Dust Extract Research Articles

In Silico Analysis of Binding Sites for a Novel ssDNA Aptamer Specific to Verrucarin A and Detection in Dust Extracts.

An aptamer is a single-stranded oligonucleotide that serves as a chemical antibody with a high specificity and binding affinity that can recognize a wide range of molecules. Effective modification and truncation of aptamers can enhance their binding affinities to particular targets while also broadening their application for uses, such as biosensors. However, a conventional trial-and-error methodology hinders this process. Herein, we demonstrate an in silico method to elucidate the binding site of single-stranded DNA aptamer specific to verrucarin A, a mycotoxin produced by molds in indoor buildings that causes adverse effects in living organisms. The novel ssDNA aptamer exhibited a binding affinity of 29.5 nM, demonstrating a relatively strong affinity compared to those of previously reported typical aptamers for small molecules. Furthermore, the selected aptamer was highly specific toward verrucarin A among structurally related mycotoxins (i.e., verrucarol and zearalenone). The specific binding site of the aptamer predicted via molecular dynamics and molecular docking simulations was highly consistent with the results observed via truncation, single base mutation, and circular dichroism experiments. The fluorescence assay revealed limits of detection and quantification of 4.1 and 12 nM for the aptamer, respectively. Comparing our developed aptasensor with LC-MS/MS methodology revealed that it could detect verrucarin A levels in phosphate-buffered saline and dust extracts with robust precision and consistency. Our findings provide insight for future studies exploring interaction mechanisms with intended targets and practical sensing applications, such as point-of-care detection of verrucarin A.

Coconut dust extract as a pitting corrosion inhibitor for reinforcing steel in concrete in the presence of chlorides

Coconut dust extract as a pitting corrosion inhibitor for reinforcing steel in concrete in the presence of chlorides

The study of Thai herbal plant extract as a potential therapeutic food ingredient for preventing the effects of airborne pollutants via in vitro model

Thai herbal plant is known as medicinal plant material for several treatments of diseases particularly non-communicable diseases (NCDs). This work aimed to investigate the potentiality of three plant extracts, including Bat flower (TCE), Vietnamese Coriander (POE), and Indian Pennywort (Centell), which can be a therapeutic food ingredient, in the protection of blood vessels caused by the effect of airborne through the in vitro model. The vascular smooth muscle cell (VSMC), A7r5 rat aortic cell, was used for cell culture and determined their activity after being treated with dust and plant extracts at different concentrations. The dust was prepared at 0-400 μg/mL, and the plant extracts were prepared as powder by freeze dryer before further use. The toxicity test, antioxidant activity, and cell apoptosis as well as wound healing properties were examined. The results showed the POE was highest the antioxidant activity (TPC: 1156.02±35.78 mg gallic acid/g sample and DPPH: 949.45±31.97 μmol Trolox/g sample) when compared to TCE and Centell (p<0.05). The maximum concentration of plant extracts treated cells was not over 500 μg/mL for cell toxicity. The VSMC cell apoptosis depended on increasing the dust concentration manner. There was a positive effect of plant extracts on wound repair in the blood vessels after being treated with TCE at a concentration of 100 μg/mL. According to the results, it could be suggested that plant extracts, especially TCE can be a food ingredient that plays a vital role in preventing the blood vessel from the airborne effects caused by PM10 receiving. Also, these data help and be useful for healthy food or therapeutic food development for reducing the risk factor of arteriosclerotic effects.

Aconitate decarboxylase 1 mediates the acute airway inflammatory response to environmental exposures.

Environmental lipopolysaccharide (LPS) and microbial component-enriched organic dusts cause significant lung disease. These environmental exposures induce the recruitment and activation of distinct lung monocyte/macrophage subpopulations involved in disease pathogenesis. Aconitate decarboxylase 1 (Acod1) was one of the most upregulated genes following LPS (vs. saline) exposure of murine whole lungs with transcriptomic profiling of sorted lung monocyte/macrophage subpopulations also highlighting its significance. Given monocyte/macrophage activation can be tightly linked to metabolism, the objective of these studies was to determine the role of the immunometabolic regulator ACOD1 in environmental exposure-induced lung inflammation. Wild-type (WT) mice were intratracheally (i.t.) instilled with 10 μg of LPS or saline. Whole lungs were profiled using bulk RNA sequencing or sorted to isolate monocyte/macrophage subpopulations. Sorted subpopulations were then characterized transcriptomically using a NanoString innate immunity multiplex array 48 h post-exposure. Next, WT and Acod1-/- mice were instilled with LPS, 25% organic dust extract (ODE), or saline, whereupon serum, bronchoalveolar lavage fluid (BALF), and lung tissues were collected. BALF metabolites of the tricarboxylic acid (TCA) cycle were quantified by mass spectrometry. Cytokines/chemokines and tissue remodeling mediators were quantitated by ELISA. Lung immune cells were characterized by flow cytometry. Invasive lung function testing was performed 3 h post-LPS with WT and Acod1-/- mice. Acod1-/- mice treated with LPS demonstrated decreased BALF levels of itaconate, TCA cycle reprogramming, decreased BALF neutrophils, increased lung CD4+ T cells, decreased BALF and lung levels of TNF-α, and decreased BALF CXCL1 compared to WT animals. In comparison, Acod1-/- mice treated with ODE demonstrated decreased serum pentraxin-2, BALF levels of itaconate, lung total cell, neutrophil, monocyte, and B-cell infiltrates with decreased BALF levels of TNF-α and IL-6 and decreased lung CXCL1 vs. WT animals. Mediators of tissue remodeling (TIMP1, MMP-8, MMP-9) were also decreased in the LPS-exposed Acod1-/- mice, with MMP-9 also reduced in ODE-exposed Acod1-/- mice. Lung function assessments demonstrated a blunted response to LPS-induced airway hyperresponsiveness in Acod1-/- animals. Acod1 is robustly upregulated in the lungs following LPS exposure and encodes a key immunometabolic regulator. ACOD1 mediates the proinflammatory response to acute inhaled environmental LPS and organic dust exposure-induced lung inflammation.

Zinc Protects against Swine Barn Dust-Induced Cilia Slowing.

Agricultural workers exposed to organic dust from swine concentrated animal feeding operations (CAFOs) have increased chances of contracting chronic lung disease. Mucociliary clearance represents a first line of defense against inhaled dusts, but organic dust extracts (ODEs) from swine barns cause cilia slowing, leading to decreased bacterial clearance and increased lung inflammation. Because nutritional zinc deficiency is associated with chronic lung disease, we examined the role of zinc supplementation in ODE-mediated cilia slowing. Ciliated mouse tracheal epithelial cells were pretreated with 0-10 µg/mL ZinProTM for 1 h, followed by treatment with 5% ODE for 24 h. Cilia beat frequency (CBF) and protein kinase C epsilon (PKCε) activity were assayed. ODE treatment resulted in cilia slowing after 24 h, which was reversed with 0.5 and 1.0 µg/mL ZinPro pre-treatment. No zinc protection was observed at 50 ng/mL, and ciliated cells detached at high concentrations (100 µg/mL). ZinPro alone produced no changes in the baseline CBF and showed no toxicity to the cells at concentrations of up to 10 µg/mL. Pre-treatment with ZinPro inhibited ODE-stimulated PKCε activation in a dose-dependent manner. Based on ZinPro's superior cell permeability compared to zinc salts, it may be therapeutically more effective at reversing ODE-mediated cilia slowing through a PKCε pathway. These data demonstrate that zinc supplementation may support the mucociliary transport apparatus in the protection of CAFO workers against dust-mediated chronic lung disease.

Microbial Assessment in A Rare Norwegian Book Collection: A One Health Approach to Cultural Heritage.

Microbial contamination poses a threat to both the preservation of library and archival collections and the health of staff and users. This study investigated the microbial communities and potential health risks associated with the UNESCO-classified Norwegian Sea Trade Archive (NST Archive) collection exhibiting visible microbial colonization and staff health concerns. Dust samples from book surfaces and the storage environment were analysed using culturing methods, qPCR, Next Generation Sequencing, and mycotoxin, cytotoxicity, and azole resistance assays. Penicillium sp., Aspergillus sp., and Cladosporium sp. were the most common fungi identified, with some potentially toxic species like Stachybotrys sp., Toxicladosporium sp., and Aspergillus section Fumigati. Fungal resistance to azoles was not detected. Only one mycotoxin, sterigmatocystin, was found in a heavily contaminated book. Dust extracts from books exhibited moderate to high cytotoxicity on human lung cells, suggesting a potential respiratory risk. The collection had higher contamination levels compared to the storage environment, likely due to improved storage conditions. Even though overall low contamination levels were obtained, these might be underestimated due to the presence of salt (from cod preservation) that could have interfered with the analyses. This study underlines the importance of monitoring microbial communities and implementing proper storage measures to safeguard cultural heritage and staff well-being.

Health risk assessment of heavy metal(loid)s in road dust via dermal exposure pathway from a low latitude plateau provincial capital city: The importance of toxicological verification

The human health risk assessment through the dermal exposure of metal (loid)s in dust from low latitude and high geological background plateau cities was largely unknown. In this study, the road dust samples were harvested from a typical low-latitude plateau provincial capital city Kunming, Southwest China. The total concentration and dermal bioaccessibility of heavy metal (loid)s in road dust were determined, and their health risks as well as cytotoxicity on human skin keratinocytes were also assessed. The average concentrations of As (28.5 mg/kg), Cd (2.65 mg/kg), Mn (671 mg/kg), and Zn (511 mg/kg) exceeded the soil background values. Arsenic had the highest bioaccessibility after 2 h (3.79%), 8 h (4.24%), and 24 h (16.6%) extraction. The dermal pathway when bioaccessibility is considered has a higher hazard quotient than the conventional method using total metal(loid)s in the dust. In addition, toxicological verification suggested that the dust extracts suppressed the cell viability, increased the reactive oxygen species (ROS) level and DNA damage, and eventually activated the mitochondria-mediated apoptosis pathway, evidenced by the upregulation of Caspase-3/9, Bax, and Bak-1. Cadmium was positively correlated with the mRNA expression of Bax. Taken together, our data indicated that both dermal bioaccessibility and cytotoxicity should be considered for accurate human skin health risk assessment of heavy metal(loid)s in road dust, which may provide new insight for accurate human health risk assessment and environmental management.

Targeting transitioning lung monocytes/macrophages as treatment strategies in lung disease related to environmental exposures

BackgroundEnvironmental/occupational exposures cause significant lung diseases. Agricultural organic dust extracts (ODE) and bacterial component lipopolysaccharide (LPS) induce recruited, transitioning murine lung monocytes/macrophages, yet their cellular role remains unclear.MethodsCCR2 RFP+ mice were intratracheally instilled with high concentration ODE (25%), LPS (10 μg), or gram-positive peptidoglycan (PGN, 100 μg) for monocyte/macrophage cell-trafficking studies. CCR2 knockout (KO) mice and administration of intravenous clodronate liposomes strategies were employed to reduce circulating monocytes available for lung recruitment following LPS exposure. Lung tissues and bronchoalveolar lavage fluid (BALF) were collected. Pro-inflammatory and/or pro-fibrotic cytokines, chemokines, and lung extracellular matrix mediators were quantitated by ELISA. Infiltrating lung cells including monocyte/macrophage subpopulations, neutrophils, and lymphocytes were characterized by flow cytometry. Lung histopathology, collagen content, vimentin, and post-translational protein citrullination and malondialdehyde acetaldehyde (MAA) modification were quantitated. Parametric statistical tests (one-way ANOVA, Tukey’smultiple comparison) and nonparametric statistical (Kruskal–Wallis, Dunn’s multiple comparison) tests were used following Shapiro–Wilk testing for normality.ResultsIntratracheal instillation of ODE, LPS, or PGN robustly induced the recruitment of inflammatory CCR2+ CD11cintCD11bhi monocytes/macrophages and both CCR2+ and CCR2− CD11c−CD11bhi monocytes at 48 h. There were also increases in CCR2+ CD4+ and CD8+ T cells and NK cells. Despite reductions in LPS-induced lung infiltrating CD11cintCD11bhi cells (54% reduction), CCR2 knockout (KO) mice were not protected against LPS-induced inflammatory and pro-fibrotic consequences. Instead, compensatory increases in lung neutrophils and CCL2 and CCL7 release occurred. In contrast, the depletion of circulating monocytes through the administration of intravenous clodronate (vs. vehicle) liposomes 24 h prior to LPS exposure reduced LPS-induced infiltrating CD11cintCD11bhi monocyte-macrophage subpopulation by 59% without compensatory changes in other cell populations. Clodronate liposome pre-treatment significantly reduced LPS-induced IL-6 (66% reduction), matrix metalloproteinases (MMP)-3 (36%), MMP-8 (57%), tissue inhibitor of metalloproteinases (61%), fibronectin (38%), collagen content (22%), and vimentin (40%). LPS-induced lung protein citrullination and MAA modification, post-translational modifications implicated in lung disease, were reduced (39% and 48%) with clodronate vs. vehicle liposome.ConclusionHighly concentrated environmental/occupational exposures induced the recruitment of CCR2+ and CCR2− transitioning monocyte-macrophage and monocyte subpopulations and targeting peripheral monocytes may reduce the adverse lung consequences resulting from exposures to LPS-enriched inhalants.

Lung-delivered IL-10 therapy elicits beneficial effects via immune modulation in organic dust exposure-induced lung inflammation

Efficacious therapeutic options capable of resolving inflammatory lung disease associated with environmental and occupational exposures are lacking. This study sought to determine the preclinical therapeutic potential of lung-delivered recombinant interleukin (IL)-10 therapy following acute organic dust exposure in mice. Here, C57BL/6J mice were intratracheally instilled with swine confinement organic dust extract (ODE) (12.5%, 25%, 50% concentrations) with IL-10 (1 μg) treatment or vehicle control intratracheally-administered three times: 5 hr post-exposure and then daily for 2 days. The results showed that IL-10 treatment reduced ODE (25%)-induced weight loss by 66% and 46% at Day 1 and Day 2 post-exposure, respectively. IL-10 treatment reduced ODE (25%, 50%)-induced lung levels of TNFα (–76%, −83% [reduction], respectively), neutrophil chemoattractant CXCL1 (–51%, −60%), and lavage fluid IL-6 (–84%, −89%). IL-10 treatment reduced ODE (25%, 50%)-induced lung neutrophils (–49%, −70%) and recruited CD11cintCD11b+ monocyte-macrophages (–49%, −70%). IL-10 therapy reduced ODE-associated expression of antigen presentation (MHC Class II, CD80, CD86) and inflammatory (Ly6C) markers and increased anti-inflammatory CD206 expression on CD11cintCD11b+ cells. ODE (12.5%, 25%)-induced lung pathology was also reduced with IL-10 therapy. In conclusion, the studies here showed that short-term, lung-delivered IL-10 treatment induced a beneficial response in reducing inflammatory consequences (that were also associated with striking reduction in recruited monocyte-macrophages) following acute complex organic dust exposure.

SCREENING OF ALPHA-GLUCOSIDASE INHIBITORY ACTIVITY FROM TWO PRODUCTS OF THE CAPSULIZED JAMU CINNAMON EXTRACT (CINNMOMUM BURMANNII)


 Cinnamon (Cinnamomim burmannii) found in the markets, comes in many forms with one of them being a type of jamu which the cinnamon dust is capsulized. The capsulized jamu is claimed to be beneficial on treating diabetes melitus. The effects of antidiabetics on some products of the capsulized jamu is suspected to work through the alpha-glucosidase enzyme inhibition activites contained in them. The aim of this research is to verify the activities of some capsulized cinnamon dust extract in jamu (C. burmannii) found in the markets on its effect to inhibit alpha-glucosidase activity and to know its IC50 value. Experiment is done by using analytic experiments using two different products (product A and product B) and by using acarbose 50mg as a positive control factor. Enzyme activity are then calculated using UV-Vis spectrophotometer on a 410 nm wavelength. The result of this research is alpha-glucosidase enzyme inhibition activity found in product A and B are 155,104 µg/mL and 6.795,893 µg/mL, wherease the acarbose as a positive control are 47,466 µg/mL. The conclusion of this research is alpha-glucosidase enzyme inhibition activity found on the products as IC50 shows that product A has a better alpha-glucosidase enzyme inhibition activity than product B. However, when compared to the acarbose as the positive control, product A has a lesser alpha glucosidase enzyme inhibition activity.
 Kata kunci : Cinnamomum burmannii, diabetes mellitus, alpha glucosidase inhibition.
 

Endocrine disrupting potential of total and bioaccessible extracts of dust from seven different types of indoor environment

Information on the indoor environment as a source of exposure with potential adverse health effects is mostly limited to a few pollutant groups and indoor types. This study provides a comprehensive toxicological profile of chemical mixtures associated with dust from various types of indoor environments, namely cars, houses, prefabricated apartments, kindergartens, offices, public spaces, and schools. Organic extracts of two different polarities and bioaccessible extracts mimicking the gastrointestinal conditions were prepared from two different particle size fractions of dust. These extracts were tested on a battery of human cell-based bioassays to assess endocrine disrupting potentials. Furthermore, 155 chemicals from different pollutant groups were measured and their relevance for the bioactivity was determined using concentration addition modelling. The exhaustive and bioaccessible extracts of dust from the different microenvironments interfered with aryl hydrocarbon receptor, estrogen, androgen, glucocorticoid, and thyroid hormone (TH) receptor signalling, and with TH transport. Noteably, bioaccessible extracts from offices and public spaces showed higher estrogenic effects than the organic solvent extracts. 114 of the 155 targeted chemicals were detectable, but the observed bioactivity could be only marginally explained by the detected chemicals. Diverse toxicity patterns across different microenvironments that people inhabit throughout their lifetime indicate potential health and developmental risks, especially for children. Limited data on the endocrine disrupting potency of relevant chemical classes, especially those deployed as replacements for legacy contaminants, requires further study.

Immune modulation by rural exposures and allergy protection.

Growing up on traditional farms protects children from the development of asthma and allergies. However, we have identified distinct asthma-protective factors, such as poultry exposure. This study aims to examine the biological effect of rural exposure in China. We recruited 67 rural children (7.4 ± 0.9 years) and 79 urban children (6.8 ± 0.6 years). Depending on the personal history of exposure to domestic poultry (DP), rural children were further divided into those with DP exposure (DP+ , n = 30) and those without (DP- , n = 37). Blood samples were collected to assess differential cell counts and expression of immune-related genes. Dust samples were collected from poultry stables inside rural households. Invivo activities of nasal administration of DP dust extracts were tested in an ovalbumin-induced asthma model. There was a stepwise increase in the percentage of eosinophils (%) from rural DP+ children (median = 1.65, IQR = [1.28, 3.75]) to rural DP- children (3.40, [1.70, 6.50]; DP+ vs. DP- , p = .087) and to the highest of their urban counterparts (4.00, [2.00, 7.25]; urban vs. DP+ , p = .017). Similarly, rural children exhibited reduced mRNA expression of immune markers, both at baseline and following lipopolysaccharide (LPS) stimulation. Whereas LPS stimulation induced increased secretion of Th1 and proinflammatory cytokines in rural DP+ children compared to rural DP- children and urban children. Bronchoalveolar lavage of mice with intranasal instillation of dust extracts from DP household showed a significant decrease in eosinophils as compared to those of control mice (p < .05). Furthermore, DP dust strongly inhibited gene expression of Th2 signature cytokines and induced IL-17 expression in the murine asthma model. Immune responses of rural children were dampened compared to urban children and those exposed to DP had further downregulated immune responsiveness. DP dust extracts ameliorated Th2-driven allergic airway inflammation in mice. Determining active protective components in the rural environment may provide directions for the development of primary prevention of asthma.

Evaluation of the efficiency of coconut dust extract as a corrosion inhibitor for steel reinforcement in concrete by mass spectrometry

Ethanol extraction was employed to isolate a range of compounds from waste products derived from coconut fiber production (coconut dust) in Ben Tre, Vietnam. Phytochemical screening confirmed the presence of flavonoids, tannins, polyphenols, saponins, alkaloids, flobatannins, and anthraquinones among the extracted substances. FT-IR spectroscopy analysis supported the identification of oxygen and nitrogen atoms within functional groups (e.g., O–H, N–H, C–O) and aromatic rings, characteristic of typical corrosion inhibitors. Mass spectrometry investigations indicated that when St3 steel was exposed to an alkaline solution lacking chlorides, a passive film composed of FeOOH formed on the surface. However, upon the addition of NaCl at a concentration of 1.00 mol/dm3, FeCl, FeCl2Cl–, and FeCl3Cl– compounds were detected across the analyzed surface, while peaks corresponding to FeOO– were absent. Remarkably, areas with the highest concentration of particles corresponded to regions exhibiting visible corrosion damage under magnification. The addition of 2.00 g/dm3 of coconut dust extract to the chloride solution prevents the formation of Fe and Cl compounds on the steel surface. Consequently, only peaks characteristic of FeOO– and organic fragments containing oxygen atoms from the extract were observed. Based on these results, it can be assumed that coconut dust extract has the potential to inhibit local (pitting) corrosion of low-carbon steel (St3) when exposed to aqueous alkaline solutions simulating concrete pore liquid containing chlorides. The addition of 2.00 g/dm3 of the extract has been shown to prevent pitting formation at a chloride concentration of 1.00 mol/dm3. Conversely, in the absence of the extract, visible local corrosion damage was observed upon magnification. These findings provide a basis for further exploration of the protective properties of coconut dust extract as an environment-friendly corrosion inhibitor for mild steel in concrete environments containing chlorides.

Road dust exposure and human corneal damage in a plateau high geological background provincial capital city: Spatial distribution, sources, bioaccessibility, and cytotoxicity of dust heavy metals

Ocular surface diseases are common in the plateau city, Kunming China, the continued daily exposure to heavy metals in dust may be an important inducement. In this study, the 150 road dust samples from five functional areas in Kunming were collected. The concentrations, distribution, possible sources, and bioaccessibility of heavy metals were analyzed. The adverse effects of dust extracts on human corneal epithelial cells and the underlying mechanisms were also assessed. The concentrations (mg·kg−1) of As (19.1), Cd (2.67), Cr (90.5), Cu (123), Pb (78.4), and Zn (389) in road dust were higher than the soil background, with commercial and residential areas showing the highest pollution. Their bioaccessibility in artificial tears was As (6.59 %) > Cu (5.11 %) > Ni (1.47 %) > Cr (1.17 %) > Mn (0.84 %) > Cd (0.76 %) > Zn (0.50 %) > Pb (0.31 %). The two main sources of heavy metals included tire and mechanical abrasion (24.5 %) and traffic exhaust (21.6 %). All dust extracts induced cytotoxicity, evidenced by stronger inhibition of cell viability, higher production of ROS, and altered mRNA expression of antioxidant enzymes and cell cycle-related genes, with commercial- areas-2 (CA2)-dust extract showing the greatest oxidative damage and cell cycle arrest. Our data may provide new evidence that dust exposure in high geological background cities could trigger human cornea damage.

Effects of Indoor Dust Exposure on Lung Cells: Association of Chemical Composition with Phenotypic and Lipid Changes in a 3D Lung Cancer Cell Model.

Indoor dust is a key contributor to the global human exposome in urban areas since the population develops most of its activities in private and public buildings. To gain insight into the health risks associated with this chronic exposure, it is necessary to characterize the chemical composition of dust and understand its biological impacts using reliable physiological models. The present study investigated the biological effects of chemically characterized indoor dust extracts using three-dimensional (3D) lung cancer cell cultures combining phenotypic and lipidomic analyses. Apart from the assessment of cell viability, reactive oxygen species (ROS) induction, and interleukin-8 release, lipidomics was applied to capture the main lipid changes induced as a cellular response to the extracted dust compounds. The application of chemometric tools enabled the finding of associations between chemical compounds present in dust and lipidic and phenotypic profiles in the cells. This study contributes to a better understanding of the toxicity mechanisms associated with exposure to chemical pollutants present in indoor dust.

Coconut coir dust extract as a novel green corrosion inhibitor for carbon steel in the chloride-contaminated concrete pore solution

The potential of coconut coir dust to inhibit corrosion, especially the pitting of rebars in concrete was tapped by electrochemical techniques. Electrochemical impedance spectroscopy and linear polarization results show that both deionized water and ethanol extracts of coconut coir dust can slow down corrosion development by forming a protective film even after long-term exposure to chloride and the latter performs better and is more stable. Cyclic potentiodynamic polarization results further show that ethanol extract at a concentration of 0.1 g/L can significantly delay the initiation of pitting. This inhibitor has exhibited the highest inhibition efficiency, which can be sustained at over 90 % even after six months of immersion in solutions with high chloride concentration, but increasing the concentration of the inhibitor does not result in any additional improvement in its efficiency. Critical chloride concentration for corrosion initiation prediction and corrosion resistance evaluation was also discussed.

Respiratory exposure to agricultural dust extract promotes increased intestinal Tnfα expression, gut barrier dysfunction, and endotoxemia in mice.

Concentrated animal feeding operations (CAFOs) are responsible for the production of global greenhouse gases and harmful environmental pollutants including hydrogen sulfide, ammonia, and particulate matter. Swine farmers are frequently exposed to organic dust that is proinflammatory in the lung and are thus at greater risk of developing pneumonia, asthma, and other respiratory conditions. In addition to respiratory disease, air pollutants are directly associated with altered gastrointestinal (GI) physiology and the development of GI diseases, thereby highlighting the gut-lung axis in disease progression. Instillation of hog dust extract (HDE) for 3 wk has been reported to promote the development of chronic airway inflammation in mice, however, the impact of HDE exposure on intestinal homeostasis is poorly understood. We report that 3-wk intranasal exposure of HDE is associated with increased intestinal macromolecule permeability and elevated serum endotoxin concentrations in C57BL/6J mice. In vivo studies also indicated mislocalization of the epithelial cell adhesion protein, E-cadherin, in the colon as well as an increase in the proinflammatory cytokine, Tnfα, in the proximal colon. Moreover, mRNA expression of the Paneth cell-associated marker, Lyz1, was increased the proximal colon, whereas the expression of the goblet cell marker, Muc2, was unchanged in the epithelial cells of the ileum, cecum, and distal colon. These results demonstrate that airway exposure to CAFOs dusts promote airway inflammation and modify the gastrointestinal tract to increase intestinal permeability, induce systemic endotoxemia, and promote intestinal inflammation. Therefore, this study identifies complex physiological consequences of chronic exposure to organic dusts derived from CAFOs on the gut-lung axis.NEW & NOTEWORTHY Agricultural workers have a higher prevalence of occupational respiratory symptoms and are at greater risk of developing respiratory diseases. However, gastrointestinal complications have also been reported, yet the intestinal pathophysiology is understudied. This work is novel because it emphasizes the role of an inhaled environmental pollutant on the development of intestinal pathophysiological outcomes. This work will provide foundation for other studies evaluating how agricultural dusts disrupts host physiology and promotes debilitating gastrointestinal and systemic disorders.

Asthma-protective agents in dust from traditional farm environments

Growing up on traditional European or US Amish dairy farms in close contact with cows and hay protects children against asthma, and airway administration of extracts from dust collected from cowsheds of those farms prevents allergic asthma in mice. This study sought to begin identifying farm-derived asthma-protective agents. Our work unfolded along 2 unbiased and independent but complementary discovery paths. Dust extracts (DEs) from protective and nonprotective farms (European and Amish cowsheds vs European sheep sheds) were analyzed by comparative nuclear magnetic resonance profiling and differential proteomics. Bioactivity-guided size fractionation focused on protective Amish cowshed DEs. Multiple invitro and invivo functional assays were used in both paths. Some of the proteins thus identified were characterized by in-solution and in-gel sodium dodecyl sulfate-polyacrylamide gel electrophoresis enzymatic digestion/peptide mapping followed by liquid chromatography/mass spectrometry. The cargo carried by these proteins was analyzed by untargeted liquid chromatography-high-resolution mass spectrometry. Twelve carrier proteins of animal and plant origin, including the bovine lipocalins Bos d 2 and odorant binding protein, were enriched in DEs from protective European cowsheds. Apotent asthma-protective fraction of Amish cowshed DEs (≈0.5% of the total carbon content of unfractionated extracts) contained 7 animal and plant proteins, including Bos d 2 and odorant binding protein loaded with fatty acid metabolites from plants, bacteria, and fungi. Animals and plants from traditional farms produce proteins that transport hydrophobic microbial and plant metabolites. When delivered to mucosal surfaces, these agents might regulate airway responses.

Toxicity Assessment of Urban Dust from Barranquilla, a Colombian Caribbean City, using Caenorhabditis elegans

Urban dust is a reservoir of potentially toxic elements (PTEs) that can be incorporated into aquatic ecosystems where they bioaccumulate and biomagnify causing toxic effects. The aim of this work was to assess the PTEs’ concentrations and toxicity to Caenorhabditis elegans of inorganic extracts from urban dust of Barranquilla, the largest Colombian Caribbean city. Trace elements were analyzed by inductively couple plasma-mass spectrometry. PTEs concentration decreased in the order Sr > Cu > Ba > Mo > Se > Cr > V > Ni > As > Zn > Rb > Mn > Sb > Co > Sn > Cd > La > Ce >Tl ≈ Bi > Ag ≈ Pb. Inorganic extracts from urban dust affected physiological parameters in the nematode, such as survival, growth and locomotion. Lethality showed a positive relation with Sr and negative with V. Growth displayed a negative association with Mo. Expression of mtl-2, sod-4, and unc-25 genes was induced by PTEs. The results suggest that C. elegans is a sensitive organism capable of responding to exposure to urban dust extracts, being a suitable sensor for the implementation of warning systems related to risks to biota associated with air pollution.

Analysis and Pollution Assessment of Brominated Flame Retardants (PBDEs, DBDPE, and BTPBE) in Settled Dust from E-waste and Vehicle Processing Areas in Northern Vietnam

Polybrominated diphenyl ethers (PBDEs), decabromodiphenyl ethane (DBDPE), and 1,2-bis(2,4,6-tribromophenoxy)ethane (BTBPE) are typical brominated flame retardants (BFRs), which were widely added to polymeric and textile materials to meet fire safety requirements. PBDEs (including commercial penta-, octa-, and deca-BDE mixtures) have been classified as persistent organic pollutants (POPs) under the Stockholm Convention, while DBDPE and BTBPE are considered as PBDE replacements. In the present study, concentrations of PBDEs (major congeners of technical PBDE mixtures such as BDE-28, 47, 99, 100, 153, 154, 183, 197, 207, and 209), DBDPE, and BTBPE were simultaneously analyzed in settled dust samples collected from e-waste and end-of-life vehicle (ELV) processing areas in northern Vietnam. The dust samples were extracted by using an ultrasonic processor subsequently by acetone and acetone/hexane (1:1) mixture for 10 min each time. The dust extract was treated with concentrated sulfuric acid and activated silica gel to remove interferences. BFRs were analyzed by using gas chromatography/mass spectrometry (GC/MS) equipped with a DB-5ht column. The mass spectrometer was operated at electron capture negative ionization (ECNI) and selected ion monitoring (SIM) mode. Concentrations of total PBDEs, DBDPE, and BTBPE ranged from 77 to 240,000 (median 6000), from &lt;20 to 240,000 (median 5500), and from &lt;10 to 9200 (median 160) ng/g, respectively. Concentrations of BFRs in the e-waste dust were significantly higher than those measured in the ELV dust, suggesting e-waste processing activities as potential sources of BFRs in dust. Among BFRs analyzed, BDE-209 and DBDPE were the most predominant compounds, implying intensive application of deca-BDE mixtures and alternative formulations.