No acute effects of an exposure to 50 ppm acetaldehyde on the upper airways

Muttray, Axel; Gosepath, Jan; Brieger, Jürgen; Faldum, Andreas; Pribisz, A.; Mayer-Popken, Otfried; Jung, Detlev; Roßbach, Bernd; Mann, Wolf J.; Letzel, Stephan

doi:10.1007/s00420-008-0354-9

Cited by 12 publications

(4 citation statements)

References 41 publications

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“…148 AA is produced during the manufacture of numerous industrial products including many plastics and synthetic rubber. 149 It is also found in tobacco smoke and formed endogenously through the action of alcohol dehydrogenase 1B (ALDH1B) following ethanol consumption. 150 AA can then be detoxified to acetic acid by ALDH2.…”

Section: Acrolein (Vi)mentioning

confidence: 99%

DNA Adducts as Biomarkers To Predict, Prevent, and Diagnose Disease—Application of Analytical Chemistry to Clinical Investigations

Hernandez-Castillo

Termini

Shuck

2019

Chem. Res. Toxicol.

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Characterization of the chemistry, structure, formation, and metabolism of DNA adducts has been one of the most significant contributions to the field of chemical toxicology. This work provides the foundation to develop analytical methods to measure DNA adducts, define their relationship to disease, and establish clinical tests. Monitoring exposure to environmental and endogenous toxicants can predict, diagnose, and track disease as well as guide therapeutic treatment. DNA adducts are one of the most promising biomarkers of toxicant exposure owing to their stability, appearance in numerous biological matrices, and characteristic analytical properties. In addition, DNA adducts can induce mutations to drive disease onset and progression and can serve as surrogate markers of chemical exposure. In this perspective, we highlight significant advances made within the past decade regarding DNA adduct quantitation using mass spectrometry. We hope to expose a broader audience to this field and encourage analytical chemistry laboratories to explore how specific adducts may be related to various pathologies. One of the limiting factors in developing clinical tests to measure DNA adducts is cohort size; ideally, the cohort would allow for model development and then testing of the model to the remaining cohort. The goals of this perspective article are to (1) provide a summary of analyte levels measured using state-of-the-art analytical methods, (2) foster collaboration, and (3) highlight areas in need of further investigation. 289 10. Crotonaldehyde (CrA, VII) and Acetaldehyde (AA, VIII) 290 11. 4-Aminobiphenyl (4-ABP, IX) 290 12. 1,3-Butadiene (BD, X) 290 13. 4-Hydroxy-nonenal (HNE, XI) and 4-Oxo-nonenal (ONE, XII) 293 14. Benzene (XIII) 294 15. Benzo[a]pyrene (BP, XIV) 294 16. Aflatoxin (AFB1, XV) 295 17. 4-(Methylnitrosamino)-1-(3-pyridyl)-butanone (NNK, XVI) and N′-Nitrosonornicotine (NNN, XVII) 295 18. Aristolochic Acid (XVIII) 295 19.

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Section: Acrolein (Vi)mentioning

confidence: 99%

DNA Adducts as Biomarkers To Predict, Prevent, and Diagnose Disease—Application of Analytical Chemistry to Clinical Investigations

Hernandez-Castillo

Termini

Shuck

2019

Chem. Res. Toxicol.

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“…The following parameter were investigated: mucociliary transport time before and after exposure, interleukin-1β and interleukin 8 in nasal secretions, as well as mRNA-levels of interleukins-1β, 6 and 8, tumor necrosis factor- α, granulocyte-macrophage colony-stimulating factor, monocyte chemotactic protein 1, and cyclooxygenases 1 and 2 in nasal epithelial cells were measured after exposure (Muttray et al 2009). …”

Section: Part 3: Recommendation For the Derivation Of Occupational Exmentioning

confidence: 99%

Sensory irritation as a basis for setting occupational exposure limits

Bartsch²,

et al. 2014

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There is a need of guidance on how local irritancy data should be incorporated into risk assessment procedures, particularly with respect to the derivation of occupational exposure limits (OELs). Therefore, a board of experts from German committees in charge of the derivation of OELs discussed the major challenges of this particular end point for regulatory toxicology. As a result, this overview deals with the question of integrating results of local toxicity at the eyes and the upper respiratory tract (URT). Part 1 describes the morphology and physiology of the relevant target sites, i.e., the outer eye, nasal cavity, and larynx/pharynx in humans. Special emphasis is placed on sensory innervation, species differences between humans and rodents, and possible effects of obnoxious odor in humans. Based on this physiological basis, Part 2 describes a conceptual model for the causation of adverse health effects at these targets that is composed of two pathways. The first, “sensory irritation” pathway is initiated by the interaction of local irritants with receptors of the nervous system (e.g., trigeminal nerve endings) and a downstream cascade of reflexes and defense mechanisms (e.g., eyeblinks, coughing). While the first stages of this pathway are thought to be completely reversible, high or prolonged exposure can lead to neurogenic inflammation and subsequently tissue damage. The second, “tissue irritation” pathway starts with the interaction of the local irritant with the epithelial cell layers of the eyes and the URT. Adaptive changes are the first response on that pathway followed by inflammation and irreversible damages. Regardless of these initial steps, at high concentrations and prolonged exposures, the two pathways converge to the adverse effect of morphologically and biochemically ascertainable changes. Experimental exposure studies with human volunteers provide the empirical basis for effects along the sensory irritation pathway and thus, “sensory NOAEChuman” can be derived. In contrast, inhalation studies with rodents investigate the second pathway that yields an “irritative NOAECanimal.” Usually the data for both pathways is not available and extrapolation across species is necessary. Part 3 comprises an empirical approach for the derivation of a default factor for interspecies differences. Therefore, from those substances under discussion in German scientific and regulatory bodies, 19 substances were identified known to be human irritants with available human and animal data. The evaluation started with three substances: ethyl acrylate, formaldehyde, and methyl methacrylate. For these substances, appropriate chronic animal and a controlled human exposure studies were available. The comparison of the sensory NOAEChuman with the irritative NOAECanimal (chronic) resulted in an interspecies extrapolation factor (iEF) of 3 for extrapolating animal data concerning local sensory irritating effects. The adequacy of this iEF was confirmed by its application to additional substances with lower data density (acet...

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“…Acetaldehyde toxicity has also been reviewed in several publications. Eye irritation has been reported in human volunteers exposed to acetaldehyde concentrations of as low as 50 ppm, while nose and throat irritation was also reported in individuals after exposure to acetaldehyde at concentrations typically greater than 100-200 ppm [23][24][25]. Limited information is available on the health effects of propionaldehyde.…”

Section: Introductionmentioning

confidence: 99%

An Unrecognized Hazard in E-Cigarette Vapor: Preliminary Quantification of Methylglyoxal Formation from Propylene Glycol in E-Cigarettes

Azimi

Keshavarz

Luna

et al. 2021

IJERPH

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Up to 95% of the liquid volume in an e-cigarette consists of propylene glycol. Previous research has shown that propylene glycol can generate diacetyl and formaldehyde when heated. New research shows that propylene glycol can also generate methylglyoxal, an alpha di-carbonyl compound recently shown to cause epithelial necrosis at even lower concentrations than diacetyl, the flavoring chemical associated with bronchiolitis obliterans (“Popcorn Lung”). We analyzed chemical emissions from 13 JUUL pod flavors. Diacetyl and methylglyoxal was detected in 100% of samples with median concentration (range) of 20 µg/m3 (less than limit of quantification: 54 µg/m3) and 4219 µg/m3 (677–15,342 µg/m3), respectively. We also detected acetaldehyde (median concentration: 341 µg/m3) and propionaldehyde (median concentration: 87 µg/m3) in all samples. The recent evidence that methylglyoxal is more cytotoxic to airway epithelial cells than diacetyl makes this an urgent public health concern. Current smokers considering e-cigarettes as a smoking cessation tool, and never users, who may be under the impression that e-cigarettes are harmless, need information on emissions and potential risks to make informed decisions.

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No acute effects of an exposure to 50 ppm acetaldehyde on the upper airways

Abstract: An acute exposure to 50 ppm acetaldehyde did not cause any adverse effects in test subjects.

Cited by 12 publications

References 41 publications

DNA Adducts as Biomarkers To Predict, Prevent, and Diagnose Disease—Application of Analytical Chemistry to Clinical Investigations

DNA Adducts as Biomarkers To Predict, Prevent, and Diagnose Disease—Application of Analytical Chemistry to Clinical Investigations

Sensory irritation as a basis for setting occupational exposure limits

An Unrecognized Hazard in E-Cigarette Vapor: Preliminary Quantification of Methylglyoxal Formation from Propylene Glycol in E-Cigarettes

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