Biofilm-mediated bioremediation of xenobiotic pollutants is an environmental friendly biological technique. In this study, 36 out of 55 bacterial isolates developed biofilms in glass test tubes containing salt-optimized broth plus 2% glycerol (SOBG). Scanning electron microscopy, Fourier transform infrared (FTIR) spectroscopy, and Congo red- and Calcofluor binding results showed biofilm matrices contain proteins, curli, nanocellulose-rich polysaccharides, nucleic acids, lipids, and peptidoglycans. Several functional groups including –OH, N–H, C–H, CO, COO⁻, –NH₂, PO, C–O, and C–C were also predicted. By sequencing, ten novel biofilm-producing bacteria (BPB) were identified, including Exiguobacterium indicum ES31G, Kurthia gibsonii ES43G, Kluyvera cryocrescens ES45G, Cedecea lapagei ES48G, Enterobacter wuhouensis ES49G, Aeromonas caviae ES50G, Lysinibacillus sphaericus ES51G, Acinetobacter haemolyticus ES52G, Enterobacter soli ES53G, and Comamonas aquatica ES54G. The Direct Red (DR) 28 (a carcinogenic and mutagenic dye used in dyeing and biomedical processes) decolorization process was optimized in selected bacterial isolates. Under optimum conditions (SOBG medium, 75 mg L⁻¹ dye, pH 7, 28 °C, microaerophilic condition and within 72 h of incubation), five of the bacteria tested could decolorize 97.8% ± 0.56–99.7% ± 0.45 of DR 28 dye. Azoreductase and laccase enzymes responsible for biodegradation were produced under the optimum condition. UV–Vis spectral analysis revealed that the azo (−NN−) bond peak at 476 nm had almost disappeared in all of the decolorized samples. FTIR data revealed that the foremost characteristic peaks had either partly or entirely vanished or were malformed or stretched. The chemical oxygen demand decreased by 83.3–91.3% in the decolorized samples, while plant probiotic bacterial growth was indistinguishable in the biodegraded metabolites and the original dye. Furthermore, seed germination (%) was higher in the biodegraded metabolites than the parent dye. Thus, examined BPB could provide potential solutions for the bioremediation of industrial dyes in wastewater.

Accurate quantification of nanoplastics (NPs) in complex matrices remains a challenge, especially for biological samples containing high content of organic matters. Herein, a new method extracting and quantifying polystyrene (PS) NPs from biological samples was developed. The extraction included alkaline digestion, centrifugation, and cloud point extraction (CPE), and the quantification included gold nanoparticles formation and labeling on surfaces of the extracted NPs and thereafter measurement with single particle inductively coupled plasma mass spectrometry (SP-ICP-MS). Results show that 25% tetramethylammonium hydroxide solution was an effective alkaline digestion solution for biological matrices, and CPE after centrifugation (3000 rpm, 10 min) was applicable to purify and enrich PS NPs with different sizes (100 and 500 nm) and surface functionalities (-COOH and –NH₂ modifications) from the digestion solution. The efficiency of Au labeling on PS NPs surface was improved by about 70% in the presence of 100 μM cetyltrimethylammonium bromide. The performance of the quantification method was examined by extraction and measurement of PS NPs spiked in four representative organism samples including bacteria, algae, nematode, and earthworm, and was further validated by analyzing the accumulated PS NPs in exposed nematodes. Good recovery rates (65 ± 10%–122 ± 22%) were achieved for spiking levels of 5–50 μg g⁻¹; the limit of detection was 3.7 × 10⁷ particles g⁻¹, corresponding to the mass concentration of about 0.02 and 2.5 μg g⁻¹ for the 100 nm and 500 nm PS NPs, respectively. The established extraction and quantification methods are efficient and sensitive, providing a useful approach for further exploring the environmental behavior and toxicity of NPs.

Litterfall mercury (Hg) input has been regarded as the dominant Hg source in montane forest floor. To depict combining effects of vegetation, climate and topography on accumulation of Hg in montane forests, we comprehensively quantified litterfall Hg deposition and decomposition in a serial of subtropical forests along an elevation gradient on both leeward and windward slopes of Mt. Ailao, Southwest China. Results showed that the average litterfall Hg deposition increased from 12.0 ± 4.2 μg m⁻² yr⁻¹ in dry-hot valley shrub at 850–1000 m, 14.9 ± 6.8 μg m⁻² yr⁻¹ in mixed conifer-broadleaf forest at 1250–2400 m, to 23.1 ± 8.3 μg m⁻² yr⁻¹ in evergreen broadleaf forest at 2500–2650 m. Additionally, the windward slope forests had a significantly higher litterfall Hg depositions at the same altitude because the larger precipitation promoted the greater litterfall biomass production. The one-year litter Hg decomposition showed that the Hg mass of litter in dry-hot valley shrub decreased by 29%, while in mixed conifer-broadleaf and evergreen broadleaf forests increased by 22–48%. The dynamics of Hg in decomposing litter was controlled by the temperature mediated litter decomposition rate and the additional adsorption of environmental Hg during decomposition. Overall, our study highlights the litterfall mediated atmospheric mercury inputs and sequestration increase with the montane elevation, thus driving a Hg enhanced accumulation in the high montane forest.

Wastewater treatment plants (WWTPs) are among the main hotspots of antibiotic resistance genes (ARGs) in the environment. Previously, we demonstrated that, by increasing anthropogenic pollution, the antibiotic resistome persisted in the microbial community of rivers and lakes, independently by changes in community composition. In this study, we reanalysed the data to test for the relation of metal resistance genes (MRGs), plasmids, and integrons to the persistence of the antibiotic resistome. The experiment consisted in replicated co-cultures of riverine or lacustrine microbial communities and WWTP effluents in different proportions. Samples before (T0) and after a short period of incubation (TF) were collected and community metagenomic data were obtained by shotgun sequencing. The data were processed to annotate MRGs, plasmids, and integrases. The integrases stabilized in the aquatic environment following the degree of contamination with effluent water (in particular in one site), whereas MRGs and plasmids showed stochastic trajectories. These results confirm the potential correlation between integrons and anthropogenic pollution, and the reliability of intI1 as a pollution marker. Only in one site MRGs, plasmids, and ARGs were correlated, highlighting their partial contribution to the persistence of ARGs in surface waters.

Epidemiological studies have indicated that exposure to ambient air-borne fine particulate matter (PM2.5) is associated with many cardiopulmonary diseases; however, the underlying pathological mechanisms of PM2.5-induced lung injury remain unknown. In this study, we aimed to assess the impact of acute or prolonged exposure to water-insoluble fractions of PM2.5 (PM2.5 particulate) on lung injury and its molecular mechanisms. Balb/c mice were randomly exposed to PM2.5 once (acute exposure) or once every three days for a total of 6 times (prolonged exposure). Lung, BALF and blood samples were collected, and pulmonary pathophysiological alterations were analyzed. Nrf2 knockout mice were adapted to assess the involvement of Nrf2 in lung injury, and transcriptomic analysis was performed to delineate the mechanisms. Through transcriptomic analysis and validation of Nrf2 knockout mice, we found that acute exposure to PM2.5 insoluble particulates induced neutrophil infiltration-mediated airway inflammation, whereas prolonged exposure to PM2.5 insoluble particulate triggered lung fibrosis by decreasing the transcriptional activity of Nrf2, which resulted in the downregulated expression of antioxidant-related genes. In response to secondary LPS exposure, prolonged PM2.5 exposure induced more severe lung injury, indicating that prolonged PM2.5 exposure induced Nrf2 inhibition weakened its antioxidative defense capacity against oxidative stress injury, leading to the formation of pulmonary fibrosis and increasing its susceptibility to secondary bacterial infection.

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 cement industry is the second largest source of anthropogenic mercury (Hg) emissions in Europe, accounting for 11% of global anthropogenic Hg emissions. The main objective of this study was to examine the influence of Hg emissions from the Salonit Anhovo cement plant on Hg levels measured in the ambient air at Vodarna, 1 km downwind from the flue gas chimney. The findings reveal that the plant raw mill operational status plays an important role in Hg concentrations in the flue gas emitted from the plant. Emitted total gaseous mercury was, on average, higher (49.4 μg/m³) when raw mills were in the direct mode (both raw mills-off) and lower (23.4 μg/m³) in the combined mode (both raw mills-on). The average Hg concentrations in Vodarna were 3.14 ng/m³ for gaseous elemental mercury, 53.7 pg/m³ for gaseous oxidised mercury, and 41.9 pg/m³ for particulate bound mercury for the whole measurement period. Atmospheric Hg speciation in Vodarna, coupled with plant emissions and wind data, has revealed that the total gaseous mercury emitted from the cement plant is clearly related to all Hg species measured in Vodarna. Wind blowing from the northeastern quadrant (mostly NE, ENE) is responsible for the elevated Hg levels in Vodarna, where gaseous oxidised mercury levels are highly linked to the cement plant emissions. However, elevated levels of Hg species in the absence of northeastern winds indicate potential inputs from other unknown local sources as well as inputs from regional and global transport mechanisms.

Cadmium (Cd) is an environmentally polluted toxic heavy metal and seriously risks food safety and human health through food chain. Mining genetic potentials of plants is a crucial step for limiting Cd accumulation in rice crops and improving environmental quality. This study characterized a novel locus in rice genome encoding a Cd-binding protein named OsHIPP16, which resides in the nucleus and near plasma membrane. OsHIPP16 was strongly induced by Cd stress. Histochemical analysis with pHIPP16::GUS reveals that OsHIPP16 is primarily expressed in root and leaf vascular tissues. Expression of OsHIPP16 in the yeast mutant strain ycf1 sensitive to Cd conferred cellular tolerance. Transgenic rice overexpressing OsHIPP16 (OE) improved rice growth with increased plant height, biomass, and chlorophyll content but with a lower degree of oxidative injury and Cd accumulation, whereas knocking out OsHIPP16 by CRISPR-Cas9 compromised the growth and physiological response. A lifelong trial with Cd-polluted soil shows that the OE plants accumulated much less Cd, particularly in brown rice where the Cd concentrations declined by 11.76–34.64%. Conversely, the knockout oshipp16 mutants had higher levels of Cd with the concentration in leaves being increased by 26.36–35.23% over the wild-type. These results suggest that adequate expression of OsHIPP16 would profoundly contribute to Cd detoxification by regulating Cd accumulation in rice, suggesting that both OE and oshipp16 mutant plants have great potentials for restricting Cd acquisition in the rice crop and phytoremediation of Cd-contaminated wetland soils.

Freshwater ecosystems play a key role in global greenhouse gas estimations and carbon budgets, and algal blooms are widespread owing to intensified anthropological activities. However, little is known about greenhouse gas dynamics in freshwater experiencing frequent algal blooms. Therefore, to explore the spatial and temporal variations in methane (CH₄) and carbon dioxide (CO₂), seasonal field investigations were performed in the Northwest Bay of Lake Chaohu (China), where there are frequent algal blooms. From the highest site in the nearshore to the pelagic zones, the CH₄ concentration in water decreased by at least 80%, and this dynamic was most obvious in warm seasons when algal blooms occurred. CH₄ was 2–3 orders of magnitude higher than the saturated concentration, with the highest in spring, which makes this bay a constant source of CH₄. However, unlike CH₄, CO₂ did not change substantially, and river mouths acted as hotspots for CO₂ in most situations. The highest CO₂ concentration appeared in winter and was saturated, whereas at other times, CO₂ was unsaturated and acted as a sink. The intensive photosynthesis of rich algae decreased the CO₂ in the water and increased dissolved oxygen and pH. The increase in CH₄ in the bay was attributed to the mineralization of autochthonous organic carbon. These findings suggest that frequent algal blooms will greatly absorb more CO₂ from atmosphere and increasingly release CH₄, therefore, the contribution of the bay to the lake's CH₄ emissions and carbon budget will be major even though it is small. The results of this study will be the same to other shallow lakes with frequent algal bloom, making lakes a more important part of the carbon budget and greenhouse gases emission.