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.

The Central Plains Economic Region (CPER) located along the transport path to the Beijing-Tianjin-Hebei area has experienced severe PM₂.₅ pollution in recent years. However, few modeling studies have been performed on the sources of PM₂.₅, especially the impacts of emission reduction strategies. In this study, the Nested Air Quality Prediction Model System (NAQPMS) with an online tracer-tagging module was adopted to investigate source sectors of PM₂.₅ and a series of sensitivity tests were conducted to investigate the impacts of different sector-based mitigation strategies on PM₂.₅ pollution. The response surfaces of pollutants to sector-based emission changes were built. The results showed that resident-related sector (resident and agriculture), fugitive dust, traffic and industry emissions were the main sources of PM₂.₅ in Zhengzhou, contributing 49%, 19%, 15% and 13%, respectively. Response surfaces of pollutants to sector-based emission changes in Henan revealed that the combined reduction of resident-related sector and industry emissions efficiently decreased PM₂.₅ in Zhengzhou. However, reduced emissions in only the Henan region barely satisfied the national air quality standard of 75 μg/m³, whereas a 50%–60% reduction in resident-related sector and industry emissions over the whole region could reach this goal. On severely polluted days, even a 60% reduction in these two sectors over the whole region was insufficient to satisfy the standard of 75 μg/m³. Moreover, a reduction in traffic emissions resulted in an increase in the O₃ concentration. The results of the response surface method showed that PM₂.₅ in Zhengzhou decreased by 19% in response to the COVID-19 lockdown, which approached the observed reduction of 21%, indicating that the response surface method could be employed to study the impacts of the COVID-19 lockdown on air pollution. This study provides a scientific reference for the formulation of pollution mitigation strategies in the CPER.

Flue gas desulfurized gypsum (FGD gypsum), mainly originates from thermal power plants, smelters, and large-scale enterprise boilers. This article reviews the production in China and the latest beneficial utilizations of FGD gypsum. China is a large coal-consuming country and has always had serious SO₂ emissions. Therefore, the Chinese government has implemented a large number of desulfurization measures since 2006. With continually increasing energy consumption and increasingly stringent environmental requirements, the production of FGD gypsum has exceeded 10⁸ tons. The basic properties and the current beneficial applications of FGD gypsum are summarized here. The practical application of FGD gypsum in four fields—building materials, agriculture, material synthesis, and soil—and its impact on the environment, are analyzed. Finally, a new direction is proposed for the future utilization of FGD gypsum.

This study investigates changes in air quality conditions during the restricted COVID-19 lockdown period in 2020 across 21 metropolitan areas in the Middle East and how these relate to surface urban heat island (SUHI) characteristics. Based on satellite observations of atmospheric gases from Sentinel-5, results indicate significant reductions in the levels of atmospheric pollutants, particularly nitrogen dioxide (NO₂), sulfur dioxide (SO₂), and carbon monoxide (CO). Air quality improved significantly during the middle phases of the lockdown (April and May), especially in small metropolitan cities like Amman, Beirut, and Jeddah, while it was less significant in “mega” cities like Cairo, Tehran, and Istanbul. For example, the concentrations of NO₂ in Amman, Beirut, and Jeddah decreased by −56.6%, −43.4%, and −32.3%, respectively, during April 2020, compared to April 2019. Rather, there was a small decrease in NO₂ levels in megacities like Tehran (−0.9%) and Cairo (−3.1%). Notably, during the lockdown period, there was a decrease in the mean intensity of nighttime SUHI, while the mean intensity of daytime SUHI experienced either an increase or a slight decrease across these locations. Together with the Gulf metropolitans (e.g. Kuwait, Dubai, and Muscat), the megacities (e.g. Tehran, Ankara, and Istanbul) exhibited anomalous increases in the intensity of daytime SUHI, which may exceed 2 °C. Statistical relationships were established to explore the association between changes in the mean intensity and the hotspot area in each metropolitan location during the lockdown. The findings indicate that the mean intensity of SUHI and the spatial extension of hotspot areas within each metropolitan had a statistically significant negative relationship, with Pearson's r values generally exceeding - 0.55, especially for daytime SUHI. This negative dependency was evident for both daytime and nighttime SUHI during all months of the lockdown. Our findings demonstrate that the decrease in primary pollutant levels during the lockdown contributed to the decrease in the intensity of nighttime SUHIs in the Middle East, especially in April and May. Changes in the characteristics of SUHIs during the lockdown period should be interpreted in the context of long-term climate change, rather than just the consequence of restrictive measures. This is simply because short-term air quality improvements were insufficient to generate meaningful changes in the region's urban climate.

The bioaccumulation and adverse effects of organophosphorus flame retardants (OPFRs) on human health have become a global concern. China produces the largest amount of OPFRs globally and has the highest global market share. However, little is known about its emission level and environmental cycling, thereby causing uncertainties in the assessment of the environmental and health impacts of OPFRs. We developed a gridded annual OPFRs emission inventory at 1/4° longitude by 1/4° latitude resolution over China from 2014 to 2018. The results show that the annual OPFRs emissions increased from approximately 670 tons/yr in 2014 to 1000 tons/yr in 2018 in China. Higher OPFR emissions were identified in Jiangxi, Shandong, Beijing-Tianjin-Hebei (BTH), Yangtze River Delta (YRD), and Pearl River Delta (PRD). In total, 2400 tons of OPFRs were released into the atmosphere during the multi-year period, in which production accounting for 56.6% of total OPFR emissions in China. An atmospheric transport model, the Canadian Model for Environmental Transport of Organochlorine Pesticides (CanMETOP), was employed to verify the gridded emission inventory and elucidate the atmospheric environmental fate of OPFRs. Modeled OPFRs in the air and soil agreed reasonably well with observed data, suggesting that the developed inventory was, to a large extent, reliable. The modeled atmospheric and surface soil concentrations of OPFRs across China ranged from 0 to 119 ng/m³ and 0 to 428 ng/g, respectively. East China is subjected to more intense OPFR contamination than the rest of the country. The results provide a valuable dataset and assessment of OPFRs, which may aid policy-makers and the scientific community in developing emission control strategies and evaluating the health and environmental consequences of OPFRs in China.

Long-term exposure to air pollutants, especially particulates, in adulthood is related to cardiovascular diseases and vascular markers of atherosclerosis. However, whether vascular changes in children is related to exposure to air pollutants remains unknown. This study examined whether childhood exposure to air pollutants was related to a marker of cardiovascular risk, carotid intima–media thickness (CIMT) in children aged 11–12 years old. Longitudinal Study of Australian Children (LSAC) recruited parents and their children born in 2003–4. Among the participants, CheckPoint examination was conducted when the children were 11–12 years old. Ultrasound of the right carotid artery was performed using standardized protocols. Average and maximum far-wall CIMT, carotid artery distensibility, and elasticity were quantified using semiautomated software. Annual and life-time exposure to air pollutants was estimated using satellite-based land-use regression by residential postcodes. A total of 1063 children (50.4% girls) with CIMT data, serum cholesterol, and modeled estimates of NO₂ and PM₂.₅ exposure for the period 2003 to 2015 were included. The average and maximum CIMT, carotid distensibility, and elasticity were 497 μm (standard deviation, SD 58), 580 μm (SD 44), 17.4% (SD 3.2), and 0.48%/mmHg (SD 0.09), respectively. The life-time average concentrations of PM₂.₅ and NO₂ were 6.4 μg/m³ (SD 1.4) and 6.4 ppb (SD 2.4), respectively. Both average and maximum CIMT were significantly associated with average ambient PM₂.₅ concentration (average CIMT: +5.5 μm per μg/m³, 95% confidence interval, CI 2.4 to 8.5, and maximum CIMT: +4.9 μm per μg/m³, CI 2.3 to 7.6), estimated using linear regression, adjusting for potential confounders. CIMT was not significantly related to NO₂ exposure. Carotid artery diameter, distensibility, and elasticity were not significantly associated with air pollutants. We conclude that life-time exposure to low levels of PM₂.₅ in children might have measurable adverse impacts on vascular structure by age 11–12 years.

Perfluorooctane sulfonate (PFOS) is one of the most widely used and distributed perfluorinated compounds proven to cause adverse health outcomes. Datasets of ecotoxico-genomics and proteomics have given greater insights for PFOS toxicological effect. However, the molecular mechanisms of hepatotoxicity of PFOS on post-translational modifications (PTMs) regulation, which is most relevant for regulating the activity of proteins, are not well elucidated. Protein glycosylation is one of the most ubiquitous PTMs associated with diverse cellular functions, which are critical towards the understanding of the multiple biological processes and toxic mechanisms exposed to PFOS. Here, we exploit the multilayered glycoproteomics to quantify the global protein expression levels, glycosylation sites, and glycoproteins in PFOS exposure and wild-type mouse livers. The identified 2439 proteins, 1292 glycosites, and 799 glycoproteins were displayed complex heterogeneity in PFOS exposure mouse livers. Quantification results reveal that 241 dysregulated proteins (fold change ≥ 2, p < 0.05) in PFOS exposure mouse livers were involved in the lipid and xenobiotic metabolism. While, 16 overexpressed glycoproteins were exclusively related to neutrophil degranulation, cellular responses to stress, protein processing in endoplasmic reticulum (ER). Moreover, the interactome and functional network analysis identified HP and HSP90AA1 as the potential glycoprotein biomarkers. These results provide unique insights into a deep understanding of the mechanisms of PFOS induced hepatotoxicity and liver disease. Our platform of multilayered glycoproteomics can be adapted to diverse ecotoxicological research.

The impact of oil exploration and production activities on the environment of sub-saharan African countries is not well studied. This study aimed at determining concentrations, sources, and bioaccumulation of 13 polycyclic aromatic hydrocarbons (PAHs) in sediments and fish from the White Nile near Melut oil fields, South Sudan. The study also assessed the ecological and human health risk associated with PAHs in this aquatic system. Total (∑₁₃) PAH concentrations ranged from 566 to 674 ng g⁻¹dry weight (dw) in sediments, while those in fish were 191–1143 ng g⁻¹ wet weight (ww). ∑₁₃PAH concentrations were significantly higher in C. gariepinus than in other fish species. Low molecular weight PAHs (LPAHs) dominated the profile of PAHs in sediments (constituted 95% of ∑₁₃PAHs) and fish (97% of ∑₁₃PAHs). Compared to Sediment Quality Guidelines of the United States Oceanic and Atmospheric Administration, the levels of LPAHs in this study were all above the threshold effect limits, but below the probable effect level, while those of high molecular weight PAHs (HPAHs) were all below the lowest effect levels. The carcinogenic potency equivalent concentrations of PAHs in L. niloticus and C. gariepinus were above the US EPA screening level; suggesting consumption of these species could adversely affect human health. Biota-sediment accumulation factor values (range: 0.006–3.816 g OC g⁻¹ lipid) for PAHs showed high bioaccumulation of LPAHs in fish muscle, and that bioaccumulation decreased with increase in hydrophobicity of the compounds. This is possibly because LPAHs have higher aqueous solubilities which increases their bioavailability through water-gill transfers compared to HPAHs. Profiles of PAHs in the White Nile environment indicate predominant contribution from petrogenic sources, which could be attributed to presence of crude oil reservoirs and oil production operations. More research into the levels of other environmental pollutants in the oil-rich area is recommended.