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      E-cigarettes and health risks: more to the flavour than just the name

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          Abstract

          Rationale: The growing interest in regulating flavoured E-liquids must incorporate understanding of the "flavouring profile" of each E-liquid - which flavourants (flavouring chemicals) are present and at what concentrations not just focussing on the flavour on the label. Methods: We investigated the flavouring profile of 10 different flavoured E-liquids. We assessed bronchial epithelial cell viability and apoptosis, phagocytosis of bacteria and apoptotic cells by macrophages after exposure to E-cigarette vapour extract (EVE). And validated in normal human bronchial epithelial cells (NHBE) and alveolar macrophages (AMs) from healthy donors. We also assessed cytokine release and validated in the saliva from E-cigarette users. Results: Increased necrosis/apoptosis (16.1-64.5% apoptosis) in 16HBE cells was flavour dependent, and NHBEs showed an increased susceptibility to flavours. In THP-1 differentiated macrophages phagocytosis was also flavour dependent, with alveolar macrophages (AM) also showing increased susceptibility to flavours. Furthermore, Banana and Chocolate were shown to reduce surface expression of phagocytic target recognition receptors on alveolar macrophages. Banana and Chocolate increased IL-8 secretion by NHBE, whilst all 4 flavours reduced AM IL-1β secretion which was also reduced in the saliva of E-cigarette users compared with healthy controls. Flavourant profiles of E-liquids varied from simple 2 compound mixtures to complex mixtures containing over a dozen flavourants. E-liquids with high benzene content, complex flavouring profiles, high chemical concentration had the greatest impacts. Conclusions: The flavourant profile of E-liquids is key to disruption of the airway status quo by increasing bronchial epithelial cell apoptosis, causing alveolar macrophage phagocytic dysfunction and altering airway cytokines.

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          Most cited references 51

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          Essential involvement of interleukin-8 (IL-8) in acute inflammation.

           T Akahoshi,  T Wada,  N Sekido (1994)
          Neutrophil infiltration into inflammatory sites is one of the hallmarks of acute inflammation. Locally produced chemotactic factors are presumed to mediate the sequence of events leading to the infiltration at inflammatory sites. Interleukin-8 (IL-8), a novel leukocyte chemotactic activating cytokine (chemokine), is produced by various types of cells upon stimulation with inflammatory stimuli and exerts a variety of functions on leukocytes, particularly, neutrophils in vitro. However, no definitive evidence has been presented on its role in recruiting and activating neutrophils in the lesions of various types of inflammatory reactions. We administered a highly specific neutralizing antibody against IL-8 in several types of acute inflammatory reactions, including lipopolysaccharide (LPS)-induced dermatitis, LPS/IL-1-induced arthritis, lung reperfusion injury, and acute immune complex-type glomerulonephritis. Anti-IL-8 treatment prevented neutrophil-dependent tissue damage as well as neutrophil infiltration in these conditions. These results suggest that IL-8 plays a causative role in acute inflammation by recruiting and activating neutrophils.
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            Carbonyl compounds in electronic cigarette vapors: effects of nicotine solvent and battery output voltage.

            Glycerin (VG) and propylene glycol (PG) are the most common nicotine solvents used in e-cigarettes (ECs). It has been shown that at high temperatures both VG and PG undergo decomposition to low molecular carbonyl compounds, including the carcinogens formaldehyde and acetaldehyde. The aim of this study was to evaluate how various product characteristics, including nicotine solvent and battery output voltage, affect the levels of carbonyls in EC vapor. Twelve carbonyl compounds were measured in vapors from 10 commercially available nicotine solutions and from 3 control solutions composed of pure glycerin, pure propylene glycol, or a mixture of both solvents (50:50). EC battery output voltage was gradually modified from 3.2 to 4.8V. Carbonyl compounds were determined using the HPLC/DAD method. Formaldehyde and acetaldehyde were found in 8 of 13 samples. The amounts of formaldehyde and acetaldehyde in vapors from lower voltage EC were on average 13- and 807-fold lower than in tobacco smoke, respectively. The highest levels of carbonyls were observed in vapors generated from PG-based solutions. Increasing voltage from 3.2 to 4.8V resulted in a 4 to more than 200 times increase in formaldehyde, acetaldehyde, and acetone levels. The levels of formaldehyde in vapors from high-voltage device were in the range of levels reported in tobacco smoke. Vapors from EC contain toxic and carcinogenic carbonyl compounds. Both solvent and battery output voltage significantly affect levels of carbonyl compounds in EC vapors. High-voltage EC may expose users to high levels of carbonyl compounds. © The Author 2014. Published by Oxford University Press on behalf of the Society for Research on Nicotine and Tobacco. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
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              Alveolar macrophages from subjects with chronic obstructive pulmonary disease are deficient in their ability to phagocytose apoptotic airway epithelial cells.

              Chronic obstructive pulmonary disease is a highly prevalent, complex disease, usually caused by cigarette smoke. It causes serious morbidity and mortality and costs the global community billions of dollars per year. While chronic inflammation, extracellular matrix destruction and increased airway epithelial cell apoptosis are reported in chronic obstructive pulmonary disease, the understanding of the basic pathogenesis of the disease is limited and there are no effective treatments. We hypothesized that the accumulation of apoptotic airway epithelial cells chronic obstructive pulmonary disease in could be due to defective phagocytic clearance by alveolar macrophages. There have been no previous studies of the phagocytic capacity of alveolar macrophages in chronic obstructive pulmonary disease using physiologically relevant apoptotic airway epithelial cells as phagocytic targets. We developed a phagocytosis assay whereby cultured 16HBE airway epithelial cells were induced to apoptosis with ultraviolet radiation and stained with mitotracker green. Alveolar macrophages from bronchoalveolar lavage from eight control and six chronic obstructive pulmonary disease subjects were analysed following 1.5 h incubation with apoptotic airway epithelial cells, then staining with macrophage marker anti CD33. CD33+/mitotracker green + events (i.e., alveolar macrophages which had phagocytosed apoptotic airway epithelial cells) were analysed using flow cytometry. Phagocytosis of polystyrene microbeads was investigated in parallel. A significantly reduced proportion of alveolar macrophages from chronic obstructive pulmonary disease subjects ingested apoptotic airway epithelial cells compared with controls (11.6 +/- 4.1% for chronic obstructive pulmonary disease versus 25.6 +/- 9.2% for control group). Importantly, the deficiency was not observed using polystyrene beads, suggesting that the failure to resolve epithelial damage in chronic obstructive pulmonary disease may result, at least partially, from specific defects in phagocytic ability of alveolar macrophages to ingest apoptotic airway epithelial cells.
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                Author and article information

                Journal
                American Journal of Physiology-Lung Cellular and Molecular Physiology
                American Journal of Physiology-Lung Cellular and Molecular Physiology
                American Physiological Society
                1040-0605
                1522-1504
                December 09 2020
                Affiliations
                [1 ]Department of Thoracic Medicine, Royal Adelaide Hospital, Australia
                [2 ]Medicine, UC San Diego and VASDHS, United States
                [3 ]Department of Occupational and Environmental Health, School of Public Health, Univerity of Adelaide, Australia
                [4 ]Pulmonary Critical Care Section, VA San Diego Healthcare System, United States
                [5 ]Department of Medicine, UC San Diego and VASDHS, United States
                [6 ]Lung Research Laboratory, University of Adelaide, Australia
                [7 ]Department of Medicine, University of California, San Diego, United States
                [8 ]School Of Medicine, University of Adelaide, Australia
                Article
                10.1152/ajplung.00370.2020
                © 2020

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