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).

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).

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).

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).

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.

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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 contains two data files: 1) Adult cigarette use prevalence and 2) Adult tobacco use prevalence in California. Tobacco use includes cigarettes, cigars, little cigars or cigarillos, pipe tobacco, smokeless tobacco (e.g. chew, snuff, snus), hookah, or electronic smoking devices (e.g. e-cigarettes, vape pens, pod mods). See the individual file description for more information on each data file. The California Behavioral Risk Factor Surveillance System (BRFSS) is an on-going telephone survey of randomly selected adults, which collects information on a wide variety of health-related behaviors, including current cigarette and tobacco usage. Data are collected monthly from a random sample of the California population aged 18 years and older. The BRFSS has been conducted since 1984 by the California Department of Public Health in collaboration with the Centers for Disease Control and Prevention (CDC).

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