Last data update: Jul 18, 2025. (Total: 49602 publications since 2009)
Records 1-2 (of 2 Records) |
Query Trace: Burns ES[original query] |
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Peracetic acid effects on human bronchial cells in an air liquid interface
Burns ES , Olgun NS , Friend SA , McKinney WG , Sinsel EW , Reynolds JS , Leonard SS . PLoS One 2025 20 (5) e0322926 Peracetic acid (PAA) is an organic peroxide commonly used as a disinfectant or sterilizing agent across many industries such as in agriculture, water treatment plants, and healthcare facilities. PAA is versatile, effective, and is considered environmentally friendly due to its decomposition products which include acetic acid, oxygen, and water. However, occupational researchers recognize that it is also highly corrosive as well as a strong oxidizer, and exposure to peracetic acid can severely irritate the respiratory system and this mixture can even act as an asthmagen. To determine the effect of PAA exposure to human airways, normal human bronchial epithelial cells (NHBE) were cultured at the air liquid interface and then exposed to PAA vapors generated across four separate concentrations: 0, 3, 12, and 24 ppm during four-hour exposure periods. Cells were allowed time to recover post-exposure for four and twenty-four hours prior to analysis. Cellular response and toxicity were assessed through metabolic assays for cell viability and cytotoxicity, cell layer integrity (using transepithelial electrical resistance (TEER) measures), and ELISA assays for endothelin-1 (ET-1) (pro-inflammatory mediator and vasoconstrictor) and pro-inflammatory cytokines (IL-6, IL-8). Histological changes were examined for presence of mucosubstances and overall tissue layer structure. PAA exposure had a significant effect on cytotoxicity wherein cytotoxic effect increased with dose concentration and recovery duration. Conversely, cell viability decreased significantly with dose and recovery period. Furthermore, exposure to PAA lowered transepithelial resistance significantly between controls and exposure conditions. ET-1, IL-6, and IL-8 were also assessed from culture fluid and were found to respond to dosage and recovery length. Histology suggested an injury response and cell layer disruptions at 12 ppm exposure and showed indicators of cell death at 24 ppm. Our findings suggest that PAA induces cell damage and a pro-inflammatory response in human bronchial cells with increasing dose and recovery time that reflects increased cell mortality at higher concentrations. Future work will extend this study to the human nasal epithelium to discern health effects across airway tissues. |
Comparative in vitro toxicity of compositionally distinct thermal spray particulates in human bronchial cells
Burns ES , Harner RE , Kodali V , Afshari AA , Antonini JM , Leonard SS . Toxicol Rep 2024 13 Thermal spray, in general, is a process that involves forcing a melted substance, such as metal or ceramic in the form of wire or powder, onto the surface of a targeted object to enhance its desired surface properties. In this paper, the melted substance is metal wire generated by an electric arc and forcibly coated on a rotary iron substrate using compressed air. This thermal process is referred to as double-wire arc thermal spray. The particles generated through these methods fall within the nanometer to micrometer agglomerate size range. There is concern regarding potential human health outcomes as these particles exhibit a similarity in particle morphology to welding fumes. Thermal spray wires with zinc (PMET540), iron and chromium (PMET731), and nickel (PMET885) as primary metal compositions were used to generate particulate via an electric arc wire thermal spray generator for exposure to human bronchial cells (BEAS-2B) to examine comparative toxicity ranging from 0 to 200 µg/mL. Resulting cellular viability was assessed through live cell counts, and percent cytotoxicity was measured as a function of LDH release. Oxidative stress, genotoxicity, and alteration in total antioxidant capacity were evaluated through DNA damage (COMET analysis) and antioxidant concentration at 0, 3.125, 25, and 100 µg/mL. Protein markers for endothelin-1 (ET-1), interleukin-6 (IL-6), and interleukin-8 (IL-8) were also assessed to determine inflammation and endothelial alteration. Results: indicate modulation of oxidative stress response in a material and dose dependent manner. PMET540 exhibited the greatest cytotoxic effect between wires and across doses. DNA damage and antioxidant concentration induced by PMET540 were significantly higher than other wires at higher doses (DNA damage increased at 25 and 100 µg/mL; Antioxidant concentration increased at 100 µg/mL). However, ET-1 concentration significantly increased only after application of 100 µg/mL PMET885. IL-6 and IL-8 were most highly expressed in BEAS2B culture after 25 µg/mL exposure to PMET540 (99.4 % Zn). This data suggests that metal composition of thermal spray wires dictates the diverse response in human bronchial cells. © 2024 |
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