scholarly journals E-Cigarette Use: Device Market, Study Design, and Emerging Evidence of Biological Consequences

2021 ◽  
Vol 22 (22) ◽  
pp. 12452
Author(s):  
Hunter T. Snoderly ◽  
Timothy R. Nurkiewicz ◽  
Elizabeth C. Bowdridge ◽  
Margaret F. Bennewitz
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Study Design ◽  
Electronic Cigarettes ◽  
Public Awareness ◽  
Emerging Diseases ◽  
Cellular Level ◽  
Cigarette Use ◽  
Pulmonary Endothelium ◽  
Chronic Use

Electronic cigarettes are frequently viewed as a safer alternative to conventional cigarettes; however, evidence to support this perspective has not materialized. Indeed, the current literature reports that electronic cigarette use is associated with both acute lung injury and subclinical dysfunction to the lung and vasculature that may result in pathology following chronic use. E-cigarettes can alter vascular dynamics, polarize innate immune populations towards a proinflammatory state, compromise barrier function in the pulmonary endothelium and epithelium, and promote pre-oncogenic phenomena. This review will summarize the variety of e-cigarette products available to users, discuss current challenges in e-cigarette study design, outline the range of pathologies occurring in cases of e-cigarette associated acute lung injury, highlight disease supporting tissue- and cellular-level changes resulting from e-cigarette exposure, and briefly examine how these changes may promote tumorigenesis. Continued research of the mechanisms by which e-cigarettes induce pathology benefit users and clinicians by resulting in increased regulation of vaping devices, informing treatments for emerging diseases e-cigarettes produce, and increasing public awareness to reduce e-cigarette use and the onset of preventable disease.

scholarly journals Vaping-induced lung injury: brief report for the practicing clinician

2020 ◽  
Vol 2020 (8) ◽  
Author(s):  
Bashar Khiatah ◽  
Alex Murdoch ◽  
Charles Hubeny ◽  
Carl Constantine ◽  
Amanda Frugoli
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Case Vignette ◽  
Cigarette Use ◽  
Lung Injuries ◽  
Teenagers And Young Adults ◽  
The Usa ◽  
Physician Awareness ◽  
Harmful Effects

ABSTRACT The USA is witnessing an outbreak of vaping-induced lung injuries associated with the drastic rise in e-cigarette use, especially among teenagers and young adults. Our understanding of the harmful effects of these products is expanding as an increasing amount of consumers seek medical care for lung-related illnesses. The knowledge of the long-term sequelae of e-cigarette use is limited due to their novelty, but a growing association exists between use and acute lung injury. We describe a case vignette of vaping-induced lung injury to increase physician awareness and discuss the applicability of preliminary diagnostic criteria.

Secondhand smoke from electronic cigarette resulting in hypersensitivity pneumonitis

2020 ◽  
Vol 13 (3) ◽  
pp. e233381 ◽  
Author(s):  
Panagis Galiatsatos ◽  
Erin Gomez ◽  
Cheng Ting Lin ◽  
Peter B Illei ◽  
Pali Shah ◽  
...  
Keyword(s):  
Lung Injury ◽  
Secondhand Smoke ◽  
Hypersensitivity Pneumonitis ◽  
Electronic Cigarettes ◽  
Electronic Cigarette ◽  
Cigarette Use ◽  
Diagnostic Investigation ◽  
Health Related ◽  
The Usa ◽  
Exposure To Secondhand Smoke

Cases of vaping-induced lung injury have increased in the USA, resulting in a heterogeneous collection of pneumonitis patterns in persons who used electronic cigarettes. Hypersensitivity pneumonitis has been documented in several cases of first-hand electronic cigarette use; however, secondhand smoke health-related consequences have not been fully understood. We present a case of the patient who developed hypersensitivity pneumonitis secondary to exposure to secondhand smoke from electronic cigarette. We summarise the presentation and diagnostic investigation, as well as the management of this case.

scholarly journals Oxidative lipidomics of hyperoxic acute lung injury: mass spectrometric characterization of cardiolipin and phosphatidylserine peroxidation

2010 ◽  
Vol 299 (1) ◽  
pp. L73-L85 ◽  
Author(s):  
Yulia Y. Tyurina ◽  
Vladimir A. Tyurin ◽  
A. Murat Kaynar ◽  
Valentyna I. Kapralova ◽  
Karla Wasserloos ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Molecular Species ◽  
Caspase 3 ◽  
Ionization Mass ◽  
Individual Molecular Species ◽  
Pulmonary Endothelium ◽  
Anionic Phospholipids ◽  
Pulmonary Endothelial Cells

Reactive oxygen species have been shown to play a significant role in hyperoxia-induced acute lung injury, in part, by inducing apoptosis of pulmonary endothelium. However, the signaling roles of phospholipid oxidation products in pulmonary endothelial apoptosis have not been studied. Using an oxidative lipidomics approach, we identified individual molecular species of phospholipids involved in the apoptosis-associated peroxidation process in a hyperoxic lung. C57BL/6 mice were killed 72 h after exposure to hyperoxia (100% oxygen). We found that hyperoxia-induced apoptosis (documented by activation of caspase-3 and -7 and histochemical terminal deoxynucleotidyl transferase dUTP-mediated nick-end labeling staining of pulmonary endothelium) was accompanied by nonrandom oxidation of pulmonary lipids. Two anionic phospholipids, mitochondria-specific cardiolipin (CL) and extramitochondrial phosphatidylserine (PS), were the two major oxidized phospholipids in hyperoxic lung. Using electrospray ionization mass spectrometry, we identified several oxygenation products in CL and PS. Quantitative assessments revealed a significant decrease of CL and PS molecular species containing C18:2, C20:4, C22:5, and C22:6 fatty acids. Similarly, exposure of mouse pulmonary endothelial cells (MLEC) to hyperoxia (95% oxygen; 72 h) resulted in activation of caspase-3 and -7 and significantly decreased the content of CL molecular species containing C18:2 and C20:4 as well as PS molecular species containing C22:5 and C22:6. Oxygenated molecular species were found in the same two anionic phospholipids, CL and PS, in MLEC exposed to hyperoxia. Treatment of MLEC with a mitochondria-targeted radical scavenger, a conjugate of hemi-gramicidin S with nitroxide, XJB-5-131, resulted in significantly lower oxidation of both CL and PS and a decrease in hyperoxia-induced changes in caspase-3 and -7 activation. We speculate that cytochrome c driven oxidation of CL and PS is associated with the signaling role of these oxygenated species participating in the execution of apoptosis and clearance of pulmonary endothelial cells, thus contributing to hyperoxic lung injury.

Lung Biopsy Findings in Severe Pulmonary Illness Associated With E-Cigarette Use (Vaping)

2019 ◽  
Author(s):  
Sanjay Mukhopadhyay ◽  
Mitra Mehrad ◽  
Pedro Dammert ◽  
Andrea V Arrossi ◽  
Rakesh Sarda ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Lung Biopsy ◽  
Diffuse Alveolar Damage ◽  
Lung Damage ◽  
Cigarette Use ◽  
Lipoid Pneumonia ◽  
Lung Biopsies ◽  
Severe Lung

Abstract Objectives The aim of this report is to describe the lung biopsy findings in vaping-associated pulmonary illness. Methods Lung biopsies from eight patients with vaping-associated pulmonary illness were reviewed. Results The biopsies were from eight men (aged 19-61 years) with respiratory symptoms following e-cigarette use (vaping). Workup for infection was negative in all cases, and there was no evidence for other etiologies. Imaging showed diffuse bilateral ground-glass opacities in all patients. Most recovered with corticosteroid therapy, while one died. Lung biopsies (seven transbronchial, one surgical) showed acute lung injury, including organizing pneumonia and/or diffuse alveolar damage. Common features were fibroblast plugs, hyaline membranes, fibrinous exudates, type 2 pneumocyte hyperplasia, and interstitial organization. Some cases featured a sparse interstitial chronic inflammatory infiltrate. Although macrophages were present within the airspaces in all cases, this feature was not prominent, and findings typical of exogenous lipoid pneumonia were absent. Conclusions The histopathology of acute pulmonary illness related to e-cigarette use (vaping) is characterized by acute lung injury patterns, supporting the contention that vaping can cause severe lung damage.

Ventilator-induced lung injury: in vivo and in vitro mechanisms

2002 ◽  
Vol 283 (4) ◽  
pp. L678-L682 ◽  
Author(s):  
Michael A. Matthay ◽  
Sunita Bhattacharya ◽  
Donald Gaver ◽  
Lorraine B. Ware ◽  
Lina H. K. Lim ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Barrier Properties ◽  
Pulmonary Endothelium ◽  
Ventilator Induced Lung Injury ◽  
Proinflammatory Responses ◽  
Substantial Progress ◽  
Made In

A lung-protective ventilator strategy significantly reduces mortality in patients with acute lung injury. Substantial progress has been made in understanding how mechanical stress can injure the lung, both in terms of alterations in barrier properties of the pulmonary endothelium and epithelium as well as in stimulating proinflammatory responses of macrophages and neutrophils.

Protective effect of hydrogen sulfide in a murine model of acute lung injury induced by combined burn and smoke inhalation

2008 ◽  
Vol 115 (3) ◽  
pp. 91-97 ◽  
Author(s):  
Aimalohi Esechie ◽  
Levente Kiss ◽  
Gabor Olah ◽  
Eszter M. Horváth ◽  
Hal Hawkins ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Murine Model ◽  
Smoke Inhalation ◽  
In Vivo Studies ◽  
Protective Effects ◽  
Pulmonary Endothelium ◽  
Anti Inflammatory

Acute lung injury results in a severe inflammatory response, which leads to priming and activation of leucocytes, release of reactive oxygen and reactive nitrogen species, destruction of pulmonary endothelium, extravasation of protein-rich fluid into the interstitium and formation of oedema. Recently, H2S (hydrogen sulfide) has been shown to decrease the synthesis of pro-inflammatory cytokines, reduce leucocyte adherence to the endothelium and subsequent diapedesis of these cells from the microvasculature in in vivo studies, and to protect cells in culture from oxidative injury. In the present study, we hypothesized that a parenteral formulation of H2S would reduce the lung injury induced by burn and smoke inhalation in a novel murine model. H2S post-treatment significantly decreased mortality and increased median survival in mice. H2S also inhibited IL (interleukin)-1β levels and significantly increased the concentration of the anti-inflammatory cytokine IL-10 in lung tissue. Additionally, H2S administration attenuated protein oxidation following injury and improved the histological condition of the lung. In conclusion, these results suggest that H2S exerts protective effects in acute lung injury, at least in part through the activation of anti-inflammatory and antioxidant pathways.

Pathophysiology of Neonatal Lung Injury

1991 ◽  
Vol 7 (S1) ◽  
pp. 56-60
Author(s):  
Richard D. Bland
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Ventilatory Support ◽  
Fetal Lung ◽  
Amniotic Cavity ◽  
Pulmonary Endothelium ◽  
Young Infants ◽  
Neonatal Lung ◽  
High Concentrations ◽  
Protein Rich

Respiratory distress in newborn and young infants often develops as a result of acute lung injury, in which disruption of the normal barrier function of the pulmonary endothelium and epithelium causes protein-rich interstitial and alveolar edema. Several conditions may initiate acute lung injury, including aspiration of meconium or gastric contents, bacterial or viral infection, overzealous resuscitation, and birth associated with incomplete lung development that requires ventilatory support with positivepressure mechanical ventilation and high concentrations of inspired oxygen. The latter condition usually occurs after premature birth, but it also may occur as a consequence of impaired fetal lung growth secondary to diaphragmatic hernia or chest compression from lack of liquid in the amniotic cavity. Acute lung injury sometimes progresses to a chronic form of lung disease, which is characterized by edema, fibrosis, airway distortion, and nonuniform inflation of the lungs.

scholarly journals Cross-Sectional Association Between Lifetime Use of Electronic Cigarettes With or Without Marijuana and Self-Reported Past 12-Month Respiratory Symptoms as well as Lifetime Respiratory Diseases in U.S. Adults

2020 ◽  
Vol 22 (Supplement_1) ◽  
pp. S70-S75
Author(s):  
Zidian Xie ◽  
Dongmei Li
Keyword(s):  
Respiratory Symptoms ◽  
Respiratory Diseases ◽  
Respiratory Health ◽  
Electronic Cigarettes ◽  
Public Awareness ◽  
Smoking History ◽  
Health Study ◽  
Cigarette Use ◽  
Cross Sectional ◽  
Potential Health

Abstract Introduction The use of electronic cigarettes (vaping), especially with marijuana, has become increasingly popular among adults. Aims and Methods The Population Assessment of Tobacco and Health study Wave 4 data on 33 606 adult participants who indicated ever using electronic cigarettes were included in the study. By controlling for confounding variables (such as age and smoking history), multivariable weighted logistic regression models were used to examine the cross-sectional association between lifetime e-cigarette use with or without marijuana and self-reported past 12-month respiratory symptoms as well as lifetime respiratory diseases. Results Compared to adults who never vaped, adults who had ever vaped with marijuana had a significantly higher association with self-reported past 12-month respiratory symptoms but not lifetime respiratory diseases. Compared to adults who had ever vaped without marijuana, adults who had ever vaped at least sometimes with marijuana had a significantly greater risk of having wheezing/whistling in the chest (adjusted odds ratio [aOR] = 1.21, 95% confidence interval [CI]: 1.01, 1.44), chest sounded wheezy during or after exercise (aOR = 1.59, 95% CI: 1.31, 1.93), and had a dry cough at night (aOR = 1.35, 95% CI: 1.16, 1.57), while adults who had ever vaped rarely with marijuana had a significantly greater risk of having wheezing/whistling in the chest (aOR = 1.31, 95% CI: 1.06, 1.61), chest sounded wheezy during or after exercise (aOR = 1.24, 95% CI: 1.01, 1.52), and had a dry cough at night (aOR = 1.24, 95% CI: 1.04, 1.47). Conclusions Lifetime e-cigarette use with marijuana is associated with self-reported past 12-month respiratory symptoms in adults. Implications The use of e-cigarettes with marijuana has become prevalent in recent years. Our cross-sectional study suggests that there may be respiratory health symptoms associated with ever vaping with marijuana that is independent of nicotine vaping, which should raise public awareness of potential health risks associated with the use of e-cigarettes with marijuana. Further longitudinal studies on the respiratory health effects of e-cigarette use with marijuana are warranted.

scholarly journals Smouldering ashes: burning questions after the outbreak of electronic cigarette or vaping-associated lung injury (EVALI)

2020 ◽  
Vol 96 (1141) ◽  
pp. 686-692
Author(s):  
Gabor Zoltan Xantus ◽  
Anna V Gyarmathy ◽  
Carole Ann Johnson
Keyword(s):  
Lung Injury ◽  
Electronic Cigarettes ◽  
Public Awareness ◽  
Real Life ◽  
Vitamin E Acetate ◽  
Control And Prevention ◽  
The Usa ◽  
To Come ◽  
Counterfeit Products

In the summer of 2019, the Center for Disease Control and Prevention (CDC) declared an emergency of electronic cigarettes and/or vaping (vaping)-associated lung injury (EVALI) in the USA. The outbreak abated by January 2020, which the CDC attributed to heightened public awareness, ‘user actions to reduce risk’ and potentially the removal of vitamin E acetate (VEA) from vaping products (VEA is an oily chemical cutting agent, strongly associated with the disease). Even though the EVALI outbreak appears to be over, numerous epidemiological and medical questions are left still open. First, why were there practically no cases outside the USA, which represents nearly a quarter of the global vaping market? Comparative studies to map the differences in device/fluids/user habits between countries might be needed urgently. Second, what is the pathomechanism that sickens vapers irrespective of VEA exposure? VEA was only confirmed in about half of the cases and the presumed toxicity is yet to be determined. Aetiology/epidemiology focused research is needed to investigate/interpret the broader context to explain the outbreak. Third, could any socioeconomic/environmental factors have influenced the course of the outbreak? Finally, what should we expect in the years to come? Was EVALI a serious but reversible emergency medicine condition or is vaping as detrimental to long-term health as smoking? Besides the complex legislative, regulatory, ethical aspects of EVALI, biomedical research is also difficult: in-vitro experiments have limited inferential value to real real-life vaping due to its complexity; user habits are self-reported and under-researched; there is an active black market pouring unknown quality counterfeit products and, in the USA, federal restrictions limit cannabis research. Vaping is a toxicological, multidimensional conundrum; therefore, stringent quality control, transparent legal/ethical boundaries, meticulous international research and user education are paramount to prevent potential future outbreaks and determine the parameters safe vaping (if these exist).

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