Figure 1.

Pathways of inflammatory signaling. E-cig aerosols induce the expression of pattern-recognition receptors such as TLR and the secretion of pro-inflammatory cytokines such as IL1B and TNFα and their respective receptors, particularly in response to menthol-flavored e-cigs. In the oral cavity (left part of the figure), e-cig vape affects the healthy oral microbiota by inhibiting commensals and favoring growth and biofilm formation of cariogenic bacteria, especially in the presence of sweet flavors containing sugar. IL4 suppression further supports colonization with pathogenic bacteria. In human airway epithelial cells (right part of the figure), e-cig aerosols also increase inflammatory cytokines, such as IL6 and IL8, secreted by macrophages in response to, for example, cinnamon- and caramel-flavored e-vape containing ethyl maltol. Acrolein, found in e-cig vape, inhibits the Fc receptor and function of neutrophils. Additionally, exposure to even a 100% propylene glycol e-cig liquid without flavors and nicotine results in increased mucus concentration, trapping bacteria and viruses and leading to IL8-mediated inflammation relevant to lung disease and COPD.