SCIREQ recently attended this year’s Society For Research On Nicotine and Tobacco (SRNT 2021) Annual Meeting!
This year’s theme was focused on social justice issues, health inequality, and importantly, action to correct health disparities of nicotine and tobacco. Here are some highlights of what we learned in this year’s meeting!
Dr. Tarran et al. looked at tobacco smoke exposure in Primary Human Bronchial Epithelial cells and found that it increased ACE2 activity. The researchers also noted that intracellular Ca2+, cAMP signalling, and nicotine might play a role in increased ACE2 activity. Research shows that enhanced ACE2 activity promotes SARS-CoV-2 binding and infection, which could lead to increased susceptibility of COVID19. Further, Dr. Gomperts and her group showed that direct exposure to SARS-CoV-2 and cigarette smoke has impacts on the stem cell-derived airway repair response and, as a result, increases infection severity.
Dr. Vanscheeuwijck and his team characterized the toxicity of 28 e-cigarette flavouring substances in a 90-day subchronic inhalation study. They found that the biological effects from the exposure were like the effects seen after nebulized nicotine exposure. There were few adaptive changes in the white blood cell differential counts, including increased neutrophil and decreased lymphocyte counts, which returned to normal after the 42-day recovery period. The nicotine exposure also resulted in lower levels of energy metabolism parameters but was resolved after the recovery period.
Interestingly, Dr. Vanscheeuqijck found that the flavoring substances did not induce a substantial response when looking at the transcriptome level. Additionally, there were no apparent additive and synergistic toxic effects observed among the substances.
Dr. Alexandra Noel’s research highlighted the carbonyl profiles of electronic nicotine delivery system (ENDS) flavorings and their effects on redox signaling in lung cells and dysregulated gene expression. Her lab looked at Strawberry, Catalan cream, and vanilla flavored aerosols with 12-18mg/mL of nicotine.
Using the inExpose e-cigarette vape generation extension, her lab found that vanilla-flavored ENDS aerosols contain more harmful compounds overall than Strawberry or Catalan cream and increased inflammation and oxidative stress. Additionally, the aerosols had ketones and impacted Reactive Oxygen Species and Nitric Oxide signaling.
Dr. Goniewicz and his team exposed mice to tobacco using IQOS and tobacco cigarettes to study the impact heated tobacco products have on lung tissue and inflammation. Analysis of the mice’s lung infiltrating cells showed substantially increased numbers of neutrophils in mice following CS inhalation compared to IQOS aerosol or air inhalation. Additionally, there was a noticeable reduction of macrophages in the lungs from IQOS aerosol inhalation compared to air and CS exposures.
Cigarette smoke exposure but not aerosols from IQOS significantly enhanced numbers of CD4+ and CD8+ T cells in the lungs compared to air control. In contrast, researchers found significantly lower numbers of CD19+B cells in lungs following IQOS versus cigarette smoke exposure.
Further researchers at the University of Oklahoma Medical Research Foundation found that e-cigarette aerosol exposures can change the expression of several components of antioxidant and inflammasome pathways. Their study suggests that e-cigarette aerosols carry high levels of reactive oxygen species and can alter the cellular antioxidant and inflammatory responses worsening the oral health of e-cig users.
Dr. Thanavala presented their studies on how JUUL aerosols containing nicotine salts (nicotine benzoate, nicotine salicylate, and nicotine levulinate) impact primary human small airway epithelial cells (SAECs). They found that nicotine salt containing JUUL aerosols had more cytotoxic effects in SAEC cells than freebase nicotine. Between the nicotine salts studied, nicotine benzoate aerosols specifically are more toxic to SAEC cells. Nicotine salts tend to induce more lung damage in comparison to freebase nicotine. However, acute exposures to either freebase nicotine or nicotine salts lessened the lungs’ antioxidant potential in mice.
The pH of e-cigarette liquid can also impact distribution within the respiratory tract. Dr. Kiran K. Solingapuram Sai from Wake Forest University Baptist Medical Center presented his findings on the effect of electronic cigarette liquid pH on retention of 11C-Nicotine in a respiratory tract model. They found more regional distribution in the upper airways with e-cigarettes in comparison to combustible e-cigarette smoke. The aerosol of combustible e-cigarettes is more acidic. Therefore, it traps the nicotine as the protonated form, which does not evaporate within the tar particles. This, in turn, allows the nicotine to travel more deeply into the lungs. Additionally, the retention of nicotine in the respiratory tract is dependent on the e-liquid pH, and lowering the pH reduces
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