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Abstract Dust events are concerning due to their potential to cause environmental pollution and health issues by carrying numerous particles from various regions. However, the risks of airborne bacteria from dust have not yet been thoroughly investigated. This study aimed to reveal the particle size distribution, antibiotic resistance, microbial community structure, and diversity of airborne bacteria by using culture methods, and assess the potential health risks by calculating the dose expectation $$(\overline{d })$$ ( d ¯ ) , daily short-term intake (STI), and Hazard Index (HI) during an extreme dust event in urban Beijing (China). Airborne bacteria were sampled before, during, and the day after a severe dust event in March 2021 in Beijing using the six-stage impactor. The major findings were as follows: (1) airborne bacterial concentration increased during the dust event, and inhalable bacteria account for 67.93%. The Hazard Index (HI) of cultivable and inhalable airborne bacteria in men, women, and children exposed to dust events was up to 1.42 and 1.54 times higher than that in individuals who were not exposed, respectively. HI was 1.52 times higher in children than in men when exposed to the dust event. (2) The percentage of Gram-positive bacteria (GPB) resistant to different antibiotics was altered. The abundance of ciprofloxacin-resistant bacteria increased by 24.51%, while that of clindamycin-resistant bacteria decreased by 34.64%. The $$\overline{d }$$ d ¯ , STI, and HI of antibiotic-resistant bacteria per breath for men, women, and children after the dust event were 14 times greater than those before the dust event. (3) The diversity of airborne bacteria increased throughout the dust event. Opportunistic bacteria were found after the dust event. From a health perspective, airborne bacteria during extreme dust events should be further studied for their sources, changes, human exposure, and so forth. Government-scale measures are necessary to control dust dissemination. Graphical Abstract

Lipids play a crucial role in a range of physiological processes, with a particular significance during the early development stages. However, our understanding of lipid remodeling in cold-water salmon species during these critical early developmental phases remains limited. To address this, a comprehensive lipidomic study was conducted using rainbow trout (Oncorhynchus mykiss) as a model and four critical developmental stages were selected for analysis (i.e., newly fertilized eggs, eyed stage, post-hatch sac-fry stage, and swim-up stage). As expected, our results demonstrated significant lipid alterations during early development of rainbow trout. Through fuzzy c-mean clustering analysis, our study further provided a detailed description on the dynamic changes and regulation of the lipidome. Most unsaturated phosphatidylcholines (PCs) excluding very long-chain polyunsaturated PCs and all polyunsaturated triacylglycerols (TGs) were continuously consumed, suggesting that they are the major energy sources and/or precursor substances for early-stage development in rainbow trout. Gradual increases in very long-chain polyunsaturated phosphatidylethanolamines (PEs) and PCs, phosphatidylserines (PSs), as well as saturated and monounsaturated sphingomyelins (SMs) were observed in this study, which may closely associate with retina and brain development, and the myelination process. Additionally, diacylglycerol (DG), a well-known second messenger, displayed continuous synthesis throughout embryogenesis in this study. In addition to the abovementioned lipid dynamics, our study also found distinct patterns of change in certain glycerophospholipids (GP) isomers, while all glycerolipid (GL) isomers exhibited consistent trends in alteration, indicating different GP isomers may have different biological functions or activities for early development. Overall, this study emphasized the significant roles of lipids during the early development of rainbow trout and served as an informational data set for fish development-related research.

Antimicrobial resistance poses a significant threat to public health and social development worldwide. This study aimed to investigate the effectiveness of silver nanoparticles (AgNPs) in treating multidrug-resistant bacterial infections. Eco-friendly spherical AgNPs were synthesized using rutin at room temperature. The biocompatibility of both polyvinyl pyrrolidone (PVP) and mouse serum (MS)-stabilized AgNPs was evaluated at 20 μg/mL and showed a similar distribution in mice. However, only MS-AgNPs significantly protected mice from sepsis caused by the multidrug-resistant Escherichia coli (E. coli) CQ10 strain (p = 0.039). The data revealed that MS-AgNPs facilitated the elimination of Escherichia coli (E. coli) in the blood and the spleen, and the mice experienced only a mild inflammatory response, as interleukin-6, tumor necrosis factor-α, chemokine KC, and C-reactive protein levels were significantly lower than those in the control group. The results suggest that the plasma protein corona strengthens the antibacterial effect of AgNPs in vivo and may be a potential strategy for combating antimicrobial resistance.

Antimony (Sb) poses a significant threat to human health due to sharp increases in its exploitation and application globally, but few studies have explored the pathophysiological mechanisms of acute hepatotoxicity induced by Sb exposure. We established an in vivo model to comprehensively explore the endogenous mechanisms underlying liver injury induced by short-term Sb exposure. Adult female and male Sprague-Dawley rats were orally administrated various concentrations of potassium antimony tartrate for 28 days. After exposure, the serum Sb concentration, liver-to-body weight ratio, and serum glucose levels significantly increased in a dose-dependent manner. Body weight gain and serum concentrations of biomarkers of hepatic injury (e.g., total cholesterol, total protein, alkaline phosphatase, and the aspartate aminotransferase/alanine aminotransferase ratio) decreased with increasing Sb exposure. Through integrative non-targeted metabolome and lipidome analyses, alanine, aspartate, and glutamate metabolism; phosphatidylcholines; sphingomyelins; and phosphatidylinositols were the most significantly affected pathways in female and male rats exposed to Sb. Additionally, correlation analysis showed that the concentrations of certain metabolites and lipids (e.g., deoxycholic acid, N-methylproline, palmitoylcarnitine, glycerophospholipids, sphingomyelins, and glycerol) were significantly associated with hepatic injury biomarkers, indicating that metabolic remodeling may be involved in apical hepatotoxicity. Our study demonstrated that short-term exposure to Sb induces hepatotoxicity, possibly through a glycolipid metabolism disorder, providing an important reference for the health risks of Sb pollution.

Jasmine flower residue (JFR) is a by-product retained in the production process of jasmine tea and can be used as an unconventional feed due to its rich nutrient value. This study aimed to evaluate the effects of the addition of JFR to the diet of goats on their meat quality and flavor. Twenty-four castrated Nubian male goats were randomly divided into two groups and fed a mixed diet containing 10% JFR (JFR, n = 12) or a conventional diet (CON, n = 12) for 45 days. Meat quality and flavor were measured at the end of the treatment. The addition of JFR to the diet could reduce the shear force of the longissimus dorsi muscle, as well as, the cross-sectional area and diameter of muscle fibers, indicating that the addition of JFR improved meat quality. JFR also increased the content of glutamic acid and ω-3 polyunsaturated fatty acid (C18:3n3 and C20:5N3) and reduced the content of C24:1 and saturated fatty acid (C20:0 and C22:0). In addition, the use of JFR increased the content of acetaldehyde and hexanal in the meat. Furthermore, JFR introduced new volatile components in the meat. The umami, saltiness, and richness of the meat also improved. In conclusion, the addition of jasmine flower residue to the diet can improve the meat quality and flavor of goat.

Background: Air pollution is associated with accelerated biological ages determined by DNA methylation (DNAm) patterns, imposing further risks of age-related adverse effects. However, little is known about the independent and joint effects of exposure to gaseous organic chemicals that may share a common source. Methods: We conducted a panel study with the 3-day exposure assessment monthly among 73 Chinese healthy elderly people aged 60 to 69 years in Jinan, Shandong province during September 2018 to January 2019. Exposure to 26 ambient organic chemical contaminants were measured by wearable passive samplers, including volatile organic compounds, polycyclic aromatic hydrocarbons (PAHs), phthalates (PAEs), nitroaromatics (NIs), polybrominated diphenyl ethers, chlorinated hydrocarbons, and organophosphate esters. The Illumina MethylationEPIC BeadChip was used to measure DNA methylation levels in blood samples, and based on which, epigenetic ageing biomarkers, including Hannum clock, Horvath clock, DNAm PhenoAge, DNAm GrimAge, and DNAm estimator of telomere length (DNAmTL) were calculated. Linear mixed effect models were used to estimate the linear associations between 3-day personal chemical exposure and the epigenetic biomarkers, Weighted quantile sum (WQS) regression and the Bayesian kernel machine regression (BKMR) model were further used to evaluate the effect of chemical mixtures. Results: Multiple linear mixed effects regression models showed that DNAmPhenoAge acceleration was significantly and positively associated with exposure to PAEs, NIs, and PAHs in healthy elderly individuals. Both WQS regression and BKMR models showed a significant positive association with DNAmPhenoAge acceleration with chemical exposures, in which the effect of di-n-butyl phthalate exposure showed the greatest importance. Conclusion: These findings suggest that exposure to a mixture of airborne chemicals significantly increase the acceleration of the epigenetic biomarker of phenotypic age. These findings serve to identify toxic chemicals in the air and facilitate the evaluation of their potentially severe health effects.

Summary: Recent studies have shown that PM2.5 may activate the hypothalamus-pituitary-adrenal (HPA) axis by inducing hormonal changes, potentially explaining the increase in neurological and cardiovascular risks. In addition, an association between PM2.5 and gut microbiota and metabolites was established. The above evidence represents crucial parts of the gut-brain axis (GBA). In view of this evidence, we proposed a hypothesis that PM2.5 exposure may affect the HPA axis through the gastrointestinal tract microbiota pathway (GBA mechanism), leading to an increased risk of neurological and cardiovascular diseases. We conducted a real-world prospective repeated panel study in Jinan, China. At each visit, we measured real-time personal PM2.5 and collected fecal and blood samples. A linear mixed-effects model was used to analyze the association between PM2.5 and serum biomarkers, gut microbiota, and metabolites. We found that PM2.5 was associated with increased serum levels of hormones, especially the adrenocorticotropic hormone (ACTH) and cortisol, which are reliable hormones of the HPA axis. Gut microbiota and tryptophan metabolites and inflammation, which are important components of the GBA, were significantly associated with PM2.5. We also found links between PM2.5 and changes in the nervous and cardiovascular outcomes, e.g., increases of 19.77% (95% CI: −36.44, 125.69) in anxiety, 1.19% (95% CI: 0.65, 1.74) in fasting blood glucose (FBG), 2.09% (95% CI: 1.48, 2.70) in total cholesterol (TCHOL), and 0.93% (95% CI: 0.14, 1.72) in triglycerides (TG), were associated with 10 μg/m3 increase in PM2.5 at the lag 0–72 h, which represent the main effects of GBA. This study indicated the link between PM2.5 and the microbiota GBA for the first time, providing evidence of the potential mechanism for PM2.5 with neurological and cardiovascular system dysfunction.

The emerging and spreading of multi-drug resistant (MDR) bacteria have been becoming one of the most severe threats to human health. Enhancing oxidative stress as mimicking immune system was considered as a potential strategy to fight against infection of MDR bacteria. In this study, we investigated the antibacterial efficiency of such a strategy which combines silver nanoparticles (AgNPs) with ebselen. The results showed that AgNPs and ebselen combination had significant synergistic killing effects both on Escherichia coli (E. coli) and Staphylococcus aureus (S. aureus) in vitro, including model strains of China Veterinary Culture Collection and MDR clinical isolates, which is similar as the combination of silver ion and ebselen. AgNPs exhibited to be a strong inhibitor of bacterial thioredoxin reductase, same as a free silver ion. Ebselen mitigated the cytotoxicity of AgNPs to HeLa cells. However, in a bacteria-cell coexistence condition, the synergistic bactericidal effect was only observed on S. aureus (p

Human exposure to OPEs is pervasive and should be of great concern due to associations with adverse health effects, especially in susceptible populations. In this study, body burdens and exposure pathways of OPEs were investigated for 76 healthy elderly people in Jinan, China based on the measured OPE and metabolite concentrations in human bio-samples (whole blood and urine) and paired environmental matrices (air and dust), as well as food frequency questionnaire. Eight of 16 OPEs and 5 of 11 metabolites were detected in > 50% of whole blood and urine samples, respectively. Tri(1-chloro-2-propyl) phosphate (TCIPP), tris(2-chloroethyl) phosphate (TCEP), tri-phenyl phosphate (TPHP), and 2-ethylhexyl di-phenyl phosphate (EHDPP) were frequently detected and abundant in whole blood, while their corresponding metabolites were detected at low frequencies or levels in urine. The reduced metabolic and/or excretory capacity of elderly people may be an important reason, implying a higher health risk to them. Fourteen OPEs had over 50% detection frequencies in indoor air and dust, while 6 di-esters in indoor dust. Tris(2-ethylhexyl) phosphate (TEHP) in indoor dust and tri-n-butyl phosphate (TnBP) in indoor air were positively correlated with paired levels in blood but not with their metabolites (BEHP and DnBP) in urine. Combined with the direct intakes of BEHP and DBP from dust, blood is indicated as more suitable biomarker for TEHP and TnBP exposure. High consumption frequencies of several foods were associated with higher blood concentrations of three OPEs and urinary levels of four di-OPEs, indicating the importance of dietary exposure pathway. Estimated daily total intakes of OPEs via inhalation, dust ingestion, and dermal absorption ranged from 2.78 to 42.0 ng/kg bw/day, which were far less than the reference dosage values. Further studies were warranted to explore the potential health effects of OPE exposure in the elderly populations.

The health impact of airborne contaminants has been challenging to assess due to current limitations in measurement technologies. The emergence of wearable passive samplers coupled with high resolution mass spectrometry (HR-MS) chemical analysis has enabled comprehensive characterization of personal exposures. We conducted a repeated-measure study among 84 older adults in Jinan, China, as part of the Biomarkers for Air Pollutants Exposure (China BAPE) study. Study objectives were: 1) to characterize the occurrence, magnitude, and distribution of personal exposure to airborne contaminants; 2) to evaluate the temporal variation of chemical exposures across the study population; and 3) to identify behavioral and environmental factors that influence the observed variance in chemical exposures. The FreshAir wristband was worn by participants for three consecutive days each month from September 2018 to January 2019 and collected with paired time-activity logs. Passive air samplers were also deployed in parallel at a local outdoor air monitoring station. Spearman’s Rho trend test and trajectory cluster analysis were used to identify exposure trends and variation patterns, respectively. Out of the 70 airborne compounds of potential concern screened, 26 compounds from 10 chemical classes were found to be above detection thresholds across >70% of the study population. Personal exposures were predominantly characterized by nine polycyclic aromatic hydrocarbons (PAHs), four phthalates, three nitroaromatics, and two volatile organic compounds (VOCs). Phthalate personal exposures were positively correlated with outdoor temperatures while the inverse relationship was observed for certain PAHs (p

Personal exposure to air pollution is affected by its concentration in the microenvironment and individual time-activity patterns. To investigate personal black carbon (BC) exposure levels and identify their potential determinants, we conducted a panel study among 67 elderly residents aged 60–69 years in Jinan, China. Personal BC exposure was measured using portable real-time monitors, while corresponding ambient BC concentrations and meteorological conditions were also collected from the local central site. Time-activity and household characteristics were recorded. A linear mixed-effects model was used to identify potential determinants of personal BC exposure. The daily average personal BC exposure concentration was 4.1 ± 2.0 μg/m3 (±standard deviation, SD), which was significantly lower than the ambient concentration (4.6 ± 2.5 μg/m3) (p

BACKGROUND: Evidence suggested that abiotic airborne exposures may be associated with changes in body composition. However, more evidence is needed to identify key pollutants linked to adverse health effects and their underlying biomolecular mechanisms, particularly in sensitive older adults. OBJECTIVES: Our research aimed to systematically assess the relationship between abiotic airborne exposures and changes in body composition among healthy older adults, as well as the potential mediating mechanisms through the serum lipidome. METHODS: From September 2018 to January 2019, we conducted a monthly survey among 76 healthy adults (60–69 years old) in the China Biomarkers of Air Pollutant Exposure (BAPE) study, measuring their personal exposures to 632 abiotic airborne pollutions using MicroPEM and the Fresh Air wristband, 18 body composition indicators from the InBody 770 device, and lipidomics from venous blood samples. We used an exposome-wide association study (ExWAS) and deletion/substitution/addition (DSA) model to unravel complex associations between exposure to contaminant mixtures and body composition, a Bayesian kernel machine regression (BKMR) model to assess the overall effect of key exposures on body composition, and mediation analysis to identify lipid intermediators. RESULTS: The ExWAS and DSA model identified that 2,4,5-T methyl ester (2,4,5-TME), 9,10-Anthracenedione (ATQ), 4b,8-dimethyl-2-isopropylphenanthrene, and 4b,5,6,7,8,8a,9,10-octahydro-(DMIP) were associated with increased body fat mass (BFM), fat mass indicators (FMI), percent body fat (PBF), and visceral fat area (VFA) in healthy older adults [Bonferroni-Hochberg false discovery rate (FDRBH)<0.05]. The BKMR model demonstrated a positive correlation between contaminants (anthracene, ATQ, copaene, di-epi-a-cedrene, and DMIP) with VFA. Mediation analysis revealed that phosphatidylcholine [PC, PC(16:1e/18:1), PC(16:2e/18:0)] and sphingolipid [SM, SM(d18:2/24:1)] mediated a significant portion, ranging from 12.27% to 26.03% (푝-value <0.05), of the observed increase in VFA. DISCUSSION: Based on the evidence from multiple model results, ATQ and DMIP were statistically significantly associated with the increased VFA levels of healthy older adults, potentially regulated through lipid intermediators. These findings may have important implications for identifying potentially harmful environmental chemicals and developing targeted strategies for the control and prevention of chronic diseases in the future, particularly as the global population is rapidly aging. [ABSTRACT FROM AUTHOR]

BACKGROUND: Insulin resistance (IR) affects the development of type 2 diabetes mellitus (T2DM), which is also influenced by accumulated fine particle air pollution [particulate matter (PM) with aerodynamic diameter of <2.5 µm (PM2.5)] exposure. Previous experimental and epidemiological studies have proposed several potential mechanisms by which PM2.5 contributes to IR/T2DM, including inflammation imbalance, oxidative stress, and endothelial dysfunction. Recent evidence suggests that the imbalance of the gut microbiota affects the metabolic process and may precede IR. However, the underlying mechanisms of PM2.5, gut microbiota, and metabolic diseases are unclear. OBJECTIVES: We investigated the associations between personal exposure to PM2.5 and fasting blood glucose and insulin levels, the IR index, and other related biomarkers. We also explored the potential underlying mechanisms (systemic inflammation and sphingolipid metabolism) between PM2.5 and insulin resistance and the mediating effects between PM2.5 and sphingolipid metabolism. METHODS: We recruited 76 healthy seniors to participate in a repeated-measures panel study and conducted clinical examinations every month from September 2018 to January 2019. Linear mixed-effects (LME) models were used to analyze the associations between PM2.5 and health data (e.g., functional factors, the IR index, inflammation and other IR-related biomarkers, metabolites, and gut microbiota). We also performed mediation analyses to evaluate the effects of mediators (gut microbiota) on the associations between exposures (PM2.5) and featured metabolism outcomes. RESULTS: Our prospective panel study illustrated that exposure to PM2.5 was associated with an increased risk of higher IR index and functional biomarkers, and our study provided mechanistic evidence suggesting that PM2.5 exposure may contribute to systemic inflammation and altered sphingolipid metabolism. DISCUSSION: Our findings demonstrated that PM2.5 was associated with the genera of the gut microbiota, which partially mediated the association between PM2.5 and sphingolipid metabolism. These findings may extend our current understanding of the pathways of PM2.5 and IR. [ABSTRACT FROM AUTHOR]