A safer alternative? Investigating the impact of e-cigarettes on pulmonary inflammation, tissue repair, and infectious disease


E-cigarettes (e-cigs) are often marketed and perceived as safer substitutes for traditional tobacco products. These devices use batteries to aerosolize and deliver nicotine, avoiding the formation of toxic combustion compounds that occurs when conventional cigarettes are burned. Nevertheless, both known and potential toxins have been identified in e-cig vapor. Some of these, such as volatile carbon compounds and nitrosamines, are also found in tobacco smoke. Others may be derived from the solvent and flavoring components of e-cig fluid. Little conclusive data exist on the safety of e-cigarettes, particularly when exposure occurs repeatedly over many years. Given that annual e-cig use in the US is now growing exponentially, particularly among adolescents and young adults, comprehensive studies of the health effects of these devices are urgently needed. Environmental stressors like tobacco smoke and e-cigarette vapor can have multiple effects on the respiratory system. Cytotoxicity, whether immediate or delayed, is one of these. In addition, changes in gene transcription may occur as the lung activates various stress, inflammatory, and tissue repair pathways. Resident alveolar macrophage (MΦ) cells are key players in these responses. Depending on environmental cues, they can assume pro- or anti-inflammatory phenotypes (M1 and M2 respectively), regulating the delicate balance between inflammation and tissue repair. Over time, exposure to toxins can dysregulate these functions, leading to pathological inflammation, increased susceptibility to infections, and carcinogenesis. We hypothesized that components in e-cigarette vapor induce cytotoxicity and cell damage in the lung. Exposure to e-cigs was also predicted to upregulate inflammatory and stress responses, especially when acting synergistically with common respiratory infectious agents. Bone marrow macrophages were used as in vitro models of alveolar macrophages. We assessed the effects of treatment with e-cigarette extract (ECE), both alone and in conjunction with influenza virus or Streptococcus pneumoniae, on cell viability, transcriptional activity, and phenotype.


Yu, Tammy, "A safer alternative? Investigating the impact of e-cigarettes on pulmonary inflammation, tissue repair, and infectious disease" (2015). Summer Research Symposium. Brown Digital Repository. Brown University Library. https://doi.org/10.26300/v1eh-6z97



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    Each year, Brown University showcases the research of its undergraduates at the Summer Research Symposium. More than half of the student-researchers are UTRA recipients, while others receive funding from a variety of Brown-administered and national programs and fellowships and go …