Data include assessment of transepithelial electrical resistance, lactate dehydrogenase, toxicity scores, pro-inflammatory cytokines, and modulation of gene expression in human airway epithelial cells exposed to burn pit smoke condensates. This dataset is associated with the following publication: Ghosh, A., A. Payton, S. Gallant, K. Rogers, T. Mascenik, E. Hickman, C. Love, K. Schichlein, T. Smyth, Y.H. Kim, J. Rager, M. Gilmour, S. Randell, and i. Jspers. Burn pit smoke condensate-mediated toxicity in human airway epithelial cells. CHEMICAL RESEARCH IN TOXICOLOGY. American Chemical Society, Washington, DC, USA, 37(5): 791-803, (2024).

This dataset provides information about how short-term inhalation of burn pit smoke particles, specifically plastic smoke particles, causes significant toxicity in human nasal epithelial cells and how toxicity caused by inhaled emissions from plastic incinerations could contribute to the development of sinonasal disease associated with burn pits and other environmental particulate matter exposures. This dataset is associated with the following publication: Rogers, K., E. WaMaina, A. Barber, S. Masood, C. Love, Y.H. Kim, M. Gilmour, and i. Jaspers. Emissions from plastic incineration induce inflammation, oxidative stress, and impaired bioenergetics in primary human respiratory epithelial cells. TOXICOLOGICAL SCIENCES. Society of Toxicology, RESTON, VA, 199(2): 301-315, (2024).

This dataset provides information on the gene regulation by single and repeated exposure to lower dose of burn pit smoke condensates and biological changes at 48 hrs post-exposure depending on different combustion conditions. The findings suggest that exposure to burn pit smoke condensates may impart a lasting adverse impact on human respiratory health, and the sustained effects depend on the waste source material and combustion condition. This dataset is associated with the following publication: Ghosh, A., K. Rogers, S. Gallant, S. Brocke, A. Speen, Y.H. Kim, I. Gilmour, S. Randell, and i. jaspers. Simulated burn pit smoke condensates cause sustained impact on human airway epithelial cell. TOXICOLOGICAL SCIENCES. Society of Toxicology, RESTON, VA, 204(1): 2-8, (2025).

The dataset consists of 2 revised files. The excel file shows all of the individual data used in calculation of the tables and figures. Each table and figure has data stored on a separate tab of the file. The zip file consists of 5 GraphPad Prism files which show the statistics and graphs used in the paper. The names of the 5 files indicate which figures and tables are analyzed statistically and the graphs generated from the data. This dataset is associated with the following publication: Hargrove, M., Y.H. Kim, C. King, C. Wood, M. Gilmour, J. Dye, and S. Gavett. Smoldering and Flaming Biomass Wood Smoke Inhibit Respiratory Responses in Mice. INHALATION TOXICOLOGY. Taylor & Francis, Inc., Philadelphia, PA, USA, 31(6): 236-247, (2019).

There is increasing evidence for a close link between the upper and the lower respiratory tracts and the fact that rhinitis has an important impact on asthma. Several clinical and experimental observations suggest a similar immunopathology between the upper and lower airways in allergic subjects. The common inflammatory process that develops in the respiratory tract explains some of the complex interactions among different clinical diseases such as rhinitis, sinusitis, asthma, bronchial hyperresponsiveness and viral infections. There are also non-inflammatory mechanisms that may contribute to the link between rhinitis and asthma. Moreover, the outcomes of various pharmacological treatments of rhinitis have recently provided further support for the hypothesis of the united airways. We discuss some of the recent observations on the nose-lung interaction and some of the novel therapeutic approaches used to treat rhinitis and asthma that arise from this.

Data include: trans-epithelial electrical resistance, FITC-dextran permeability, cell viability and gene expression (RNA and protein). This dataset is associated with the following publication: Faber, S., N. McNabb, P. Ariel, E. Aungst, and S. McCullough. Exposure Effects Beyond the Epithelial Barrier: Trans-Epithelial Induction of Oxidative Stress by Diesel Exhaust Particulates in Lung Fibroblasts in an Organotypic Human Airway Model. TOXICOLOGICAL SCIENCES. Society of Toxicology, RESTON, VA, 177(1): 140-155, (2020).

Frontiers in Toxicology paper, Differential transcriptomic alterations in nasal versus lung tissue of acrolein-exposed rats, 2023 Alewel DI. This dataset is associated with the following publication: Alewel, D., T. Jackson, K. Rentschler, M. Schladweiler, A. Astriab Fisher, S. Gavett, P. Evansky, and U. Kodavanti. Differential transcriptomic alterations in nasal versus lung tissue of acrolein-exposed rats. Frontiers in Toxicology. Frontiers, Lausanne, SWITZERLAND, 27(5): 1280230, (2023).

Exposure of the airways to cigarette smoke (CS) is the primary risk factor for developing several lung diseases such as Chronic Obstructive Pulmonary Disease (COPD). CS consists of a complex mixture of over 6000 chemicals including the highly reactive α,β-unsaturated aldehyde acrolein. Acrolein is thought to be responsible for a large proportion of the non-cancer disease risk associated with smoking. Emerging evidence suggest a key role for CS-induced abnormalities in mitochondrial morphology and function in airway epithelial cells in COPD pathogenesis. Although in vitro studies suggest acrolein-induced mitochondrial dysfunction in airway epithelial cells, it is unknown if in vivo inhalation of acrolein affects mitochondrial content or the pathways controlling this. In this study, rats were acutely exposed to acrolein by inhalation (nose-only; 0-4 ppm), 4 hours/day for 1 or 2 consecutive days (n=6/group). Subsequently, the activity and abundance of key constituents of mitochondrial metabolic pathways as well as expression of critical proteins and genes controlling mitochondrial biogenesis and mitophagy were investigated in lung homogenates. A transient decreasing response in protein and transcript abundance of subunits of the electron transport chain complexes was observed following acrolein inhalation. Moreover, acrolein inhalation caused a decreased abundance of key regulators associated with mitochondrial biogenesis, respectively a differential response on day 1 versus day 2. Abundance of components of the mitophagy machinery was in general unaltered in response to acrolein exposure in rat lung. Collectively, this study demonstrates that acrolein inhalation acutely and dose-dependently disrupts the molecular regulation of mitochondrial metabolism in rat lung. Hence, understanding the effect of acrolein on mitochondrial function will provide a scientifically supported reasoning to shortlist aldehydes regulation in tobacco smoke. This dataset is not publicly accessible because: EPA does not own the data and therefore EPA does not have right to publish the data. It can be accessed through the following means: Data can be obtained from corresponding author of the paper. Format: The data in this paper are collected from lung tissue that were isolated from air or acrolein-exposed Wistar Kyoto rats. All data are derived from lung tissue assessment of many biological markers associated with mitochondrial homeostasis. For these data n=8 animals were used for each group of samples. This dataset is associated with the following publication: Tulen, C., S. Snow , P. Leermakers, U. Kodavanti, F. van Schooten, A. Opperhuizen, and A. Remels. Acrolein inhalation acutely affects the regulation of mitochondrial metabolism in rat lung. TOXICOLOGY. Elsevier Science Ltd, New York, NY, USA, 469(153129): 1, (2022).