Nicotine promotes e-cigarette vapour-induced lung inflammation and structural alterations

Area of Science:

• Pulmonary Medicine
• Toxicology
• Cell Biology

Background:

• Electronic cigarettes (e-cigarettes) are popular smoking alternatives.
• E-cigarette vapor can cause acute lung injury.
• The specific role of nicotine in e-cigarette vapor's long-term effects on the lungs is unclear.

Purpose of the Study:

• To investigate the long-term effects of nicotine-containing e-cigarette vapor (ECV) versus nicotine-free e-cigarette vapor (NF ECV) on mouse lungs.
• To determine the specific contribution of nicotine to e-cigarette-induced lung pathology.

Main Methods:

• In vitro exposure of cells to e-cigarette vapor extracts (ECVE and NF ECVE).
• Acute inhalation exposure of isolated lungs to ECV and NF ECV.
• Long-term in vivo inhalation exposure of mice to ECV and NF ECV for 8 months.

Main Results:

• Nicotine-containing e-cigarette vapor extract (ECVE) reduced pulmonary arterial smooth muscle cell proliferation.
• Acute exposure to nicotine-containing e-cigarette vapor (ECV) increased pulmonary endothelial permeability.
• Long-term ECV exposure in mice led to significant increases in inflammatory cells (lymphocytes) in bronchoalveolar fluid and lung tissue, elevated cytokines, and structural lung changes (increased airspace).
• Nicotine-free e-cigarette vapor (NF ECV) caused milder inflammatory and structural changes compared to ECV.

Conclusions:

• Nicotine is a key component driving significant inflammation and lung tissue damage in e-cigarette vapor.
• While non-nicotine components of e-cigarette vapor can induce some cellular effects and mild pulmonary alterations, nicotine exacerbates these effects.
• The findings highlight nicotine's critical role in the adverse pulmonary outcomes associated with e-cigarette use.