Method to access data for Brett R. Winters et al., 'E-Cigarette Liquids and Aldehyde Flavoring Agents Inhibit CYP2A6 Activity in Lung Epithelial Cells' in ACS Omega, Vol 8, Issue 12, pg 11261-11266, 2023; DOI https://doi.org/10.1021/acsomega.2c08258, PMC10061538. This dataset is not publicly accessible because: Data was not shared by lead author. It can be accessed through the following means: To request data, contact lead author Brett Winters at brwinters@cytokinetics.com. Format: N/A. This dataset is associated with the following publication: Winters, B., P. Clapp, S. Simmons, T. Kochar, I. Jaspers, and M. Madden. E-Cigarette Liquids and Aldehyde Flavoring Agents Inhibit CYP2A6 Activity in Lung Epithelial Cells. ACS Omega. American Chemical Society, Washington, DC, USA, 8(12): 11261-11266, (2023).

Most of the data illustrates the effects that some e-cigarette flavoring agents, as well as some of the chemical components of those flavoring agents, directly have on the cytochrome P450 2A6 enzyme activity. This dataset is associated with the following publication: Winters, B., T. Kochar, P. Clapp, I. Jaspers, and M. Madden. Impact of E-Cigarette Flavoring Agents on Activity of Microsomal Recombinant CYP2A6, The Primary Nicotine-Metabolizing-Enzyme. CHEMICAL RESEARCH IN TOXICOLOGY. American Chemical Society, Washington, DC, USA, 33(7): 1689-1697, (2020).

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).

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).

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).

Background Free radicals generated in biological systems by cigarette smoke (CS) inhalation can cause oxidative stress in tissues, resulting in lipid peroxidation (LPO). In view of the antioxidant properties of α-tocopherol (AT), in the present study, effects of AT on antioxidant defence system and LPO were investigated in mice inhaling CS for different time intervals. Results Male Balb/c mice were fed orally with AT (5 I.U./Kg.b.wt.) and /or exposed to CS for 2, 4, 6 or 8 weeks. No effect was observed on body growth, diet consumption, water intake and lung weight due to AT and /or CS treatment in any of the groups as compared to their control counterparts. After two weeks of treatment, no change in LPO, reduced glutathione (GSH) levels and antioxidant enzymes were observed except for glutathione reductase (GR) which increased in all the treated groups. A significant increase in pulmonary LPO levels was observed in mice exposed to CS inhalation for 4, 6 or 8 weeks. There was a gradual increase in the LPO levels as the extent of CS inhalation increased from 4 to 8 weeks. However, the extent of increase in LPO levels due to CS exposure for 4, 6 or 8 weeks in the mice treated with AT was comparatively less. A significant decrease in the GSH levels was also observed in all the animals exposed to CS for 4, 6 or 8 weeks. There was a significant increase in the activities of catalase, glutathione peroxidase (GSH-Px) and GR observed in all the groups exposed to CS for 4,6 or 8 weeks. The increase in above antioxidant enzymes seems to be insufficient to combat the oxidative stress posed by CS inhalation. There was a marked decrease observed in the LPO levels in the animals treated with AT alone for 4, 6, or 8 weeks, when compared to their control counterparts. However, the supplementation of AT for 4, 6 or 8 weeks demonstrated a significant increase in GSH levels. Conclusion It appears from our studies that AT exhibits its antioxidant role either directly by scavenging the oxidative species or indirectly by modulating the GSH levels.

Data include assessment of pro-inflammatory cytokines, epithelial integrity, bulk RNA sequencing, and gene expression changes in human airway epithelial cells exposed to burn pit smoke condensates. This dataset is associated with the following publication: Ghosh, A., K. Rogers, S. Gallant, Y.H. Kim, J. Rager, I. Gilmour, S. Randell, and i. Jaspers. Effects of simulated smoke condensate generated from combustion of selected military burn pit contents on human airway epithelial cells. Particle and Fibre Toxicology. BioMed Central Ltd, London, UK, 21: 41, (2024).

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).

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).