The accumulation of human-derived debris in the oceans is a global concern and a serious threat to marine wildlife. There is a volume of evidence that points to deleterious effects of marine debris (MD) on cetaceans in terms of both entanglement and ingestion. This review suggests that about 68% of cetacean species are affected by interacting with MD with an increase in the number of species reported to have interacted with it over the past decades. Despite the growing body of evidence, there is an ongoing debate on the actual effects of plastics on cetaceans and, in particular, with reference to the ingestion of microplastics and their potential toxicological and pathogenic effects. Current knowledge suggests that the observed differences in the rate and nature of interactions with plastics are the result of substantial differences in species-specific diving and feeding strategies. Existing projections on the production, use and disposal of plastics suggest a further increase of marine plastic pollution. In this context, the contribution of the ongoing COVID-19 pandemic to marine plastic pollution appears to be substantial, with potentially serious consequences for marine life including cetaceans. Additionally, the COVID-19 pandemic offers an opportunity to investigate the direct links between industry, human behaviours and the effects of MD on cetaceans. This could help inform management, prevention efforts, describe knowledge gaps and guide advancements in research efforts. This review highlights the lack of assessments of population-level effects related to MD and suggests that these could be rather immediate for small populations already under pressure from other anthropogenic activities. Finally, we suggest that MD is not only a pollution, economic and social issue, but also a welfare concern for the species and populations involved.

Microorganisms are essential for modifying arsenic morphology, mobility, and toxicity. Still, knowledge of the microorganisms responsible for arsenic metabolism in specific arsenic-contaminated fields, such as metallurgical plants is limited. We sampled on-field soils from three depths at 70 day intervals to explore the distribution and transformation of arsenic in the soil. Arsenic-metabolizing microorganisms were identified from the mapped gene sequences. Arsenic metabolism pathways were constructed with metagenomics and AsChip analysis (a high-throughput qPCR chip for arsenic metabolism genes). It has been shown in the result that 350 genera of arsenic-metabolizing microorganisms carrying 17 arsenic metabolism genes in field soils were identified, as relevant to arsenic reduction, arsenic methylation, arsenic respiration, and arsenic oxidation, respectively. Arsenic reduction genes were the only genes shared by the 10 high-ranking arsenic-metabolizing microorganisms. Arsenic reduction genes (arsABCDRT and acr3) accounted for 73.47%–78.11% of all arsenic metabolism genes. Such genes dominated arsenic metabolism, mediating the reduction of 14.11%–19.86% of As(V) to As(III) in 0–100 cm soils. Arsenic reduction disrupts microbial energy metabolism, DNA replication and repair and membrane transport. Arsenic reduction led to a significant decrease in the abundance of 17 arsenic metabolism genes (p < 0.0001). The critical role of arsenic-reducing microorganisms in the migration and transformation of arsenic in metallurgical field soils, was emphasized with such results. These results were of pronounced significance for understanding the transformation behavior of arsenic and the precise regulation of arsenic in field soil.

Silicosis is a disease mainly caused by pulmonary interstitial fibrosis caused by long-term inhalation of dust with excessively high content of free SiO₂. Transdifferentiation of lung fibroblasts into myofibroblasts is an important cellular basis for silicosis, but the key transcription factors (TFs) involved in this process are still unclear. In order to explore the biological regulation of transcription factor PPARγ/LXRα in silica-induced pulmonary fibrosis, this study explored the molecular mechanism of PPARγ/LXRα involved in regulating transcription factors related to SiO₂-induced lung injury at the cellular level and in animal models. ChIP-qPCR detected that PPARγ directly regulated the transcriptional activity of the LXRα gene promoter, while the PPARγ agonist RSG increased the expression of LXRα. In addition, we demonstrated in the cell model that upregulation of LXRα can inhibit silica-mediated fibroblast transdifferentiation, accompanied by an increase in the expression of SREBF1, PLTP and ABCA1. The results of LXRα silencing experiment matched those of overexpression experiment. These studies explored the role of LXRα in plasticity and phenotypic transformation between lung fibroblasts and myofibroblasts. Therefore, inhibiting or reversing the transdifferentiation of lung fibroblasts to myofibroblasts by intervening PPARγ/LXRα may provide a new therapeutic target for the treatment of silicosis.

The effects of catalytic hydrothermal (HT) pretreatment on animal manure followed by the addition of hydrochar on the nutrients recovery have not yet been investigated using a combination of chemical, microscopic, and spectroscopic techniques. Therefore, a catalytic HT process was employed to pretreat swine manure without additives (manure-HT) and with H₂O₂ addition (manure-HT- H₂O₂) to improve the conversion efficiency of labile or organic phosphorus (P) to inorganic phase. Then, a Ca–Al layered double hydroxide hydrochar (Ca/Al LDH@HC) derived from corn cob biomass was synthesized and applied to enhance P sorption. Scanning electron microscopy (SEM), and three-dimensional excitation emission matrix (3D-EEM), X-ray photoelectron spectroscopy (XPS), P k-edge X-ray absorption near edge structure (XANES), were used to elucidate the mechanisms of P release and capture. The H₂O₂ assisted HT treatment significantly enhanced the release of inorganic P (251.4 mg/L) as compared to the untreated manure (57.2 mg/L). The 3D-EEM analysis indicated that the labile or organic P was transformed and solubilized efficiently along with the deconstruction of manure components after the H₂O₂ assisted HT pretreatment. Application of Ca/Al LDH@HC improved the removal efficiency of P from the derived P-rich HT liquid. This sorption process was conformed to the pseudo-second-order model, suggesting that chemisorption was the primary mechanism. The results of SEM and P k-edge XANES exhibited that Ca, as the dominated metal component, could act as a reaction site for the formation of phosphate precipitation. These results provide critical findings about recovering P from manure waste, which is useful for biowastes management and nutrients utilization, and mitigating unintended P loss and potential environmental risks.

In recent years, biochar has become of considerable interest for environmental applications, it can be used as a catalyst for sulfides reduction of perchloroethylene, but the crucial role of biochar properties played in catalyzing dechlorination remained ambiguous investigation. To pinpoint the critical functional groups, the modified biochars were respectively produced by HNO₃, KOH and H₂O₂ with similar dimensional structures but different functional groups. Combined with the adsorption and catalytic results of different biochars, the acid-modified biochar had the best catalytic performance (99.9% removal) due to the outstanding specific surface area and ample functional groups. According to characterization and DFT results, carboxyl and pyridine nitrogen exhibited a positive correlation with the catalytic rate, indicating that their contribution to catalytic performance. Customizing biochar with specific functional groups removed depth demonstrated that the carboxyl was essential component. Further, alkaline condition was conducive to catalytic reduction, while tetrachloroethylene cannot be reduced under acidic conditions, because HS⁻ and S²⁻ mainly existed in alkaline environment and the sulfur-containing nucleophilic structure formed with biochar was more stable under this condition. Overall, this study opens new perspectives for in situ remediation by biochar in chlorinated olefin polluted anoxic environment and promotes our insight of modifying for biochar catalyst design.

Arsenic (As) and cadmium (Cd), two major carcinogenic heavy metals, enters into human food chain by the consumption of rice or rice-based food products. Both As and Cd disturb plant-nutrient homeostasis and hence, reduces plant growth and crop productivity. In the present study, As/Cd modulated responses were studied in non-basmati (IR-64) and basmati (PB-1) rice varieties, at physiological, biochemical and transcriptional levels. At the seedling stage, PB-1 was found more sensitive than IR-64, in terms of root biomass; however, their shoot phenotype was comparable under As and Cd stress conditions. The ionomic data revealed significant nutrient deficiencies in As/Cd treated-roots. The principal component analysis identified NH₄⁺ as As-associated key macronutrient; while, NH₄⁺/NO₃⁻ and K⁺ was majorly associated with Cd mediated response, in both IR-64 and PB-1. Using a panel of 21 transporter gene expression, the extent of nutritional deficiency was ranked in the order of PB-1(As)<IR-64(As)<PB-1(Cd)<IR-64(Cd). A feed-forward model is proposed to explain nutrient deficiency induced de-regulation of gene expression, as observed under Cd-treated IR-64 plants, which was also validated at the level of sulphur metabolism related enzymes. Using urea supplementation, as nitrogen-fertilizer, significant mitigation was observed under As stress, as indicated by 1.018- and 0.794-fold increase in shoot biomass in IR-64 and PB-1, respectively compared to that of control. However, no significant amelioration was observed in response to supplementation of urea under Cd or potassium under As/Cd stress conditions. Thus, the study pinpointed the relative significance of various macronutrients in regulating As- and Cd-tolerance and will help in designing suitable strategies for mitigating As and/or Cd stress conditions.

Biodegradation of microplastics (MPs) in contaminated biowastes has received big scientific attention during the past few years. The aim here is to study the impacts of livestock manure biochar (LMBC) on the biodegradation of polyhydroxyalkanoate microplastics (PHA-MPs) during composting, which have not yet been verified. LMBC (10% wt/wt) and PHA-MPs (0.5% wt/wt) were added to a mixture of pristine cow manure and sawdust for composting, whereas a mixture without LMBC served as the control (CK). The maximum degradation rate of PHA-MPs (22–31%) was observed in the thermophilic composting stage in both mixtures. LMBC addition significantly (P < 0.05) promoted PHA-MPs degradation and increased the carbon loss and oxygen loading of PHA-MPs compared to CK. Adding LMBC accelerated the cleavage of C–H bonds and oxidation of PHA-MPs, and increased the O–H, CO and C–O functional groups on MPs. Also, LMBC addition increased the relative abundance of dominant microorganisms (Firmicutes, Proteobacteria, Deinococcus-Thermus, Bacteroidetes, Ascomycota and Basidiomycota) and promoted the enrichment of MP-degrading microbial biomarkers (e.g., Bacillus, Thermobacillus, Luteimonas, Chryseolinea, Aspergillus and Mycothermus). LMBC addition further increased the complexity and connectivity between dominant microbial biomarkers and PHA-MPs degradation characteristics, strengthened their positive relationship, thereby accelerated PHA-MPs biodegradation, and mitigated the potential environmental and human health risk. These findings provide a reference point for reducing PHA-MPs in compost and safe recycling of MPs contaminated organic wastes. However, these results should be validated with other composting matrices and conditions.

Perfluorooctanesulfonic acid (PFOS) is a persistent anthropogenic chemical that can affect the thyroid hormone system in humans and animals. In adults, thyroid hormones (THs) are regulated by the hypothalamic-pituitary-thyroid (HPT) axis, but also by organs such as the liver and potentially the gut microbiota. PFOS and other xenobiotics can therefore disrupt the TH system at various locations and through different mechanisms. To start addressing this, we exposed adult male rats to 3 mg PFOS/kg/day for 7 days and analysed effects on multiple organs and pathways simultaneously by transcriptomics. This included four primary organs involved in TH regulation, namely hypothalamus, pituitary, thyroid, and liver. To investigate a potential role of the gut microbiota in thyroid hormone regulation, two additional groups of animals were dosed with the antibiotic vancomycin (8 mg/kg/day), either with or without PFOS. PFOS exposure decreased thyroxine (T4) and triiodothyronine (T3) without affecting thyroid stimulating hormone (TSH), resembling a state of hypothyroxinemia. PFOS exposure resulted in 50 differentially expressed genes (DEGs) in the hypothalamus, 68 DEGs in the pituitary, 71 DEGs in the thyroid, and 181 DEGs in the liver. A concomitant compromised gut microbiota did not significantly change effects of PFOS exposure. Organ-specific DEGs did not align with TH regulating genes; however, genes associated with vesicle transport and neuronal signaling were affected in the hypothalamus, and phase I and phase II metabolism in the liver. This suggests that a decrease in systemic TH levels may activate the expression of factors altering trafficking, metabolism and excretion of TH. At the transcriptional level, little evidence suggests that the pituitary or thyroid gland is involved in PFOS-induced TH system disruption.

Research on per- and polyfluoroalkyl substances (PFAS) in freshwater ecosystems has focused primarily on legacy compounds and little is still known on the presence of emerging PFAS. Here, we investigated the occurrence of 60 anionic, zwitterionic, and cationic PFAS in a food web of the St. Lawrence River (Quebec, Canada) near a major metropolitan area. Water, sediments, aquatic vegetation, invertebrates, and 14 fish species were targeted for analysis. Levels of perfluorobutanoic acid (PFBA) in river water exceeded those of perfluorooctanoic acid (PFOA) or perfluorooctane sulfonate (PFOS), and a zwitterionic betaine was observed for the first time in the St. Lawrence River. The highest mean PFAS concentrations were observed for the benthopelagic top predator Smallmouth bass (Micropterus dolomieu, Σ₆₀PFAS ∼ 92 ± 34 ng/g wet weight whole-body) and the lowest for aquatic plants (0.52–2.3 ng/g). Up to 33 PFAS were detected in biotic samples, with frequent occurrences of emerging PFAS such as perfluorobutane sulfonamide (FBSA) and perfluoroethyl cyclohexane sulfonate (PFECHS), while targeted ether-PFAS all remained undetected. PFOS and long-chain perfluorocarboxylates (C10–C13 PFCAs) dominated the contamination profiles in biota except for insects where PFBA was predominant. Gammarids, molluscs, and insects also had frequent detections of PFOA and fluorotelomer sulfonates, an important distinction with fish and presumably due to different metabolism. Based on bioaccumulation factors >5000 and trophic magnification factors >1, long-chain (C10–C13) PFCAs, PFOS, perfluorodecane sulfonate, and perfluorooctane sulfonamide qualified as very bioaccumulative and biomagnifying. Newly monitored PFAS such as FBSA and PFECHS were biomagnified but moderately bioaccumulative, while PFOA was biodiluted.