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Background:There are > 7,000 e-cigarette flavors currently marketed. Flavoring chemicals gained notoriety in the early 2000s when inhalation exposure of the flavoring chemical diacetyl was found to be associated with a disease that became known as “popcorn lung.” There has been limited research on flavoring chemicals in e-cigarettes.Objective:We aimed to determine if the flavoring chemical diacetyl and two other high-priority flavoring chemicals, 2,3-pentanedione and acetoin, are present in a convenience sample of flavored e-cigarettes.Methods:We selected 51 types of flavored e-cigarettes sold by leading e-cigarette brands and flavors we deemed were appealing to youth. E-cigarette contents were fully discharged and the air stream was captured and analyzed for total mass of diacetyl, 2,3-pentanedione, and acetoin, according to OSHA method 1012.Results:At least one flavoring chemical was detected in 47 of 51 unique flavors tested. Diacetyl was detected above the laboratory limit of detection in 39 of the 51 flavors tested, ranging from below the limit of quantification to 239 μg/e-cigarette. 2,3-Pentanedione and acetoin were detected in 23 and 46 of the 51 flavors tested at concentrations up to 64 and 529 μg/e-cigarette, respectively.Conclusion:Because of the associations between diacetyl and bronchiolitis obliterans and other severe respiratory diseases observed in workers, urgent action is recommended to further evaluate this potentially widespread exposure via flavored e-cigarettes.Citation:Allen JG, Flanigan SS, LeBlanc M, Vallarino J, MacNaughton P, Stewart JH, Christiani DC. 2016. Flavoring chemicals in e-cigarettes: diacetyl, 2,3-pentanedione, and acetoin in a sample of 51 products, including fruit-, candy-, and cocktail-flavored e-cigarettes. Environ Health Perspect 124:733–739; http://dx.doi.org/10.1289/ehp.1510185

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Lipids of the renal cortex and outer stripe of outer medulla were analyzed in rats during ischemia and 2 hr after blood reflow. After 15 min of ischemia, there were marked elevations of free fatty acids (FFA) and diacylglycerol (DG), increasing further at 60 min. Percentile increases were greater for polyunsaturated FFA. These elevations were accompanied by alterations in phospholipids (PL): Elevations of lysophosphatidylcholine (LPC) at 15 min, phosphatidic acid at 15 and 60 min, and declines of phosphatidylcholine and phosphatidylinositol at 60 min. Triacylglycerol (TG) showed only modest decline, at 60 min, and in insufficient degree to account for increments in FFA and DG. Two hours after 15 min of ischemia, LPC returned to control levels and other PL were normal except phosphatidylinositol which was decreased, and phosphatidic acid, which remained elevated. FFA and DG approached or reached control values. Two hours after 60 min of ischemia, LPC, FFA, DGs and phosphatidic acid remained elevated; phosphatidylcholine and phosphatidylinositol remained decreased. Histological injury was seen 2 and 24 hr after blood reflow only in kidneys injured by 60 min of ischemia. Thus, irreversible ischemic damage correlates with persistent abnormalities of phosphatidylcholine metabolism and persistent elevations of FFA, LPC, and DG. It is not known whether lipids break down at normal or accelerated rates during ischemia. In this context, accumulation of lipid breakdown products in ischemic cells may be due to failure of their reutilization, or disposal. Similarly, depletion of phospholipids during ischemia may be due to the inability of cells to reconstitute the lipid following degradation.(ABSTRACT TRUNCATED AT 250 WORDS)

Further evaluation of workplace exposures or independent investigations of similar occupational groups may clarify the interpretation of associations observed in this study.