Citations

Abstract Rationale Secondhand exposure to electronic nicotine products is driven by exhaled emissions. Eliminating heat and combustion may reduce exhaled toxic carbonyls. Methods In a 4-day within-subject crossover, six adults each used four devices after 24-hour abstinence: an NHNC nebulization device (Bluesky), a coil-heated ENDS (RELX), a heated-tobacco device (IQOS), and a heated aerosol device (Marlboro). For each condition, paired pre-use exhaled blank and post-use exhaled samples were collected; 50 L of exhaled breath was captured post-use. Nicotine and 12 carbonyls were quantified (DNPH/activated-carbon with HPLC). Primary endpoint: within-subject change (Δ, post-pre) in total carbonyls (μg/50 L). Secondary: Δ acetaldehyde and Δ acrolein. Results The exhaled carbonyls(within-subject change, post-pre) in total differed markedly across devices: Bluesky (non-heated, non-combustion; NHNC) 0.85 ± 6.99, RELX 4.41 ± 2.58, IQOS 62.38 ± 21.77, Marlboro 80.73 ± 20.24 (p = 0.0015). Bluesky had significantly lower total exhaled carbonyls than IQOS (p = 0.0077) and Marlboro (p = 0.0021, μg/50 L; mean±SD), with a nonsignificant trend versus RELX (p = 0.945). For acetaldehyde, Bluesky was lower than all three (Bluesky 0.20 ± 0.16 vs. RELX 1.93 ± 0.86, p = 0.016; vs IQOS 43.08 ± 16.70, p = 0.0044; vs Marlboro 65.40 ± 13.69, p = 0.00025, μg/50 L). For acrolein, average exhaled volume was 0.54 ± 6.94 (Bluesky), 1.35 ± 2.05 (RELX), 7.94 ± 6.07 (IQOS), and −1.86 ± 5.09 (Marlboro); pairwise differences vs Bluesky were not significant after correction (p ≥ 0.37, μg/50 L). Conclusions In a controlled, within-subject comparison using exhaled breath as a proxy for secondhand aerosol, the NHNC nebulization device (Bluesky) produced near-zero average increment in total exhaled carbonyls, whereas heated devices—particularly heated-tobacco—showed order-of-magnitude higher increases. These descriptive data support the hypothesis that removing heat and combustion from nicotine aerosolization can materially reduce exhaled carbonyl burden relevant to secondhand exposure. Larger, randomized studies with standardized capture and enhanced nicotine quantification are warranted. This abstract is funded by: Pneuma Respiratory.Inc

Type 2 diabetes is an emerging global health epidemic. Foundations for new therapies are arising from understanding interactions between body systems. Bone‐derived factors that reduce RANKL (receptor activator of NF‐kappa B ligand) signaling in the liver may prevent insulin resistance and the onset of type 2 diabetes. Here we demonstrate that deletion of the epigenetic regulator, Hdac3, in Osx1‐expressing osteoprogenitors prevents insulin resistance induced by high fat diet by increasing serum and skeletal gene expression levels of osteoprotegerin (Opg), a natural inhibitor of RANKL signaling. Removal of one Opg allele in mice lacking Hdac3 in Osx1+ osteoprogenitors increases the insulin resistance of the Hdac3‐deficient mice on a high fat diet. Thus, Hdac3‐depletion in osteoblasts increases expression of Opg, subsequently preserving insulin sensitivity. The Hdac inhibitor vorinostat also increased Opg transcription and histone acetylation of the Opg locus. These results define a new mechanism by which bone regulates systemic insulin sensitivity.