Tobacco smoke and e-cigarettes
Epidemiological studies and meta-analyses indicate that pre- or
post-natal maternal smoking increases the risk of wheezing and asthma in
children ≤2 years40 and that secondhand smoke during
infancy without prior exposure in utero leads to an enhanced risk of
food sensitization and eczema.41Tobacco smoke and
e-cigarettes may mediate their effects via a number of inflammatory
mechanisms. For instance, tobacco smoke provokes oxidative
stress42 which leads to upregulation of
TSLP43 and IL-3344 suggestive of a
pro type-2 inflammation in the lungs. In addition, phagocytic activity
of alveolar macrophages from smokers is reduced compared to
non-smokers.45 Repetitive exposure to cigarette smoke
in normal human airway epithelial cells was found to impact the adhesive
intercellular junctions and disrupt monolayer integrity. Cortical
tension of epithelial cells was observed due to increased actin polymer
levels, which further destabilized cell adhesion.46Tobacco smoke may also mediate its effect through microbiome dysbiosis.
A study found that sensitization to Staphylococcus aureusenterotoxins is increased in smokers with asthma, and it may be a marker
of eosinophilic inflammation and severe asthma.45E-cigarettes were also found to be associated with inflammation. A study
found that e-cigarette vapors and cigarette smoke altered virulence of
key lung pathogens (Haemophilus influenzae, Streptococcus
pneumoniae, Staphylococcus aureus and Pseudomonas aeruginosa ), which
may increase bacterial persistence and inflammatory
potential.47