Woodsmoke marker levoglucosan: Kinetics in a self-experiment

Moshammer, Hanns; Weiß, Stefan; Neuberger, Manfred

doi:10.2478/s13382-012-0023-9

Cited by 7 publications

(2 citation statements)

References 10 publications

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“…59 Review of the nicotine levels in teabacco demonstrated that teabacco is on a similar scale to commercial tobacco with respect to (Z)-9-Octadecenamide Nicotine lozengedispersion aid in surface coatings. 43 Not toxic 1,6-Anhydro-β-D-Glucopyranose Bible paper and teapyrolysis of carbohydrates, such as starch 85 and cellulose 86,87 Not toxic, 44 excreted in urine 88…”

Section: Identification Of Compounds By Gc-msmentioning

confidence: 99%

Constituents of “teabacco”: A forensic analysis of cigarettes made from diverted nicotine replacement therapy lozenges in smoke‐free prisons

Mitchell

Puljević

Coomber

et al. 2018

Drug Testing and Analysis

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Following the implementation of prison smoke-free policies, there have been reports of prisoners creating substitute cigarettes made from nicotine replacement therapy patches or lozenges infused with tea leaves ("teabacco"). No studies have analyzed the chemical constituents of teabacco made from nicotine lozenges, so as to document any potential related health hazards. Teabacco samples were made by a participant who reported creating teabacco while incarcerated in a smoke-free prison in Queensland, Australia, and the process was video-recorded for replication in a laboratory. A simple linear smoking system captured the teabacco smoke for analysis. Inductively coupled plasma optical emission spectroscopy (ICP-OES) was used to analyze elemental composition and gas chromatography coupled with a mass spectrometer (GC-MS) analyzed the captured smoke using the National Institute of Standards and Technology mass spectral library. Analyses determined that quantities of copper, aluminum, and lead concentrations, and levels of inhaled total particulate matter, were above recommended guidelines for safe ingestion. Analysis of teabacco smoke using GC-MS identified potentially toxic compounds catechol and nicotine. However, our findings show that smoking this form of teabacco is less harmful than smoking teabacco made from nicotine patches, or smoking traditional tobacco cigarettes. Considering the limited potential health harm of smoking teabacco made from lozenges, and that nicotine lozenges represent the only form of smoking cessation support for individuals entering smoke-free prisons, we caution against the removal of nicotine lozenges from Queensland's prisons, at least until further research directly establishes health harms associated with this form of teabacco.

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Section: Identification Of Compounds By Gc-msmentioning

confidence: 99%

Constituents of “teabacco”: A forensic analysis of cigarettes made from diverted nicotine replacement therapy lozenges in smoke‐free prisons

Mitchell

Puljević

Coomber

et al. 2018

Drug Testing and Analysis

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“…Levoglucosan is generally considered non-toxic however its presence in biofluids, such as urine, has been suggested as a biomarker for WS exposure and thus exposure to more toxic compounds such as polyaromatic hydrocarbons 47 . However, levoglucosan has a short half-life in the body whereby >70% of it has been excreted within 7 hours of exposure 47 . Guaiacol, a methoxyphenol compound, is produced through the pyrolysis of lignin and has also been proposed as a marker of WS exposure.…”

Section: Discussionmentioning

confidence: 99%

Soluble Wood Smoke Extract Promotes Barrier Dysfunction in Alveolar Epithelial Cells through a MAPK Signaling Pathway

Zeglinski

Turner

Zhou

et al. 2019

Sci Rep

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Wildfire smoke induces acute pulmonary distress and is of particular concern to risk groups such as the sick and elderly. Wood smoke (WS) contains many of the same toxic compounds as those found in cigarette smoke (CS) including polycyclic aromatic hydrocarbons, carbon monoxide, and free radicals. CS is a well-established risk factor for respiratory diseases such as asthma and COPD. Limited studies investigating the biological effects of WS on the airway epithelium have been performed. Using a cell culture-based model, we assessed the effects of a WS-infused solution on alveolar epithelial barrier function, cell migration, and survival. The average geometric mean of particles in the WS was 178 nm. GC/MS analysis of the WS solution identified phenolic and cellulosic compounds. WS exposure resulted in a significant reduction in barrier function, which peaked after 24 hours of continuous exposure. The junctional protein E-cadherin showed a prominent reduction in response to increasing concentrations of WS. Furthermore, WS significantly repressed cell migration following injury to the cell monolayer. There was no difference in cell viability following WS exposure. Mechanistically, WS exposure induced activation of the p44/42, but not p38, MAPK signaling pathway, and inhibition of p44/42 phosphorylation prevented the disruption of barrier function and loss of E-cadherin staining. Thus, WS may contribute to the breakdown of alveolar structure and function through a p44/42 MAPK-dependent pathway and may lead to the development and/or exacerbation of respiratory pathologies with chronic exposure.

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