Perfluorooctane sulfonate (PFOS) is among the most commonly per- and poly-fluoroalkyl substances (PFAS) found in environmental samples. Nevertheless, the effect of this legacy persistent organic contaminant has never been investigated on corals to date. Corals are the keystone organisms of coral reef ecosystems and sensitive to rising ocean temperatures, but it is not understood how the combination of elevated temperature and PFOS exposure will affect them. Therefore, the aims of the present study were (1) to evaluate the time-dependent bioconcentration and depuration of PFOS in the scleractinian coral Stylophora pistillata using a range of PFOS exposure concentrations, and (2) to assess the individual and combined effects of PFOS exposure and elevated seawater temperature on key physiological parameters of the corals. Our results show that the coral S. pistillata rapidly bioconcentrates PFOS from the seawater and eliminates it 14 days after ceasing the exposure. We also observed an antagonistic effect between elevated temperature and PFOS exposure. Indeed, a significantly reduced PFOS bioconcentration was observed at high temperature, likely due to a loss of symbionts and a higher removal of mucus compared to ambient temperature. Finally, concentrations of PFOS consistent with ranges observed in surface waters were non-lethal to corals, in the absence of other stressors. However, PFOS increased lipid peroxidation in coral tissue, which is an indicator of oxidative stress and enhanced the thermal stress-induced impairment of coral physiology. This study provides valuable insights into the combined effects of PFOS exposure and ocean warming for coral's physiology. PFOS is usually the most prevalent but not the only PFAS defected in reef waters, and thus it will be also important to monitor PFAS mixture concentrations in the oceans and to study their combined effects on aquatic wildlife.

Billions of disposable face masks are consumed daily due to the COVID-19 pandemic. The role of these masks as a source of nanoplastics (NPs) and microplastics (MPs) in the environment has not been studied in previous studies. We quantified and characterized face mask released particles and evaluated their potential for accumulation in humans and marine organisms. More than one billion of NPs and MPs were released from each surgical or N95 face mask. These irregularly-shaped particles sized from c. 5 nm to c. 600 μm. But most of them were nano scale sized <1 μm. The middle layers of the masks had released more particles than the outer and inner layers. That MPs were detected in the nasal mucus of mask wearers suggests they can be inhaled while wearing a mask. Mask released particles also adsorbed onto diatom surfaces and were ingested by marine organisms of different trophic levels. This data is useful for assessing the health and environmental risks of face masks.

Marine coastal contamination caused by human activity is a major issue worldwide. The implementation of effective pollution monitoring programs, especially in coastal areas, is important and urgent. The use of biological, physiological, or biochemical measurements to monitor the impacts of pollution has garnered increasing interest, particularly for the development of new non-invasive tools to assess water pollution. Fish skin mucus is in direct contact with the marine environment, making it a favourable microenvironment for the formation of biofilm bacterial communities. In this study, we developed a non-invasive technique, sampling fish skin mucus to determine and analyse bacterial community composition using next-generation sequencing. We hypothesised that bacterial communities associated with the skin mucus of a common harbour benthic blennioid triplefin fish, Forsterygion capito, would reflect conditions of different marine environments. We detected clear differences in bacterial community alpha-diversity between contaminated and reference sites. Beta-diversity analysis also revealed differences in the bacterial community structure of the skin mucus of fish inhabiting different geographical areas. The relative abundance of different bacterial orders varied among sites, as determined by linear discriminant analysis (LDA) and effect size (LEfSe) analyses. The observed variation in bacterial community compositions correlated more strongly with variation in hydrocarbons than to various metal concentrations. Using advanced DNA sequencing technologies, we have developed a novel non-invasive, low-cost and effective tool to monitor the impacts of pollution through analysis of the bacterial communities associated with fish skin mucus.

Some studies have indicated that formaldehyde, a ubiquitous environmental pollutant, can induce or aggravate allergic asthma. Epidemiological studies have also shown that the relative humidity indoors may be an independent and a key factor associated with the aggravation of allergic asthma. However, the synergy of humidity and formaldehyde on allergic asthma and the mechanism underlying this effect remain largely unknown. In this study, we aim to determine the effect of high relative humidity and/or formaldehyde exposure on allergic asthma and explore the underlying mechanisms. Male Balb/c mice were modeled with ovalbumin (OVA) and exposure to 0.5 mg/m3 formaldehyde and/or different relative humidity (60%/75%/90%). Histopathological changes, pulmonary function, Th1/Th2 balance, the status of mucus hypersecretion and the levels of inflammatory factors were detected to assess the exacerbation of allergic asthma. The levels of the transient receptor potential vanilloid 4 (TRPV4), calcium ion and the activation of p38 mitogen-activated protein kinases (p38 MAPK) were detected to explore the underlying mechanisms. The results showed that exposure to high relative humidity or to 0.5 mg/m3 formaldehyde alone had a slight, but not significant, affect on allergic asthma. However, the pathological response and airway hyperresponsiveness (AHR) were greatly aggravated by simultaneous exposure to 0.5 mg/m3 formaldehyde and 90% relative humidity. Blocking TRPV4or p38 MAPK using HC-067047 and SB203580 respectively, effectively alleviated the exacerbation of allergic asthma induced by this simultaneous exposure to formaldehyde and high relative humidity. The results show that when formaldehyde and high relative humidity are present this can enhance the activation of the TRPV4 ion channel in the lung leading to the aggravation of the p38 MAPK activation, resulting in the exacerbation of inflammation and hypersecretion of mucus in the airways.

Manmade antibiotics are emerging organic pollutants widely detected in the marine environment. In this study, 14 out of 19 target antibiotics were detected in corals collected from coastal and offshore regions in the South China Sea. The average total antibiotic concentrations (∑19ABs) in the two regions were similar: 28 ng/g for coastal corals and 31 ng/g for offshore corals, based on dry tissue weight (dw). Fluoroquinolones (FQs) were predominant antibiotics in the coastal corals (mean ∑FQs: 18 ng/g dw), while sulfonamides (SAs) predominated in the offshore corals (mean ∑SAs: 23 ng/g dw). However, corals living in coastal regions tend to excrete more mucus than corals in offshore habitat. We found 53% by average of ∑19ABs in the mucus of the coastal corals; while in offshore corals, most antibiotics (88% by average) were accumulated in the tissues. In addition, the tissue-mucus mass distribution differs among individual antibiotics. Sulfonamides were mainly accumulated in tissues while fluoroquinolones were present mainly in mucus. The results of this study suggest that mucus played an important role in the bioaccumulation of antibiotics by corals. It may resist the bioaccumulation of antibiotics by coral tissue, especially for the coastal corals. Additionally, corals were compared with other marine biotas in the study area and found to be more bioaccumulative towards antibiotics.

Since only a few studies have investigated effects of microplastics (MPs) by routes other than ingestion, this study was designed to analyze the accumulation patterns and transfer of toxic substances associated with microplastic exposure by simple attachment to (1) adult zebrafish (Danio rerio) gills and (2) zebrafish embryos. Two sizes of fluorescently labelled polymers (1–5 and 10–20 μm) loaded with the model polycyclic aromatic hydrocarbon (PAH) benzo[a]pyrene (BaP) were used to analyze fate, accumulation and transfer of microplastic-associated persistent organic pollutants (POPs) on gills and embryos.Results indicate that microplastics did not permanently accumulate at high amounts in adult zebrafish gills after 6 nor 24 h of incubation: Most particles only superficially adhered to the mucus layer on the filaments, which is constantly being excreted. In contrast, the smaller and heavier MPs (1–5 μm) accumulated in high numbers on the surface of zebrafish egg chorions. In both exposure scenarios, transfer of BaP could be visualized with fluorescence microscopy: A prominent BaP signal was visible both in gill filaments and arches after 6 and 24 h incubation and in zebrafish embryos after exposure to BaP-spiked microplastics. Furthermore, the gill EROD (Ethoxyresorufin-O-deethylase) assay showed a clear trend to CYP 1A (Cytochrom P450 1 A) induction via exposure to BaP-spiked microplastics. However, BaP from spiked microplastics did not reach sufficiently high concentrations to be able to induce morphological effects in the fish embryo toxicity test (FET). In contrast, control exposure to waterborne BaP did induce effects in the FET.As a conclusion, microplastics can also transfer POPs not only via ingestion, but also by simple attachment to epithelia or via the water column. However, further studies are needed to clarify if these interactions are of environmental concern relative to waterborne exposure to toxic substances.

Increasing use of metal and metal oxide nanoparticles [Me(O)NPs] in products means many will inevitably find their way into marine systems. Their likely fate here is sedimentation following hetero-aggregation with natural organic matter and/or free anions, putting benthic, sediment-dwelling and filter feeding organisms most at risk. In marine systems, Me(O)NPs can absorb to micro-organisms with potential for trophic transfer following consumption. Filter feeders, especially bivalves, accumulate Me(O)NPs through trapping them in mucus prior to ingestion. Benthic in-fauna may directly ingest sedimented Me(O)NPs. In fish, uptake is principally via the gut following drinking, whilst Me(O)NPs caught in gill mucus may affect respiratory processes and ion transport. Currently, environmentally-realistic Me(O)NP concentrations are unlikely to cause significant adverse acute health problems, however sub-lethal effects e.g. oxidative stresses have been noted in many organisms, often deriving from dissolution of Ag, Cu or Zn ions, and this could result in chronic health impacts.

The effects on the growth of tomato seedlings and cadmium accumulation of earthworm mucus and a solution of amino acids matching those in earthworm mucus was studied through a hydroponic experiment. The experiment included four treatments: 5 mg Cd L⁻¹ (CC), 5 mg Cd L⁻¹ þ 100 mL L⁻¹ earthworm mucus (CE), 5 mg Cd L⁻¹ þ 100 mL L⁻¹ amino acids solution (CA) and the control (CK). Results showed that, compared with CC treatment, either earthworm mucus or amino acids significantly increased tomato seedling growth and Cd accumulation but the increase was much higher in the CE treatment compared with the CA treatment. This may be due to earthworm mucus and amino acids significantly increasing the chlorophyll content, antioxidative enzyme activities, and essential microelement uptake and transport in the tomato seedlings. The much greater increase in the effect of earthworm mucus compared with amino acid treatments may be due to IAA-like substances in earthworm mucus.

Polystyrene nanoparticles (PSNPs) are a newly emerging pollutant in the natural environment. However, due to the lack of sufficient toxicological studies in mammals, the potential effects of PSNPs on human health remain largely undefined. Therefore, in this study, young mice aged four weeks old were subjected to oral administration of 0, 0.2, 1, or 10 mg/kg PSNPs for 30 days. Our results demonstrated for the first time that oral exposure to PSNPs affected the expressions of mucus secretion-related genes and altered the community composition of intestinal microbiota, although this treatment did not cause behavioral impairments in young mice. No significant alterations in inflammatory or oxidative stress-related indicators were observed in the liver, lung, intestine, cortex or serum of PSNPs-treated animals. Moreover, exposure to PSNPs did not cause pathological changes in the liver, lung, or cortex tissues. Notably, although oral administration of PSNPs did not produce obvious toxic effects in the major organs of young mice, the possible toxicity of PSNPs remains unresolved and it may depend on the dose, exposure route and species. The potential hazardous effects of PSNPs still need to be systematically assessed, especially for children who are susceptible to exposure to nanoparticles.

Fine particulate matter 2.5 (PM2.5) exposure leads to the progress of pulmonary disease. It has been reported that N6-methyladenosine (m6A) modification was involved in various biological processes and diseases. However, the critical role of m6A modification in pulmonary disease during PM2.5 exposure remains elusive. Here, we revealed that lung inflammation and mucus production caused by PM2.5 were associated with m6A modification. Both in vivo and in vitro assays demonstrated that PM2.5 exposure elevated the total level of m6A modification as well as the methyltransferase like 3 (METTL3) expression. Integration analysis of m6A RNA immunoprecipitation-seq (meRIP-seq) and RNA-seq discovered that METTL3 up-regulated the expression level and the m6A modification of Interleukin 24 (IL24). Importantly, we explored that the stability of IL24 mRNA was enhanced due to the increased m6A modification. Moreover, the data from qRT-PCR showed that PM2.5 also increased YTH N6-Methyladenosine RNA Binding Protein 1 (YTHDF1) expression, and the up-regulated YTHDF1 augmented IL24 mRNA translation efficiency. Down-regulation of Mettl3 reduced Il24 expression and ameliorated the pulmonary inflammation and mucus secretion in mice exposed to PM2.5. Taken together, our finding provided a comprehensive insight for revealing the significant role of m6A regulators in the lung injury via METTL3/YTHDF1-coupled epitranscriptomal regulation of IL24.