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.

Numerous applications exist for graphene-based materials, such as graphene oxide (GO) nanosheets. Increased concentrations of GO nanosheets in the environment have the potential to have a large negative effect on the aquatic environment, with consequences for benthic organisms, such as polychaetes. The polychaete Hediste diversicolor mobilises the sediments, hence altering the availability of contaminants and the nutrients biogeochemical cycle. As such, this study proposes to assess the effects of different GO nanosheet concentrations on the behaviour, feeding activity, mucus production, regenerative capacity, antioxidant status, biochemical damage and metabolism of H. diversicolor. This study evidenced that H. diversicolor exposed to GO nanosheets had a significantly lower ability to regenerate their bodies, took longer to feed and burrow into the sediment and produced more mucus. Membrane oxidative damage (lipid peroxidation) increased in exposed specimens. The increased metabolic rate (ETS) evidenced a higher energy expenditure in exposed organisms (high use of ready energy sources – soluble sugars) to fight the toxicity induced by GO nanosheets, such as SOD activity. The increase in SOD activity was enough to reduce reactive oxygen species (ROS) induced by GO on cytosol at the lowest concentrations, avoiding the damage on proteins (lower PC levels), but not on membranes (LPO increase). This study revealed that the presence of GO nanosheets, even at the lower levels tested, impaired behavioural, physiological, and biochemical traits in polychaetes, suggesting that the increase of this engineered nanomaterial in the environment can disturb these benthic organisms, affecting the H. diversicolor population. Moreover, given the important role of this group of organisms in coastal and estuarine food webs, the biogeochemical cycle of nutrients, and sediment oxygenation, there is a real possibility for repercussions into the estuarine community.

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.

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.

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.

Around the globe, worsening air pollution is spawning major public health and environmental concerns, especially in the poorest and most populous cities. As a major secondary air pollutant, ozone is a potential risk factor for exacerbated asthma, although the underlying mechanisms remain uncertain. In this study, we aim to investigate the role of ozone on asthma exacerbation using a classic asthmatic model with allergic airway inflammation by treating Balb/c mice with ovalbumin (OVA). Our study shows ozone exposure significantly exacerbated OVA-induced asthmatic phenotypes, including serum immunoglobulin, Th cytokines, inflammatory cell counts, mucus production, airway remodeling, and airway hyper-responsiveness (AHR). Interestingly, expression of transient receptor potential cation channel subfamily V member1 (TRPV1) was also significantly elevated in ozone-exacerbated asthmatic mice and that treatment with TRPV1 antagonist effectively suppressed AHR, airway inflammation and remodeling. The underlying mechanisms of these effects may be associated with suppression of neuropeptide calcitonin gene-related peptide (CGRP) and thymic stromal lymphopoietin (TSLP), an epithelial cell-derived cytokine. Base on the role of TRPV1 in allergic asthma, this study further revealed that inhibition of TRPV1 by TRPV1 antagonist has significant anti-inflammatory effects on ozone-induced asthma exacerbation in this study. Induction of TRPV1 expression may be an important mechanism underlying the increased risks for asthma after exposure to environmental pollutants.

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.

Microplastic (MP) vector effects have been well described in the literature but surprisingly little is in known about the impact of MPs on the intestinal uptake of contaminants. The present study aimed to determine whether the intestinal fate of Ag was affected by the presence of polyethylene MP beads. Ag (added as ¹¹⁰ᵐAg) was introduced into the lumen of rainbow trout (Oncorhynchus mykiss) anterior/mid-intestine gut sac preparations as Ag only, Ag and MPs (co-exposure) and Ag-incubated MPs (where Ag was adsorbed to the MP). Results show that after 3 h exposure the distribution of accumulated Ag between the four intestinal compartments (mucus layer, mucosal epithelium, muscle layer and serosal saline) was not affected by either MP condition when compared to Ag alone (p > 0.05, One way ANOVA). Across all treatment groups mucus layer binding dominated (54.2–72.6%) whereas relatively little Ag was transported to the blood compartment (i.e. combined muscle layer and serosal saline compartments, 8.5–15.0%). Accompanying adsorption/desorption studies were performed in relevant media. Over 24 h, 60.6± 2.9% of the available Ag in artificial freshwater adhered to the surface of the PE MPs. In pH adjusted luminal fluids (pH 2.2, 4.1, 7.4 and 9.8) that span the range of conditions encountered within the rainbow trout digestive tract, there was almost complete dissociation at acidic pHs within 3 h (<2% remaining on MPs at both pH 2.2 and pH 4.1). Such pHs are typical of piscine stomach. Based on our finding we suggest that following the ingestion of MPs with adsorbed pollutants, desorption would occur prior to entering the site of uptake. The MPs themselves have no impact on the trans-epithelial transport of the contaminant, but the net result of the MP vector effect is to potentially introduce labile contaminant forms into the intestine.

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.