In recent years, e-cigarettes have been marketed as an alternative to cigarette smoking that is less damaging to health. However, there is a lack of scientific evidence to support this assertation that they are a safer alternative to cigarettes. This study aimed to evaluate the effect of e-cigarettes on key respiratory pathogens which included S. aureus (SA), P. aeruginosa (PA), H. influenzae (HI), S. pneumoniae (SP) and M. catarrhalis (MCAT).

Results from this study have shown that neat e-liquids can reduce bacterial viability with particular flavours causing significant reductions in bacterial viability. It was found that e-liquids contained numerous chemical compounds some of which had antimicrobial properties. The greater the number of chemical compounds present in the e-liquid the greater the reduction in bacterial viability. E-liquid induced antimicrobial pressure affected HI, MCAT and SP isolates to a greater degree than PA and SA isolates.

It was discovered that both vaped and neat e-liquids increased biofilm formation in PA and SA isolates whilst decreasing biofilm formation in HI, SP and MCAT isolates. The vaping of the e-liquids indicated that PGVG and flavours had significant effects on biofilm formation in bacteria. Additionally, e-cigarette vapour extract (ECVE) exposure modified the expression of two PA virulence factors, pyoverdine and pyocyanin. The chemical components of e-liquids components can act as environmental stressors resulting in modification of important bacterial virulence factors.

Exposing respiratory bacteria to ECVE or cigarette smoke extract (CSE) before infection was found to result in significant increases and decreases in the release of IL-8 and IL-6 and activation of NF-κB in human cells. The degree of effect on cell inflammation appeared to be dependent on the bacterial isolate and whether it was exposed to ECVE or CSE. The exposure of respiratory isolates to ECVE or CSE can modulate the host immune response to infection.

Overall, the study shows that e-cigarette exposure can induce changes in key respiratory pathogens associated with chronic lung diseases. These changes could impact host-bacterial interactions and may increase bacterial persistence and inflammatory potential.