Abstract Title

The Potential Role of E-Cigarettes In Diffuse Alveolar Damage

Presenter Name

Samir Khan

RAD Assignment Number

1802

Abstract

Purpose: The prevalence of e-cigarette usage has increased in non-smokers and those planning to quit smoking. Although the potential long term adverse effects have not been studied in humans, studies have shown that certain components of e-cigarette fluid may lead to the release of cytotoxic components implicated in the pathogenesis of diffuse alveolar damage (DAD), a histopathological diagnosis that is commonly associated with acute respiratory distress syndrome (ARDS). This literature review describes the potential association between e-cigarettes and diffuse alveolar damage while making reference to relevant associated studies.

Methods: An English literature review of studies that examine the potential cytotoxic effects of E-cigarette fluid components in relation to the pathophysiology of diffuse alveolar damage.

Results: To date, no longitudinal studies have been performed on humans to show the toxicity of e-cigarette vapor on the human lung. However, studies have shown different mechanisms by which the compounds in e-cigarette vapor lead to the destruction of alveolar epithelial cells in-vitro.

The major component of e-cigarette vapor, propylene glycol, has been shown by in-vitro studies to be cytotoxic to alveolar type II epithelial cells. Glycerol, another component of e-cigarettes, was also found to be cytotoxic in a dose-dependent pattern. Moreover, lactate dehydrogenase, a common byproduct of cell death, was found elevated in alveolar cells exposed to e-cigarette vapor when compared to alveolar cell controls exposed to clean air, suggestive of cell death.

Interleukin-6 (IL-6), a proinflammatory cytokine, was found to be elevated in a dose dependent pattern after young healthy non-smokers hTBE cells (human tracheobronchial epithelial cells) were exposed to e-cigarette fluid. Furthermore, there was an increase in fibroblast growth factor (FGF) in alveolar cells, which is also part of the pathogenesis of DAD.

Conclusion: Diffuse alveolar damage is a life-threatening condition with a high mortality rate. The evidence of adverse effects demonstrated by the in-vitro studies described above suggests an association between e-cigarette use and diffuse alveolar damage. Just as studies were able to reveal the harmful effects of tobacco products in the past, this literature review introduces a new avenue of investigation to assess the long-term effects of e-cigarettes on humans.

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The Potential Role of E-Cigarettes In Diffuse Alveolar Damage

Purpose: The prevalence of e-cigarette usage has increased in non-smokers and those planning to quit smoking. Although the potential long term adverse effects have not been studied in humans, studies have shown that certain components of e-cigarette fluid may lead to the release of cytotoxic components implicated in the pathogenesis of diffuse alveolar damage (DAD), a histopathological diagnosis that is commonly associated with acute respiratory distress syndrome (ARDS). This literature review describes the potential association between e-cigarettes and diffuse alveolar damage while making reference to relevant associated studies.

Methods: An English literature review of studies that examine the potential cytotoxic effects of E-cigarette fluid components in relation to the pathophysiology of diffuse alveolar damage.

Results: To date, no longitudinal studies have been performed on humans to show the toxicity of e-cigarette vapor on the human lung. However, studies have shown different mechanisms by which the compounds in e-cigarette vapor lead to the destruction of alveolar epithelial cells in-vitro.

The major component of e-cigarette vapor, propylene glycol, has been shown by in-vitro studies to be cytotoxic to alveolar type II epithelial cells. Glycerol, another component of e-cigarettes, was also found to be cytotoxic in a dose-dependent pattern. Moreover, lactate dehydrogenase, a common byproduct of cell death, was found elevated in alveolar cells exposed to e-cigarette vapor when compared to alveolar cell controls exposed to clean air, suggestive of cell death.

Interleukin-6 (IL-6), a proinflammatory cytokine, was found to be elevated in a dose dependent pattern after young healthy non-smokers hTBE cells (human tracheobronchial epithelial cells) were exposed to e-cigarette fluid. Furthermore, there was an increase in fibroblast growth factor (FGF) in alveolar cells, which is also part of the pathogenesis of DAD.

Conclusion: Diffuse alveolar damage is a life-threatening condition with a high mortality rate. The evidence of adverse effects demonstrated by the in-vitro studies described above suggests an association between e-cigarette use and diffuse alveolar damage. Just as studies were able to reveal the harmful effects of tobacco products in the past, this literature review introduces a new avenue of investigation to assess the long-term effects of e-cigarettes on humans.