Vaping additives cannabinoid oil and vitamin E acetate adhere to and damage the human airway epithelium.

E-cigarette, or vaping product use-associated lung injury (EVALI), is a severe respiratory disorder that caused a sudden outbreak of hospitalized young people in 2019. Using cannabis oil containing vaping products, including vitamin E acetate contaminants, was found to be strongly associated with EVALI. However, the underlying tissue impacts of the condition are still largely unknown. Here, we focused on the vehicle cannabinoid oil (CBD oil) and contaminant vitamin E acetate (VEA) effects on airway epithelial cells. Primary human bronchial epithelial (HBE) cultures were exposed to e-liquid aerosols that contained CBD oil and VEA in combination or the common e-liquid components PG/VG with and without nicotine. Cell viability analysis indicated dramatically increased cell death counts after 3 days of CBD exposure, and this effect was even higher after CBD + VEA exposure. Microscopic examination of the cultures revealed cannabinoid and VEA depositions on the epithelial surfaces and cannabinoid accumulation in exposed cells, followed by cell death. These observations were supported by proteomic analysis of the cell secretions that exhibited increases in known markers of airway epithelial toxicity, such as xenobiotic enzymes, factors related to oxidative stress response, and cell death indicators. Overall, our study provides insights into the association between cannabinoid oil and vitamin E acetate vaping and lung injury. Collectively, our results suggest that the adherent accumulation of CBD oil on airway surfaces and the cellular uptake of both CBD oil- and VEA-containing condensates cause elevated metabolic stress, leading to increased cell death rates in human airway epithelial cultures.

Potential for release of pulmonary toxic ketene from vaping pyrolysis of vitamin E acetate.

A combined analytical, theoretical, and experimental study has shown that the vaping of vitamin E acetate has the potential to produce exceptionally toxic ketene gas, which may be a contributing factor to the upsurge in pulmonary injuries associated with using e-cigarette/vaping products. Additionally, the pyrolysis of vitamin E acetate also produces carcinogen alkenes and benzene for which the negative long-term medical effects are well recognized. As temperatures reached in vaping devices can be equivalent to a laboratory pyrolysis apparatus, the potential for unexpected chemistries to take place on individual components within a vape mixture is high. Educational programs to inform of the danger are now required, as public perception has grown that vaping is not harmful.

Aerosolized vitamin E acetate causes oxidative injury in mice and in alveolar macrophages.

Although vitamin E acetate (VEA) is suspected to play a causal role in the development of electronic-cigarette, or vaping, product use-associated lung injury (EVALI), the underlying biological mechanisms of pulmonary injury are yet to be determined. In addition, no study has replicated the systemic inflammation observed in humans in a murine EVALI model, nor investigated potential additive toxicity of viral infection in the setting of exposure to vaping products. To identify the mechanisms driving VEA-related lung injury and test the hypothesis that viral infection causes additive lung injury in the presence of aerosolized VEA, we exposed mice to aerosolized VEA for extended times, followed by influenza infection in some experiments. We used mass spectrometry to evaluate the composition of aerosolized VEA condensate and the VEA deposition in murine or human alveolar macrophages. Extended vaping for 28 days versus 15 days did not worsen lung injury but caused systemic inflammation in the murine EVALI model. Vaping plus influenza increased lung water compared with virus alone. Murine alveolar macrophages exposed to vaped VEA hydrolyzed the VEA to vitamin E with evidence of oxidative stress in the alveolar space and systemic circulation. Aerosolized VEA also induced cell death and chemokine release and reduced efferocytotic function in human alveolar macrophages in vitro. These findings provide new insights into the biological mechanisms of VEA toxicity.

Exploring the potential neurotoxicity of vaping vitamin E or vitamin E acetate.

Serious adverse health effects have been reported with the use of vaping products, including neurologic disorders and e-cigarette or vaping product use-associated lung injury (EVALI). Vitamin E acetate, likely added as a diluent to cannabis-containing products, was linked to EVALI. Literature searches were performed on vitamin E and vitamin E acetate-associated neurotoxicity. Blood brain barrier (BBB) penetration potential of vitamin E and vitamin E acetate were evaluated using cheminformatic techniques. Review of the literature showed that the neurotoxic potential of inhalation exposures to these compounds in humans is unknown. Physico-chemical properties demonstrate these compounds are lipophilic, and molecular weights indicate vitamin E and vitamin E acetate have the potential for BBB permeability. Computational models also predict both compounds may cross the BBB via passive diffusion. Based on literature search, no experimental nonclinical studies and clinical information on the neurotoxic potential of vitamin E via inhalation. Neurotoxic effects from pyrolysis by-product, phenyl acetate, structurally analogous to vitamin E acetate, suggests vitamin E acetate has potential for central nervous system (CNS) impairment. Cheminformatic model predictions provide a theoretical basis for potential CNS permeability of these inhaled dietary ingredients suggesting prioritization to evaluate for potential hazard to the CNS.

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

"E-Cigarette (e-cig) Vaping-Associated Acute Lung Injury" (EVALI) has been linked to vitamin-E-acetate (VEA) and Δ-9-tetrahydrocannabinol (THC), due to their presence in patients' e-cigs and biological samples. Lacking standardized methodologies for patients' data collection and comprehensive physicochemical/toxicological studies using real-world-vapor exposures, very little data are available, thus the underlying pathophysiological mechanism of EVALI is still unknown. This review aims to provide a comprehensive and critical appraisal of existing literature on clinical/epidemiological features and physicochemical-toxicological characterization of vaping emissions associated with EVALI. The literature review of 161 medical case reports revealed that the predominant demographic pattern was healthy white male, adolescent, or young adult, vaping illicit/informal THC-containing e-cigs. The main histopathologic pattern consisted of diffuse alveolar damage with bilateral ground-glass-opacities at chest radiograph/CT, and increased number of macrophages or neutrophils and foamy-macrophages in the bronchoalveolar lavage. The chemical analysis of THC/VEA e-cig vapors showed a chemical difference between THC/VEA and the single THC or VEA. The chemical characterization of vapors from counterfeit THC-based e-cigs or in-house-prepared e-liquids using either cannabidiol (CBD), VEA, or medium-chain triglycerides (MCT), identified many toxicants, such as carbonyls, volatile organic compounds, terpenes, silicon compounds, hydrocarbons, heavy metals, pesticides and various industrial/manufacturing/automotive-related chemicals. There is very scarce published toxicological data on emissions from THC/VEA e-liquids. However, CBD, MCT, and VEA emissions exert varying degrees of cytotoxicity, inflammation, and lung damage, depending on puffing topography and cell line. Major knowledge gaps were identified, including the need for more systematic-standardized epidemiological surveys, comprehensive physicochemical characterization of real-world e-cig emissions, and mechanistic studies linking emission properties to specific toxicological outcomes.

The role of vitamin E acetate (VEA) and its derivatives in the vaping associated lung injury: systematic review of evidence.

Small scale observational evidence suggested that Vitamin E (VE) might play beneficial role in human and animal respiratory conditions of various origin by stabilizing surfactant functions. The intra-aleveolar VE level is directly proportionate to the lung's response to inflammation. Electronic cigarette or vaping associated lung injury was a dominantly respiratory syndrome in the United States with seemingly strong association between potential Vitamin E acetate inhalation exposure and the onset of symptoms. This systematic review intended to assess if there was previous evidence of any potential respiratory/gastrointestinal toxicity associated with Vitamin E acetate or any of its derivatives. A systematic review was constructed and prospectively registered at PROSPERO to search important clinical databases between 2000 and 2020 for full text human articles investigating the effect of VEA or any of its derivatives administered via any route (oral/parenteral/aerosolised) in adults with any respiratory conditions. Out of 363 records investigating the effect of VEA and/or its derivatives/isomers in (any) lung injury (inflammatory, oxidative, infective, asthma/COPD) seven articles qualified. The papers reported various surrogate outcomes (APACHEII score, spirometry, etc) with equivocal results. There was one case report of harmful exposure to both Vitamin E (intramuscular) and Vitamin E acetate (topical). The present review found evidence of neither harm nor any significant clinical improvement associated with the administration of VEA or any derivatives via any route in adult inflammatory lung conditions however, the articles were of low-level evidence. Further studies are needed to correct flaws in research to explore the role of Vitamin E in pulmonology.

Dose-Dependent Pulmonary Toxicity of Aerosolized Vitamin E Acetate.

Electronic-cigarette, or vaping, product use-associated lung injury (EVALI) is a syndrome of acute respiratory failure characterized by monocytic and neutrophilic alveolar inflammation. Epidemiological and clinical evidence suggests a role of vitamin E acetate (VEA) in the development of EVALI, yet it remains unclear whether VEA has direct pulmonary toxicity. To test the hypotheses that aerosolized VEA causes lung injury in mice and directly injures human alveolar epithelial cells, we exposed adult mice and primary human alveolar epithelial type II (AT II) cells to an aerosol of VEA generated by a device designed for vaping oils. Outcome measures in mice included lung edema, BAL analysis, histology, and inflammatory cytokines; in vitro outcomes included cell death, cytokine release, cellular uptake of VEA, and gene-expression analysis. Comparison exposures in both models included the popular nicotine-containing JUUL aerosol. We discovered that VEA caused dose-dependent increases in lung water and BAL protein compared with control and JUUL-exposed mice in association with increased BAL neutrophils, oil-laden macrophages, multinucleated giant cells, and inflammatory cytokines. VEA aerosol was also toxic to AT II cells, causing increased cell death and the release of monocyte and neutrophil chemokines. VEA was directly absorbed by AT II cells, resulting in the differential gene expression of several inflammatory biological pathways. Given the epidemiological and clinical characteristics of the EVALI outbreak, these results suggest that VEA plays an important causal role.

Culprit or correlate? An application of the Bradford Hill criteria to Vitamin E acetate.

Vitamin E acetate (VEA) has come under significant scrutiny due to its association with e-cigarette, or vaping, product use-associated lung injury (EVALI). In 1965, Sir Austin Bradford Hill proposed a set of criteria used to critically assess an association for causality. In this article, we apply the Bradford Hill causation criteria to VEA and the EVALI outbreak to clarify what further areas of study are needed to strengthen the causal argument. Additionally, we highlight the need for systematized approaches to rapidly identify the cause of mass poisoning events of unknown etiology.

E-cigarette or vaping product use-associated lung injury in the pediatric population: imaging features at presentation and short-term follow-up.

BACKGROUND: Cases of e-cigarette or vaping product use-associated lung injury (EVALI) have rapidly reached epidemic proportions, yet there remain limited reports within the literature on the associated imaging findings. OBJECTIVE: We describe the most common imaging findings observed on chest computed tomography (CT) and chest radiograph (CXR) at presentation and at short-term follow-up at our major pediatric hospital. MATERIALS AND METHODS: A retrospective review of the electronic medical records was performed on all patients with suspected EVALI who were treated at a major pediatric hospital and 11 patients were included for analysis. Two board-certified pediatric radiologists then categorized the CXRs as either normal or abnormal, and further performed a systematic review of the chest CTs for imaging findings in the lungs, pleura and mediastinum. Interrater discordance was reconciled by consensus review. RESULTS: The 11 patients (9 males:2 females) ranged in age from 14 to 18 years. Gastrointestinal and constitutional symptoms were present in all patients, whereas shortness of breath and cough were reported in 5/11 and 6/11 patients, respectively. The CXR was abnormal in 10/11 patients, whereas all chest CTs were abnormal. The most common CT findings included consolidation, ground-glass opacities, interlobular septal thickening, lymphadenopathy and crazy-paving pattern. Almost all patients demonstrated subpleural sparing, and less than half also demonstrated peribronchovascular sparing. There was complete or near-complete resolution of imaging abnormalities in 5/6 patients with a median follow-up duration of 114 days. CONCLUSION: Pulmonary opacities with subpleural and peribronchovascular sparing was a commonly observed pattern of EVALI in the pediatric population at this institution. A CXR may not be sufficiently sensitive in diagnosing EVALI, and radiologists and clinicians should exercise caution when excluding EVALI based on the lack of a pulmonary opacity. Caution should also be exercised when excluding EVALI solely based on the lack of respiratory symptoms. Despite extensive pulmonary involvement at presentation, findings may resolve on short-term follow-up imaging.

Inhalation Toxicology of Vaping Products and Implications for Pulmonary Health.

E-cigarettes have a liquid that may contain flavors, solvents, and nicotine. Heating this liquid generates an aerosol that is inhaled into the lungs in a process commonly referred to as vaping. E-cigarette devices can also contain cannabis-based products including tetrahydrocannabinol (THC), the psychoactive component of cannabis (marijuana). E-cigarette use has rapidly increased among current and former smokers as well as youth who have never smoked. The long-term health effects are unknown, and emerging preclinical and clinical studies suggest that e-cigarettes may not be harmless and can cause cellular alterations analogous to traditional tobacco smoke. Here, we review the historical context and the components of e-cigarettes and discuss toxicological similarities and differences between cigarette smoke and e-cigarette aerosol, with specific reference to adverse respiratory outcomes. Finally, we outline possible clinical disorders associated with vaping on pulmonary health and the recent escalation of acute lung injuries, which led to the declaration of the vaping product use-associated lung injury (EVALI) outbreak. It is clear there is much about vaping that is not understood. Consequently, until more is known about the health effects of vaping, individual factors that need to be taken into consideration include age, current and prior use of combustible tobacco products, and whether the user has preexisting lung conditions such as asthma and chronic obstructive pulmonary disease (COPD).

Stable Ozonides with Vitamin E Acetate versus Corticosteroid in the Treatment of Lichen Sclerosus in Foreskin: Evaluation of Effects on Inflammation.

BACKGROUND: Lichen sclerosus (LS) is a disease of the skin of unclear etiology that can occur in the foreskin. Topical therapy with corticosteroids is recommended, but they can have side effects. OBJECTIVES: We aimed to compare the effects of ozonides with vitamin E acetate (OZOILE) versus topical corticosteroid in children undergoing circumcision. METHOD: Twenty children undergoing circumcision were treated before surgery: 10 children with OZOILE cream and 10 with 0.1% mometasone furoate once a day for 7 days. Ten age-matched patients with LS of the foreskin without any treatment were recruited as controls. Transcript levels of proinflammatory and anti-inflammatory cytokines and e-cadherin were evaluated in removed foreskins by qRT-PCR. RESULTS: OZOILE and steroid topical treatment produced a similar reduction of TNF-α and IL-1ß mRNA levels in foreskins from patients with LS when compared to untreated patients (p < 0.001). OZOILE and steroid treatment caused an increase in the transcript levels of IL-13 and e-cadherin in the foreskin of patients affected by LS in comparison to untreated foreskin (p < 0.001). CONCLUSIONS: On the basis of our biochemical data, a randomized clinical trial might be useful to verify the actual clinical effect of OZOILE as alternative treatment to corticosteroids in children affected by LS of the foreskin.

Anti-Inflammatory and Tissue Regenerative Effects of Topical Treatment with Ozonated Olive Oil/Vitamin E Acetate in Balanitis Xerotica Obliterans.

Balanitis xerotica obliterans (BXO) is a chronic inflammatory skin disorder, considered the male genital variant of lichen sclerosus. Anti-inflammatory drugs are commonly used in BXO. We evaluated the effects of an innovative formulation of ozonated olive oil with vitamin E acetate (OZOILE®) on the inflammatory status and tissue remodeling in male children with BXO. The mRNA transcripts of proteins involved either in inflammation or in dynamics of tissue regeneration were analyzed by quantitative real-time PCR, in foreskins affected by BXO removed from patients untreated or treated with OZOILE® cream for 7 days before circumcision. We found a significant reduction in mRNA levels of IL-1ß, TNF-α, INF-γ, transglutaminase 2 and NOS2 in foreskins treated with OZOILE® in comparison to untreated ones (p < 0.001). No significant differences were observed in NF-κB activation in the specimens obtained from treated and untreated patients. Hence, OZOILE® treatment up-regulated hypoxia-inducible factor (HIF)-1alpha, vascular endothelial growth factor (VEGF) and E-cadherin gene expression (p < 0.001). The treatment with OZOILE® showed effective results in children affected by BXO by reducing the inflammatory process and stimulating mechanisms for tissue regeneration of the foreskin. A randomized clinical trial on a large number of children affected by BXO might be useful to verify the efficacy of topical treatment with OZOILE®.

An in vitro evaluation of e-vapor products: The contributions of chemical adulteration, concentration, and device power.

Homemade e-liquids and power-adjustable vaping devices may carry higher risks than commercial formulations and fixed-power devices. This study used human macrophage-like and bronchial epithelial (NHBE) cell cultures to investigate toxicity of homemade e-liquids containing propylene glycol and vegetable glycerin (PG/VG), nicotine, vitamin E acetate (VEA), medium-chain fatty acids (MCFAs), phytol, and cannabidiol (CBD). SmallAir™ organotypic epithelial cultures were exposed to aerosols generated at different power settings (10-50 W). Carbonyl levels were measured, and endpoints reflecting epithelial function (ciliary beating frequency [CBF]), integrity (transepithelial electrical resistance [TEER]), and structure (histology) were investigated. Treatment with nicotine or VEA alone or with PG/VG did not impact cell viability. CBD, phytol, and lauric acid caused cytotoxicity in both culture systems and increased lipid-laden macrophages. Exposure of SmallAir™ organotypic cultures to CBD-containing aerosols resulted in tissue injury and loss of CBF and TEER, while PG/VG alone or with nicotine or VEA did not. Aerosols generated with higher power settings had higher carbonyl concentrations. In conclusion, the presence and concentration of certain chemicals and device power may induce cytotoxicity in vitro. These results raise concerns that power-adjustable devices may generate toxic compounds and suggest that toxicity assessments should be conducted for both e-liquid formulations and their aerosols.

The implications of Vitamin E acetate in E-cigarette, or vaping, product use-associated lung injury.

In the summer of 2019, a cluster of cases were observed with users of battery-operated or superheating devices presenting with multiple symptoms, such as dyspnea, cough, fever, constitutional symptoms, gastrointestinal upset, and hemoptysis, that is now termed e-cigarette, or vaping, product use-associated lung injury (EVALI). The Centers for Disease Control and Prevention reported 2807 cases within the USA leading to at least 68 deaths as of February 18, 2020. The heterogeneous presentations of EVALI make diagnosis and treatment difficult; however, treatment focused on identifying and removal of the noxious substance and providing supportive care. Vitamin E acetate (VEA) is a likely cause of this lung injury, and others have reported other components to play a possible role, such as nicotine and vegetable glycerin/propylene glycol. EVALI is usually observed in adolescents, with a history of vaping product usage within 90 days typically containing tetrahydrocannabinol, and presenting on chest radiograph with pulmonary infiltrates or computed tomography scan with ground-glass opacities. Diagnosis requires a high degree of suspicion to diagnose and exclusion of other possible causes of lung disease. Here, we review the current literature to detail the major factors contributing to EVALI and primarily discuss the potential role of VEA in EVALI. We will also briefly discuss other constituents other than just VEA, as a small number of EVALI cases are reported without the detection of VEA, but with the same clinical diagnosis.

Comparative study of lung toxicity of E-cigarette ingredients to investigate E-cigarette or vaping product associated lung injury.

No comparative study has yet been performed on the respiratory effects of individual E-cigarette ingredients. Here, lung toxicity of individual ingredients of E-cigarette products containing nicotine or tetrahydrocannabinol was investigated. Mice were intratracheally administered propylene glycol (PG), vegetable glycerin (VG), vitamin E acetate (VEA), or nicotine individually for two weeks. Cytological and histological changes were noticed in PG- and VEA-treated mice that exhibited pathophysiological changes which were associated with symptoms seen in patients with symptoms of E-cigarette or Vaping Use-Associated Lung Injuries (EVALI) or E-cigarette users. Compared to potential human exposure situations, while the VEA exposure condition was similar to the dose equivalent of VEA content in E-cigarettes, the PG condition was about 47-137 times higher than the dose equivalent of the daily PG intake of E-cigarette users. These results reveal that VEA exposure is much more likely to cause problems related to EVALI in humans than PG. Transcriptomic analysis revealed that PG exposure was associated with fibrotic lung injury via the AKT signaling pathway and M2 macrophage polarization, and VEA exposure was associated with asthmatic airway inflammation via the mitogen-activated protein kinase signaling pathway. This study provides novel insights into the pathophysiological effects of individual ingredients of E-cigarettes.

Cannabidiol and Δ8-Tetrahydrocannabinol: Cannabinoids of Rising Interest and Concern.

Although much is known about Δ9-tetrahydrocannabinol and its inactive open ring isomer, cannabidiol, far less is known about the effects, metabolism, and pharmacodynamics of Δ9-tetrahydrocannabinol's double-bond isomer, Δ8-tetrahydrocannabinol. With the passage of the so-called United States "Farm Bill," which was made law in order to allow legal hemp cultivation in the United States, more needs to be known about the effects of Δ8-tetrahydrocannabinol, a double-bond isomer of Δ9-tetrahydrocannabinol, and cannabidiol (CBD), which is an open-ring isomer of Δ8-tetrahydrocannabinol. It is the aim of the review to summarize current knowledge of Δ8-tetrahydrocannabinol and CBD, including the pharmacodynamics and pharmacokinetics of CBD. Also, plant genetics, the effect of cannabinoids on the current topic of viral entry into mammalian cells, and the current practice of vaping, dabbing, and dripping are covered.

Can social media monitoring help identify the next EVALI? An examination of Reddit posts about vitamin E acetate and Dank Vapes.

BACKGROUND: Scientists identified vitamin E acetate (VEA) and "Dank Vapes" (a fake brand of tetrahydrocannabinol [THC] vaping products) as contributors to the 2019-2020 outbreak of e-cigarette, or vaping, product use-associated lung injury (EVALI). On social media, people who post about vaping or THC discussed the causes of EVALI. We examined whether Reddit conversations may have served as early signals of the outbreak. METHODS: We collected Reddit posts from March 2018 to February 2020 on vaping- and THC-related subreddits that mentioned VEA or Dank Vapes. We identified peaks in post volume, examined post content, and used natural language processing to identify terms most characteristic of posts. RESULTS: There were almost no posts about VEA before EVALI. Subsequently, there were two peaks, both referencing media coverage of scientific findings that linked VEA to EVALI. Discussion regularly referenced concerns about the legitimacy of Dank Vapes before EVALI; peaks in posts were largely unrelated to scientific findings or media coverage of those findings. The terms most characteristic of VEA posts were EVALI-related; those most characteristic of Dank Vapes posts were about quality or legitimacy. CONCLUSIONS: Although posts about VEA and Dank Vapes did not predict the outbreak, the public health community could use social media to encourage people who vape or use THC to report future health concerns (e.g., through FDA's Safety Reporting Portal). Researchers and regulators could also use social media to see if potentially problematic products, such as Dank Vapes, have a history of concern among individuals who use those products.

Adolescent e-cigarette or vaping product use-associated lung injury: A case series and review of the literature.

BACKGROUND: Adolescent e-cigarette or vaping product use-associated lung injury (EVALI) has increased in prevalence, and while cases describing various pulmonary manifestations have been reported, reports on the presentations and outcomes in teenage patients are sparse. METHODS: We retrospectively describe eight EVALI patients with different presentations, laboratory and imaging findings, treatment, and concomitant diagnoses. We review the literature and describe how our analysis adds to the literature. FINDINGS: Eight males, aged 15-18 years of age presented with various symptoms. Four patients were Caucasian while four were of Hispanic origin. All patients presented with respiratory symptoms; six also had GI symptoms; five were hypoxemic; all but one patient admitted to using products containing tetrahydrocannabinol (THC). All patients had changes on imaging with ground-glass opacities. One patient underwent lung biopsy and bronchoscopy showing eosinophilic pneumonia. All patients received antimicrobial therapies without improvement until systemic steroids were administered. Six patients underwent pulmonary function testing, and five required medications for newly diagnosed persistent asthma. One patient developed pulmonary hypertension, which resolved after treatment. One patient required noninvasive ventilation. No patients were positive for SARS-CoV2. Two had coinfections with other microbes. Five patients required escalation of asthma therapies at follow-up with pulmonology. CONCLUSION: This analysis of eight adolescent males hospitalized for EVALI highlights the unpredictable spectrum of disease presentation and management. These patients can be misdiagnosed without proper screening and may have residual respiratory complications necessitating outpatient management by a pulmonologist.

Analysis of the Aerosol Generated from Tetrahydrocannabinol, Vitamin E Acetate, and Their Mixtures.

E-cigarette, or vaping, product use-associated lung injury (EVALI) outbreak was linked to vitamin E acetate (VEA) used as a solvent for tetrahydrocannabinol (THC). Several studies were conducted to assess the products of VEA (and THC/VEA mixtures) thermal degradation as a result of vaporizing/aerosolizing from a traditional type (coil-cotton wick) and ceramic type coil vape pens. The particle size distribution (PSD) of VEA aerosol and the temperature VEA and THC/VEA mixtures are heated to were also measured for a few types of traditional and ceramic vape pens. The current study assessed the PSD of the aerosol generated from THC, VEA, and a number of THC/VEA mixtures using a dab-type vape pen under two different temperature settings and two puffing flow rates. Thermal degradation of THC, VEA, and THC/VEA mixtures were also assessed, and coil temperature was measured. Results showed the dependence of the PSD upon the chemical content of the aerosolized mixture as well as upon the puffing flow rate. Minimal thermal degradation was observed. Flaws in the vape pen's design, which most likely affected results, were detected. The suitability of VEA, THC, and THC/VEA mixtures with certain types of vape pens was discussed.

Examining the temporality of vitamin E acetate in illicit THC-containing e-cigarette, or vaping, products from a public health and law enforcement response to EVALI - Utah, 2018-2020.

BACKGROUND: In the summer of 2019, e-cigarette, or vaping, product use-associated lung injury (EVALI) was detected in the United States. Multiple agencies reported illicit tetrahydrocannabinol (THC)-containing e-cigarette, or vaping, products containing vitamin E acetate (VEA) as a substance of concern. METHODS: As an expansion of the Utah Department of Health's response to EVALI, the Utah Public Health Laboratory and the Utah Department of Public Safety screened 170 products from 96 seizures between October 2018 and January 2020. Using Pearson's correlation coefficient, we analyzed the temporal correlation of national, and Utah specific case counts, and the percentage of seizures indicating VEA by month. RESULTS: The findings indicate strong and significant correlations between seizures indicating VEA and both the national (r = 0.70, p = 0.002) and Utah specific (r = 0.78, p < 0.001) case counts. CONCLUSION: These findings underscore that VEA should not be added to e-cigarettes, or vaping, products and the importance of collaboration with law enforcement when responding to outbreaks associated with illicit substances.