Exposure Chamber Research Articles

The Specific and Total CO2 Emission Activity of Wood-Decaying Fungi and Their Response to Increases in Temperature.

The CO2 emission activity of xylotrophic fungi responding to an increase in temperature in the range of 10-30 °C with pure dikaryotic cultures of Fomes fomentarius s. str., F. inzengae, Fomitopsis betulina, F. pinicola, and Phellinus igniarius was analyzed. Emission activity was assessed by the difference in CO2 concentration in 0.5 L exposure chambers with Petri dishes with mycelium growing on agar at the beginning of exposure and an hour later using a Gasmet DX-4030 FTIR spectrometer (Gasmet Technologies Oy, Finland), error measurements ±50 ppm. Specific (μg CO2/cm2/h) and total (μg CO2/h) emission activity and its relationship with temperature and size (area) of the mycelium were assessed. It is shown that in the range of 10-30 °C, the specific and total CO2 emission activity of the mycelium is closely and positively related to temperature. Specific emission, which is an indicator of the respiratory activity of the mycelium, does not depend on its size; its only driver is temperature, the relationship with which is linear: an increase in temperature by 10 °C causes an increase in the specific emission activity of the mycelium by 1.7 times. The total CO2 emission activity, which is an indicator of the total amount of CO2 emitted, is directly proportional to the specific emission activity and the size of the mycelium. In the range of 10-30 °C, an increase in temperature causes an almost equal increase in both the specific emission activity of the mycelium (Q10 1.7) and its growth (Q10 1.5) and causes an exponential increase in the total emission of CO2. This must be taken into account when predicting CO2 emissions from woody debris under climate change, as it could potentially contribute to accelerating climate change.

Field study on the uptake pathways and their contributions to the accumulation of organophosphate esters, phthalates, and polycyclic aromatic hydrocarbons in upland rice

Plant uptake of organic contaminants generally occurs through either root, gas-phase foliar, or particle-phase foliar uptake. Understanding these pathways is essential for food-system practitioners to reduce human exposures, and to clean contaminated-sites with phytoremediation. Herein, we conducted a field-based experiment using an improved specific exposure chamber to elucidate the uptake pathways of organophosphate esters, phthalates, and polycyclic aromatic compounds, and quantitatively assessed their contributions to organic contaminant accumulations in field-grown rice. For most target compounds, all three uptake pathways (root, foliar gas, and foliar particle uptakes) contributed substantially to the overall contaminant burden in rice. Compounds with lower octanol–water partition coefficients (Kow) were more readily translocated from roots to leaves, and compounds with higher octanol−air partition coefficients (Koa) tended to enter rice leaves mostly through particle deposition. Most compounds were mostly stored in the inner leaves (55.3–98.2 %), whereas the relatively volatile compounds were more readily absorbed by the waxy layer and then transferred to the inner leaves. Air particle desorption was a key process regulating foliar uptake of low-volatility compounds. The results can help us to better understand and predict the environmental fate of those contaminants, and develop more effective management strategies for reducing their human exposure through food ingestion.

Chronic PM2.5 exposure disrupts intestinal barrier integrity via microbial dysbiosis-triggered TLR2/5-MyD88-NLRP3 inflammasome activation

BackgroundPM2.5, a known public health risk, is increasingly linked to intestinal disorders, however, the mechanisms of its impact are not fully understood. PurposeThis study aimed to explore the impact of chronic PM2.5 exposure on intestinal barrier integrity and to uncover the underlying molecular mechanisms. MethodsC57BL/6 J mice were exposed to either concentrated ambient PM2.5 (CPM) or filtered air (FA) for six months to simulate urban pollution conditions. We evaluated intestinal barrier damage, microbial shifts, and metabolic changes through histopathology, metagenomics, and metabolomics. Analysis of the TLR signaling pathway was also conducted. ResultsThe mean concentration of PM2.5 in the CPM exposure chamber was consistently measured at 70.9 ± 26.8 μg/m³ throughout the study period. Our findings show that chronic CPM exposure significantly compromises intestinal barrier integrity, as indicated by reduced expression of the key tight junction proteins Occludin and Tjp1/Zo-1. Metagenomic sequencing revealed significant shifts in the microbial landscape, identifying 35 differentially abundant species. Notably, there was an increase in pro-inflammatory nongastric Helicobacter species and a decrease in beneficial bacteria, such as Lactobacillus intestinalis, Lactobacillus sp. ASF360, and Eubacterium rectale. Metabolomic analysis further identified 26 significantly altered metabolites commonly associated with intestinal diseases. A strong correlation between altered bacterial species and metabolites was also observed. For example, 4 Helicobacter species all showed positive correlations with 13 metabolites, including Lactate, Bile acids, Pyruvate and Glutamate. Additionally, increased expression levels of TLR2, TLR5, Myd88, and NLRP3 proteins were noted, and their expression patterns showed a strong correlation, suggesting a possible involvement of the TLR2/5-MyD88-NLRP3 signaling pathway. ConclusionsChronic CPM exposure induces intestinal barrier dysfunction, microbial dysbiosis, metabolic imbalance, and activation of the TLR2/5-MyD88-NLRP3 inflammasome. These findings highlight the urgent need for intervention strategies to mitigate the detrimental effects of air pollution on intestinal health and identify potential therapeutic targets.

Surface Finish Optimization of Vapor Smoothened PLA Fabricated Parts with Microstructural Analysis

Additive Manufacturing (AM) is a product creation method done layer-by-layer. This process tends to create an unwanted feature known as staircase effect. Vapor smoothing is considered a viable solution for polymer-based AM products to minimized surface roughness. Research literature concerning vapor smoothing of polylactic acid (PLA) parts generally limited unlike its ABS counterpart. This research aims to identify optimum level for both chamber temperature and exposure time of the AM product. Two methods were used to compare their outputs with one another. The two methods are surface roughness tester and optical microscopy. The results provided an impressive 50.88 and 62.72% improvement based on the two test methods. Lastly, a contour-plot was generated to provide future users a guideline if they want to conduct research similar study.

Home-made low-cost dosemeter for photon dose measurements in radiobiological experiments and for education in the field of radiation sciences

Reliable dosimetry systems are crucial for radiobiological experiments either to quantify the biological consequences of ionizing radiation or to reproduce results by other laboratories. Also, they are essential for didactic purposes in the field of radiation research. Professional dosemeters are expensive and difficult to use in exposure facilities with closed exposure chambers. Consequently, a simple, inexpensive, battery-driven dosemeter was developed that can be easily built using readily available components. Measurements were performed to validate its readout with photons of different energy and dose rate and to demonstrate the applicability of the dosemeter. It turned out that the accuracy of the dose measurements using the developed dosemeter was better than 10%, which is satisfactory for radiobiological experiments. It is concluded that this dosemeter can be used both for determining the dose rates of an exposure facility and for educational purposes.

Low-vacuum SEM imaging and viability test of L929 cells exposed to a Euro 6 diesel exhaust gas mixture in a BAT-CELL chamber in comparison with hydrocarbons emission

Exhaust emissions, which count among the most common causes of premature death worldwide, can cause irreversible changes in cells, leading to their damage or degeneration. In this research, L929 line cells were observed after exposure in the BAT-CELL chamber to exhaust gases emitted from a Euro 6 compression-ignition engine. Real road traffic conditions were simulated, taking into account air resistance while driving at speeds of 50 km/h, 120 km/h and idling engine. Morphological analysis of the cells was performed using an environmental scanning electron microscope. It has been observed that diesel exhaust fumes can cause inflammation, which can induce apoptosis or leads to necrotic cell death. The impact of the vehicle exhaust gases can inhibit cell proliferation by almost three times. Moreover, a correlation has been observed between the speed of the inflammatory reaction in cells and the presence of specific hydrocarbon compounds that determine the toxicity of exhaust gases. Research has shown that the toxicity of the emitted exhaust gases has been the highest at the driving speed of 120 km/h. In order to reduce the harmful effects of exhaust emissions, ecological alternatives and the supplementation of legal provisions regarding the compounds subject to limitation are necessary.

The Underlying Mechanism of Poisoning after the Accidental Inhalation of Aerosolised Waterproofing Spray.

Waterproofing sprays can cause acute respiratory symptoms after inhalation, including coughing and dyspnoea shortly after use. Here, we describe two cases where persons used the same brand of waterproofing spray product. In both cases the persons followed the instructions on the product and maximized the ventilation by opening windows and doors; however, they still became affected during the application of the product. Products with the same batch number as that used in one case were tested for their effect on respiration patterns of mice in whole-body plethysmographs and lung surfactant function inhibition in vitro. The product was used in spraying experiments to determine the particle size distribution of the aerosol, both using a can from one case and a can with an identical batch number. In addition, the aerosols in the mouse exposure chamber were measured. Aerosol data from a small-scale exposure chamber and data on the physical and temporal dimensions of the spraying during one case were used to estimate the deposited dose during the spraying events. All collected data point to the spraying of the waterproofing product being the reason that two people became ill, and that the inhibition of lung surfactant function was a key component of this illness.

Exposure to fine particulate matter 2.5 from wood combustion smoke causes vascular changes in placenta and reduce fetal size

During gestation, maternal blood flow to the umbilical cord and placenta increases, facilitating efficient nutrient absorption, waste elimination, and effective gas exchange for the developing fetus. However, the effects of exposure to wood smoke during this period on these processes are unknown. We hypothesize that exposure to PM2.5, primarily sourced from wood combustion for home heating, affects placental vascular morphophysiology and fetal size. We used exposure chambers that received either filtered or unfiltered air. Female rats were exposed to PM2.5 during pre-gestational and/or gestational stages. Twenty-one days post-fertilization, placentas were collected via cesarean section. In these placentas, oxygen diffusion capacity was measured, and the expression of angiogenic factors was analyzed using qPCR and immunohistochemistry. In groups exposed to PM2.5 during pre-gestational and/or gestational stages, a decrease in fetal weight, crown-rump length, theoretical and specific diffusion capacity, and an increase in HIF-1α expression were observed. In groups exposed exclusively to PM2.5 during the pre-gestational stage, there was an increase in the expression of placental genes Flt-1, Kdr, and PIGF. Additionally, in the placental labyrinth region, the expression of angiogenic factors was elevated. Changes in angiogenesis and angiogenic factors reflect adaptations to hypoxia, impacting fetal growth and oxygen supply. In conclusion, this study demonstrates that exposure to PM2.5, emitted from wood smoke, in both pre-gestational and gestational stages, affects fetal development and placental health. This underscores the importance of addressing air pollution in areas with high levels of wood smoke, which poses a significant health risk to pregnant women and their fetuses.

EXPOSURE TO AIR POLLUTION FINE PARTICULATE MATTER (PM2.5) ALTERS SYSTEMIC AND TISSUE-SPECIFIC COMPONENTS OF THE RENIN-ANGIOTENSIN SYSTEM

Objective: Previous studies have implicated air pollution fine particulate matter (PM2.5) in various cardiovascular cardiometabolic and renal disease states. However, the molecular mechanisms by which these pollutants mediate these comorbidities have not been fully elucidated. Dysregulation of the renin-angiotensin system (RAS) may be one potential mechanism. This study aimed to investigate the participation of the RAS in air pollution-associated pathologies. Design and method: To study the impact of PM2.5 on systemic and tissue components of the RAS, male 8-week-old Balb/C mice were exposed to filtered air (FA) or urban air (UA) from Buenos Aires City, in whole-body exposure chambers for 14 weeks. Levels of main RAS components including angiotensin-converting enzyme (ACE) and ACE2, as well as AT1, AT2, and Mas receptors (R) abundance, were determined in kidney, heart, and lung tissue by Western Blotting (WB) and their corresponding mRNA expression was detected by RT-qPCR. Circulating angiotensin (Ang) II levels were determined by radioimmunoassay. Results: Exposure to air pollution resulted in increased mRNA levels of ACE and MasR, and increased protein levels of ACE in the kidney; upregulated mRNA and protein abundance of cardiac and pulmonary AT2R and MasR, together with increased levels of proteins nitrated at Tyr residues in both kidney and lung homogenates, indicative of nitrosative stress in these tissues. In addition, exposure to PM2.5 was associated with increased levels of circulating Ang II, indicative of an exacerbation of the RAS. Conclusions: Our findings indicate that chronic exposure to air pollution induces an altered expression of both tissue and systemic components of the RAS. Given that both the AT2R and the MasR have been ascribed to participate in tissue-repair mechanisms, the upregulation of these receptors detected in mouse heart and lung after chronic exposure to polluted air could represent a mechanism of tissue protection against damage induced by PM2.5.

Rhinoconjunctivitis severity induced by cat exposure influences early and late asthmatic responses: Evidence from an environmental exposure chamber.

The impact of allergic rhinoconjunctivitis on the early (EAR) and late asthmatic response (LAR) has yet to be assessed during optimal allergen exposure conditions. We aimed to assess predictive factors of the EAR and LAR and to evaluate the relation between rhinitis, conjunctivitis and asthma induced by cat allergen exposure in an environmental exposure chamber (EEC). Data from two cohort studies involving asthmatic patients with cat allergy who performed a cat allergen exposure challenge in ALYATEC EEC were analysed. Spirometry, visual analogue scale (VAS) for asthma, VAS for rhinitis, Total Nasal Symptoms Score, Total Ocular Symptoms Score (TOSS), Rhinoconjunctivitis Total Symptoms Score and Abelson score were used to assess asthma, rhinitis and conjunctivitis during and after exposure. An EAR occurred in 65.1% of patients, 32.1% of whom had a LAR. The diameter of the prick test to cat allergens and non-specific bronchial hypersensitivity level were independent risk factors for EAR (p < .05). No independent risk factors for LAR were identified. Rhinoconjunctivitis severity during exposure correlated with the asthma VAS during EAR and LAR (p < .05). Allergen exposure time needed to trigger an EAR correlated with the Abelson score during exposure (p < .05). The asthma VAS and TOSS during exposure correlated with faster LAR occurrence (p < .05). Prick test size and non-specific bronchial hypersensitivity level were confirmed as independent predictive factors of EAR during allergen exposure in an EEC. This study demonstrated the relation between the severity of rhinitis, conjunctivitis and asthma induced by allergen exposure for both EAR and LAR.

Clinical validation of grass pollen exposure chamber in patients with allergic rhinitis triggered by timothy grass.

The fluctuation in concentrations of airborne allergens frequently presents a challenge to assessing the efficacy of allergen immunotherapy (AIT) in 'field' studies. Allergen exposure chambers (AECs) are specialized medical installations developed to expose individuals to allergens at defined and consistent concentrations under a controlled environment. The aim of the study was to validate the provocation test with timothy grass pollen as well as to assess its safety in the AEC in patients with allergic rhinitis. In the ALLEC® AEC, varying concentrations of timothy grass pollen were dispersed. Allergic symptoms were measured by total nasal symptom score (TNSS), acoustic rhinometry, peak nasal inspiratory flow (PNIF) and nasal discharge volume. Lung function, assessed through peak expiratory flow rate (PEFR) and forced expiratory volume in the first second (FEV1), was used to evaluate safety. The consistency of the test was proved by the stability of environmental conditions, including temperature, humidity and CO2 levels, as well as constant concentrations of grass pollen at predetermined levels ranging from 1000 to 10,000 particles per cubic meter (p/m3). Allergic individuals developed symptoms at concentrations of 3000 p/m3 and above, across all measured endpoints. Lung function was not affected throughout all the challenges. The reproducibility of symptoms was confirmed throughout the tests. The concentration of 8000 p/m3 together with a challenge duration of 120 min was found to be optimal. The study demonstrates that the ALLEC® grass pollen exposure chamber provides a reliable and safe method for inducing repeatable symptoms in patients with allergic rhinitis. This approach can be effectively applied for allergy diagnostics and clinical endpoint determination during AIT.

Ascorbic acid attenuates gasoline-induced testicular toxicity, sperm quality deterioration, and testosterone imbalance in rats.

The present study evaluated the protective effect of ascorbic acid (ASCB) against gasoline fumes (PET) induced testicular oxidative stress, sperm toxicity, and testosterone imbalance in Wistar rats. Twenty-four (24) male albino rats (75 ± 16g) were randomized into three experimental groups (N = 8). The control group: received normal saline, PET group: exposed to PET 6h daily by inhalation in an exposure chamber and PET + 200mg ASCB/kg body weight group: exposed to PET 6h daily by inhalation and administered ASCB per os. Treatment of ASCB and PET exposure was done thrice and five times weekly for a period of 10weeks respectively. ASCB co-treatment prevented PET-induced increases in the oxidative stress markers (glutathione, glutathione S-transferase, superoxide dismutase, catalase, hydrogen peroxide generation, nitric oxide, and lipid peroxidation) and serum testosterone concentration (p < .05). Sperm quality was low and those with damaged heads and tails increased alongside histological injuries in the PET-exposed rats, which were also minimized with ASCB administration. ASCB protected against PET-induced oxidative stress, sperm, and testis damage in rats.

Acute Inhalation Toxicity Study of 3-Methoxybutyl Acetate in Sprague-Dawley Rats

3-Methoxybutyl acetate is an organic solvent used in a wide range of industrial and consumer applications, such as coatings, adhesives, chemical intermediates, paints, and washing products. We conducted an acute inhalation toxicity study of 3-Methoxybutyl acetate using an inhalation exposure system (nose-only) in Sprague-Dawley rats. Male and female rats were exposed to 3-Methoxybutyl acetate for 4 h/day. The tests were conducted according to the Organisation for Economic Cooperation and Development Guidelines for the Testing of Chemicals (OECD TG) 436. The analytical concentrations of the exposure chamber were 9.76 ± 0.51 mg/L. Clinical signs, mean body weight changes, and gross necropsy results were observed. No deaths, abnormal clinical signs, gross findings at necropsy, or abnormal mean body weight changes related to exposure to the test substance were observed in either sex. Based on these results, we suggested that 3-Methoxybutyl acetate does not have acute toxic effects at the technically acceptable concentration of 10 mg/L.

SULPHUR DIOXIDE INDUCED OXIDATIVE AND HISTOPATHOLOGICAL DAMAGE TO THE OVARIES OF FEMALE RATS (Rattus rattus)

The aim of the study was to examine the toxic effect of sulphur dioxide on the ovaries of female rats. The effect of different concentrations of SO2 (0, 5, 10 and 15 ppm) on antioxidant enzymes and histopathological changes were investigated in ovaries of female rats under natural and experimental conditions. Naturally exposed, house rats, Rattus rattus (Group I) were collected from agricultural fields alongside the road in Ludhiana, India and acclimatized for 1 month in laboratory. Laboratory-bred house rats were divided into four groups. Group II (control rats), III, IV and V were first exposed to the filtered air in 1 m3 exposure chamber for 5 h day-1for 28 days and then treated with 0, 5, 10 and 15 ppm of SO2, respectively. SO2 treatment showed significant increase in lipid peroxidation (LPO) levels, followed by significant decrease in the activities of superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), glutathione-S-transferase (GST) and GSH-PX in ovaries of female rats. The results revealed that SO2 can cause oxidative damage to the ovaries of female rats. The increase in LPO and decrease in other enzymes was more prominent at higher SO2 concentration as compared to the other tested concentrations.

Abstract 5521: Nicotine promotes perineural brain metastasis of lung cancer by activating GABAergic neurons

Abstract Tobacco smoking significantly increases the incidence of brain metastasis. However, the pathological mechanism by which smoking promotes brain metastasis through modulating brain microenvironment is yet poorly understood. We previously showed that the incidence of brain metastasis is associated with nicotine intake. Nicotine enhanced polarization of M2 pro-tumor microglia, which promoted brain metastasis. In addition to the immune surveillance role, microglial cells also control neuronal synapse formation. Microglial cells promote neuron synapse formation in the developing brain, whereas microglia depletion suppresses synapse density. Furthermore, microglia-secreted microRNAs (miRNAs) have been shown to promote synaptic formation by targeting synapse-related genes of the DKK-Wnt family. Neurons are one of the most abundant cell types in the brain, and they are highly specialized for cell-to-cell signal activation. However, little is known about the roles of neurons in brain metastasis of lung cancer. We hypothesize that nicotine stimulates microglia to secrete exosomal miR-32-3p, which promotes brain metastasis by augmenting GABAergic synaptic formation and hence releasing GABA that serves as a metabolic substrate to fuel tumor cell growth. We also hypothesize that inhibiting the GABA transporter of tumor cells suppresses brain metastasis by blocking the GABA shunt. We found that lung cancer patients with a smoking history had significantly higher synaptic formation and the expression of GABA transporter in brain metastasis. To investigate the effect of smoking and nicotine intake on brain metastasis in vivo, mice were intracardially transplanted with lung cancer brain metastasis cells (H2030BrM and PC9BrM) followed by administration of nicotine or cigarette smoke exposure in a smoking chamber. We found that smoking and nicotine increased M2 microglia polarization, synaptic formation, and the expression of GABA in mouse brain metastasis. Furthermore, nicotine increased the secretion of miR-32-3p from nicotine-pretreated microglia, which promoted GABA release from GABAergic neurons. Treating H2030BrM and PC9BrM cells with conditioned medium (CM) obtained from neurons exposed to CM derived from nicotine-treated microglia exosomes resulted in increased tumor growth through the activation of the GABA shunt pathway. Blocking GABA transporter 1 (GAT1) by CRISPR/Cas9 or a small molecule of GAT1 inhibitor suppressed the GABAergic neuron-induced tumor progression. Our results indicate that nicotine-activated microglia enhanced GABA release from neurons followed by the promotion of GABA shunt in tumor cells and that a GAT inhibitor serves as a promising therapeutic tool for the treatment of lung cancer patients with brain metastasis. Citation Format: Shih-Ying Wu, Abhishek Tyagi, Ravindra Pramod Deshpande, Kerui Wu, Eleanor Cecile Smith, Kounosuke Watabe. Nicotine promotes perineural brain metastasis of lung cancer by activating GABAergic neurons [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 5521.

Assessing the Impact of Sepiolite-Based Bio-Pigment Infused with Indigo Extract on Appearance and Durability of Water-Based White Primer.

The objective of this study is to evaluate how two varying amounts of sepiolite-based powder, infused with indigo extract, affect the appearance and durability of a water-based, white primer. To examine the influence of this eco-friendly pigment on the coatings' overall appearance, assessments were performed for color, gloss, and surface roughness. Additionally, the coatings were investigated through optical and electron microscopic observations, to evaluate the distribution of the pigment within the polymer matrix. The effect of the pigment on the coating's durability was assessed through accelerated tests, including exposure in a salt spray chamber and a UV-B chamber. These tests aimed to evaluate the emergence of defects and changes in the appearance of the samples over time. Furthermore, the impact of different quantities of sepiolite-based powder on the coating's ability to act as a barrier was assessed using liquid resistance tests and contact angle measurements. These evaluations aimed to understand how the coating responded to various liquids and its surface properties concerning repellency or absorption. In essence, this study underscores the considerable influence of the eco-friendly pigment, demonstrating its capacity to introduce unique color and texture variations in the paint. Moreover, the inclusion of the pigment has enhanced the coating's color stability, its ability to act as a barrier, and its overall durability when exposed to harsh environments.

Flow Rate and Wall Shear Stress Characterization of a Biomimetic Aerosol Exposure System.

Current in vitro emissions and exposure systems lack biomimicry, use unrealistic flow conditions, produce unrealistic dose, and provide inaccurate biomechanical cues to cell cultures, limiting ability to correlate in vitro outcomes with in vivo health effects. A biomimetic in vitro system capable of puffing aerosol and clean air inhalation may empower researchers to investigate complex questions related to lung injury and disease. A biomimetic aerosol exposure system (BAES), including an electronic cigarette adapter, oral cavity module (OCM), and bifurcated exposure chamber (BEC) was designed and manufactured. The fraction of aerosol deposited in transit to a filter pad or lost as volatiles was 0.116±0.021 in a traditional emissions setup versus 0.098 ± 0.015 with the adapter. The observed flowrate was within 5% of programed flowrate for puffing (25 mL/s), puff-associated respiration (450 mL/s), and tidal inhalation (350 mL/s). The maximum flowrate observed in the fabricated BAES was 450 mL/s, exceeding the lower target nominal wall shear stress of 0.025 Pa upstream of the bifurcation and fell below the target of 0.02 Pa downstream. This in vitro system addresses several gaps observed in commercially available systems and may be used to study many inhaled aerosols. The current work illustrates how in silico models may be used to correlate results of an in vitro study to in vivo conditions, rather than attempting to design an in vitro system that performs exactly as the human respiratory tract.

Effects of uptake pathways on the accumulation, translocation, and metabolism of OPEs in rice: An emphasis on foliar uptake

The often-overlooked importance of foliar absorption on the plant uptake of organic pollutants was investigated by an exposure chamber test. Rice seedlings were exposed to organophosphate esters (OPEs) through 8 scenarios arranged from 3 major uptake pathways: root uptake via solution, foliar uptake via gas, and foliar uptake via particles, to identify the contributions of these 3 uptake pathways and their influences on the translocation and metabolism of OPEs in rice. The concentration of OPEs in rice tissues showed an “additive effect” with the increase of exposure pathways. OPEs in rice shoots mainly originated from foliar uptake through particle (29.6 %–63.5 %) and gaseous (28.5 %–49.4 %) absorptions rather than root uptake (7.86 %–24.2 %) under the exposure condition. In comparison with stomal absorption, wax layer penetration was the main pathway for most OPEs to enter into leaves, especially for those compounds with high octanol-air partition coefficients. Although the subcellular distributions of OPEs in the rice tissues of the foliar exposure were slightly different from those of the root exposure, hydrophobic OPEs were mainly stored in the cell wall with hydrophilic OPEs mainly in the cytosol. The translocation of OPEs from the exposed tissue to the unexposed tissue were significantly negatively correlated with their octanol-water partition coefficients, but their basipetal translocation were limited. The result suggested that the translocation of OPEs within rice is prioritized over their degradation. This study deepens our understanding of the processes behind OPE uptake by rice and highlights the importance of foliar uptake, especially for those via particle absorption.

A Replicate Phase III Clinical Trial to Assess the Reproducibility of Efficacy and Safety of Reproxalap Ophthalmic Solution (0.25%) Compared to Vehicle in Participants With Seasonal Allergic Conjunctivitis (AC) Using the Environmental Exposure Chamber (EEC)

A Replicate Phase III Clinical Trial to Assess the Reproducibility of Efficacy and Safety of Reproxalap Ophthalmic Solution (0.25%) Compared to Vehicle in Participants With Seasonal Allergic Conjunctivitis (AC) Using the Environmental Exposure Chamber (EEC)

Exploring polyamide 11 as a novel renewable resource-based filler in wood paint: Investigating aesthetic aspects and durability impact of the composite coating

The aim of this study is to assess the impact of different quantities of polyamide 11 powder on the visual appeal, durability, and multi-functionality of a water-based wood paint. To investigate the effect of this bio-based additive on the overall appearance of the coatings, measurements for color, gloss, and surface roughness were conducted. Additionally, various tests were performed to quantify the influence of these environmentally friendly additives on the mechanical properties of the coatings, including hardness, surface friction coefficient, and resistance to abrasion. Moreover, the effect of varying amounts of polyamide 11 powder on the coating's barrier capabilities was evaluated through liquid resistance tests, contact angle measurements, and water uptake assessment. Finally, the influence of the bio-based additive on the layers' durability was evaluated by subjecting them to exposure in a xenon arc light chamber. The degradation of the samples was monitored through colorimetric inspections to assess any changes or deterioration. In summary, this study underscores the significant impact of varying the quantity of polyamide 11 powder, showcasing its ability to not only introduce distinct texture to the paint but also significantly enhance the mechanical properties of the composite layer. Importantly, these improvements are achieved without compromising the barrier properties and durability of the acrylic matrix coating.