Ketenes comprise a unique class of cumulene molecules with the general formula RR'C=C=O. Initially described by Wedekind as a reactive intermediate in 1901, Staudinger reported the first synthesis and characterization of a ketene molecule, diphenyl ketene (R=R'=Ph), in 1905. Since that time, despite their relative instability, ketenes have served as valuable reagents and intermediates in organic synthesis. Currently, however, the smallest homolog (R=R'=H, ketene, ethenone) of the series is receiving attention as a potentially significant public health hazard, since it has been identified in aerosols generated by commercial vaping products. The chemical and toxicological properties of ketene mirror those of phosgene (Cl 2 C=O), a WW-I chemical warfare agent, as a reactive acylating agent and respiratory poison. There is a lack of human toxicity data for ketene exposure. The available animal data was obtained mainly prior to 1950. Exposure to animals causes alveolar damage and a delayed onset of pulmonary toxicity leading to death by pulmonary edema. Similar to phosgene, the delayed effects result from the non-enzymatic acylation of lung proteins, as opposed to direct irritation. The Acute Exposure Guideline Levels (AEGL)-3 (life-threatening levels) for ketene are 0.24 ppm for 10 min and 0.088 ppm for 8 h. Vitamin E acetate (VEA) has been linked to the 2019-2020 e-cigarette or vaping product use-associated lung injury (EVALI) epidemic, in large part due to VEA's prevalence in patient samples. In 2020, Wu and O'Shea reported the formation of ketene when heating and vaping VEA, indicating an additional possible link between ketene and EVALI. There is general agreement that EVALI is caused by chemical toxicant inhalation. However, to date, neither ketene, VEA, nor any other specific chemical has been conclusively proven to be the causative agent of EVALI. Moreover, although there has been a significant decline since 2020, cases continue to be observed throughout the US. Regardless of whether VEA-derived ketene is a primary cause of EVALI, any source of exposure to ketene may put one at risk for significant lung injury. Recently, we reported that four acetylated cannabinoids (acetylated ∆ 8 -and ∆ 9 -THC, CBN, and CBD; Figure ), produce ketene emissions under real-world vaping conditions, from either a vape pen or dab platform, including at levels in range of NIOSH (National Institute for Occupational Safety & Health) thresholds. Interestingly, aerosolized THC products had been reported to cause acute respiratory syndromes prior to the EVALI outbreak. 11 The strong experimental evidence for ketene emissions arising from vaping cannabinoid acetates or VEA raises two issues. First, since ketene is too reactive and shortlived to be characterized as an intact molecule under common laboratory conditions, vaping studies to date have employed the well-known method of trapping ketene with a nucleophile (i.e., benzylamine) for characterization as the corresponding N-benzylacetamide. Since amines are relatively non-selective reagents, their use for ketene trapping and determination should ideally be limited to relatively well-defined systems that do not contain molecules that can react to form the same N-benzylacetamide product as ketene. However, manufacturers are not required to disclose most vaping product ingredients and, moreover, heating and vaping produces aerosols containing complex chemical mixtures.