Abstract
Little cigars (LCs) are regulated differently than cigarettes, allowing them to be potentially targeted at youth/young adults. We exposed human bronchial epithelial cultures (HBECs) to air or whole tobacco smoke from cigarettes vs. LCs. Chronic smoke exposure increased the number of dead cells, lactate dehydrogenase release, and interleukin-8 (IL-8) secretion and decreased apical cilia, cystic fibrosis transmembrane conductance regulator (CFTR) protein levels, and transepithelial resistance. These adverse effects were significantly greater in LC-exposed HBECs than cigarette exposed cultures. LC-exposure also elicited unique gene expression changes and altered the proteomic profiles of airway apical secretions compared to cigarette-exposed HBECs. Gas chromatography-mass spectrometry (GC-MS) analysis indicated that LCs produced more chemicals than cigarettes, suggesting that the increased chemical load of LCs may be the cause of the greater toxicity. This is the first study of the biological effects of LCs on pulmonary epithelia and our observations strongly suggest that LCs pose a more severe danger to human health than cigarettes.
Highlights
Tobacco smoke is inhaled by 1.3 billion people worldwide and remains a major risk factor for several diseases including many types of cancer, cardiovascular disease and chronic obstructive pulmonary disease (COPD)[1]
Using surface airway epithelia obtained directly from human lungs, we found that Little cigars (LCs) exerted greater cytotoxicity and pro-inflammatory cytokine secretion and wrought greater changes at both the gene and protein levels
human bronchial epithelial cultures (HBECs) have previously been shown to be predictive of outcomes in both cystic fibrosis patients and smokers[21], suggesting that their use is valid
Summary
Tobacco smoke is inhaled by 1.3 billion people worldwide and remains a major risk factor for several diseases including many types of cancer, cardiovascular disease and chronic obstructive pulmonary disease (COPD)[1]. A well-hydrated ASL is required to maintain mucus clearance, a key component of the lung’s innate defense system. The CFTR is a cAMP-regulated anion channel whose function is absolutely required for ASL hydration and to maintain mucociliary clearance and the sterility of lungs, as indicated by the genetic disease cystic fibrosis[8]. Despite little being known about the health effects of LCs, these products are perceived as less harmful than cigarettes by young adults[13]. The detrimental effects of tobacco exposure are counteracted by the lung’s innate defense system that works to limit the damages caused by smoke by providing anti-oxidants and by removing inhaled toxicants[15]. We exposed primary, well-differentiated HBECs to air and tobacco smoke from Kentucky research cigarettes, and LCs to evaluate their relative effects on airway epithelial viability/function
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