Microbial Toxins in Nicotine Vaping Liquids

Lee, Mi-Sun; Christiani, David C.

doi:10.1164/rccm.201911-2178le

Cited by 4 publications

(2 citation statements)

References 3 publications

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“…The demonstration of the toxicity of VEA does not exclude the possibility of other interacting insults in patients with EVALI, which may include subclinical toxicity from nicotine-containing e-cigarettes (35), microbial or toxin contamination of the devices (36), and the ongoing use of combustible marijuana or tobacco products (37). Moreover, the lack of direct lung injury observed with brief exposures to aerosol from nicotine pod devices (JUUL) should not be interpreted as evidence of their safety.…”

Section: Discussionmentioning

confidence: 99%

Dose-Dependent Pulmonary Toxicity of Aerosolized Vitamin E Acetate

Matsumoto

Fang

Traber³

et al. 2020

Am J Respir Cell Mol Biol

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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.

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Section: Discussionmentioning

confidence: 99%

Dose-Dependent Pulmonary Toxicity of Aerosolized Vitamin E Acetate

Matsumoto

Fang

Traber³

et al. 2020

Am J Respir Cell Mol Biol

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“…Some of these factors have been found to play a major role in the formation of toxins, such as the production of high levels of formaldehyde with the application of high wattage or high temperature (8,9) and production of carbonyls with combinations of wick length and coil design (10). Toxic metals and other substances have also been detected in e-liquids and e-cigarette aerosols, which may be due to the materials used to make the devices (11)(12)(13)(14)(15)(16)(17)(18)(19) (Figure 1).…”

Section: The Spectrum Of Vaping Exposuresmentioning

confidence: 99%

Vaping and Lung Inflammation and Injury

Park

Alexander

Christiani

2022

Annu. Rev. Physiol.

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The use of electronic (e)-cigarettes was initially considered a beneficial solution to conventional cigarette smoking cessation. However, paradoxically, e-cigarette use is rapidly growing among nonsmokers, including youth and young adults. In 2019, this rapid growth resulted in an epidemic of hospitalizations and deaths of e-cigarette users (vapers) due to acute lung injury; this novel disease was termed e-cigarette or vaping use-associated lung injury (EVALI). Pathophysiologic mechanisms of EVALI likely involve cytotoxicity and neutrophilic inflammation caused by inhaled chemicals, but further details remain unknown. The undiscovered mechanisms of EVALI are a barrier to identifying biomarkers and developing therapeutics. Furthermore, adverse effects of e-cigarette use have been linked to chronic lung diseases and systemic effects on multiple organs. In this comprehensive review, we discuss the diverse spectrum of vaping exposures, epidemiological and clinical reports, and experimental findings to provide a better understanding of EVALI and the adverse health effects of chronic e-cigarette exposure. Expected final online publication date for the Annual Review of Physiology, Volume 84 is February 2022. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.

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