We tested the postulate that 1) a fulvic acid (FA)-like substance is included in cigarette smoke and wood smoke particles and 2) exposure of respiratory epithelial cells to this substance results in a disruption of iron homeostasis associated with both a cell deficiency of the metal and inflammatory response. It was concluded that 1) FA-like substance is included in cigarette smoke and wood smoke particle and 2) respiratory epithelial cell exposure to this substance results in a disruption of iron homeostasis associated with both a cell deficiency of the metal and inflammatory response. This dataset is associated with the following publication: Gonzalez, D., J. Soukup, M. Madden, M. Hays, J. Berntsen, S. Paulson, and A. Ghio. A fulvic acid-like substance participates in the pro-inflammatory effects of cigarette smoke and wood smoke particles.. CHEMICAL RESEARCH IN TOXICOLOGY. American Chemical Society, Washington, DC, USA, 33(4): 999-1009, (2020).

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).

Figure 2. Cell non-heme iron concentrations following 4 (A) and 24 (B) hr exposures of BEAS-2B cells to media, carbon black treated with air (CB-Air), carbon black treated with ozone (CB-O3), and Suwanee River fulvic acid (SRFA). Incubations were without and with 200 μM FAC. Exposures to CB-Air, CB-O3, and SRFA did not impact cell non-heme iron relative to media at either time point. Exposure to FAC increased cell non-heme iron but co-exposure with CB-O3 was associated with significantly increased non-heme iron concentrations at both 4 (A) and 24 (B) hr. Exposures of BEAS-2B cells to FAC increased cell ferritin levels after 24 hr relative to media alone (C). However, co-exposure of CB-O3, and SRFA with FAC was associated with significantly elevated cell ferritin concentrations (C). Two-way ANOVA indicated that both addition of FAC and exposure group significantly impacted cell non-heme iron. Figure 3. Release of IL-8 and IL-6 after 24 hr exposure of BEAS-2B cells to media, carbon black treated with air (CB-Air), carbon black treated with ozone (CB-O3), and Suwanee River fulvic acid (SRFA). Exposure to CB-O3 and SRFA significantly increased the release of IL-8 and IL-6. FAC treatment significantly diminished this response. This dataset is associated with the following publication: Ghio, A., D.H. Gonzalez, S.E.P. Paulson, J. Soukup, L. Dailey, M. Madden, B. Mahler, S.A. Elmore, M.C. Schladweiler, and U. Kodavanti. Ozone reacts with carbon black to produce a fulvic acid-like substance and increase an inflammatory effect. TOXICOLOGIC PATHOLOGY. Society of Toxicology, RESTON, VA, 48(7): 887-898, (2020).

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).

This dataset includes physico-chemical characteristics of biomass smoke of three different fuels (oak, peat, and eucalyptus) generated from a tube furnace system at two different combustion phases (smoldering and flaming) and also provides comparisons of lung toxicity outcomes after inhalation and aspiration exposures to the biomass smoke. This dataset is associated with the following publication: Kim, Y.H., C. King, Q. Krantz, M.M. Hargrove, I. George, J. McGee, L. Copeland, M. Hays, M. Landis, M. Higuchi, S. Gavett, and M. Gilmour. The role of fuel type and combustion phase on the toxicity of biomass smoke following inhalation exposure in mice. Archives of Toxicology. Springer, New York, NY, USA, 93(6): 1501-1513, (2019).

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).

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).

This dataset includes physico-chemical characteristics of biomass smoke of five different fuels (red oak, peat, pine needles, pine, and eucalyptus) generated from a tube furnace system at two different combustion phases (smoldering and flaming) and also provides two toxicological outcomes (lung toxicity in mice and mutagenicity in Salmonella) associated with exposures to the biomass smoke PM collected by a cryo-trap system. This dataset is associated with the following publication: Kim, Y.H., S. Warren, T. Krantz, C. King, R. Jaskot, W.T. Preston, B. George, M. Hays, M. Landis, M. Higuchi, D. DeMarini, and I. Gilmour. Mutagenicity and Lung Toxicity of Smoldering Versus Flaming Emissions from Various Biomass Fuels: Implications for Health Effects from Wildland Fires. ENVIRONMENTAL HEALTH PERSPECTIVES. National Institute of Environmental Health Sciences (NIEHS), Research Triangle Park, NC, USA, 126(1): 1, (2018).

This study sought to examine whether mild preexisting allergic airways disease enhances the response of the lungs to burn pit smoke emissions. The findings indicate that exposure to house dust mite (HDM) antigen sensitizes the mouse lungs to make them more susceptible to burn pit smoke-induced dysfunction, in both the inflammatory response to burn pit smoke and in the accumulation of airway mucus. This suggests that changes in cilia and mucociliary clearance (MCC) induced by asthma that are amplified by inhalation of burn pit smoke, followed by a feedback loop of enhanced inflammation induced by the accumulating mucus, appears a likely mechanism. This dataset is associated with the following publication: Belfield-Simpson, L., J. Martin, M.K. McPeek, A. Livraghi-Butrico, H. Dang, Y.H. Kim, I. Gilmour, and C. Doerschuk. Combustion products of burn pit constituents induce more changes in asthmatic than non-asthmatic murine lungs. Particle and Fibre Toxicology. BioMed Central Ltd, London, UK, 22: 21, (2025).