Reducing toxic reactive carbonyl species in e-cigarette emissions: testing a harm-reduction strategy based on dicarbonyl trapping

Abstract

Reducing the concentration of reactive carbonyl species (RCS) in e-cigarette emissions represents a major goal to control their potentially harmful effects. Here, we adopted a novel strategy of trapping carbonyls present in e-cigarette emissions by adding polyphenols in e-liquid formulations. Our work showed that the addition of gallic acid, hydroxytyrosol and epigallocatechin gallate reduced the levels of carbonyls formed in the aerosols of vaped e-cigarettes, including formaldehyde, methylglyoxal and glyoxal. Liquid chromatography mass spectrometry analysis highlighted the formation of covalent adducts between aromatic rings and dicarbonyls in both e-liquids and vaped samples, suggesting that dicarbonyls were formed in the e-liquids as degradation products of propylene glycol and glycerol before vaping. Short-term cytotoxic analysis on two lung cellular models showed that dicarbonyl-polyphenol adducts are not cytotoxic, even though carbonyl trapping did not improve cell viability. Our work sheds lights on the ability of polyphenols to trap RCS in high carbonyl e-cigarette emissions, suggesting their potential value in commercial e-liquid formulations.

Fig. 1. Heat-map showing the concentration of carbonyls and dicarbonyls in the aerosols of vaped e-cigarettes after addition of phenolic compounds in the e-liquid formulations. The addition of polyphenols reduced carbonyl and dicarbonyl concentration in the corresponding aerosols. Data were subjected to one-way ANOVA and significant differences (P ≤ 0.05) between means were determined using Tukey's test. Lowercase letters denote differences between treatments for each reactive carbonyl species. Each block is the mean value of three replicates ± SE, n = 3. C, control (model e-liquid system); EGCG, epigallocatechin gallate; nd, not detected; ns, not significant. Other carbonyls were area summed from known and unknown peaks as previously reported by Stephens et al., 2019. Boxes without letters, below limit of quantification.

Fig. 2. The reduction of polyphenols in the e-liquid (SEL) and aerosol condensate samples. GA, gallic acid; HT, hydroxytyrosol, EGCG, epigallocatechin gallate.

Fig. 3. Molecular structures and their exact masses of hypothesized adducts. Abbreviations used: HT, hydroxytyrosol, EGCG, epigallocatechin gallate, DOPAL, 3,4-dihydroxyphenylacetaldehyde, GO, glyoxal, MGO, methylglyoxal.

Fig. 4. The formation of adducts between phenolic compounds and dicarbonyls in e-liquid (SEL) and aerosol condensate samples after addition of phenolic compounds in the e-liquid formulations. DOPAL, 3,4-dihydrophenyl-acetaldehyde; EGCG, epigallocatechin gallate; GA, gallic acid; GO, glyoxal; MGO, methylglyoxal.

Fig. 5. Putative pathway leading to the formation of the epigallocatechin gallate adduct (m/z [M − H]⁻ 567) as degradation product of the EGCG plus two methylglyoxal residues.

Fig. 6. Short-term cytotoxic effect of e-cigarette aerosols on two lung cellular models, alveolar (A549) and bronchial (BEAS-2B) cell lines. Data were subjected to one-way ANOVA and significant differences (P ≤ 0.05) between means were determined using Tukey's test. Asterisks indicate differences between treatments of the same dilution in relation to the control water. Bars are the mean value of three replicates ± SE, n = 3. CC, condensed control; EGCG, epigallocatechin gallate; GA, gallic acid; HT, hydroxytyrosol.