Effects of E-Cigarette Aerosols with Varying Levels of Nicotine on Biomarkers of Oxidative Stress and Inflammation in Mice (original) (raw)
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American journal of physiology. Lung cellular and molecular physiology, 2018
Electronic cigarettes (e-cig) are advertised as a less harmful nicotine delivery system or as a new smoking cessation tool. We aimed to assess the in vivo effects of e-cigarette vapor in the lung and to compare them to those of cigarette smoke (CS). We exposed C57BL/6 mice for either 3 days or 4 weeks to ambient air, CS or e-cig vapor containing: i) propylene glycol/vegetable glycerol (1:1; PG:VG-Sol), ii) PG:VG with nicotine (G:VG-N), or iii) PG:VG with nicotine and flavor (PG:VG- N+F) and determined oxidative stress, inflammation and pulmonary mechanics. E-cig vapors, especially PG:VG- N+F, increased bronchoalveolar lavage fluid (BALF) cellularity, Muc5ac production, as well as BALF and lung oxidative stress markers at least comparably and in many cases more than CS. BALF protein content at both time points studied was only elevated in the PG:VG- N+F group. After 3 days, PG:VG-Sol altered tissue elasticity, static compliance and airway resistance, while after 4 weeks, CS was the o...
PLOS ONE, 2015
Oxidative stress and inflammatory response are the key events in the pathogenesis of chronic airway diseases. The consumption of electronic cigarettes (e-cigs) with a variety of e-liquids/e-juices is alarmingly increasing without the unrealized potential harmful health effects. We hypothesized that electronic nicotine delivery systems (ENDS)/e-cigs pose health concerns due to oxidative toxicity and inflammatory response in lung cells exposed to their aerosols. The aerosols produced by vaporizing ENDS e-liquids exhibit oxidant reactivity suggesting oxidants or reactive oxygen species (OX/ROS) may be inhaled directly into the lung during a "vaping" session. These OX/ROS are generated through activation of the heating element which is affected by heating element status (new versus used), and occurs during the process of e-liquid vaporization. Unvaporized e-liquids were oxidative in a manner dependent on flavor additives, while flavors containing sweet or fruit flavors were stronger oxidizers than tobacco flavors. In light of OX/ROS generated in ENDS e-liquids and aerosols, the effects of ENDS aerosols on tissues and cells of the lung were measured. Exposure of human airway epithelial cells (H292) in an air-liquid interface to ENDS aerosols from a popular device resulted in increased secretion of inflammatory cytokines, such as IL-6 and IL-8. Furthermore, human lung fibroblasts exhibited stress and morphological change in response to treatment with ENDS/e-liquids. These cells also secrete increased IL-8 in response to a cinnamon flavored e-liquid and are susceptible to loss of cell viability by ENDS e-liquids. Finally, exposure of wild type C57BL/6J mice to aerosols produced from a popular e-cig increase pro-inflammatory cytokines and diminished lung glutathione levels which are critical in maintaining cellular redox balance. Thus, exposure to e-cig aerosols/ juices incurs measurable oxidative and inflammatory responses in lung cells and tissues that could lead to unrealized health consequences.
American Journal of Physiology-Lung Cellular and Molecular Physiology, 2019
The effects of e-cigarette (e-cig) aerosol inhalation by nonsmokers have not been examined to date. The present study was designed to evaluate the acute response to aerosol inhalation of non-nicotinized e-cigarettes in terms of oxidative stress and indices of endothelial activation in human pulmonary microvascular endothelial cells (HPMVEC). Ten smoking-naïve healthy subjects (mean age ± SD = 28.7 ± 5.5 yr) were subjected to an e-cig challenge, following which their serum was monitored for markers of inflammation [C-reactive protein (CRP) and soluble intercellular adhesion molecule (sICAM)] and nitric oxide metabolites (NOx). The oxidative stress and inflammation burden of the circulating serum on the vascular network was also assessed by measuring reactive oxygen species (ROS) production and induction of ICAM-1 expression on HPMVEC. Our results show that serum indices of oxidative stress and inflammation increased significantly ( P < 0.05 as compared with baseline), reaching a p...
E-cigarette aerosols induce lower oxidative stress in vitro when compared to tobacco smoke
Toxicology mechanisms and methods, 2016
Tobacco smoking is a risk factor for various diseases. The underlying cellular mechanisms are not fully characterized, but include oxidative stress, apoptosis, and necrosis. Electronic-cigarettes (e-cigarettes) have emerged as an alternative to and a possible means to reduce harm from tobacco smoking. E-cigarette vapor contains significantly lower levels of toxicants than cigarette smoke, but standardized methods to assess cellular responses to exposure are not well established. We investigated whether an in vitro model of the airway epithelium (human bronchial epithelial cells) and commercially available assays could differentiate cellular stress responses to aqueous aerosol extracts (AqE) generated from cigarette smoke and e-cigarette aerosols. After exposure to AqE concentrations of 0.063-0.500 puffs/mL, we measured the intracellular glutathione ratio (GSH:GSSG), intracellular generation of oxidant species, and activation of the nuclear factor erythroid-related factor 2 (Nrf2)-co...
Drug and Chemical Toxicology, 2021
An electronic cigarette is a rechargeable device that produces an inhaled aerosol containing varying levels of nicotine, and inorganic and organic toxicants and carcinogenic compounds. The aerosol is generated by heating a solution of propylene glycol and glycerin with nicotine and flavoring ingredients at a high temperatures. The e-cigarette was developed and marketed as a safer alternative to the regular cigarette which is known to be injurious to human health. However, published studies suggest that the aerosol of e-cigarette can also have adverse health effects. The main objective of this review is to briefly describe some consequences of e-cigarette smoking, and to present data showing that the resulting increased oxidative stress and inflammation are likely to be involved in effecting to lung damage. The aerosol contains varying amounts of organic and inorganic toxicants as well as carcinogens, which might serve as the source of such deleterious events. In addition, the aerosol also contains nicotine, which is known to be addictive. E-cigarette smoking releases these toxicants into the air leading to inhalation by non-smokers in residential or work place areas. Unlike regular tobacco smoke, the long-term consequences of direct and secondhand exposure to e-cigarette aerosol have not been extensively studied but based on available data, e-cigarette aerosol should be considered harmful to human health
Toxicology Research and Application
Cigarette smoking causes serious diseases, including lung cancer, atherosclerotic coronary artery disease, peripheral vascular disease, chronic bronchitis, and emphysema. While cessation remains the most effective approach to minimize smoking-related disease, alternative non-combustible tobacco-derived nicotine-containing products may reduce disease risks among those unable or unwilling to quit. E-vapor aerosols typically contain significantly lower levels of smoke-related harmful and potentially harmful constituents; however, health risks of long-term inhalation exposures are unknown. We designed a 7-month inhalation study in C57BL/6 mice to evaluate long-term respiratory toxicity of e-vapor aerosols compared to cigarette smoke and to assess the impact of smoking cessation (Cessation group) or switching to an e-vapor product (Switching group) after 3 months of exposure to 3R4F cigarette smoke (CS). There were no significant changes in in-life observations (body weights, clinical si...
International Journal of Molecular Sciences, 2020
The use of electronic nicotine delivery systems (ENDS), also known as electronic-cigarettes (e-cigs), has raised serious public health concerns, especially in light of the 2019 outbreak of e-cig or vaping product use-associated acute lung injury (EVALI). While these cases have mostly been linked to ENDS that contain vitamin E acetate, there is limited research that has focused on the chronic pulmonary effects of the delivery vehicles (i.e., without nicotine and flavoring). Thus, we investigated lung function and immune responses in a mouse model following exposure to the nearly ubiquitous e-cig delivery vehicles, vegetable glycerin (VG) and propylene glycol (PG), used with a specific 70%/30% ratio, with or without vanilla flavoring. We hypothesized that mice exposed sub-acutely to these e-cig aerosols would exhibit lung inflammation and altered lung function. Adult female C57BL/6 mice (n = 11–12 per group) were exposed to filtered air, 70%/30% VG/PG, or 70%/30% VG/PG with a French v...
Inflammation and Oxidative Stress from E-cigarette Exposure: Implications for COPD and Asthma
Journal of Pharmaceutical Research International
Currently, little is known about the effects of e-cigarette use on chronic respiratory diseases, due to their relative novelty. This review compiles data on the cellular effects of e-cigarette use with population data on disease incidence to determine potential risk for COPD and asthma development, two of the most prevalent respiratory diseases. We searched the Google Scholar database for studies on e-cigarette exposure and levels of inflammation and oxidative stress in human cells and e-cigarette users, as well a population studies analyzing e-cigarette use and respiratory disease incidence. All reviewed studies found significant increases in inflammatory biomarkers, as well as pro-inflammatory cytokines, demonstrating a correlation between e-cigarette use and a pro-inflammatory affect. Our findings suggest e-cigarette vapor contains reactive oxygen species, and that exposure increases cellular oxidation and lowers antioxidant power. Every population study we reviewed found signifi...
A brief review on cigarette induced cellular damage
INTERNATIONAL JOURNAL OF EXPERIMENTAL RESEARCH AND REVIEW, 2020
Cigarette smoking has become one of the most common addictions in context to the present scenario of tobacco consumption. Comprising of nearly 7000 chemicals, cigarette smoke have both free radicals and oxidizing agents in both smoke tar and gas phase, both of which can cause oxidative stress in human health. Long time smoking causes decreased serum immunoglobulin level but increased level of auto– antibodies. During chronic oxidative stress resulting from cigarette smoking, cells secrete mucus and increased viscosity of mucus in airways makes it susceptible to bacterial infection. Furthermore, chronic exposure of lungs to tobacco smoke causes unfolded protein response, ER stress and altered ceramide metabolism. Apart from the above mentioned facts, Cigarette smoking can also cause senescence resulting in abnormal wound healing that exaggerates pathogenesis of COPD. Although there are several management therapies available for COPD management, but the permanent cellular damages due ...
2021
Supplemental Material, sj-pdf-3-tor-10.1177_2397847321995875 for A 7-month inhalation toxicology study in C57BL/6 mice demonstrates reduced pulmonary inflammation and emphysematous changes following smoking cessation or switching to e-vapor products by Ashutosh Kumar, Ulrike Kogel, Marja Talikka, Celine Merg, Emmanuel Guedj, Yang Xiang, Athanasios Kondylis, Bjoern Titz, Nikolai V Ivanov, Julia Hoeng, Manuel Peitsch, Joshua Allen, Amit Gupta, Anthony Skowronek and K Monica Lee in Toxicology Research and Application