Aquaculture activities in southern Chile demand floating devices to produce electricity powered by diesel generators. It has been recently proposed to replace this fuel with propane. However, little is known about the behaviour and possible environmental impacts of an accidental release of propane underwater. In this study we evaluated the impact of water temperature and salinity on the saturation and further release of propane under controlled laboratory experiments. Results showed that under extreme environmentally relevant scenarios (high and low temperature and salinity), propane saturated the water more quickly. However, while it is important to consider that saturation times can be similar (∼2 h), the magnitudes of propane dissolved can be different. Experiments showed that cold waters (5 °C) propane is dissolved twice than warm waters (20 °C). Residence time was more affected by water temperature and almost independent of water salinity. Propane may take at least 2 days to be released from waters (around 90% of the initial amount dissolved under laboratory conditions).Additionally, we evaluated the impact on dissolved oxygen displacement and the embryotoxicity of the dissolved fraction by using Zebrafish Embryo Toxicity Assay. Results showed that dissolved oxygen was quickly removed. However, the levels of dissolved oxygen were promptly recovered in the studied systems. We also observed that propane can generate genotoxic effects (3–10% mortality), but after 2 days the system can be almost free of propane and the effects may become much lower. Comparatively with the literature, propane showed to be less toxic than diesel and it is a viable and less environmentally hazardous replacement for diesel.

Microcystin-LR (MC-LR) and glyphosate (GLY) have been classified as a Group 2B and Group 2A carcinogens for humans, respectively, and frequently found in aquatic ecosystems. However, data on the potential hazard of MC-LR and GLY exposure to the fish gut are relatively scarce. In the current study, a subacute toxicity test of zebrafish exposed to MC-LR (35 μg L⁻¹) and GLY (3.5 mg L⁻¹), either alone or in combination was performed for 21 d. The results showed that MC-LR or/and GLY treatment reduced the mRNA levels of tight junction genes (claudin-5, occludin, and zonula occludens-1) and altered the levels of diamine oxidase and D-lactic, indicating increased intestinal permeability in zebrafish. Furthermore, MC-LR and/or GLY treatment remarkably increased the levels of intestinal IL-1β and IL-8 but decreased the levels of IL-10 and TGF-β, indicating that MC-LR and/or GLY exposure induced an inflammatory response in the fish gut. MC-LR and/or GLY exposure also activated superoxide dismutase and catalase, generally upregulated the levels of p53, bax, bcl-2, caspase-3, and caspase-9, downregulated the levels of caspase-8 and caused notable histological injury in the fish gut. Moreover, MC-LR and/or GLY exposure also significantly altered the microbial community in the zebrafish gut and the expression of miRNAs (miR-146a, miR-155, miR-16, miR-21, and miR-223). Chronic exposure to MC-LR and/or GLY can induce intestinal damage in zebrafish, and this study is the first to demonstrate an altered gut microbiome and miRNAs in the zebrafish gut after MC-LR and GLY exposure.

The presence of ultrafine plastics particles and its potential to concentrate and transport organic contaminants in aquatic environments have become a major concern in recent years. Specifically, the uptake of hazardous chemicals by plastics particles may affect the distribution and bioavailability of the chemicals. In this study, the adsorption of tetracycline (TC), an antibiotic frequently found in aquatic environments, on high-density polyethylene (PE) particles with the average size of 45 μm, was investigated. The PE particles were characterized for surface acidity for the first time. Results showed that pH controls the surface charge of PE particles. TC adsorption onto PE particles was rapid as expected following the pseudo-second-order rate law (r² > 0.99). Polar forces in addition to specific chemical interactions, such as hydrogen bonding and hydrophophilicity controlled TC adsorption onto PE particles. Parameters, including pH, dissolved organic matter, ionic strength, major cations and anions affected TC adsorption onto PE micro-particles. Results indicated that PE particles can function as a carrier of antibiotics in the aquatic environment, which potentially imposes ecosystem and human health risks.

Knowledge of the toxic potential of polycyclic aromatic hydrocarbons (PAHs) has increased over time. Much of this knowledge is about the 16 United States - Environmental Protection Agency (US - EPA) priority PAHs; however, there are other US – EPA non-priority PAHs in the environment, whose toxic potential is underestimated. We conducted a systematic review of in vitro, in vivo, and in silico studies to assess the genotoxicity, mutagenicity, and carcinogenicity of 13 US - EPA non-priority parental PAHs present in the environment. Electronic databases, such as Science Direct, PubMed, Scopus, Google Scholar, and Web of Science, were used to search for research with selected terms without time restrictions. After analysis, following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) protocol, 249 articles, published between 1946 and 2020, were selected and the quality assessment of these studies was performed. The results showed that 5-methylchrysene (5-MC), 7,12-dimethylbenz[a]anthracene (7,12-DMBA), cyclopenta[cd]pyrene (CPP), and dibenzo[al]pyrene (Db[al]P) were the most studied PAHs. Moreover, 5-MC, 7,12-DMBA, benz[j]aceanthrylene (B[j]A), CPP, anthanthrene (ANT), dibenzo[ae]pyrene (Db[ae]P), and Db[al]P have been reported to cause mutagenic effects and have been being associated with a risk of carcinogenicity. Retene (RET) and benzo[c]fluorene (B[c]F), the least studied compounds, showed evidence of a strong influence on the mutagenicity and carcinogenicity endpoints. Overall, this systematic review provided evidence of the genotoxic, mutagenic, and carcinogenic endpoints of US - EPA non-priority PAHs. However, further studies are needed to improve the future protocols of environmental analysis and risk assessment in severely exposed populations.

Cyanobacterial harmful algal blooms (CyanoHABs) have been found to transmit from N₂ fixer-dominated to non-N₂ fixer-dominated in many freshwater environments when the supply of N decreases. To elucidate the mechanisms underlying such “counter-intuitive” CyanoHAB species succession, metatranscriptomes (biotic data) and water quality-related variables (abiotic data) were analyzed weekly during a bloom season in Harsha Lake, a multipurpose lake that serves as a drinking water source and recreational ground. Our results showed that CyanoHABs in Harsha Lake started with N₂-fixing Anabaena in June (ANA stage) when N was high, and transitioned to non-N₂-fixing Microcystis- and Planktothrix-dominated in July (MIC-PLA stage) when N became limited (low TN/TP). Meanwhile, the concentrations of cyanotoxins, i.e., microcystins were significantly higher in the MIC-PLA stage. Water quality results revealed that N species (i.e., TN, TN/TP) and water temperature were significantly correlated with cyanobacterial biomass. Expression levels of several C- and N-processing-related cyanobacterial genes were highly predictive of the biomass of their species. More importantly, the biomasses of Microcystis and Planktothrix were also significantly associated with expressions of microbial genes (mostly from heterotrophic bacteria) related to processing organic substrates (alkaline phosphatase, peptidase, carbohydrate-active enzymes) and cyanophage genes. Collectively, our results suggest that besides environmental conditions and inherent traits of specific cyanobacterial species, the development and succession of CyanoHABs are regulated by co-occurring microorganisms. Specifically, the co-occurring microorganisms can alleviate the nutrient limitation of cyanobacteria by remineralizing organic compounds.

Microplastics pollution in marine environments is concerning. Microplastics persist and accumulate in various sections of the ocean where they present opportunity for micropollutant accumulation and microbial colonisation. Even though biofilm formation on plastics was first reported in the 1970's, it is only in recent years were plastic associated biofilms have gained research attention. Plastic surfaces pose a problem as they are a niche ready for colonisation by diverse biofilm assemblages, composed of specific bacterial communities and putative pathogens prone to acquiring ARGs and resistance in the biofilm. However, the nature of antibiotic resistance on aquatic plastic debris is not yet fully understood and remains a concern. Given the inevitable increase of plastic production and waste generation, microplastics released into the environment may prove to be problematic. This review explores microplastic waste in the ocean and possible concerns that may arise from the presence of microplastics in conjunction with favourable conditions for the development and dispersal of antibiotic resistance in the ocean and food web.

Phenanthrene (Phe), among the most ubiquitous polycyclic aromatic hydrocarbons (PAHs) existing in nature and foodstuffs, has severe effects on hepatic lipids metabolism. However, the detailed mechanism involved is still unknown. For environmental chemicals can disturb intestinal microbiota, which plays a vital role in lipids metabolism, we hypothesized that oral exposure to Phe may disrupt the intestinal microbiota, leading to the induction of an abnormal inflammatory response and lipid metabolism dysfunction. Herein, male mice were orally exposed to Phe (0.05, 0.5 and 5 mg/kg/2d) for ten weeks and the results showed that long term exposure to Phe induced significant alteration in relative Bacteroidetes, Firmicutes and Proteobacteria abundance in male mice. Histopathological anomalies, and significantly increased hepatic levels of free fatty acid, cholesterol and triglyceride were observed as well. The expression of hepatic proteins linked to lipid metabolism including peroxisome proliferator-activated receptors (PPARs), liver X receptor β (LXRβ) and retinoid X receptors (RXRs) were upregulated. The importance of the gut microbiota in Phe-altered lipid metabolism disorder was further confirmed by fecal microbiota transplantation (FMT). FMT intervention boosted microbial diversity and attenuated Phe-induced elevation in liver somatic index and hepatic total lipids levels. These results demonstrated that environmental-level Phe altered the composition of gastrointestinal bacteria and subsequently induced hepatic lipid metabolism disorder. These results would be helpful for understanding the health risk posed by Phe.

With the widespread use of plastics and nanotechnology products, nanoplastics (NPs) have become a potential threat to human health. It is of great practical significance to study and evaluate the distribution of NPs in mice as mammal models and their entry, transport, and cytotoxicity in human cell lines. In this study, we detected the tissue distribution of fluorescent polystyrene nanoplastics (PS-NPs) in mice and assessed their endocytosis, transport pathways, and cytotoxic effects in GES-1 cells. We found that PS-NPs were clearly visible in gastric, intestine, and liver tissues of mice and in GES-1 cells treated with PS-NPs. Entry of PS-NPs into GES-1 cells decreased with the inhibition of caveolae-mediated endocytosis (nystatin), clathrin-mediated endocytosis (chlorpromazine HCl), micropinocytosis (ethyl-isopropyl amiloride), RhoA (CCG-1423), and F-actin polymerization (lantrunculin A). Rac1 inhibitors (NSC 23766) had no significant effect on PS-NPs entering GES-1 cells. F-actin levels significantly decreased in CCG-1423-pretreated GES-1 cells exposed to PS-NPs. GES-1 cell ultrastructural features indicated that internalized PS-NPs can be encapsulated in vesicles, autophagosomes, lysosomes, and lysosomal residues. RhoA, F-actin, RAB7, and LAMP1 levels in PS-NPs-treated GES-1 cells were remarkably up-regulated and the Rab5 level was significantly down-regulated compared to levels in untreated cells. PS-NPs treatment decreased cell proliferation rates and increased cell apoptosis. The formation of autophagosomes and autolysosomes and levels of LC3II increased with the length of PS-NPs treatment. The results indicated that cells regulated endocytosis in response to PS-NPs through the RhoA/F-actin signaling pathway and internalized PS-NPs in the cytoplasm, autophagosomes, or lysosomes produced cytotoxicity. These results illustrate the potential threat of NPs pollution to human health.