Introduction: Rhinitis is one of the most prevalent chronic respiratory diseases worldwide. There is emerging evidence suggesting that the indoor microbiome may contribute the onset and exacerbation of rhinitis symptoms, but comprehensive studies on this topic remain scarce.Methods: In this study, we assessed the microbiome assemblage of settled air dust collected in Petri dishes in 86 dormitory rooms of Shanxi University, China using 16s rRNA sequencing. A self-administered questionnaire, including questions about rhinitis symptoms and personal information, was completed by 357 students residing in these dormitories. Logistic and linear regression model was applied to examine the associations between environmental characteristics, indoor microbiome, and rhinitis.Results: The most abundant genera in the dormitories were Ralstonia (15.6%), Pelomonas (11.3%), Anoxybacillus (9.3%) and Ochrobactrum (6.2%). Taxa richness in the class of Actinobacteria and Fusobacteriia was negatively/protectively associated with rhinitis (p<0.05). Six bacterial genera, including those from Actinobacteria (Actinomyces), Fusobacteriia (Fusobacterium), and Bacteroidetes (Prevotella and Capnocytophaga), were negatively/protectively associated with rhinitis. Conversely, seven genera, predominantly from Alphaproteobacteria and Betaproteobacteria (Sphingomonas, Caulobacter, uncharacterized Caulobacteraceae and Comamonadaceae), were positively associated with rhinitis. Living in higher floor level and higher indoor PM_2.5 concentrations were associated with a higher abundance of taxa potentially protective against rhinitis and a lower abundance of taxa potentially increasing the risk of rhinitis (P<0.01). However, having curtain indoor and higher indoor CO₂ concentrations were associated with a lower abundance of taxa potentially protective against rhinitis and a higher abundance of taxa potentially increasing the risk of rhinitis (P<0.01).Discussion: This study enhances our understanding of the complex interactions between environmental characteristics, indoor microbiomes, and rhinitis, shedding light on potential strategies to manipulate indoor microbiome for disease prevention and control.

Background: The World Health Organization has indicated that airport noise is strongly associated with cardiovascular disease, with vascular inflammation identified as the primary mechanism. Therefore, long-term exposure to airport noise is considered far more harmful than other types of noise. However, there remains a lack of research into the mechanisms underlying long-term exposure to airport noise and harm to the human body. Methods: A mouse model was established and exposed to airport noise at a maximum sound pressure level of 95 dB(A) and an equivalent continuous sound pressure level of 72 dB(A) for 12 h per day over a period of 100 days. Quantitative polymerase chain reaction (qPCR) was used to detect the mRNA expression levels of pro-inflammatory and anti-inflammatory factors. Enzyme-linked immunosorbent assay (ELISA) was used to detect LPS, LTA, TMA, and TMAO levels. Intestinal flora composition was analyzed by 16S rDNA sequencing, and targeted metabolomics was employed to determine the levels of serum short-chain fatty acids. Results: Long-term airport noise exposure significantly increased systolic blood pressure, diastolic blood pressure, and mean blood pressure (p < 0.05); significantly increased the mRNA expression levels of oxidative stress parameters (nuclear matrix protein 2, 3-nitrotyrosine, and monocyte chemoattractant protein-1) (p < 0.05); significantly increased pro-inflammatory factors (interleukin 6 and tumor necrosis factor alpha) (p < 0.05); significantly decreased the mRNA expression level of anti-inflammatory factor interleukin 10 (p < 0.05); and significantly increased the content of LPS and LTA (p < 0.05). The composition of the main flora in the intestinal tract was structurally disordered, and there were significant differences between the noise-exposed and control groups at the levels of the phylum, family, and genus of bacteria. β-diversity of the principal component analysis diagrams was clearly distinguished. Compared with those of the control group, TMA-producing bacteria and levels of TMA and TMAO were significantly reduced, and the serum ethanoic acid and propanoic acid levels of the noise-exposed group were significantly decreased (p < 0.05). Conclusions: Long-term airport noise exposure causes significant elevation of blood pressure and structural disruption in the composition of the intestinal flora in mice, leading to elevated levels of oxidative stress and inflammation, resulting in metabolic disorders that lead to significant changes in the production of metabolites.

Long-term exposure to noise can cause irreversible hearing loss. Considering that there is no effective drug treatment, it is important to seek preventive treatment for noise-induced hearing loss (NIHL). Although astragaloside IV (AS-IV) protects against NIHL by reducing serum inflammatory factors, there is scarce information on the regulation of inflammatory factors by AS-IV to prevent NIHL. We investigated the hearing thresholds and relationship between the serum levels of inflammatory cytokines and intestinal microbiota of c57bl/6j mice exposed to noise (103 dB SPL 4 h·d⁻¹) for 7 days, treated with or without AS-IV. Our results revealed a lower hearing threshold and lower serum levels of TNF-α, TNF-γ, IL-6, IL-1β, and IFN-γ in the mice treated with AS-IV. Additionally, AS-IV increased the abundance levels of the phylum Firmicutes, class Bacillus, order Lactobacillus, and family Lactobacillus (p < 0.05), and decreased those of the phylum Bacteroidetes and order Bacteroidales (p < 0.05). Lactobacillus and Bacilli negatively correlated with TNF-α, TNF-γ, and IL-1β; Erysipelotrichaceae negatively correlated with INF-γ; and Clostridiales positively correlated with IL-1β. In conclusion, AS-IV reduces the elevation of hearing thresholds in mice, preventing hearing loss in mice exposed to noise, and under the intervention of AS-IV, changes in the levels of inflammatory factors correlate with intestinal flora. We suggest that AS-IV improves intestinal flora and reduces inflammation levels in c57bl/6j mice exposed to noise.

Background: The role of the indoor microbiome in sick building syndrome (SBS) is well-recognized, yet prior studies have been limited to single-center analyses, limiting a broader understanding and applicability of their findings. Methods: We conducted a multicenter indoor microbiome and metabolome investigation for SBS, involving 1139 middle school students across three regions in Malaysia (Johor Bahru, Terengganu, and Penang). Using high-throughput amplicon sequencing and untargeted LC-MS, indoor microbiome and metabolites were characterized from classroom dust samples. Results: The study found that the prevalence of SBS symptoms was high across all three centers (51.0% to 54.6%). Environmental characteristics, including indoor NO₂ and CO₂ concentrations and total weight of indoor dust, were positively associated with SBS (p < 0.01, linear regression). Curtobacterium in Terengganu was negatively associated with SBS, and Clostridium perfringens in Johor Bahru was positively associated with SBS (p < 0.01, FDR < 0.05). Whereas all identified fungal taxa, including an uncharacterized uc_f_Auriculariaceae_sp., Duportella kuehneroides, and Wallemia mellicola, were positively associated with SBS (p < 0.01, FDR < 0.05) in Johor Bahru and Terengganu. Mediation analysis revealed that the adverse health effects of NO₂ on SBS were partially mediated by the increased abundance of uc_f_Auriculariaceae_sp. (p < 0.05, total effect mediated 51.40%). Additionally, potential protective metabolites (S-adenosylmethionine, N-acetylserotonin, sphinganine, 4-hydroxy-2-quinolone, and (2E,4Z,8E)-Colneleic acid) were mainly derived from environmental microorganisms, conferring protective effects against nasal symptoms and tiredness. In contrast, synthetic chemicals were associated with higher SBS symptoms, inducing eye and nasal symptoms. Conclusions: This study emphasizes both the significance of fostering a balanced indoor microbiome/metabolite and the necessity to reduce exposure to deleterious substances, providing new insights for future targeted intervention strategies.

Porous activated carbons (AC-AN and AC-AO) for toluene adsorption were prepared starting from brewer’s grain biomass pretreated with microorganisms (Aspergillus niger van Tieghem for AC-AN and Aspergillus oryzae RIB40 for AC-AO). The structures and chemical properties of the three activated carbon materials (AC-AN, AC-AO, and AC that was not pretreated with microorganisms) were characterized by N₂ adsorption–desorption isotherms, scanning electron microscopy (SEM), transmission electron microscopy (TEM), Fourier-transform infrared spectroscopy (FTIR), Raman spectroscopy, X-ray diffraction (XRD), and X-ray photoelectron spectroscopy (XPS). The adsorption behavior of the three activated carbons for toluene was studied and correlated with the physical and chemical properties of these materials. The results suggested that the activated carbons prepared by microbial pretreatment had a rougher morphology, higher specific surface area, richer pore structure, fewer oxygen-containing functional groups on the surface, and better adsorption performance for toluene (increased by 31.5% and 18.3% with AC-AN and AC-AO, respectively) compared with the untreated activated carbon (AC). The Thomas model was used to fit the toluene adsorption data, indicating that the rich pore structure accelerated the kinetic process of toluene adsorption. Therefore, appropriate microbial pretreatment of the feedstock that is used to prepare activated carbon can effectively improve its adsorption capacity towards toluene.