An electronic cigarette (e-cig) generates aerosols by vaporizing the e-liquid, which mainly consists of propylene glycol (PG), vegetable glycerin (VG), and nicotine. Understanding the effects of e-liquid main compositions on e-cig aerosols is important for exposure assessment. This study investigated how the PG/VG ratio and nicotine content affect e-cig aerosol emissions and dynamics. A tank-based e-cig device with 10 different flavorless e-liquid mixtures (e.g., PG/VG ratios of 0/100, 10/90, 30/70, 50/50, and 100/0 with 0.0% or 2.4% nicotine) was used to puff aerosols into a 0.46 m³ stainless steel chamber for 0.5 h. Real-time measurements of particle number concentration (PNC), fine particulate matter (PM_2.5), and particle size distributions were conducted continuously throughout the puffing and the following 2-h decay period. During the decay period, particle loss rates were determined by a first-order log-linear regression and used to calculate the emission factor. The addition of nicotine in the e-liquid significantly decreased the particle number emission factor by 33%. The PM_2.5 emission factor significantly decreased with greater PG content in the e-liquid. For nicotine-free e-liquids, increasing the PG/VG ratio resulted in increased particle loss rates measured by PNC and PM_2.5. This pattern was not observed with nicotine in the e-liquids. The particle loss rates, however, were significantly different with and without nicotine especially when the PG/VG ratios were greater than 30/70. Compared with nonvolatile diethyl-hexyl subacute (DEHS) aerosols, e-cig particle concentration decayed faster inside the chamber, presumably due to evaporation. These results have potential implications for assessing human exposure to e-cig aerosols.

Objective: Since the introduction in 2004, global usage of e-cigarettes (ECs) has risen exponentially. However, the risks of ECs on oral health are uncertain. The purpose of this study is to understand if EC aerosol exposure impacts the gene pathways of normal human oral keratinocytes (NHOKs), particularly the unfolded protein response (UPR) pathway. Materials and methods: EC aerosols were generated reproducibly with a home-made puffing device and impinged into the culture medium for NHOKs. DNA microarrays were used to profile the gene expression changes in NHOKs treated with EC aerosols, and the Ingenuity Pathway Analysis (IPA) was used to reveal signaling pathways altered by the EC aerosols. Quantitative PCR was used to validate the expression changes of significantly altered genes. Results: DNA microarray profiling followed by IPA revealed a number of signaling pathways, such as UPR, cell cycle regulation, TGF-β signaling, NRF2-mediated oxidative stress response, PI3K/AKT signaling, NF-κB signaling, and HGF signaling, activated by EC aerosols in NHOKs. The UPR pathway genes, C/EBP homologous protein (CHOP), activating transcription factor 4 (ATF4), X box binding protein 1 (XBP1), and inositol-requiring enzyme 1 alpha (IRE1α) were all significantly up-regulated in EC aerosol-treated NHOKs whereas immunoglobulin heavy-chain binding protein (BIP) and PRKR-like ER kinase (PERK) were slightly up-regulated. qPCR analysis results were found to be well correlated with those from the DNA microarray analysis. The most significantly changed genes in EC aerosol-treated NHOKs versus untreated NHOKs were CHOP, ATF4, XBP1, IRE1α and BIP. Meanwhile, Western blot analysis confirmed that CHOP, GRP78 (BIP), ATF4, IRE1α and XBP1s (spliced XBP1) were significantly up-regulated in NHOKs treated with EC aerosols. Conclusion: Our results indicate that EC aerosols up-regulate the UPR pathway genes in NHOKs, and the induction of UPR response is mediated by the PERK - EIF2α - ATF4 and IRE1α - XBP1 pathways.

Pollutants in tailpipe emissions can be highly elevated around roadways, and in early mornings the pollution plume can extend hundreds of meters into surrounding neighborhoods. Solid sound walls and vegetation barriers are commonly used to mitigate noise, but they also help mitigate near-road air pollution. Here we assess the effectiveness of barriers consisting of vegetation only and of a combination of vegetation and a solid sound wall (combination barrier) in reducing pollution concentrations downwind of roads, under stable atmospheric stability and calm to light wind conditions. Because there was no practical (no barrier) control site in the area, we primarily compare the two barrier types to each other and explore the importance of atmospheric conditions. Using measurements collected with a mobile platform, we develop concentration decay profiles of ultrafine and fine particles, oxides of nitrogen (NO and NO₂) and carbon monoxide downwind of a freeway in California with different barrier configurations and meteorological conditions. Diurnally averaged data collected with passive samplers indicate that pollution from morning rush hour has about equal impact as the entire remainder of the day, because of differences in atmospheric dispersion as the day progresses. Under calm and stable atmospheric conditions (wind speed <0.6 m/s); a vegetation-only barrier was more effective than a combination barrier with a total height that was somewhat lower than the vegetation-only barrier, by 10-24% in the first 160 m downwind. Under light winds (above ~ 0.6 but below 3 m/s) and stable conditions, the combination barrier was more effective than the vegetation barrier alone, by 6-33%, in the first 160 m from the barrier. The average particle size downwind of the vegetation-only barrier was larger than downwind of the combination barrier, indicating that particle deposition plays an important role in the reductions observed downwind of vegetation. Our results are consistent with the notion that at low wind speeds, vegetation acts as an effective barrier. Overall, adding vegetation alone or to an existing solid barrier results in lower downwind pollution concentrations, especially under low wind speeds when concentrations can be high.