Dust Extract Research Articles

Lung Inflammatory Response to Environmental Dust Exposure in Mice Suggests a Link to Regional Respiratory Disease Risk.

PurposeThe Salton Sea, California’s largest lake, is designated as an agricultural drainage reservoir. In recent years, the lake has experienced shrinkage due to reduced water sources, increasing levels of aerosolized dusts in surrounding regions. Communities surrounding the Salton Sea have increased asthma prevalence versus the rest of California; however, a connection between dust inhalation and lung health impacts has not been defined.MethodsWe used an established intranasal dust exposure murine model to study the lung inflammatory response following single or repetitive (7-day) exposure to extracts of dusts collected in regions surrounding the Salton Sea (SSDE), complemented with in vitro investigations assessing SSDE impacts on the airway epithelium.ResultsIn these investigations, single or repetitive SSDE exposure induced significant lung inflammatory cytokine release concomitant with neutrophil influx. Repetitive SSDE exposure led to significant lung eosinophil recruitment and altered expression of genes associated with allergen-mediated immune response, including Clec4e. SSDE treatment of human bronchial epithelial cells (BEAS-2B) induced inflammatory cytokine production at 5- and 24-hours post-treatment. When BEAS-2B were exposed to protease activity-depleted SSDE (PDSSDE) or treated with SSDE in the context of protease-activated receptor-1 and −2 antagonism, inflammatory cytokine release was decreased. Furthermore, repetitive exposure to PDSSDE led to decreased neutrophil and eosinophilic influx and IL-6 release in mice compared to SSDE-challenged mice.ConclusionThese investigations demonstrate potent lung inflammatory responses and tissue remodeling in response to SSDE, in part due to environmental proteases found within the dusts. These studies provide the first evidence supporting a link between environmental dust exposure, protease-mediated immune activation, and respiratory disease in the Salton Sea region.

Coconut Coir Dust Extract (CCDE) as green corrosion inhibitor for rebar’ steel in concrete environment

Coconut Coir Dust Extract (CCDE) as green corrosion inhibitor for rebar’ steel in concrete environment

Transmission of infectious laryngotracheitis virus vaccine and field strains: the role of degree of contact and transmission by whole blood, plasma and poultry dust

Understanding the mechanisms of transmission of infectious laryngotracheitis virus (ILTV) is critical to proper control as both vaccine and wild-type strains circulate within chicken flocks with potential adverse consequences. The relative efficiency of transmission by direct contact between chickens and airborne transmission has not been investigated. Furthermore, relatively high levels of ILTV DNA have been detected in poultry dust and blood but the infectivity of these is unknown. In this study, comparison of in-contact and airborne transmission of two vaccine and one field strain of ILTV revealed that all transmitted to 100% of in-contact birds by 6 days post-exposure (dpe). Airborne transmission without contact resulted in 100% transmission by 14 and 17 dpe for the wild-type and Serva vaccine virus but only 27% transmission by 21 dpe for the A20 vaccine virus. The infectivity of dust or extracts of dust and blood or plasma from infected chickens at various stages of infection was assessed by inoculation into susceptible chickens. There was no transmission by any of these materials. In conclusion, direct contact facilitated efficient ILTV transmission but the virus was unable to be transmitted by dust from infected chickens suggestive of a limited role in the epidemiology of ILTV.

Toxicological and microbiological characterization of cow stable dust

Exposure to farm environment has been shown to both protect from allergic diseases and increase the risk of respiratory syndromes. Mechanisms have been previously investigated by using farm dust extracts or specific components of dust. The use of authentic farm dust would better reflect the natural exposure. The aim of our study was to highlight the importance of proper assessment of the cow stable dust characteristics before conducting further investigations. For this purpose, we characterized microbiome and size distribution of unprocessed cow stable dust and its toxicological properties, as they have been often overlooked in search of protective factors. Stable dust samples from four Finnish dairy farms were collected by utilizing two different collection methods. Toxicological potential was analysed by stimulating co-cultures of lung epithelial and macrophage-like cells with dust. Size and mass distributions of airborne particles in the stables and bacterial and fungal microbiota of the dust were analysed. Stimulation with dust did not affect viability, but heightened oxidative stress responses and cytokine secretion, and slightly reduced the metabolic activity. There were a few differences in responses between farms, however, the differences were mainly in the intensity and not in the direction of the response. Cellular responses induced by dusts collected by different sampling methods did not differ substantially. Unprocessed stable dust samples showed relatively low direct toxicity but were able to trigger immune responses in studied cell model. This suggest that these dust collection methods could be utilized when investigating e.g. asthma-protective mechanisms.

A high docosahexaenoic acid diet alters lung inflammation and recovery following repetitive exposure to aqueous organic dust extracts

Agricultural workers, especially those who work in swine confinement facilities, are at increased risk for developing pulmonary diseases including asthma, chronic obstructive pulmonary disease, and chronic bronchitis due to exposures to fumes, vapors, and organic dust. Repetitive exposure to agricultural dust leads to unresolved inflammation, a common underlying mechanism that worsens lung disease. Besides occupational exposure to dusts, diet also significantly contributes to inflammation and disease progression. Since DHA (docosahexaenoic acid), a polyunsaturated omega-3 fatty acid and its bioactive metabolites have key roles in inflammation resolution, we rationalized that individuals chronically exposed to organic dusts can benefit from dietary modifications. Here, we evaluated the role of DHA in modifying airway inflammation in a murine model of repetitive exposure to an aqueous extract of agricultural dust (three-week exposure to swine confinement dust extract, HDE) and after a one-week resolution/recovery period. We found that mice fed a high DHA diet had significantly increased bronchoalveolar lavage fluid (BALF) levels of DHA-derived resolvins and lower TNFα along with altered plasma levels of endocannabinoids and related lipid mediators. Following the one-week recovery we identified significantly reduced BALF cellularity and cytokine/chemokine release along with increased BALF amphiregulin and resolvins in DHA diet-fed versus control diet-fed mice challenged with HDE. We further report observations on the effects of repetitive HDE exposure on lung Ym1+ and Arg-1+ macrophages. Overall, our findings support a protective role for DHA and identify DHA-derived resolvins and endocannabinoids among the potential mediators of DHA in altering airway inflammation in chronic agricultural dust exposure.

Antimony from brake dust to the combined sewer collection system via road effluent under rainy conditions.

Abrasion of the brake lining of automobiles is one of the main antimony (Sb) sources on the road. Therefore, the road effluent possibly supplies Sb to the combined sewer collection system. However, Sb in road-sewer systems has attracted little concern, although heavy metals such as copper (Cu), zinc (Zn), cadmium (Cd), and lead (Pb) in sewer water have been studied by many previous authors. We investigated the effect of road effluent on Sb in the combined sewer water by collecting road effluent, road dust, and sewer water under rainy and dry weather conditions. Sb in road effluent showed a significantly higher concentration than the other types of samples, and the Sb concentration in sewer during wet weather was significantly higher than that during dry weather. Furthermore, the Sb concentration in sewer water decreased with time during a wash-off event. Clear positive relationships between Sb and Cu and between Sb and Ba in both road effluent and road dust extract indicate the effect of brake abrasion because the brake lining contains Cu, Sb, and Ba in high concentrations. Approximately 42% of Sb load occurred during the wash-off event, while the loads of Cu and Ba were much less. Unlike Cu and Ba, we conclude that Sb in combined sewer water largely depends on road effluent in wet weather due to the wash-off of road dust, which is probably associated with brake lining abrasion.

Site environment type – The main factor of urban road dust toxicity?

The main objective of the study was to determine the effects of the water extracts of urban road dust (URD) samples on the growth inhibition and mortality rate of Heterocypris incongruens in various site environment type. We collected 24 samples of the road dust close to highways, main roads, crossroads as well as at other places i.e. residential area, and suburbs. We determined the selected metals (Al, As, Ba, Cd, Co, Cr, Cu, Ga, Mg, Mn, Mo, Ni, Pb, Rb, Sr, Ti, Tl, V and Zn) content of the water extracts of these samples as well as we tested the toxicity of the water extracts of URD samples using a commercial test Ostracodtoxkit F. We observed the lowest values of the growth inhibition of H. incongruens for residential areas and suburbs (<50%). The highest growth inhibition we found for water extracts of URD samples collected at the main roads in the Katowice urban area and crossroads in the urban areas. Although the mortality and growth inhibition of H. incongruens were related to the road traffic emissions it was impossible to clearly relate this finding with the urban site category.

Exposure to Hog Dust Extract Decreases Barrier Integrity in Caco‐2 Cells, Induces Airway Inflammation and Increases Intestinal Permeability in Mice

Agricultural enterprises, such as concentrated animal feeding operations (CAFOs), are responsible for the production of 10% of global greenhouse gases and harmful environmental pollutants including hydrogen sulfide, ammonia and particulate matter. Seasonal farm workers, especially swine farmers, are frequently exposed to organic dust that is pro-inflammatory in the lung and are thus at greater risk of developing pneumonia, asthma and other respiratory conditions. In addition to respiratory disease, these air pollutants are directly associated with altered gastrointestinal (GI) physiology and the development of GI diseases. Therefore, the aim of the current study was to identify mechanisms by which extracts of dusts derived from hog CAFOs (HDE) can disrupt intestinal homeostasis. Caco-2 BBE monolayers were seeded at 0.5x106cells/well in a Transwell system and exposed to a single dose of either 0.25%, 0.5%, 0.75%, 1% or 5% HDE. A decreasing trend was seen in monolayer integrity, determined by transepithelial electrical resistance (TEER), at 24-and 48-hours following treatment with 5% HDE (Two-Way ANOVA, p=0.1824 and p=0.2017, respectively, n=3). Moreover, 8-week-old male or female C57BL/6 mice (n=12) were intranasally exposed to saline (n=6) or 12.5% HDE (n=6) for 3 weeks. Bronchoalveolar lavage fluid from HDE-treated mice showed no changes in macrophage cell numbers (unpaired t-test, p=0.2993), but exhibited elevated total cell and neutrophil levels (unpaired t-test, p=0.0027 and p=0.0061, respectively) in comparison to saline controls. Furthermore, no significant differences were seen among the colon lengths of HDE-treated mice (8.32 ± 0.13cm SEM) to that of saline controls (9.2 ± 0.67cm SEM). Additionally, HDE increased permeability to FITC-dextran 4kDA and rhodamine B-dextran 70kDA (unpaired t-test, p<0.001). Moreover, histological changes observed by hematoxylin and eosin staining indicated epithelial cell loss and minimal-mild inflammation in the proximal and distal colon of HDE-treated mice. Together, these findings suggest that airway exposure to CAFOs dusts promotes airway inflammation and can access the gastrointestinal tract to increase regulated and/or unrestricted intestinal permeability, possibly due to intestinal epithelial cell damage. Further identification of mechanistic interactions between the respiratory and gastrointestinal systems is imperative to understand the complex physiological consequences of chronic exposure to organic dusts derived from CAFOs on the gut-lung axis.

Effects of elevated CO2 levels on lung immune response to organic dust and lipopolysaccharide

Workplaces with elevated organic dust levels such as animal feed barns also commonly have elevated levels of gasses, such as CO2. Workers exposed to such complex environments often experience respiratory effects that may be due to a combination of respirable factors. We examined the effects of CO2 on lung innate immune responses in mice co-exposed to the inflammatory agents lipopolysaccharide (LPS) and organic dust. We evaluated CO2 levels at the building recommended limit (1000 ppm) as well as the exposure limit (5000 ppm). Mice were nasally instilled with dust extracts or LPS and immediately put into chambers with a constant flow of room air (avg. 430 ppm CO2), 1000 ppm, or 5000 ppm CO2 enriched air. Results reveal that organic dust exposures tended to show decreased inflammatory responses with 1000 ppm CO2 and increased responses at 5000 ppm CO2. Conversely, LPS with addition of CO2 as low as 1000 ppm tended to inhibit several inflammatory markers. In most cases saline treated animals showed few changes with CO2 exposure, though some changes in mRNA levels were present. This shows that CO2 as low as 1000 ppm CO2 was capable of altering innate immune responses to both LPS and organic dust extracts, but each response was altered in a different fashion.

Assessing Indoor Dust Interference with Human Nuclear Hormone Receptors in Cell-Based Luciferase Reporter Assays.

Background:Per- and polyfluoroalkyl substances (PFAS), organophosphate esters (OPEs), and polybrominated diphenyl ethers (PBDEs) are hormone-disrupting chemicals that migrate from building materials into air and dust.Objectives:We aimed to quantify the hormonal activities of 46 dust samples and identify chemicals driving the observed activities.Methods:We evaluated associations between hormonal activities of extracted dust in five cell-based luciferase reporter assays and dust concentrations of 42 measured PFAS, OPEs, and PBDEs, transformed as either raw or potency-weighted concentrations based on Tox21 high-throughput screening data.Results:All dust samples were hormonally active, showing antagonistic activity toward peroxisome proliferator-activated receptor () (100%; 46 of 46 samples), thyroid hormone receptor () (89%; 41 samples), and androgen receptor (AR) (87%; 40 samples); agonist activity on estrogen receptor () (96%; 44 samples); and binding competition with thyroxine () on serum transporter transthyretin (TTR) (98%; 45 samples). Effects were observed with as little as of extracted dust. In regression models for each chemical class, interquartile range increases in potency-weighted or unknown-potency chemical concentrations were associated with higher hormonal activities of dust extracts (potency-weighted: , , ; , , ; , , ; , , ; unknown-potency: , , ; , , ), adjusted for chemicals with active, inactive, and unknown Tox21 designations.Discussion:All indoor dust samples exhibited hormonal activities, which were associated with PFAS, PBDE, and OPE levels. Reporter gene cell-based assays are relatively inexpensive, health-relevant evaluations of toxic loads of chemical mixtures that building occupants are exposed to. https://doi.org/10.1289/EHP8054

Organic dust exposure induces stress response and mitochondrial dysfunction in monocytic cells.

Exposure to airborne organic dust (OD), rich in microbial pathogen-associated molecular patterns (PAMPs), is shown to induce lung inflammation. A common manifestation in lung inflammation is altered mitochondrial structure and bioenergetics that regulate mitochondrial ROS (mROS) and feed a vicious cycle of mitochondrial dysfunction. The role of mitochondrial dysfunction in other airway diseases is well known. However, whether OD exposure induces mitochondrial dysfunction remains elusive. Therefore, we tested a hypothesis that organic dust extract (ODE) exposure induces mitochondrial stress using a human monocytic cell line (THP1). We examined whether co-exposure to ethyl pyruvate (EP) or mitoapocynin (MA) could rescue ODE exposure induced mitochondrial changes. Transmission electron micrographs showed significant differences in cellular and organelle morphology upon ODE exposure. ODE exposure with and without EP co-treatment increased the mtDNA leakage into the cytosol. Next, ODE exposure increased PINK1, Parkin, cytoplasmic cytochrome c levels, and reduced mitochondrial mass and cell viability, indicating mitophagy. MA treatment was partially protective by decreasing Parkin expression, mtDNA and cytochrome c release and increasing cell viability.

Organic dust-induced mitochondrial dysfunction could be targeted via cGAS-STING or cytoplasmic NOX-2 inhibition using microglial cells and brain slice culture models.

Organic dust (OD) exposure in animal production industries poses serious respiratory and other health risks. OD consisting of microbial products and particulate matter and OD exposure-induced respiratory inflammation are under investigation. However, the effect of OD exposure on brain remains elusive. We show that OD exposure of microglial cells induces an inflammatory phenotype with the release of mitochondrial DNA (mt-DNA). Therefore, we tested a hypothesis that OD exposure-induced secreted mt-DNA signaling drives the inflammation. A mouse microglial cell line was treated with medium or organic dust extract (ODE, 1% v/v) along with either phosphate-buffered saline (PBS) or mitoapocynin (MA, 10µmol). Microglia treated with control or anti-STING siRNA were exposed to medium or ODE. Mouse organotypic brain slice cultures (BSCs) were exposed to medium or ODE with or without MA. Various samples were processed to quantify mitochondrial reactive oxygen species (mt-ROS), mt-DNA, cytochrome c, TFAM, mitochondrial stress markers and mt-DNA-induced signaling via cGAS-STING and TLR9. Data were analyzed and a p value of ≤0.05 was considered significant. MA treatment decreased the ODE-induced mt-DNA release into the cytosol. ODE increased MFN1/2 and PINK1 but not DRP1 and MA treatment decreased the MFN2 expression. MA treatment decreased the ODE exposure-induced mt-DNA signaling via cGAS-STING and TLR9. Anti-STING siRNA decreased the ODE-induced increase in IRF3, IFN-β and IBA-1 expression. In BSCs, MA treatment decreased the ODE-induced TNF-α, IL-6 and MFN1. Therefore, OD exposure-induced mt-DNA signaling was curtailed through cytoplasmic NOX-2 inhibition or STING suppression to reduce brain microglial inflammatory response.

Development of a Data Analysis Tool to Determine the Measurement Variability of Consensus Mass Spectra.

The success of nontargeted analysis often depends on libraries containing reference mass spectra of known chemical compounds; the mass spectra of unknown compounds are compared to these reference mass spectra, leading to a probable compound identity. Typical calculations include the mean measured values for each ion m/z and intensity with no estimation of the variability of the measurement. This study presents a novel tool for the calculation of the variability of a measured mass spectrum, including the various data parameters that can impact the measured variability. Using perfluorooctanoic acid (PFOA) as the model compound, the variability of measured data-dependent fragmentation mass spectra (ddMS2) was calculated within replicate measurements of a simple solution of PFOA and a complex mixture (house dust extract) containing PFOA. The variability of the measured ddMS2 for PFOA in the solution and house dust extract were similar, with standard deviations about the measured m/z value ranging from m/z 0.00003 to 0.00015 and the standard deviations about the measured relative intensity ranging from 0.0077 to 0.0211 relative intensity units. In addition, the selected parameters for the extraction of ddMS2 from a single analytical run varied between the sample types due to the increased presence of background ions in the house dust extract. Finally, the variability of the ddMS2 spectra for PFOA in both samples was used to calculate a more robust similarity factor, informing the confidence of the identification of unknown compounds.

High-throughput analysis of lung immune cells in a combined murine model of agriculture dust-triggered airway inflammation with rheumatoid arthritis.

Rheumatoid arthritis (RA)-associated lung disease is a leading cause of mortality in RA, yet the mechanisms linking lung disease and RA remain unknown. Using an established murine model of RA-associated lung disease combining collagen-induced arthritis (CIA) with organic dust extract (ODE)-induced airway inflammation, differences among lung immune cell populations were analyzed by single cell RNA-sequencing. Additionally, four lung myeloid-derived immune cell populations including macrophages, monocytes/macrophages, monocytes, and neutrophils were isolated by fluorescence cell sorting and gene expression was determined by NanoString analysis. Unsupervised clustering revealed 14 discrete clusters among Sham, CIA, ODE, and CIA+ODE treatment groups: 3 neutrophils (inflammatory, resident/transitional, autoreactive/suppressor), 5 macrophages (airspace, differentiating/recruited, recruited, resident/interstitial, and proliferative airspace), 2 T-cells (differentiating and effector), and a single cluster each of inflammatory monocytes, dendritic cells, B-cells and natural killer cells. Inflammatory monocytes, autoreactive/suppressor neutrophils, and recruited/differentiating macrophages were predominant with arthritis induction (CIA and CIA+ODE). By specific lung cell isolation, several interferon-related and autoimmune genes were disproportionately expressed among CIA and CIA+ODE (e.g. Oasl1, Oas2, Ifit3, Gbp2, Ifi44, and Zbp1), corresponding to RA and RA-associated lung disease. Monocytic myeloid-derived suppressor cells were reduced, while complement genes (e.g. C1s1 and Cfb) were uniquely increased in CIA+ODE mice across cell populations. Recruited and inflammatory macrophages/monocytes and neutrophils expressing interferon-, autoimmune-, and complement-related genes might contribute towards pro-fibrotic inflammatory lung responses following airborne biohazard exposures in setting of autoimmune arthritis and could be predictive and/or targeted to reduce disease burden.

Application of sage herbal dust essential oils and supercritical fluid extract for the growth control of Escherichia coli in minced pork during storage

Sage has various biological activity and long tradition of the using in phytopharmaceutical preparations and, recently, in food industry. In this work, the essential oil obtained by hydrodistillation and essential oil and extract obtained by supercritical fluid extraction from sage herbal dust, waste product of filter tea factory, were screened for antimicrobial activity against Escherichia coli in the medium which simulates the conditions in meat and in real system of minced pork. The supercritical fluid extract had much lower effect to the reduction of a number of E. coli in meat simulation medium. The total inhibition of E. coli growth was achieved after 12 h and 24 h with the addition of 0.6 μl/ml of essential oil obtained by hydrodistilation and supercritical fluid extraction, respectively. The addition of essential oils and supercritical fluid extract of sage herbal dust could be used for the effective control of E. coli growth in minced meat.

Pre-exposure to hydrogen sulfide modulates the innate inflammatory response to organic dust.

Animal production units produce and store many contaminants on-site, including organic dust (OD) and hydrogen sulfide (H2S). Workers in these settings report various respiratory disease symptoms. Both OD and H2S have shown to induce lung inflammation. However, impact of co-exposure to both H2S and OD has not been investigated. Therefore, we tested a hypothesis that pre-exposure to H2S modulates the innate inflammatory response of the lungs to organic dust. In a mouse model of H2S and organic dust extract (ODE) exposure, we assessed lung inflammation quantitatively. We exposed human airway epithelial and monocytic cells to medium or H2S alone or H2S followed by ODE and measured cell viability, oxidative stress, and other markers of inflammation. Exposure to 10ppm H2S followed by ODE increased the lavage fluid leukocytes. However, exposure to 10ppm H2S alone resulted in changes in tight junctionproteins, an increase in mRNA levels of tlr2 and tlr4 as well as ncf1, ncf4, hif1α, and nrf2. H2S alone or H2S and ODE exposure decreased cell viability and increased reactive nitrogen species production. ODE exposure increased the transcripts of tlr2 and tlr4 in both in vitro and in vivo models, whereas increased nfkbp65 transcripts following exposure to ODE and H2S was seen only in in vitro model. H2S alone and H2S followed by ODE exposure increased the levels of IL-1β. We conclude that pre-exposure to H2S modulates lung innate inflammatory response to ODE.

Characterization of adipogenic, PPARγ, and TRβ activities in house dust extracts and their associations with organic contaminants

In this study, we sought to expand our previous research on associations between bioactivities in dust and associated organic contaminants. Dust samples were collected from central NC homes (n = 188), solvent extracted, and split into two fractions, one for analysis using three different bioassays (nuclear receptor activation/inhibition and adipocyte development) and one for mass spectrometry (targeted measurement of 124 organic contaminants, including flame retardants, polychlorinated biphenyls, perfluoroalkyl substances, pesticides, phthalates, and polycyclic aromatic hydrocarbons). Approximately 80% of dust extracts exhibited significant adipogenic activity at concentrations that are comparable to estimated exposure for children and adults (e.g. ~20 μg/well dust) via either triglyceride accumulation (65%) and/or pre-adipocyte proliferation (50%). Approximately 76% of samples antagonized thyroid receptor beta (TRβ), and 21% activated peroxisome proliferator activated receptor gamma (PPARγ). Triglyceride accumulation was significantly correlated with TRβ antagonism. Sixty-five contaminants were detected in at least 75% of samples; of these, 26 were correlated with adipogenic activity and ten with TRβ antagonism. Regression models were used to evaluate associations of individual contaminants with adipogenic and TRβ bioactivities, and many individual contaminants were significantly associated. An exploratory g-computation model was used to evaluate the effect of mixtures. Contaminant mixtures were positively associated with triglyceride accumulation, and the magnitude of effect was larger than for any individually measured chemical. For each quartile increase in mixture exposure, triglyceride accumulation increased by 212% (RR = 3.12 and 95% confidence interval: 1.58, 6.17). These results suggest that complex mixtures of chemicals present in house dust may induce adipogenic activity in vitro at environmental concentrations and warrants further research.

Acute toxicity assessment of indoor dust extracts by luminescent bacteria assays with Photobacterium Phosphoreum T3

In the last decades, there has been an increasing concern about the human exposure to indoor dust. Therefore, it is imperative to assess the toxicity of indoor dust and associated dust extracts. In this study, the acute toxicity assessment of indoor dust was performed using a bioluminescence test, with Photobacterium phosphoreum T3 (PPT3) chosen as the test bacterium. The different indoor dust samples were collected from residences, offices, dormitories and laboratories in Shanghai, China. Our data reveal that PPT3 is more active to water-soluble ions and organic contaminants at low concentrations, while extract solutions elicit increased bacterial toxicity at high concentrations. The results of a bioluminescence assay by PPT3 indicated that the dust organic extracts exhibited increased toxicity compared with the water exacts. Dust extracts from the laboratory exhibited the greatest bacterial toxicity when compared with office, dormitory and residence samples. Moreover, office dust exhibited higher bacterial toxicity than residence dust. Furthermore, the comprehensive toxicity of dust on PPT3 was assessed by extracts toxicity -addition (i.e. IRaddition). The calculated values were close to the corresponding experimental data. The bioluminescence test showed the indoor dust samples are weakly toxic to PPT3, which are equivalent to 0.046–0.123 mg Hg•L−1. Different dust extracts among the different sampling sites showed varying toxicity to PPT3. This study provides some important information to understand the potential health risk from different indoor environment using a rapid bioluminescence assay.

Niacinamide mitigates SASP-related inflammation induced by environmental stressors in human epidermal keratinocytes and skin.

To evaluate whether niacinamide (Nam) can mitigate production of inflammatory and senescence-related biomarkers induced by environmental stressors. Human epidermal keratinocytes were exposed to UVB, urban dust, diesel exhaust and cigarette smoke extract and treated with Nam or vehicle control. Full thickness 3-D skin organotypic models were exposed to a combination of UVB and PM2.5 and treated with Nam or vehicle control. Quantitation of the SASP-related inflammatory mediators PGE2 , IL-6 and IL-8 was performed on cultured media. UVB-exposed keratinocytes treated with and without Nam were immunostained for the senescence biomarker Lamin B1 (LmnB1). Transcriptomics profiling of cigarette smoke extract effects on keratinocytes was performed. A double-blind, placebo-controlled clinical was conducted on 40 female panellists that were pretreated on back sites for two weeks with 5% Nam or vehicle and then exposed to 1.5 minimal erythemal dose (MED) solar-simulated radiation (SSR). Treated sites were compared with non-treated exposed sites for erythema and the skin surface IL-1αRA/IL-1α inflammatory biomarkers. Ultraviolet B induced synthesis of PGE2 , IL-8 and IL-6 and reduced LmnB1 levels in keratinocytes. Urban dust and diesel exhaust only stimulated synthesis of IL-8 whereas cigarette smoke extract only stimulated levels of PGE2 . In all exposures, treatment with Nam significantly mitigated synthesis of the inflammatory mediators and restored levels of UVB-reduced LmnB1. In the 3D skin equivalent model, Nam reduced IL-8 levels stimulated by a combination of topical PM2.5 and UV exposure. In a UV challenge clinical, pretreatment with 5% Nam reduced erythema and skin surface IL-1αRA/IL-1α inflammatory biomarkers that were induced by SSR. Since it is known that Nam has anti-inflammatory properties, we tested whether Nam can inhibit environmental stress-induced inflammation and senescence-associated secretory phenotype (SASP) biomarkers. We show Nam can reduce PGE2 , IL-6 and IL-8 levels induced by environmental stressors. Additionally, in vivo pretreatment with Nam can reduce UV-induced erythema and skin surface inflammatory biomarkers. These findings add to the body of evidence that Nam can mitigate the skin's inflammatory response elicited by environmental stressors. This supports Nam can potentially inhibit senescence and premature ageing and thereby maintain skin's functionality and appearance.

Liquid chromatography-ion mobility-high resolution mass spectrometry for analysis of pollutants in indoor dust: Identification and predictive capabilities

Dust analysis provides a means to assess the degree of exposure of humans in an indoor environment to various contaminant classes such as flame retardants, pesticides and others. There is increasing interest in non-targeted acquisitions using high resolution mass spectrometry (HRMS) to better capture the contaminant profile. However, these studies are confronted with the challenge of assessing confidence in proposed identifications, particularly when authentic standards are not available. Here, we demonstrate the analysis of dust extracts representing various indoor environments (industrial e-waste processing and domestic) for high-abundance environmental contaminants using a data-independent LC-HRMS approach, incorporating ion mobility spectrometry (IMS) to provide additional characterization capability for the complex samples. Twenty-nine xenobiotic compound identifications were made based on both targeted and non-targeted processing approaches using accurate mass precursor and product ion measurement combined with an ion mobility derived collision-cross section (TWCCSN2) determination. Characterization of the repeatability of TWCCSN2 value measurements and their average relative error to compared authentic standards of 0.38% were consistent with various published studies and represent a robust measurement property. TWCCSN2 values were particularly useful in cases where confirmation after the initial dust analysis was performed using a different chromatographic method, due to the gas-phase measurement being unaffected by such changes. Observed compound TWCCSN2 values were then compared to predicted CCSN2 values obtained using two different machine-learning based predictive techniques. Results from one of the predictive programs indicates a promising avenue for use of these models for supporting compound identification in non-targeted analyses.