Journal
NICOTINE & TOBACCO RESEARCH
Volume 23, Issue 7, Pages 1160-1167Publisher
OXFORD UNIV PRESS
DOI: 10.1093/ntr/ntaa267
Keywords
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Funding
- National Heart, Lung and Blood Institute of the National Institutes of Health [RO1HL142511]
- Roswell Park Institute Alliance Foundation
- NCI [P30CA016056]
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The study found that short-term inhalation of aerosols from IQOS resulted in lung damage and proinflammatory changes similar to those caused by exposure to cigarette smoke. Both IQOS and CS exposure led to lung inflammation and immune cell infiltration, significantly higher than air-exposed controls.
Introduction: Emerging heated tobacco products (HTPs) were designed to reduce exposure to toxicants from cigarette smoke (CS) by avoiding burning tobacco and instead heating tobacco. We studied the effects of short-term inhalation of aerosols emitted from HTP called IQOS, on lung damage and immune-cell recruitment to the lungs in mice. Methods: Numerous markers of lung damage and inflammation including albumin and lung immune-cell infiltrates, proinflammatory cytokines, and chemokines were quantified in lungs and bronchoalveolar (BAL) fluid from IQOS, CS, or air-exposed (negative control) mice. Results: Importantly, as a surrogate marker of lung epithelial-cell damage, we detected significantly increased levels of albumin in the BAL fluid of both HTP- and CS-exposed mice compared with negative controls.Total numbers of leukocytes infiltrating the lungs were equivalent following both IQOS aerosols and CS inhalation and significantly increased compared with air-exposed controls. We also observed significantly increased numbers of CD4+IL-17A(+) T cells, a marker of a T-cell immune response, in both groups compared with air controls; however, numbers were the highest following CS exposure. Finally, the numbers of CD4+ROR gamma t(+)T cells, an inflammatory T-cell subtype expressing the transcription factor that is essential for promoting differentiation into proinflammatory Th17 cells, were significantly augmented in both groups compared with air-exposed controls. Levels of several cytokines in BAL were significantly elevated, reflecting a proinflammatory milieu. Conclusions: Our study demonstrates that short-term inhalation of aerosols from IQOS generates damage and proinflammatory changes in the lung that are substantially similar to that elicited by CS exposure.
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