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