Freshwater mussels are among the most endangered groups of fauna anywhere in world. The indiscriminate use of antibiotics has led to the emergence of resistant strains. These antibiotic-resistant bacteria play a key role in increasing the risk allied with the use of surface water and in spread of resistance genes. Two endangered freshwater mussel species, Margaritifera margaritifera and Potomida littoralis, were sampled at 4 sampling sites along a 50 km stretch of River Tua. Water samples were taken at same sites. Of the total of 135 isolates, 64.44% (39.26% from water and 25.19% from mussels) were coliform bacteria. Site T1, with the lowest concentration of coliform bacteria, and site T2 were the only ones where M. margaritifera was found. No E. coli isolates were found in this species and the pattern between water and mussels was similar. P. littoralis, which was present at T3/T4 sites, is the one that faces the highest concentration of bacterial toxins, which are found in treated wastewater effluents and around population centers. Sites T3/T4 have the isolates (water and mussels) with the highest resistance pattern, mainly to β-lactams. Water and P. littoralis isolates (T3/T4) showed resistance to penicillins and their combination with clavulanic acid, and to cephalosporins, precisely to a fourth generation of cephalosporin antibiotics. The analysis provides important information on the risk to water systems, as well as the need to investigate possible management measures. It is suggested that future studies on the health status of freshwater bivalves should incorporate measures to indicate bacteriological water quality.

Nowadays, the ubiquitous distribution and increasing abundance of P⁺ᴵᴵᴵ in waterbodies have caused serious concerns regarding its bioavailability and potential toxicity. However, our knowledge on these issues is relatively limited. We addressed previously unknown effects of P⁺ᴵᴵᴵ on three dominate algae species i.e. Microcystic aeruginosa (M. aeruginosa), Chlorella pyrenoidesa (C. pyrenoidesa) and Cyclotella. sp in eutrophic waterbodies in China. Remarkable declines in biomass, specific growth rate and Chl-a of algae cells treated with 0.01–0.7 mg/L P⁺ᴵᴵᴵ as sole or an alternative P source were observed, indicating P⁺ᴵᴵᴵ had an inhibitory effect on the algal growth. Besides, the intracellular enzyme activities e.g superoxide dismutase (SOD) and malondialdehyde (MDA) were significantly increased with P⁺ᴵᴵᴵ stress. M. aeruginosa and Cyclotella. sp cells seemed to be more sensitive to P⁺ᴵᴵᴵ toxicity than C. pyrenoidesa since cell membrane suffered more serious stress and destruction. These findings combined, it confirmed P⁺ᴵᴵᴵ could not be utilized as bioavailable P, but had certain toxicity to the tested algae. It indicated that the increased P⁺ᴵᴵᴵ abundance in eutrophic waterbodies would accelerate the algal cell death, which could have a positive effect against algal blooms. Our results provide new insights into assessing the ecological risks of P⁺ᴵᴵᴵ in aquatic environments.

In this short communication, we estimate that California's wildfire carbon dioxide equivalent (CO₂e) emissions from 2020 are approximately two times higher than California's total greenhouse gas (GHG) emission reductions since 2003. Without considering future vegetation regrowth, CO₂e emissions from the 2020 wildfires could be the second most important source in the state above either industry or electrical power generation. Regrowth may partly of fully occur over a long period, but due to exigencies of the climate crisis most of the regrowth will not occur quickly enough to avert greater than 1.5 degrees of warming. Global monetized damages caused by CO₂e from in 2020 wildfire emissions amount to some $7.1 billion USD. Our analysis suggests that significant societal benefits could accrue from larger investments in improved forest management and stricter controls on new development in fire-prone areas at the wildland-urban interface.

Juvenile Chinook salmon (Oncorhynchus tshawytscha) of the Sacramento River system encounter many anthropogenically-induced stressors while rearing and migrating to the Pacific Ocean. Located in a prominent agricultural region, the watershed serves as a source of notable contaminants including pesticides. Salmon rearing in riverine and floodplain areas are potentially exposed to these compounds via dietary exposure, which can vary based on selected food webs. Previous studies have suggested that juvenile Chinook salmon rearing in riverine and floodplain environments of the Sacramento River watershed are characterized by different dietary preferences, with potential for contrasting pesticide exposure between habitats. To examine the potential for pesticide exposure, juvenile Chinook salmon and known dietary items were collected in the mainstem Sacramento River and an adjacent floodplain, the Yolo Bypass, in 2019 and 2020, and analyzed for 33 pesticides, including degradates and isomers. Organochlorine pesticides including the DDX group (p,p’-DDT, p,p’-DDD and p,p’-DDE) were prevalent in all examined biota. There was a significantly greater number of total pesticide detections across all classes in zooplankton compared to macroinvertebrates, coupled with higher bifenthrin concentrations in zooplankton across regions and years, which may indicate different exposure potential depending on fish dietary preferences. Detection frequencies and concentrations of organochlorines were higher in prey items during flooding than in drought conditions, suggesting resuspension of legacy compounds. Significantly higher concentrations of organochlorines were recorded in floodplain rearing fish compared to the Sacramento River. These findings suggest that within these habitats, juvenile Chinook salmon feeding primarily on zooplankton within the water column may be exposed to a greater range of pesticides than those feeding on benthic macroinvertebrates, and that the benefits of floodplain rearing may come at a cost of increased organochlorine exposure.

Fine particulate matter (PM2.5) exposure is a significant cause of chronic obstructive pulmonary disease (COPD), but the detailed mechanisms involved in COPD remain unclear. In this study, we established PM2.5-induced COPD rat models and showed that PM2.5 induced pulmonary microvascular injury via accelerating vascular endothelial apoptosis, increasing vascular permeability, and reducing angiogenesis, thereby contributing to COPD development. Moreover, microvascular injury in COPD was validated by measurements of plasma endothelial microparticles (EMPs) and serum VEGF in COPD patients. We then performed m⁶A sequencing, which confirmed that altered N⁶-methyladenosine (m⁶A) modification was induced by PM2.5 exposure. The results of a series of experiments demonstrated that the expression of methyltransferase-like protein 16 (METTL16), an m⁶A regulator, was upregulated in PM2.5-induced COPD rats, while the expression of other regulators did not differ upon PM2.5-induction. To clarify the regulatory effect of METTL16-mediated m⁶A modification induced by PM2.5 on pulmonary microvascular injury, cell apoptosis, permeability, and tube formation, the m⁶A level in METTL16-knockdown pulmonary microvascular endothelial cells (PMVECs) was evaluated, and the target genes of METTL16 were identified from a set of the differentially expressed and m⁶A-methylated genes associated with vascular injury and containing predicted sites of METTL16 methylation. The results showed that Sulfatase 2 (Sulf2) and Cytohesin-1 (Cyth1) containing the predicted METTL16 methylation sites, exhibited higher m⁶A methylation and were downregulated after PM2.5 exposure. Further studies demonstrated that METTL16 may regulate Sulf2 expression via m⁶A modification and thereby contribute to PM2.5-induced microvascular injury. These findings not only provide a better understanding of the role played by m⁶A modification in PM2.5-induced microvascular injury, but also identify a new therapeutic target for COPD.

The use of biomass for cooking and heating is considered an important factor associated with chronic obstructive pulmonary disease (COPD), but few studies have previously addressed its underlying mechanisms. Therefore, this research aimed to evaluate the effects of biomass-related PM₂.₅ (BRPM₂.₅) exposure on 16HBE human airway epithelial cells and in mice with regard to mitochondrial dysfunction. Our study indicated that BRPM₂.₅ exposure of 16HBE cells resulted in mitochondrial dysfunction, including decreased mitochondrial membrane potential, increased expression of fission proteins-phospho-DRP1, increased mitochondrial ROS (mtROS), and decreased levels of ATP. BRPM₂.₅ altered the mitochondrial metabolism of 16HBE cells by decreasing mitochondrial oxygen consumption and glycolysis. However, Mitochondria targeted peptide SS-31 eliminated mitochondrial ROS and alleviated the ATP deficiency and proinflammatory cytokines release. BRPM2.5 exposure resulted in abnormal mitochondrial morphological alterations both in 16HBE and in lung tissue. Taken together, these results suggest that BRPM₂.₅ has detrimental effects on human airway epithelial cells, leading to mitochondrial dysfunction, abnormal mitochondrial metabolism and altered mitochondrial dynamics. The present study provides the first evidence that disruption of mitochondrial structure and mitochondrial metabolism may be one of the mechanisms of BRPM₂.₅-induced respiratory dysfunction.

Sulfur-containing organic pollutants in wastewater could threaten human health due to their high malodor and toxicity, and their conversion processes are more complex than inorganic sulfur compounds. Membrane aerated biofilm reactor (MABR), as a novel and environmentally-friendly biofilm-based technology, is able to remove inorganic sulfur in synthetic wastewater. However, it is unknown how sulfur-containing organic pollutants in actual wastewater are transformed in MABR system. This work demonstrated the feasibility of MABR to eliminate sulfur-containing organic pollutants in actual wastewater, and the removal efficiency could be reached at approximately 100%. Meanwhile, over 70% of sulfur-containing organic contaminants were transformed to SO₄²⁻ during the long-term operation. Further analysis indicated that the functional bacteria that participated in sulfur transformation and carbohydrates degradation (e.g., Chujaibacter, Microscillaceaesp., and Thiobacillus) were evidently enriched when treating actual wastewater. Moreover, the critical metabolic pathways (e.g., sulfur metabolism, glycolysis metabolism, and pyruvate metabolism), and the corresponding genetic expressions (e.g., nrrA, tauA, tauC, sorA, and SUOX) were evidently up-regulated during long-term operation, which was beneficial for the transformation of sulfur-containing organic pollutants in actual wastewater by MABR. This work would expand the application of MABR for treating the actual sulfur-containing organic wastewater and provide an in-depth understanding of the organic sulfur transformation in MABR.

Uncoupling chemical looping gasification (CLG), the organic sulfur evolution was simulated and explored qualitatively and quantitatively using typical sulfur compounds on TG-MS and temperature-programmed fixed bed. The HS radical in the reductive atmosphere easier converted to H₂S and COS. H₂O activated the evolution of S which was stably bonded to carbon, and H₂ generated from gasification and oxidation of reductive Fe by H₂O contributed to the release of sulfur. The proportion of H₂S released from sulfur compounds was greater than 87% in steam gasification, and more than 60% during CLG. Oxygen carriers promoted the conversion of sulfur to SO₂ in the mid-temperature region (500 °C–700 °C), and H₂S in the high temperature region (700 °C–900 °C). Sulfur species played a pivotal role in sulfur evolution at low temperature of CLG. The organic sulfur in mercaptan and benzyl were more easily converted and escaped than in thiophene and phenyl. The thermal stability of sulfur species, the presence of steam and OC affected the initial temperature and peak concentration of gas sulfur release as well as sulfur distribution. Consequently, CLG strengthened the sulfur evolution, and made it possible to targeted restructure the distribution of sulfur by regulating process parameters, or blending fuel with different sulfur species for emission reduction, and selective conversion of sulfur.

Aqueous film-forming foam (AFFF) has historically contained high concentrations of long-chain per-and polyfluoroalkyl substances (PFAS), which have been linked with adverse health outcomes. However, the toxicity of historical AFFFs remains largely unknown, presenting uncertainties in their risk assessment. This study assessed the toxicity of historical AFFFs by exposing human liver cells (HepG2) to various dilutions of 3M Light Water AFFF or Ansulite AFFF (0.001%, 0.002%, 0.005%, 0.009%, 0.019%, 0.038%, 0.075%, 0.15%, and 0.3%) for 24 h. The effects of the two AFFF formulations on the cell viability, intracellular reactive oxygen species (ROS) production, Nrf2-ARE activity, and DNA damage were assessed by CellTiter 96® Aqᵤₑₒᵤₛ One Solution Cell Proliferation Assay (MTS kit), dichlorofluorescein diacetate assay, luciferase assay, and alkaline Comet assay, respectively. The results revealed that the two brands of AFFFs tested were toxic to HepG2 cells at dilutions lower than the recommended 3% application formulation. Specifically, exposure to 3M Light Water AFFF or Ansulite AFFF induced a dilution-dependent decrease in cell viability, increased intracellular ROS production, and increased Nrf2-ARE activity. However, except for the highest concentration (lowest dilution) of 3M Light Water AFFF tested (0.038%.), both 3M Light Water AFFF and Ansulite AFFF did not significantly induce cellular DNA damage. Overall, 3M Light Water AFFF was more toxic than Ansulite AFFF. The findings from this study provided valuable in vitro toxicity data that may better inform the health risk assessment of these historical AFFFs.

Online monitoring of organic micropollutants (OMPs) in the aquatic environment at high temporal resolution is an upcoming technique that provides insights into their dynamics and has the potential to bring water research and management to a new level. An online monitoring setup was developed to quantify OMPs in wastewater treatment plant (WWTP) influent and effluent using automated and continuous sampling, sample preparation, online solid-phase extraction-liquid chromatography-tandem mass spectrometry analysis and data evaluation. This online monitoring setup provided high selectivity and sensitivity (limit of quantification down to 1 ng/L) as well as a stable performance during one week of constant operation whilst using a high sampling frequency of 10 min (>1000 samples). Custom automated data evaluation enabled quantification within seconds after each measurement and results were comparable to those from a commercial software. Additionally, an alarm tool was included in the evaluation application, which automatically notified the user in case a substance exceeded a predefined threshold. The online monitoring setup was applied to WWTP influent and effluent, where 57 substances were monitored over a period of one week and two days, respectively. High temporal resolution enabled the observation of periodic patterns of pharmaceuticals as well as pollution by OMPs originating from point and diffuse sources, while dynamics of OMPs in WWTP effluent were less pronounced. These new insights into the dynamics of OMPs in WWTP influent, which would not be observable using 24 h composite samples, will be a starting point for new stormwater and wastewater research and management strategies.