Understanding mercury accumulation in mosses of two subalpine forests in China.

The role of forest ecosystems in the global mercury (Hg) biogeochemical cycle is widely recognized; however, using litterfall as a surrogate to assess the Hg sink function of forests encounters limitations. We investigated the accumulation characteristics and influencing factors of Hg in mosses from two remote subalpine forests in southwestern China. The results indicated that there was high Hg accumulation in subalpine forest mosses, with average concentrations of 82 ± 49 ng g-1 for total mercury (THg) and 1.3 ± 0.8 ng g-1 for methylmercury (MeHg). We demonstrated that the accumulation capacity of Hg in mosses was significantly dependent on species and substrates (micro-habitats), the mosses on tree trunks exhibited significantly elevated Hg accumulation levels (THg 132 ± 56 ng g-1, MeHg 1.6 ± 0.2 ng g-1) compared to mosses in other substrates. The surface morphologies and biochemical components of leaf (phyllidia), such as cation exchange capacity (CEC), pectin, uronic acid, and metallothionein, play a crucial role in the accumulation of Hg by mosses. These findings provide valuable insights into Hg accumulation in forest mosses. Suggesting that the contribution of mosses Hg accumulation should be considered when assessing atmospheric Hg sinks of forests.

Insights into growth stages and genotypes in airborne Pb accumulation in Oryza sativa L. grains: Utilizing isotope fingerprinting alongside a model study.

Atmospheric exposure is an important pathway of accumulation of lead (Pb) in Oryza sativa L. grains. In this study, source contributions of soil, early atmospheric exposure, and late atmospheric exposure, along with their bioaccumulation ratios were examined both in the pot and field experiments using stable Pb isotope fingerprinting technology combined with a three-compartment accumulation model. Furthermore, genotype differences in airborne Pb accumulation among four field-grown rice cultivars were investigated using the partial least squares path model (PLS-PM) linking rice Pb accumulation to agronomic traits. The findings revealed that during the late growth period, the air-foliar-grain transfer of Pb was crucial for rice Pb accumulation. Approximately 69-82% of the Pb found in polished rice was contributed by atmospheric source, with more than 80% accumulating during the late growth stage. The air accumulation ratios of rice grains were genotype-specific and estimated to be 0.364-1.062 m3/g during the late growth. Notably, grain size exhibited the highest standardized total effects on the airborne Pb concentrations in the polished rice, followed by leaf Pb and the upward translocation efficiency of Pb. The present study indicates that mitigating the health risks associated with Pb in rice can be achieved by controlling atmospheric Pb levels during the late growth stage and choosing Japonica inbred varieties characterized by large grain size.

The European trees phyllosphere characteristics and its potential in air bioremediation.

The air pollution remediation is naturally carried out by plants. Their overground parts called phyllosphere are a type of a natural filter on which pollutants can be adsorb. Moreover, microbial communities living in phyllosphere perform a variety of biochemical processes removing also chemical pollutants. As their pollution is nowadays a burning issue especially for highly developed countries, the development of effective and ecological technologies for air treatment are of the utmost importance. The use of phyllosphere bacteria in the process of air bioremediation is a promising technology. This article reviews the role of phyllospheric bacteria in air bioremediation processes especially linked with the moderate climate plants. Research results published so far indicate that phyllosphere bacteria are able to metabolize the air pollutants but their potential is strictly determined by plant-phyllospheric bacteria interaction. The European tree species most commonly used for this purpose are also presented. The collected information filled the gap in the practical use of tree species in air bioremediation in the moderate climate zone.

A multi-omics investigation of the lung injury induced by PM2.5 at environmental levels via the lung-gut axis.

Long-term exposure to fine particulate matter (PM2.5) posed injury for gastrointestinal and respiratory systems, ascribing with the lung-gut axis. However, the cross-talk mechanisms remain unclear. Here, we attempted to establish the response networks of lung-gut axis in mice exposed to PM2.5 at environmental levels. Male Balb/c mice were exposed to PM2.5 (dose of 0.1, 0.5, and 1.0 mg/kg) collected from Chengdu, China for 10 weeks, through intratracheally instillation, and examined the effect of PM2.5 on lung functions of mice. The changes of lung and gut microbiota and metabolic profiles of mice in different groups were determined. Furthermore, the results of multi-omics were conjointly analyzed to elucidate the primary microbes and the associated metabolites in lung and gut responsible for PM2.5 exposure. Accordingly, the cross-talk network and key pathways between lung-gut axis were established. The results indicated that exposed to PM2.5 0.1 mg/kg induced obvious inflammations in mice lung, while emphysema was observed at 1.0 mg/kg. The levels of metabolites guanosine, hypoxanthine, and hepoxilin B3 increased in the lung might contribute to lung inflammations in exposure groups. For microbiotas in lung, PM2.5 exposure significantly declined the proportions of Halomonas and Lactobacillus. Meanwhile, the metabolites in gut including L-tryptophan, serotonin, and spermidine were up-regulated in exposure groups, which were linked to the decreasing of Oscillospira and Helicobacter in gut. Via lung-gut axis, the activations of pathways including Tryptophan metabolism, ABC transporters, Serotonergic synapse, and Linoleic acid metabolism contributed to the cross-talk between lung and gut tissues of mice mediated by PM2.5. In summary, the microbes including Lactobacillus, Oscillospira, and Parabacteroides, and metabolites including hepoxilin B3, guanosine, hypoxanthine, L-tryptophan, and spermidine were the main drivers. In this lung-gut axis study, we elucidated some pro- and pre-biotics in lung and gut microenvironments contributed to the adverse effects on lung functions induced by PM2.5 exposure.

Impact of fine particulate matter on liver injury: evidence from human, mice and cells.

BACKGROUND: A recently discovered risk factor for chronic liver disease is ambient fine particulate matter (PM2.5). Our research aims to elucidate the effects of PM2.5 on liver injury and the potential molecular mechanisms. METHODS AND RESULTS: A population-based longitudinal study involving 102,918 participants from 15 Chinese cities, using linear mixed-effect models, found that abnormal alterations in liver function were significantly associated with long-term exposure to PM2.5. The serum levels of alanine aminotransferase, aspartate aminotransferase, gamma-glutamyl transferase, direct bilirubin, and triglyceride increased by 2.05%, 2.04%, 0.58%, 2.99%, and 1.46% with each 10 µg/m3 increase in PM2.5. In contrast, the serum levels of total protein, albumin, and prealbumin decreased by 0.27%, 0.48%, and 2.42%, respectively. Mice underwent chronic inhalation exposure to PM2.5 experienced hepatic inflammation, steatosis and fibrosis. In vitro experiments found that hepatocytes experienced an inflammatory response and lipid metabolic dysregulation due to PM2.5, which also activated hepatic stellate cells. The down-regulation and mis-localization of polarity protein Par3 mediated PM2.5-induced liver injury. CONCLUSIONS: PM2.5 exposure induced liver injury, mainly characterized by steatosis and fibrosis. The down-regulation and mis-localization of Par3 were important mechanisms of liver injury induced by PM2.5.

Role and mechanism of miR-871-3p/Megf8 in regulating formaldehyde-induced cardiomyocyte inflammation and congenital heart disease.

OBJECTIVE AND DESIGN: We aimed to investigate the molecular mechanism underlying formaldehyde (FA)-induced congenital heart disease (CHD) using in vitro and in vivo models. MATERIALS AND SUBJECTS: Neonatal rat heart tissues and H9C2 cells were used for in vitro studies, while FA-exposed new-born rats were used for in vivo studies. TREATMENT: H9C2 cells were exposed to FA concentrations of 0, 50, 100 and 150 µM/mL for 24 h. METHODS: Whole transcriptome gene sequencing identified differentially expressed miRNAs in neonatal rat heart tissues, while Real-time quantitative PCR (RT-qPCR) assessed miR-871-3p and Megf8 expression. RNA pull-down and dual-luciferase reporter assays determined miR-871-3p and Megf8 relationships. Inflammatory cytokine expression was assessed by western blotting. A FA-induced CHD model was used to validate miR-871-3p regulatory effects in vivo. RESULTS: We identified 89 differentially expressed miRNAs, with 28 up-regulated and 61 down-regulated (fold change ≥ 2.0, P < 0.05). Inflammation (interleukin) and signalling pathways were found to control FA-induced cardiac dysplasia. miR-871-3p was upregulated in FA-exposed heart tissues, modulated inflammation, and directly targeted Megf8. In vivo experiments showed miR-871-3p knockdown inhibited FA-induced inflammation and CHD. CONCLUSION: We demonstrated miR-871-3p's role in FA-induced CHD by targeting Megf8, providing potential targets for CHD intervention and improved diagnosis and treatment strategies.

A review of the recent progress in biotrickling filters: packing materials, gases, micro-organisms, and CFD.

Organic pollutants in the air have serious consequences on both human health and the environment. Among the various methods for removing organic pollution gas, biotrickling filters (BTFs) are becoming more and more popular due to their cost-effective advantages. BTF can effectively degrade organic pollutants without producing secondary pollutants. In the current research on the removal of organic pollutants by BTF, improving the performance of BTF has always been a research hotspot. Researchers have conducted studies from different aspects to improve the removal performance of BTF for organic pollutants. Including research on the performance of BTF using different packing materials, research on the removal of various mixed pollutant gases by BTF, research on microbial communities in BTF, and other studies that can improve the performance of BTF. Moreover, computational fluid dynamics (CFD) was introduced to study the microscopic process of BTF removal of organic pollutants. CFD is a simulation tool widely used in aerospace, automotive, and industrial production. In the study of BTF removal of organic pollutants, CFD can simulate the fluid movement, mass transfer process, and biodegradation process in BTF in a visual way. This review will summarize the development of BTFs from four aspects: packing materials, mixed gases, micro-organisms, and CFD, in order to provide a reference and direction for the future optimization of BTFs.

Role of different mechanisms in pro-inflammatory responses triggered by traffic-derived particulate matter in human bronchiolar epithelial cells.

BACKGROUND: Traffic-derived particles are important contributors to the adverse health effects of ambient particulate matter (PM). In Nordic countries, mineral particles from road pavement and diesel exhaust particles (DEP) are important constituents of traffic-derived PM. In the present study we compared the pro-inflammatory responses of mineral particles and DEP to PM from two road tunnels, and examined the mechanisms involved. METHODS: The pro-inflammatory potential of 100 µg/mL coarse (PM10-2.5), fine (PM2.5-0.18) and ultrafine PM (PM0.18) sampled in two road tunnels paved with different stone materials was assessed in human bronchial epithelial cells (HBEC3-KT), and compared to DEP and particles derived from the respective stone materials. Release of pro-inflammatory cytokines (CXCL8, IL-1α, IL-1ß) was measured by ELISA, while the expression of genes related to inflammation (COX2, CXCL8, IL-1α, IL-1ß, TNF-α), redox responses (HO-1) and metabolism (CYP1A1, CYP1B1, PAI-2) was determined by qPCR. The roles of the aryl hydrocarbon receptor (AhR) and reactive oxygen species (ROS) were examined by treatment with the AhR-inhibitor CH223191 and the anti-oxidant N-acetyl cysteine (NAC). RESULTS: Road tunnel PM caused time-dependent increases in expression of CXCL8, COX2, IL-1α, IL-1ß, TNF-α, COX2, PAI-2, CYP1A1, CYP1B1 and HO-1, with fine PM as more potent than coarse PM at early time-points. The stone particle samples and DEP induced lower cytokine release than all size-fractionated PM samples for one tunnel, and versus fine PM for the other tunnel. CH223191 partially reduced release and expression of IL-1α and CXCL8, and expression of COX2, for fine and coarse PM, depending on tunnel, response and time-point. Whereas expression of CYP1A1 was markedly reduced by CH223191, HO-1 expression was not affected. NAC reduced the release and expression of IL-1α and CXCL8, and COX2 expression, but augmented expression of CYP1A1 and HO-1. CONCLUSIONS: The results indicate that the pro-inflammatory responses of road tunnel PM in HBEC3-KT cells are not attributed to the mineral particles or DEP alone. The pro-inflammatory responses seem to involve AhR-dependent mechanisms, suggesting a role for organic constituents. ROS-mediated mechanisms were also involved, probably through AhR-independent pathways. DEP may be a contributor to the AhR-dependent responses, although other sources may be of importance.

Glutaminase 1 isoform up-regulation associated with lipid metabolism disorder induced by methyl tertiary-butyl ether in male rats.

Methyl tertiary-butyl ether (MTBE) is a new unleaded gasoline additive, which is considered to be associated with abnormal lipid metabolism in many studies, but the metabolic characteristics and mechanism are still unclear. To observe the characteristics of lipid metabolism induced by MTBE and possible pathways, 21 male Wistar rats got intragastric administration for 24 weeks. The serum lipid metabolism indexes and metabolites were analyzed separately by a biochemical analyzer and untargeted metabolomics. And found that serum high-density lipoprotein cholesterol (HDL-C) levels in the exposure group were significantly reduced, and serum very low-density lipoprotein (VLDL) levels were significantly increased. In untargeted metabolomics, 190 differential metabolites were obtained. Among them, 23 metabolites were found to show the same trend in MTBE exposure groups, which might play a key role in systemic energy metabolism. Further metabolic pathways analysis showed that D-Glutamine, D-glutamate metabolism, and the other three pathways were affected by MTBE significantly. Therefore, we evaluated serum glutamine and glutamate levels and found that MTBE exposure significantly reduced glutamine levels and increased glutamate levels in rat serum and L-02 cells. Further, the key regulatory gene of glutamine metabolism, glutaminase 1 isoform (GLS1), was significantly up-regulated in rat liver and L-02 cells exposed to MTBE. While the effect of glutamine and glutamate metabolism induced by MTBE could be weakened by BPTES, an antagonist of GLS1. In conclusion, our results indicated that MTBE exposure could change the level of glutamine metabolism by promoting GLS1 expression and ultimately lead to abnormal lipid metabolism.

Fine particulate matter (PM2.5)-induced pulmonary oxidative stress contributes to increases in glucose intolerance and insulin resistance in a mouse model of circadian dyssynchrony.

Results of human and animal studies independently suggest that either ambient fine particulate matter (PM2.5) air pollution exposure or a disturbed circadian rhythm (circadian dyssynchrony) are important contributing factors to the rapidly evolving type-2-diabetes (T2D) epidemic. The objective of this study is to investigate whether circadian dyssynchrony increases the susceptibility to PM2.5 and how PM2.5 affects metabolic health in circadian dyssynchrony. We examined systemic and organ-specific changes in glucose homeostasis and insulin sensitivity in mice maintained on a regular (12/12 h light/dark) or disrupted (18/6 h light/dark, light-induced circadian dyssynchrony, LICD) light cycle exposed to air or concentrated PM2.5 (CAP, 6 h/day, 30 days). Exposures during Zeitgeber ZT3-9 or ZT11-17 (Zeitgeber in circadian time, ZT0 = begin of light cycle) tested for time-of-day PM2.5 sensitivity (chronotoxicity). Mice transgenic for lung-specific overexpression of extracellular superoxide dismutase (ecSOD-Tg) were used to assess the contribution of CAP-induced pulmonary oxidative stress. Both, CAP exposure from ZT3-9 or ZT11-17, decreased glucose tolerance and insulin sensitivity in male mice with LICD, but not in female mice or in mice kept on a regular light cycle. Although changes in glucose homeostasis in CAP-exposed male mice with LICD were not associated with obesity, they were accompanied by white adipose tissue (WAT) inflammation, impaired insulin signaling in skeletal muscle and liver, and systemic and pulmonary oxidative stress. Preventing CAP-induced oxidative stress in the lungs mitigated the CAP-induced decrease in glucose tolerance and insulin sensitivity in LICD. Our results demonstrate that circadian dyssynchrony is a novel susceptibility state for PM2.5 and suggest that PM2.5 by inducing pulmonary oxidative stress increases glucose intolerance and insulin resistance in circadian dyssynchrony.

KCNQ1 rs2237892 polymorphism modify the association between short-term ambient particulate matter exposure and fasting blood glucose: A family-based study.

BACKGROUND: The association between particulate matter and fasting blood glucose (FBG) has shown conflicting results. Genome-wide association studies have shown that KCNQ1 rs2237892 polymorphism is associated with the risk of diabetes. Whether KCNQ1 rs2237892 polymorphism might modify the association between particulate matter and FBG is still uncertain. METHODS: Data collected from a family-based cohort study in Northern China, were used to perform the analysis. A generalized additive Gaussian model was used to examine the short-term effects of air pollutants on FBG. We further conducted interaction analyses by including a cross-product term of air pollutants by rs2237892 within KCNQ1 gene. RESULTS: A total of 4418 participants were included in the study. In the single pollutant model, the FBG level increased 0.0031 mmol/L with per 10 µg/m3 elevation in fine particular matter (PM2.5) for lag 0 day. After additional adjustments for nitrogen dioxide (NO2) and sulfur dioxide (SO2), similar results were observed for lag 0-2 days. As for particulate matter with particle size below 10 µm (PM10), the significant association between the daily average concentration of the pollutant and FBG level was observed for lag 0-3 days. Additionally, rs2237892 in KCNQ1 gene modified the association between PM and FBG level. The higher risk of FBG levels associated with elevations in PM10 and PM2.5 were more evident as the number of risk allele C increased. Individuals with a CC genotype had the highest risk of elevation in FBG levels. CONCLUSION: Short-term exposures to PM2.5 and PM10 were associated with higher FBG levels. Additionally, rs2237892 in KCNQ1 gene might modify the association between the air pollutants and FBG levels.

Application of loofah and insects in a bio-trickling filter to relieve clogging.

Bio-trickling filters (BTFs) use an inert filler to purify pollutants making them prone to clogging due to bacterial accumulation. To investigate the performance of a non-inert filler in BTF and its cooperation with insects to relieve clogging, a vertical BTF was constructed with a loofah/Pall ring/polydimethylsiloxane composite filler and selected bacteria to purify toluene. The BTF was started up within 17 d and restarted within 3 d after starvation for 12-16 d. Its average removal efficiency was >90% at steady state. The maximum elimination capacity of 86.4 g·(m3·h)-1 was obtained at a volume capacity of 96.2 g·(m3·h)-1. The introduction of holometabolous insects (Clogmia albipunctata) rapidly removed the biofilm and accelerated the degradation of the loofah, which alleviated clogging. Furthermore, confocal laser scanning microscope (CLSM) observations showed that the biofilm polysaccharides were difficult to remove, while lipids were readily lost. Analysis of microbial diversity over time and space revealed that the dominant bacterium, Comamonas, was replaced by diverse microflora with no obvious dominant genus. Insect introduction and loofah migration had little effect on the evolution of microflora. This study provides a promising approach to operating BTFs with less clogging.

Aerosol physicochemical determinants of carbon black and ozone inhalation co-exposure induced pulmonary toxicity.

Air pollution accounts for more than 7 million premature deaths worldwide. Using ultrafine carbon black (CB) and ozone (O3) as a model for an environmental co-exposure scenario, the dose response relationships in acute pulmonary injury and inflammation were determined by generating, characterizing, and comparing stable concentrations of CB aerosols (2.5, 5.0, 10.0 mg/m3), O3 (0.5, 1.0, 2.0 ppm) with mixture CB + O3 (2.5 + 0.5, 5.0 + 1.0, 10.0 + 2.0). C57BL6 male mice were exposed for 3 h by whole body inhalation and acute toxicity determined after 24 h. CB itself did not cause any alteration, however, a dose response in pulmonary injury/inflammation was observed with O3 and CB + O3. This increase in response with mixtures was not dependent on the uptake but was due to enhanced reactivity of the particles. Benchmark dose modeling showed several-fold increase in potency with CB + O3 compared with CB or O3 alone. Principal component analysis provided insight into response relationships between various doses and treatments. There was a significant correlation in lung responses with charge-based size distribution, total/alveolar deposition, oxidant generation, and antioxidant depletion potential. Lung tissue gene/protein response demonstrated distinct patterns that are better predicted by either particle dose/aerosol responses (interleukin-1ß, keratinocyte chemoattractant, transforming growth factor beta) or particle reactivity (thymic stromal lymphopoietin, interleukin-13, interleukin-6). Hierarchical clustering showed a distinct signature with high dose and a similarity in mRNA expression pattern of low and medium doses of CB + O3. In conclusion, we demonstrate that the biological outcomes from CB + O3 co-exposure are significantly greater than individual exposures over a range of aerosol concentrations and aerosol characteristics can predict biological outcome.

Mass transfer characteristics and effect of flue gas used in microalgae culture.

Flue gas not only contains carbon dioxide (CO2) but also air pollutants (sulfur oxides (SOx) and nitrogen oxides (NOx)). The effective utilization of flue gas could help us to reduce the cost of microalgal biomass production. This study assessed and explored the utilization of flue gas for the absorption characteristics of different components and their biological effect in microalgal culture systems. In abiotic absorption experiments, the absorptivity of CO2 was reduced by a maximum of 3.1%, and the concentration of the available carbon source in the culture medium was decreased by 6.7% when sulfur dioxide (SO2, at 100 mg/m3) was presented in the flue gas. Meanwhile, the presence of oxygen (O2, at 4%) in the flue gas improved the absorptivity of nitric oxide (NO). When Scenedesmus dimorphus was cultured using bisulfites and nitrites (at 10 mmol/L and 8 mmol/L, respectively) as the sulfur and nitrogen sources, SOx and NOx in the flue gas did not significantly affect growth of microalgal cells and the carbohydrate, lipid, and protein content. The consumption rates of nutrient elements were calculated, which could provide an adjustment strategy for the initial gas source when culturing microalgae with the flue gas. This study indicates that the flue gas used for microalgal culture should be partially desulfurized, so that the SOx and CO2 concentrations can optimize growth of microalgal cells, while the denitrification might not be needed since the flue gas can be oxidized to utilize the NO. KEY POINTS: • The concentration of the available carbon source in the culture medium was decreased when SO2 was presented in the flue gas, and the presence of O2 in the flue gas improved the absorptivity of NO. • An adjustment strategy for the initial gas source when culturing microalgae with the flue gas was firstly proposed. • For flue gas containing 10% CO2 and 60 mg/m3 of SO2, growth of Scenedesmus dimorphus showed no difference in cell growth in normal culture conditions.

Impacts of long-term ambient particulate matter and gaseous pollutants on circulating biomarkers of inflammation in male and female health professionals.

BACKGROUND: Systemic inflammation may serve as a biological mechanism linking air pollution to poor health but supporting evidence from studies of long-term pollutant exposure and inflammatory cytokines is inconsistent. OBJECTIVE: We studied associations between multiple particulate matter (PM) and gaseous air pollutants and pro- and anti-inflammatory cytokines within two nationwide cohorts of men and women. METHODS: Data were obtained from 16,151 women in the Nurses' Health Study and 7,930 men in the Health Professionals' Follow-up Study with at least one measure of circulating adiponectin, C-Reactive Protein (CRP), Interleukin-6 (IL-6) or soluble tumor necrosis-factor receptor-2 (sTNFR-2). Exposure to PM with aerodynamic diameter ≤2.5, 2.5-10, and ≤10 µm (PM2.5, PM2.5-10, PM10) and nitrogen dioxide (NO2) was estimated using spatio-temporal models and were linked to participants' addresses at the time of blood draw. Averages of the 1-, 3-, and 12-months prior to blood draw were examined. Associations between each biomarker and pollutant were estimated from linear regression models adjusted for individual and contextual covariates. RESULTS: In adjusted models, we observed a 2.72% (95% CI: 0.43%, 5.95%), 3.11% (-0.12%, 6.45%), and 3.67% (0.19%, 7.26%) increase in CRP associated with a 10 µg/m3 increase in 1-, 3-, and 12- month averaged NO2 in women. Among men, there was a statistically significant 5.96% (95% CI: 0.07%, 12.20%), 6.99% (95% CI: 0.29%, 14.15%), and 8.33% (95% CI: 0.35%, 16.94%) increase in CRP associated with a 10 µg/m3 increase in 1-, 3-, and 12-month averaged PM2.5-10, respectively. Increasing PM2.5-10 was associated with increasing IL-6 and sTNFR-2 among men over shorter exposure durations. There were no associations with exposures to PM2.5 or PM10, or with adiponectin. Findings were robust to sensitivity analyses restricting to disease-free controls and non-movers. CONCLUSIONS: Across multiple long-term pollutant exposures and inflammatory markers, associations were generally weak. Focusing on specific pollutant-inflammatory mechanisms may clarify pathways.

Epithelial 3D-spheroids as a tool to study air pollutant-induced lung pathology.

Cigarette smoke (CS) and air pollutants (AP) activate pathological processes in bronchial epithelial cells resulting in lung function decline which severely impacts human health. Knowledge about the molecular mechanism(s) by which CS and AP induce pathology is limited. Our previous studies in 2D cultures of human bronchial epithelial (BEAS-2B) cells showed that CS exposure activates transforming growth factor-ß1 (TGF-ß1) release and signaling. Furthermore, CS exposure reduced the expression of E-cadherin, which was prevented by applying a TGF-ß1 neutralizing antibody. Exposure of BEAS-2B cells cultured in 2D to diesel exhaust particles (DEP) increased TGF-ß1 protein expression and reduced the expression of epithelial cell markers, whereas mesenchymal markers are upregulated. Conventional 2D cell culture may, however, not fully reflect the physiology of bronchial epithelial cells in vivo. To simulate the in vivo situation more closely we cultured the bronchial epithelial cells in a 3D environment in the current study. Treatment of epithelial spheroids with TGF-ß resulted in reduced E-cadherin and increased collagen I expression, indicating the activation of epithelial-to-mesenchymal transition (EMT). Similarly, exposure of spheroids to DEP induced and EMT-like phenotype. Collectively, our data indicate AP induces an EMT-like phenotype of BEAS-2B cells in 3D spheroid cultures. This opens new avenues for drug development for the treatment of lung diseases induced by AP. The 3D spheroid cell culture is a novel, innovative and physiologically relevant model for culturing a variety of cells. It is a versatile tool for both high-throughput studies and for identifying molecular mechanisms involved in bronchial epithelial cell (patho)physiology.

Adverse outcome pathway of fine particulate matter leading to increased cardiovascular morbidity and mortality: An integrated perspective from toxicology and epidemiology.

Fine particulate matter (PM2.5) exposure is a major threat to public health, and is listed as one of the leading factors associated with global premature mortality. Among the adverse health effects on multiple organs or tissues, the influence of PM2.5 exposure on cardiovascular system has drawn more and more attention. Although numerous studies have investigated the mechanisms responsible for the cardiovascular toxicity of PM2.5, the various mechanisms have not been integrated due to the variety of the study models, different levels of toxicity assessment endpoints, etc. Adverse Outcome Pathway (AOP) framework is a useful tool to achieve this goal so as to facilitate comprehensive understanding of toxicity assessment of PM2.5 on cardiovascular system. This review aims to illustrate the causal mechanistic relationships of PM2.5-triggered cardiovascular toxicity from different levels (from molecular/cellular/organ to individual/population) by using AOP framework. Based on the AOP Wiki and published literature, we propose an AOP framework focusing on the cardiovascular toxicity induced by PM2.5 exposure. The molecular initiating event (MIE) is identified as reactive oxygen species generation, followed by the key events (KEs) of oxidative damage and mitochondria dysfunction, which induces vascular endothelial dysfunction via vascular endothelial cell autophagy dysfunction, vascular fibrosis via vascular smooth muscle cell activation, cardiac dysregulation via myocardial apoptosis, and cardiac fibrosis via fibroblast proliferation and myofibroblast differentiation, respectively; all of the above cardiovascular injuries ultimately elevate cardiovascular morbidity and mortality in the general population. As far as we know, this is the first work on PM2.5-related cardiovascular AOP construction. In the future, more work needs to be done to explore new markers in the safety assessment of cardiovascular toxicity induced by PM2.5.

Olfactory bulb microglia activation mediated neuronal death in real-ambient particulate matter exposure mice with depression-like behaviors.

Growing evidence has indicated that air pollution is associated with depression, and damage of olfactory bulb (OB) is regarded as an early marker for depression. However, the toxicity of fine particulate matter (PM2.5) on OB and underlying mechanisms remains to be elucidated. In our study, a real-ambient PM2.5 exposure system was applied to explore the effects of PM2.5 on OB in C57BL/6 mice for 4 or 8 weeks. After 8 weeks exposure, the mice emerged potential depressive-like responses with reduction and disorder of cells in olfactory bulb tissues. Apoptosis and ultra-microstructure analysis indicated that the real-ambient PM2.5 exposure caused the neuronal death of OB. The immunofluorescence observation and KEGG pathway analysis revealed the real-ambient PM2.5 exposure induced microglia activation along with tumor necrosis factor α (TNFα)-mediated signaling enriched in OB of mice with depression-like behaviors. Moreover, results from ex vivo biosensor assay exhibited that PM2.5 might trigger systemic inflammation with increased levels of various proinflammatory factors to activate microglia. Further in vitro co-culture model identified that the PM2.5 evoked microglia cells activation with TNFα secretion and induced neuronal cells apoptosis via classical caspase3 signaling. Our findings provide new insights that PM2.5 induced microglia activation characterized by the release of TNFα to cause neurotoxicity either by direct action or by circulatory inflammation, resulting in OB damage, which may play a critical role in early diagnosis and pathogenic mechanisms for PM2.5 to cause depression.

Previously unaccounted atmospheric mercury deposition in a midlatitude deciduous forest.

Mercury is toxic to wildlife and humans, and forests are thought to be a globally important sink for gaseous elemental mercury (GEM) deposition from the atmosphere. Yet there are currently no annual GEM deposition measurements over rural forests. Here we present measurements of ecosystem-atmosphere GEM exchange using tower-based micrometeorological methods in a midlatitude hardwood forest. We measured an annual GEM deposition of 25.1 µg ⋅ m-2 (95% CI: 23.2 to 26.7 1 µg ⋅ m-2), which is five times larger than wet deposition of mercury from the atmosphere. Our observed annual GEM deposition accounts for 76% of total atmospheric mercury deposition and also is three times greater than litterfall mercury deposition, which has previously been used as a proxy measure for GEM deposition in forests. Plant GEM uptake is the dominant driver for ecosystem GEM deposition based on seasonal and diel dynamics that show the forest GEM sink to be largest during active vegetation growing periods and middays, analogous to photosynthetic carbon dioxide assimilation. Soils and litter on the forest floor are additional GEM sinks throughout the year. Our study suggests that mercury loading to this forest was underestimated by a factor of about two and that global forests may constitute a much larger global GEM sink than currently proposed. The larger than anticipated forest GEM sink may explain the high mercury loads observed in soils across rural forests, which impair water quality and aquatic biota via watershed Hg export.