Home
|
Inbox
|
Search
|
View Abstract
Chronic Inhalation of Unflavored Nicotine and No-Nicotine Containing Electronic Cigarette Vapor Leads to Impaired Lung Function
Description
.abstract img { width:300px !important; height:auto; display:block; text-align:center; margin-top:10px } .abstract { overflow-x:scroll } .abstract table { width:100%; display:block; border:hidden; border-collapse: collapse; margin-top:10px } .abstract td, th { border-top: 1px solid #ddd; padding: 4px 8px; } .abstract tbody tr:nth-child(even) td { background-color: #efefef; } .abstract a { overflow-wrap: break-word; word-wrap: break-word; }
A4452 - Chronic Inhalation of Unflavored Nicotine and No-Nicotine Containing Electronic Cigarette Vapor Leads to Impaired Lung Function
Author Block: V. Chun, A. Moshensky, J. Shin, A. Du, N. Nguyen, E. Le, C. J. Javier, A. Tran, R. Al Kolla, L. J. Ma, L. E. Crotty Alexander; Medicine, UCSD and VASDHS, San Diego, CA, United States.
Rationale: Electronic (e)-cigarettes have only been available on the global market since 2007. Thus, although upwards of 10% of the population are using these nicotine delivery devices, nothing is known of the long-term consequences of inhaling the vapor produced from e-cigarettes. Through the use of in vitro exposure models, we previously had found that multiple components of e-cigarette vapor alter macrophage, neutrophil and airway epithelial cell barrier function and inflammatory responses. Thus, we hypothesized that daily inhalation of heated and aerosolized propylene glycol, glycerin and nicotine would lead to repetitive injury to lung airways and parenchyma via increased epithelial permeability, and culminate in increased airway resistance and decreased lung compliance.
Methods: Male C57BL/6 mice, 6-8 weeks old, were placed in 3 groups. One group was exposed to e-cigarette vapor containing nicotine (EV) for 1 hour daily; another group was exposed to no-nicotine, vehicle control vapor only (VEH) for 1 hour daily, while controls were exposed to room air only (AIR). After six months of exposure using the InExpose system by SciReq, mice were sedated, trached and attached to the flexiVent mouse ventilator (SciReq). Baseline lung mechanics scans were conducted. Airway responsiveness was assessed with an inhaled methacholine (MCH) challenge at 0, 6, 12, and 24 mg/mL.
Results: There were no significant differences between baseline lung parameters in the three groups. There were significant differences between EV and AIR for Respiratory System Elastance (Ers), Tissue Damping (G), and Tissue Elastance (H) at 24 mg/mL of MCH. EV vs VEH was also significantly different for Tissue Elastance (H) at 24 MCH. There was a significant difference between AIR and VEH for Newtonian Resistance (Rn), a measure of central airway resistance, at 12 MCH but not at higher doses of MCH. There are also significant changes in large airway resistance with exposure to non-nicotine, vehicle only vapor (VEH) compared to exposure to room air (AIR), but the finding was not consistent at all MCH doses. This may be explained by a tolerance to a dampening effect on resistance with higher doses of MCH.
Conclusions: Our data suggest that airway resistance and lung elasticity changes occur with long-term exposure to key components of e-cigarette vapor - nicotine, propylene glycol and glycerin. This indicates that e-liquid flavors are unlikely to be the sole causes of lung toxicity, especially in the setting of long-term daily e-cigarette use.
Author Block: V. Chun, A. Moshensky, J. Shin, A. Du, N. Nguyen, E. Le, C. J. Javier, A. Tran, R. Al Kolla, L. J. Ma, L. E. Crotty Alexander; Medicine, UCSD and VASDHS, San Diego, CA, United States.
Rationale: Electronic (e)-cigarettes have only been available on the global market since 2007. Thus, although upwards of 10% of the population are using these nicotine delivery devices, nothing is known of the long-term consequences of inhaling the vapor produced from e-cigarettes. Through the use of in vitro exposure models, we previously had found that multiple components of e-cigarette vapor alter macrophage, neutrophil and airway epithelial cell barrier function and inflammatory responses. Thus, we hypothesized that daily inhalation of heated and aerosolized propylene glycol, glycerin and nicotine would lead to repetitive injury to lung airways and parenchyma via increased epithelial permeability, and culminate in increased airway resistance and decreased lung compliance.
Methods: Male C57BL/6 mice, 6-8 weeks old, were placed in 3 groups. One group was exposed to e-cigarette vapor containing nicotine (EV) for 1 hour daily; another group was exposed to no-nicotine, vehicle control vapor only (VEH) for 1 hour daily, while controls were exposed to room air only (AIR). After six months of exposure using the InExpose system by SciReq, mice were sedated, trached and attached to the flexiVent mouse ventilator (SciReq). Baseline lung mechanics scans were conducted. Airway responsiveness was assessed with an inhaled methacholine (MCH) challenge at 0, 6, 12, and 24 mg/mL.
Results: There were no significant differences between baseline lung parameters in the three groups. There were significant differences between EV and AIR for Respiratory System Elastance (Ers), Tissue Damping (G), and Tissue Elastance (H) at 24 mg/mL of MCH. EV vs VEH was also significantly different for Tissue Elastance (H) at 24 MCH. There was a significant difference between AIR and VEH for Newtonian Resistance (Rn), a measure of central airway resistance, at 12 MCH but not at higher doses of MCH. There are also significant changes in large airway resistance with exposure to non-nicotine, vehicle only vapor (VEH) compared to exposure to room air (AIR), but the finding was not consistent at all MCH doses. This may be explained by a tolerance to a dampening effect on resistance with higher doses of MCH.
Conclusions: Our data suggest that airway resistance and lung elasticity changes occur with long-term exposure to key components of e-cigarette vapor - nicotine, propylene glycol and glycerin. This indicates that e-liquid flavors are unlikely to be the sole causes of lung toxicity, especially in the setting of long-term daily e-cigarette use.
|
Home
|
Inbox
|
Search
|