industrial emissions to ongoing exposure risk. Modeling of carcinogenic risk showed that dust ingestion was the most important pathway, followed by inhalation, for both adults and children. Dermal contact to trace elements in dust was also determined to pose a carcinogenic risk for children, but not adults. Consequently, contemporary smelter operations remain an ongoing health risk to the surrounding community, in spite of recent efforts to improve emissions from the operations.

Exposure to benzo(a)pyrene (BaP) has been shown to cause mitochondrial dysfunction and injury to neural cells. Resveratrol (RSV) has been studied as an antioxidant, anti-inflammatory, anti-apoptotic, and anticancer agent and can modulate mitochondrial function in vitro and in vivo. However, the molecular mechanisms underlying RSV’s protection against mitochondrial dysfunction have not been fully elucidated. To investigate whether RSV can effectively prevent BaP-induced mitochondrial dysfunction, we tested the effects of RSV in primary neuronal models. Our results confirmed that neurons exhibited mitochondrial dysfunction and apoptosis in the mitochondrial pathway after BaP-treatment, and that pretreatment with RSV could reduce that dysfunction. Further, our results indicated that RSV pretreatment enhanced mitochondrial biogenesis via the AMPK/PGC-1α pathway and activated mitophagy via the PINK1-Parkin and AMPK/ULK1 pathways, thereby coordinating mitochondrial homeostasis. We also found that RSV could alleviate mitochondrial network fragmentation caused by BaP. This work provided insights into the role of RSV in preventing BaP-induced primary neuronal apoptosis in the mitochondrial pathway, mainly via regulation of mitochondrial biogenesis and mitophagy through AMPK pathway, thus maintaining the integrity of the mitochondrial network.

Recently, environmental risk and toxicity of neonicotinoid insecticides to honey bees have attracted extensive attention. However, toxicological understanding of neonicotinoid insecticides on gut microbiota is limited. In the present study, honey bees (Apis mellifera L.) were exposed to a series of nitenpyram for 14 days. Results indicated that nitenpyram exposure decreased the survival and food consumption of honey bees. Furthermore, 16S rRNA gene sequencing revealed that nitenpyram caused significant alterations in the relative abundance of several key gut microbiotas, which contribute to metabolic homeostasis and immunity. Using high-throughput RNA-Seq transcriptomic analysis, we identified a total of 526 differentially expressed genes (DEGs) that were significantly altered between nitenpyram-treated and control honey bee gut, including several genes related to metabolic, detoxification and immunity. In addition, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showed nitenpyram affected several biological processes, of which most were related to metabolism. Collectively, our study demonstrates that the dysbiosis of gut microbiota in honey bee caused by nitenpyram may influence metabolic homeostasis and immunity of bees, and further decrease food consumption and survival of bees.

About 11% of the global anthropogenic greenhouse gases (GHGs) emissions result from agricultural practices. Dairy manure (DM) application to soil is regarded as a best management practice due to C sequestration and improvement of soil physiochemical properties. However, GHGs emissions from the soil following the DM application could offset its advantages. Biochar (BC) is known to affect N transformation and GHGs emissions from soil. There had been considerably less focus on the BC amendment and its effects on GHGs emissions following DM application under field conditions. The objectives of this study were; i) to determine the temporal patterns and cumulative GHGs fluxes following DM and inorganic nitrogen (IN) application and, ii) to investigate BC amendment impact on DMY, GWP, direct N₂O emission factor (EFd) and the response of CH₄ emissions (RC) in DM based silage corn. To achieve these objectives a two-year field experiment was conducted with these treatments: 1) DM with high N conc. (DM₁: 0.37% N); 2) DM with low N conc. (DM₂: 0.13% N); 3) IN; 4) DM₁+BC; 5) DM₂+BC; 6) IN + BC; and 7) Control (N₀); and were laid out in randomized complete block design with four replications. BC amendment to DM₁, DM₂ and IN significantly reduced cumulative CO₂ emission by 16, 25.5 and 26.5%, CH₄ emission by 184, 200 and 293% and N₂O emission by 95, 86 and 93% respectively. It also reduced area-scaled and yield-scaled GWP, EFd, RC and enhanced DMY. Thus, BC application showed great potential to offset the negative effects of DM application i.e GHGs emissions from the silage corn cropping system. Further research is needed to evaluate soil organic carbon and nitrogen dynamics (substrates for GHG emissions) after DM and BC application on various soil types and cropping systems under field conditions.

As an important part of extracellular secondary metabolites, extracellular polymeric substances (EPS) can play a significant role in protecting cells from the threat of exogenous substances, including nanoparticles (NPs). However, the regulation mechanisms of EPS secretion under NPs exposure remain largely unknown. This study investigated the signaling pathways and molecular responses related to EPS secretion of algae (Chlorella pyrenoidosa) upon the exposures to anatase and rutile TiO₂ NPs (nTiO₂-A and nTiO₂-R, respectively) at two similar toxic (20% and 50% of algal growth inhibition) concentrations. The results showed that EPS responded to nTiO₂ stress via excess secretion and compositional variation, and nTiO₂-A induced more EPS secretion than nTiO₂-R at similar toxicity concentrations. The up-regulation of the Ca²⁺ signaling pathway might play a greater role in promoting EPS secretion under nTiO₂-R exposure compared with nTiO₂-A exposure, while the significantly increased intracellular ROS could mainly account for the increased EPS secretion under nTiO₂-A exposure. The up-regulated genes related to biological synthesis and protein metabolism and the enhanced biosynthetic metabolism might be the direct causes of the increased EPS secretion. The increased ROS could have a greater effect on the amino acid metabolism and related genes upon the exposure to nTiO₂-A than nTiO₂-R to induce more EPS secretion. More serious membrane damage caused by nTiO₂-R than nTiO₂-A would affect the intracellular inositol phospholipid metabolism more severely, while the inositol phospholipid pathway and Ca²⁺ signaling pathway might agree and communicate with each other inherently to regulate EPS secretion upon nTiO₂-R exposure. The findings address the regulation mechanisms of algal EPS secretion under nTiO₂ exposure and provide new insights into algal bio-responses to nTiO₂ exposure.

Though invertebrates are one of the largest groups of animal species in the sea and exhibit robust immune and neural responses that are crucial for their health and survival, the potential immunotoxicity and neurotoxicity of the most produced chemical bisphenol A (BPA), especially in conjunction with microplastics (MPs), still remain poorly understood in marine invertebrate species. Therefore, the impacts of exposure to BPA and MPs alone or in combination on a series of immune and neural biomarkers were investigated in the invertebrate bivalve species blood clam (Tegillarca granosa). Evident immunotoxicity as indicated by alterations in hematic indexes was observed after two weeks of exposure to BPA and MPs at environmentally realistic concentrations. The expression of four immune-related genes from the NFκB signaling pathway was also found to be significantly suppressed by the BPA and MP treatment. In addition, exposure to BPA and MPs led to an increase in the in vivo contents of three key neurotransmitters (GABA, DA, and ACh) but a decrease in the expression of genes encoding modulatory enzymes and receptors for these neurotransmitters, implying the evident neurotoxicity of BPA and MPs to blood clam. Furthermore, the results demonstrated that the toxic impacts exerted by BPA were significantly aggravated by the co-presence of MPs, which may be due to interactions between BPA and MPs as well as those between MPs and clam individuals.

Exposure to Aluminum oxide nanoparticles (Al₂O₃ NPs) has been associated with pulmonary inflammation in recent years; however, the underlying mechanism that causes adverse effects remains unclear. In the present study, we characterized microRNA (miRNA) expression profiling in human bronchial epithelial (HBE) cells exposed to Al₂O₃ NPs by miRNA microarray. Among the differentially expressed miRNAs, miR-297, a homologous miRNA in Homo sapiens and Mus musculus, was significantly up-regulated following exposure to Al₂O₃ NPs, compared with that in control. On combined bioinformatic analysis, proteomics analysis, and mRNA microarray, NF-κB-activating protein (NKAP) was found to be a target gene of miR-297 and it was significantly down-regulated in Al₂O₃ NPs-exposed HBE cells and murine lungs, compared with that in control. Meanwhile, inflammatory cytokines, including IL-1β and TNF-α, were significantly increased in bronchoalveolar lavage fluid (BALF) from mice exposed to Al₂O₃ NPs. Then we set up a mouse model with intranasal instillation of antagomiR-297 to further confirm that inhibition of miR-297 expression can rescue pulmonary inflammation via Notch pathway suppression. Collectively, our findings suggested that up-regulation of miR-297 expression was an upstream driver of Notch pathway activation, which might be the underlying mechanism involved in lung inflammation induced by exposure to Al₂O₃ NPs.