E-cigarette vaping associated acute lung injury (EVALI): state of science and future research needs

Marrocco, Antonella; Singh, Dilpreet; Christiani, David C.; Demokritou, Philip

doi:10.1080/10408444.2022.2082918

Cited by 20 publications

(30 citation statements)

References 264 publications

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“…It has been suggested that ketene gas generated upon heating VEA is the causative agents of EVALI, although other toxic or sensitizing chemicals in the inhaled vapor could also be involved in the pulmonary injury. [260][261][262][263][264] Not only the ketene 265,266 but reactive oxygen species and quinone methides, as well as other pyrolytic degradation products formed at high temperature in the vaping device, may act in a synergistic manner to cause lung damage.…”

Section: Detection and Analysismentioning

confidence: 99%

Hexahydrocannabinol and closely related semi‐synthetic cannabinoids: A comprehensive review

Ujváry¹

2023

Drug Testing and Analysis

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Since the early 2000s, there has been a turmoil on the global illicit cannabinoid market. Parallel to legislative changes in some jurisdictions regarding herbal cannabis, unregulated and cheap synthetic cannabinoids with astonishing structural diversity have emerged. Recently, semi‐synthetic cannabinoids manufactured from hemp extracts by simple chemical transformations have also appeared as recreational drugs. The burst of these semi‐synthetic cannabinoids into the market was sparked by legislative changes in the United States, where cultivation of industrial hemp restarted. By now, hemp‐derived cannabidiol (CBD), initially a blockbuster product on its own, became a “precursor” to semi‐synthetic cannabinoids such as hexahydrocannabinol (HHC), which appeared on the drug market in 2021. The synthesis and cannabimimetic activity of HHC were first reported eight decades ago in quest for the psychoactive principles of marijuana and hashish. Current large‐scale manufacture of HHC is based on hemp‐derived CBD extract, which is converted first by cyclization into a Δ8/Δ9‐THC mixture, followed by catalytic hydrogenation to afford a mixture of (9R)‐HHC and (9S)‐HHC epimers. Preclinical studies indicate that (9R)‐HHC has THC‐like pharmacological properties. The animal metabolism of HHC is partially clarified. The human pharmacology including metabolism of HHC is yet to be investigated, and (immuno)analytical methods for the rapid detection of HHC or its metabolites in urine are lacking. Herein, the legal background for the revitalization of hemp cultivation, and available information on the chemistry, analysis, and pharmacology of HHC and related analogs, including HHC acetate (HHC‐O) is reviewed.

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Section: Detection and Analysismentioning

confidence: 99%

Hexahydrocannabinol and closely related semi‐synthetic cannabinoids: A comprehensive review

Ujváry¹

2023

Drug Testing and Analysis

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“…An initial defining feature of EVALI was the presence of lipid‐laden macrophages from the lungs, 72,73 although the presence of foamy macrophages occurs in a variety of conditions and exposures including nicotine‐containing e‐cigarettes with PG/VG 24 . The changes seen in this study may have further implications for the development of acute lung injury in association with combined exposures, a scenario that is relevant for EVALI as many patients used both THC‐ and nicotine‐based e‐cigarette 74 . Moreover, symptoms of EVALI overlap with those of COVID‐19 75 .…”

Section: Discussionmentioning

confidence: 74%

“…24 The changes seen in this study may have further implications for the development of acute lung injury in association with combined exposures, a scenario that is relevant for EVALI as many patients used both THC-and nicotinebased e-cigarette. 74 Moreover, symptoms of EVALI overlap with those of COVID-19. 75 Although there is controversy on whether e-cigarette use alters COVID-19 susceptibility or severity, 76 there is evidence that e-cigarette aerosol exposure augments the inflammatory response to other types of viral infection 77,78 and is some cases may exacerbate symptoms of EVALI.…”

Section: Discussionmentioning

confidence: 99%

Chronic low‐level JUUL aerosol exposure causes pulmonary immunologic, transcriptomic, and proteomic changes

et al. 2023

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E‐cigarettes currently divide public opinion, with some considering them a useful tool for smoking cessation and while others are concerned with potentially adverse health consequences. However, it may take decades to fully understand the effects of e‐cigarette use in humans given their relative newness on the market. This highlights the need for comprehensive preclinical studies investigating the effects of e‐cigarette exposure on health outcomes. Here, we investigated the impact of chronic, low‐level JUUL aerosol exposure on multiple lung outcomes. JUUL is a brand of e‐cigarettes popular with youth and young adults. To replicate human exposures, 8‐ to 12‐week‐old male and female C57BL/6J mice were exposed to commercially available JUUL products (containing 59 mg/ml nicotine). Mice were exposed to room air, PG/VG, or JUUL daily for 4 weeks. After the exposure period, inflammatory markers were assessed via qRT‐PCR, multiplex cytokine assays, and differential cell count. Proteomic and transcriptomic analyses were also performed on samples isolated from the lavage of the lungs; this included unbiased analysis of proteins contained within extracellular vesicles (EVs). Mice exposed to JUUL aerosols for 4 weeks had significantly increased neutrophil and lymphocyte populations in the BAL and some changes in cytokine mRNA expression. However, BAL cytokines did not change. Proteomic and transcriptomic analysis revealed significant changes in numerous biological pathways including neutrophil degranulation, PPAR signaling, and xenobiotic metabolism. Thus, e‐cigarettes are not inert and can cause significant cellular and molecular changes in the lungs.

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“…The studies enrolled in our research did not provide data on e-cigarette vaping. Although e-cigarettes were often perceived as less harmful alternatives to traditional cigarettes, recent studies indicated that they could cause pulmonary inflammation, injury, and other pathological changes associated with ARDS [ 56 , 57 ]. Similar to the traditional cigarettes, e-cigarette vaping could provoke inflammatory responses and oxidative stress, activating pulmonary macrophages and epithelial cells to release proinflammatory cytokines, leading to damage in alveolar epithelial and endothelial cells [ 58 , 59 ].…”

Section: Discussionmentioning

confidence: 99%

Smoking on the risk of acute respiratory distress syndrome: a systematic review and meta-analysis

Zhang,

Xu,

et al. 2024

Crit Care

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Background The relationship between smoking and the risk of acute respiratory distress syndrome (ARDS) has been recognized, but the conclusions have been inconsistent. This systematic review and meta-analysis investigated the association between smoking and ARDS risk in adults. Methods The PubMed, EMBASE, Cochrane Library, and Web of Science databases were searched for eligible studies published from January 1, 2000, to December 31, 2023. We enrolled adult patients exhibiting clinical risk factors for ARDS and smoking condition. Outcomes were quantified using odds ratios (ORs) for binary variables and mean differences (MDs) for continuous variables, with a standard 95% confidence interval (CI). Results A total of 26 observational studies involving 36,995 patients were included. The meta-analysis revealed a significant association between smoking and an increased risk of ARDS (OR 1.67; 95% CI 1.33–2.08; P < 0.001). Further analysis revealed that the associations between patient-reported smoking history and ARDS occurrence were generally similar to the results of all the studies (OR 1.78; 95% CI 1.38–2.28; P < 0.001). In contrast, patients identified through the detection of tobacco metabolites (cotinine, a metabolite of nicotine, and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), a metabolite of tobacco products) showed no significant difference in ARDS risk (OR 1.19; 95% CI 0.69–2.05; P = 0.53). The smoking group was younger than the control group (MD − 7.15; 95% CI − 11.58 to − 2.72; P = 0.002). Subgroup analysis revealed that smoking notably elevated the incidence of ARDS with extrapulmonary etiologies (OR 1.85; 95% CI 1.43–2.38; P < 0.001). Publication bias did not affect the integrity of our conclusions. Sensitivity analysis further reinforced the reliability of our aggregated outcomes. Conclusions There is a strong association between smoking and elevated ARDS risk. This emphasizes the need for thorough assessment of patients' smoking status, urging healthcare providers to vigilantly monitor individuals with a history of smoking, especially those with additional extrapulmonary risk factors for ARDS.

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E-cigarette vaping associated acute lung injury (EVALI): state of science and future research needs

Cited by 20 publications

References 264 publications

Hexahydrocannabinol and closely related semi‐synthetic cannabinoids: A comprehensive review

Hexahydrocannabinol and closely related semi‐synthetic cannabinoids: A comprehensive review

Chronic low‐level JUUL aerosol exposure causes pulmonary immunologic, transcriptomic, and proteomic changes

Smoking on the risk of acute respiratory distress syndrome: a systematic review and meta-analysis

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