Comparative life cycle assessment of the linear and circular wine industry chains: a case study in Inner Mongolia, China.

Environmental issues and the sustainability of the wine industry receive widespread public attention, but few studies address the environmental impact of the circular wine industry chain. Therefore, we applied the life cycle assessment (LCA) method to a wine enterprise in Inner Mongolia, China, to conduct a cradle-to-gate assessment and comparative analysis on the linear and circular wine industry chain scenarios. The results show that the circular industry chain (S2) has better environmental benefits; the total value of each environmental impact category of S2 is reduced by more than 80% compared with that of the linear industry chain (S1). The global warming potential of S1 is decreased from 4.88 kg CO2eq to 0.919 kg CO2eq for S2. Viticulture is the primary source of environmental problems in all life cycle stages of both scenarios, and electricity and diesel consumption are the key factors affecting the results. Our study shows that the optimization of S2 significantly improves resource efficiency and energy utilization and alleviates the environmental burden through proper waste recycling. Finally, we proposed optimization suggestions based on S2. This study provides scientific guidance for promoting the wine industry to build a circular industry chain and optimize the industrial structure, thus promoting the sustainable development of the industry.

Steam explosion pretreatment coupling high-temperature short-time sterilization facilitating cellulose degradation and sporulation-regulatory gene expression in high-solid fermentation.

Steam explosion coupling high-temperature short-time sterilization (SE-HTST) was exploited to modify cellulosic biomass medium properties and promote high-solid fermentation (HSF). Biomass characterization analysis showed that SE-HTST enlarged microstructural pores and cavities in solid media, providing more effective space for microbial growth. Meanwhile, SE-HTST helped to release glucose from the cellulose with 35.8 ± 4.5, 20.0 ± 2.3, and 12.3 ± 5.7 mg glucose/g dry medium at 24, 48, and 72 h of fermentation, which were 3.1, 2.3, and 1.5 times higher than that in medium from conventional thermal sterilization (CTS), respectively. SE-HTST increased the viable cell and spore number of Bacillus subtilis by 1.8 and 1.6 times at 72 h of fermentation compared to CTS. Moreover, the expressions of master transcriptional gene spo0A and the early sigma factors of sigF and sigE genes gradually increased in the SE-HTST medium, showing enhanced sporulation in HSF. Therefore, SE-HTST is an effective strategy for facilitating cellulose degradation, improving glucose nutrients in biomass medium, and promoting sporulation-regulatory gene expression during high-solid fermentation, which enhances the production of microbial ecological agents using B. subtilis significantly.

Effects of drying strategies on sporulation and titer of microbial ecological agents with Bacillus subtilis.

Drying operation is beneficial to the preservation and transportation of microbial ecological agents. In this study, drying kinetics and water distribution variations in solid biomass medium during hot air drying (HAD) and vacuum freeze drying (VFD) were systematically investigated. Meanwhile, the effects of different drying strategies on the sporulation of Bacillus subtilis and the titer of microbial ecological agents were compared. The results showed that both HAD and VFD induced rapid water removal from the solid biomass medium. VFD retained bound water and maintained the porous structure of the solid medium. Both HAD and VFD induced sporulation. The expression level of sporulation-regulatory genes spo0A, sigF, and sigE followed the order 80°C-HAD > 60°C-HAD > VFD. The spore number in the medium after 80°C-HAD drying for 6 h was 0.72 × 1010/g dry medium, which was 9.1 and 12.5% larger than that of the medium with 60°C-HAD and VFD, respectively. Therefore, 80°C-HAD is an effective drying strategy for promoting sporulation, which improves the titer of microbial ecological agents with B. subtilis.

Modulation of microRNA expression by volatile organic compounds in mouse lung.

Volatile organic compounds (VOCs) are one of main pollutants indoors. Exposure to VOCs is associated with cancer, asthma disease, and multiple chemical allergies. Despite the adverse health effects of VOCs, the molecular mechanisms underlying VOCs-induced disease remain largely unknown. MicroRNAs (miRNAs), as key post-transcriptional regulators of gene expression, may influence cellular disease state. To investigate whether lung miRNA expression profiles in mice are modified by VOCs mixture exposure, 44 male Kunming mice were exposed in 4 similar static chambers, 0 (control) and 3 different doses of VOCs mixture (groups 1-3). The concentrations of VOCs mixture were as follows: formaldehyde, benzene, toluene, and xylene 3.0 + 3.3 + 6.0 + 6.0 mg/m(3) , 5.0 + 5.5 + 10.0 + 10.0 mg/m(3) , 10.0 + 11.0 + 20.0 + 20.0 mg/m(3) , respectively, which corresponded to 30, 50, and 100 times of indoor air quality standard in China, after exposure to 2 weeks (2 h/day, 5 days/week). Small RNAs in lung and protein isolated from bronchoalveolar lavage fluid (BALF) were collected and analyzed for miRNA expression using microarray analysis and for interleukin-8 (IL-8) protein levels by enzyme-linked immunosorbent assay, respectively. VOCs exposure altered the miRNA expression profiles in lung in mice. Specifically, 69 miRNAs were significantly differentially expressed in VOCs-exposed samples versus controls. Functional annotation analysis of the predicted miRNA transcript targets revealed that VOCs exposure potentially alters signaling pathways associated with cancer, chemokine signaling, Wnt signaling, neuroactive ligand-receptor interaction, and cell adhesion molecules. IL-8 isolated from BALF and nitric oxide synthase of lung increased significantly, whereas GSH of lung decreased significantly in mice exposed to VOCs. These results indicate that inhalation of VOCs alters miRNA patterns that regulate gene expression, potentially leading to the initiation of cancer and inflammatory diseases.

Potential mechanisms of neurobehavioral disturbances in mice caused by sub-chronic exposure to low-dose VOCs.

To investigate effects of neurobehavioral disturbances in mice caused by sub-chronic exposure to low-dose volatile organic compounds (VOCs) and the possible mechanism for these effects, 60 male Kunming mice were exposed in 5 similar static chambers, 0 (control) and 4 different doses of VOCs mixture (G1-4) for consecutively 90 d at 2 h/d. The concentrations of VOCs mixture were as follows: formaldehyde, benzene, toluene, and xylene 0.05 + 0.05 + 0.10 + 0.10 mg/m(3), 0.10 + 0.11 + 0.20 + 0.20 mg/m(3), 0.50 + 0.55 + 1.00 + 1.00 mg/m(3), 1.00 +1.10 + 2.00 + 2.00 mg/m(3), respectively, which corresponded to 1/2, 1, 5, and 10 times of indoor air quality standard in China. Morris water maze (MWM) and Grip strength (GS) test were performed in the last 7 weeks. One day following VOCs exposure, oxidative stress markers, neurotransmitters, and cholinergic system enzymes in brain were examined. In addition, the expressions of N-methyl-d-aspartate (NMDA) receptor in hippocampus were determined. VOCs exposure induced behavioral impairment of mice in MWM and GS test. The levels of reactive oxygen species (ROS), malondialdehyde (MDA) and glutamic acid (Glu) were significantly increased, while the acetylcholinesterase (AChE), choline acetyltransferase (ChAT) and acetylcholine (ACh) levels, and the expression of NMDA receptor were significantly decreased in VOCs exposed groups. Results showed that sub-chronic exposure to low-dose VOCs induced damage on physique and motor function, as well as impairment on learning and memory capacity of mice. Oxidative damage, abnormal metabolism of neurotransmitters and cholinergic system enzymes, and the alternation of NMDA receptor expression may be the possible mechanism for VOCs-induced neurotoxicity.

Effects of subchronic exposure to low-dose volatile organic compounds on lung inflammation in mice.

Inflammatory lung diseases are characterized by chronic inflammation and oxidant/antioxidant imbalance. Exposure to some kinds of volatile organic compounds (VOCs) leads to lung inflammation, oxidative stress, and immune modulation. However, it is suspected that sub-chronic exposure to low-dose VOCs mixture induces or aggravates lung inflammation. To clarify the effect of this exposure on lung inflammatory responses, 40 male Kunming mice were exposed in four similar static chambers, 0 (control) and three different doses of VOCs mixture (groups 1-3). The concentrations of VOCs mixture were as follows: formaldehyde, benzene, toluene, and xylene 0.10 + 0.11 + 0.20 + 0.20 mg/m(3) , 0.50 + 0.55 + 1.00 + 1.00 mg/m(3) , 1.00 + 1.10 + 2.00 + 2.00 mg/m(3) , respectively, which corresponded to 1, 5, and 10 times of indoor air quality standard in China. After 90 consecutive days of exposure (2 h/day), oxidative stress markers in lung, cellular infiltration and cytokines, chemokine, neurotrophin in bronchoalveolar lavage fluid (BALF), and immunoglobulin (Ig) in serum were examined. VOCs exposure could increase significantly reactive oxygen species (ROS) in lung, the levels of interleukin-8 (IL-8), IL-4, eotaxin, nerve growth factor (NGF), and various types of leukocytes in BALF, IgE concentration in serum. In contrast, GSH to GSSG ratio and interferon-gamma were significantly decreased following the VOCs exposure. These results indicate that the VOCs mixture-induced inflammatory response is at least partly caused by release of the ROS and mediators from the activated eosinophils, neutrophils, alveolar macrophages and epithelial cells.

Oxidative damage and genotoxic effect in mice caused by sub-chronic exposure to low-dose volatile organic compounds.

Volatile organic compounds (VOCs) are widely used as constituents of household chemicals. Although adverse health effects have been reported, long-term exposure to low-level VOCs mixture has not been studied. Especially, there is a lack of substantial information on the sensitive biomarkers and carcinogenic markers. In the present study, we examined oxidative stress and genotoxic effects of sub-chronic low-dose VOCs mixture (formaldehyde, benzene, toluene and xylene). Male Kunming mice were exposed to 0 (control) and three different doses of VOCs mixture (group 1S, 5S and 10S) for 90 d (2 h/d). Group 1S is 0.10, 0.11, 0.20 and 0.20 mg/m³, group 5S is 0.50, 0.55, 1.00 and 1.00 mg/m³, group 10S is 1.00, 1.10, 2.00 and 2.00 mg/m³, which, respectively, corresponded to 1, 5 and 10 times of indoor air quality standard (IAQS) in China. One day following VOCs exposure, oxidative stress markers in lung, 8-hydroxy-2'-deoxyguanosine in bronchoalveolar lavage fluid and genotoxicity (DNA damage) in liver were examined. Results showed that exposure to VOCs (IAQS dose) resulted in oxidative damages of lung, which were supported by the significant changes on reactive oxygen species, reduced glutathione (GSH), GSH S-transferase, total antioxidative capacity, malondialdehyde, protein carbonyl and nitric oxide (NO). Moreover, oxidative stress markers in group 5S and 10S (except NO) in lung were affected significantly. In addition, VOCs exposure also induced significantly DNA damage in liver. Our study suggested long-term VOCs inhalation at low levels caused oxidative stress and genotoxicity response in mice. Since effects were seen at the current IAQS level, further studies below this level are necessary.

Effect of exposure to volatile organic compounds (VOCs) on airway inflammatory response in mice.

Volatile organic compounds (VOCs) are the main substances causing multiple chemical sensitivity reactions in human. The effects of single VOCs exposure on airway inflammatory responses in mice lung have been reported. Previous studies have demonstrated the role of reactive oxygen species (ROS) in lung inflammation induced by single VOCs inhalation. However, effects of VOCs exposure on NO signaling and neurological signaling pathways in airway remain less clear. We exposed male Kunming mice to filtered air (0) and four types of VOCs mixture (formaldehyde, benzene, toluene, and xylene) treated air. Group 1 is 1.0, 1.1, 2.0 and 2.0 mg/m(3), group 2 is 3.0, 3.3, 6.0 and 6.0 mg/m(3), group 3 is 5.0, 5.5, 10.0 and 10.0 mg/m(3), group 4 is 10.0, 11.0, 20.0 and 20.0 mg/m(3), which respectively corresponded to 10, 30, 50 and 100 times of indoor air quality standard in China 2 hr per day, 5 days per week, for 2 weeks in the whole body exposure chamber. One day following VOCs exposure, we collected lung, bronchoalveolar lavage fluid (BALF) from each mouse and examined oxidative stress markers, cellular infiltration and production of cytokines, neurotrophin and substance P. We found that VOCs exposure influenced significantly NOS activity, GSH, or IL-6 concentration. The number of total cells, macrophages and eosinophils increased significantly in group 4. In addition, the production of interferon-gamma (IFN-γ) and substance P were significantly decreased. In contrast, neurotrophin-3 production in BALF was significantly increased in group 3 and 4. Our findings suggest that NO signaling pathways may induce airway inflammatory in short term VOCs exposure mice and the airway inflammatory response may be modulated by neurological signaling.