Based on samples tested in this study, many contain misleading information on product ingredients. The results show poor consistency between actual nicotine content analysed on ENDS cartridges and the amount labelled. These findings raise safety and efficacy concerns for current and would-be recreational users or those trying to quit smoking.

X-ray and neutron diffraction have been used to investigate the formation of solid crystalline monolayers of all of the linear carboxylic acids from C(6) to C(14) at submonolayer coverage and from C(8) to C(14) at multilayer coverages, and to characterize their structures. X-rays and neutrons highlight different aspects of the monolayer structures, and their combination is therefore important in structural determination. For all of the acids with an odd number of carbon atoms, the unit cell is rectangular of plane group pgg containing four molecules. The members of the homologous series with an even number of carbon atoms have an oblique unit cell with two molecules per unit cell and plane group p2. This odd-even variation in crystal structure provides an explanation for the odd-even variation observed in monolayer melting points and mixing behavior. In all cases, the molecules are arranged in strongly hydrogen-bonded dimers with their extended axes parallel to the surface and the plane of the carbon skeleton essentially parallel to the graphite surface. The monolayer crystal structures have unit cell dimensions similar to certain close-packed planes of the bulk crystals, but the molecular arrangements are different. There is a 1-3% compression on increasing the coverage over a monolayer.

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Solid monolayer formation by all the linear carboxylic acids from C 6 to C 20 adsorbed from their liquids to a graphite surface is demonstrated. In addition, we present the two-dimensional phase behaviour of linear monocarboxylic acid mixtures adsorbed on graphite from their liquid mixtures, determined using differential scanning calorimetry. All acid mixtures with alkyl chains that differ by two or three methylene groups (Dn ¼ 2 or 3) exhibit a significant degree of phase separation in the monolayer. Generally, the mixing tendency increases with increasing alkyl chain length for a given Dn, and with more similar chain lengths (e.g. Dn ¼ 1). We report neutron diffraction data that confirms the formation of solid acid monolayers. This structural data also allows us to compare the mixing results with a recent quantitative model for 2-D mixing. The general form of the observed behaviour agrees well with the model, although the characteristic parameters that separate complete mixing, partial mixing and phase separation are different from those found with alkane and alcohol monolayer mixtures.

Solid monolayer formation by all the linear amines from C6 to C16 adsorbed from their liquids to a graphite surface is demonstrated. Shorter homologues do not show such solid monolayer formation. The behavior is interpreted in terms of the competition between the alkyl chains, which favor solid monolayer formation, and the amine group, which does not. Nonylamine (C9) also shows evidence of a solid−solid phase transition in the monolayer prior to melting.

Objectives: Sugars in tobacco products enhance the taste and smoke characteristics of the blend. Sugars are often added to processed tobacco, particularly air-cured Burley tobacco leaves that contain virtually no sugars. The most commonly used sugars were systematically added to Burley tobacco to study the effect on aldehyde emissions in mainstream smoke. Methods: Two levels of sucrose, glucose, and fructose were added to Burley tobacco. Formaldehyde, acetaldehyde, acetone, acrolein, crotonaldehyde, propionaldehyde, and butanal in mainstream smoke were sampled on Carboxen 572 cartridges and determined by HPLC-DAD. Results: The addition of sugars to Burley tobacco resulted in an increase of the aldehydes acetaldehyde, acrolein, crotonaldehyde, propionaldehyde, and butanal in the mainstream tobacco smoke. This increase is specific, as much lower increases in tar, nicotine, and carbon monoxide levels were observed. The observed aldehyde level increases ranged from 5% to 40%. The increase was higher after the addition of fructose compared to sucrose and glucose. Conclusions: Sugars added to Burley tobacco increase the emissions of aldehydes, an important class of toxicants in tobacco smoke. Limiting sugars levels in processed tobacco may be an effective approach in tobacco product regulation to reduce the attractiveness of smoking, and the toxicants levels in cigarette smoke.

Tobacco use is associated with heart and respiratory diseases and also with a number of types of cancer.Tobacco smoke contains more than 6000 chemicals and among the most abundant ones are the aldehydes. Aldehydes have been previously shown in in vitro studies to induce intracellular oxidative stress and activation of stress signaling pathways, which are associated with cardiovascular diseases such as atherosclerosis. Also, aldehydes form one of the toxicant groups recommended for future tobacco product regulation due to its harmful effects. However, the in vitro effect of low-level aldehyde exposure has not been established. In this study, we determined the gene expression effects of aldehydes commonly found in tobacco smoke by exposing in vitro human umbilical vein epithelial cells (HUVECs) to these aldehydes.The most relevant aldehydes were used: formaldehyde, acetaldehyde, acrolein, propionaldehyde, crotonaldehyde and butyraldehyde. Sub-cytotoxic exposure levels of the different aldehydes were tested regarding cell proliferation, gene expression changes, oxidative stress responses, and DNA damage.Genes associated with cardiovascular disease development such as DEPP, ARID5B, DKK1, EGR1 and IER3 were found to be dysregulated. Gene expression responses were not related to the measurement of oxidative stress or DNA damage using a comet assay. These findings suggest that exposure to the low-level aldehydes from tobacco smoke needs to be controlled due to its effect on genes associated with cardiovascular disease.

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