A harmful effect of vaporized e-cigarette products in the alveolar-lining fluid and the lung

The lung’s delicate surfactant layer is of critical importance to the organ’s overall physiology and innate immune function. Both alveolar type II cells and alveolar macrophages are the principal subsets that maintain and catabolize surfactant at the liquid-air interface. Our study reveals that ENDS exposure disrupts both the lipid and protein components of pulmonary surfactant, increasing phospholipid pools in the airway and decreasing the expression of the regulatory surfactant proteins SP-A and SP-D. Lipid deposition and impaired immune function are distinct features of alveolar macrophages upon chronic ENDS treatment. Upon viral infection, ENDS-exposed mice exhibit increased morbidity and mortality with excessive pulmonary damage and inflammation late in infection. Of chief importance, the ENDS-mediated effects observed in our model are independent of the presence of nicotine.

The harmful effects of chronic inhalation of ENDS vapor is due to the PG/VG vehicles, which are currently considered safe solvents

long-term exposure to ENDS vapor, which delivers nicotine in amounts equal to those of conventional cigarettes, did not result in excessive lung inflammation or emphysema.
Despite these findings, mice exposed to ENDS and infected with the flu virus had significantly delayed immune responses to the infection and showed persistent lung inflammation when compared with the Air-exposed group.
Further, the increase in morbidity and mortality was independent of nicotine, indicating that the harmful effects of chronic inhalation of ENDS vapor is due to the PG/VG vehicles, which are currently considered safe solvents .

Gene expression profiling of resident alveolar macrophages is consistent with an enrichment of genes associated with lipid metabolism, thus highlighting their significant role in pulmonary surfactant homeostasis .

Chronic exposure to PG/VG uniquely promotes deposition of lipids in alveolar macrophages and disturbs the normal homeostatic process of pulmonary surfactant molecules and lipids in the lungs.

Reference:

Madison, M. C.; Landers, C. T.; Gu, B.-H.; Chang, C.-Y.; Tung, H.-Y.; You, R.; Hong, M. J.; Baghaei, N.; Song, L.-Z.; Porter, P.; Putluri, N.; Salas, R.; Gilbert, B. E.; Levental, I.; Campen, M. J.; Corry, D. B.; Kheradmand, F. Electronic Cigarettes Disrupt Lung Lipid Homeostasis and Innate Immunity Independent of Nicotine. The Journal of Clinical Investigation 2019, 129 (10), 4290. https://doi.org/10.1172/JCI128531.