Electronic cigarettes (EC) have emerged as a popular alternative to traditional tobacco products, but their impact on immune function has raised significant health concerns. This review explores the immunological effects of EC exposure, focusing on innate and adaptive immune responses. Electronic cigarette aerosol (ECA) induces widespread inflammation. These changes compromise immune cell function, impairing neutrophil chemotaxis, phagocytosis, and oxidative burst while increasing macrophage and dendritic cell recruitment and activation. ECA also disrupts epithelial barriers, increasing susceptibility to bacterial and viral infections. Studies show enhanced biofilm formation in bacteria such as Staphylococcus aureus and Streptococcus pneumoniae and impaired antiviral responses against pathogens like influenza A and SARS-CoV-2. Additionally, EC exposure modulates adaptive immunity, affecting T and B cell function and increasing systemic inflammatory markers. The long-term consequences of these immunological disruptions include heightened risks for chronic inflammatory diseases, respiratory infections, and potentially autoimmune conditions. The widespread adoption of EC, particularly among younger users, poses a growing public health challenge. As the popularity of vaping continues to rise, these immunological disruptions could result in increased healthcare burdens in the future, with higher rates of infections, chronic inflammatory diseases, and immune system-related disorders among those who begin using e-cigarettes at a young age. Understanding the full scope of EC-related health risks is essential for informing public health policies and protecting future generations from the potential long-term effects of vaping.
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