E-cigarette Aerosol Research Articles

INDICATORS OF LOCAL ORAL IMMUNITY IN USERS OF NEW TYPES OF TOBACCO PRODUCTS

Introduction. The organs and structures of the oral cavity are among the first to come into contact with the aerosol when using electronic cigarettes and heated-tobacco products, and some of the aerosol components enter various biological fluids of the mouth, inevitably provoking a response of the body to external influences. One of the markers of the response are immunoglobulins, and their analysis is intended to help in studying the effect of electronic cigarettes and heated-tobacco products on humans. Objective. The aim of the study was to estimate changes in immunoglobulins A, G and M of gingival fluid, oral fluid and saliva among users of new types of tobacco products. Material and methods. The study included 4 groups of 5 people each: regular cigarette smokers, e-cigarette users, users of tobacco heating sys-tems and non-smokers. For laboratory studies, gingival fluid, saliva and oral fluid were taken from the subjects. Results. Various changes in the concentration of immunoglobulins relative to the control group were observed in all groups of smoking patients. Conclusion. The results may indicate inhibition of the function of local immunity both when exposed to tobacco smoke and when exposed to aerosol of heated-tobacco products or electronic cigarettes, which increases the vulnerability of organs and structures of the oral cavity to pathogenic microor-ganisms.

Determination of four tobacco-specific nitrosamines in electronic cigarette liquids and aerosols by UPLC-QTOF-HRMS

To elucidate the concentrations of four tobacco-specific nitrosamines (TSNAs) in commercial e-cigarettes, analyze the correlation between TSNAs and Nicotine, and clarify the main sources of TSNAs in e-cigarettes. Ultra-high performance liquid chromatography with quadrupole time-of-flight high-resolution mass spectrometry (UPLC-QTOF-HRMS) was employed to determine the concentrations of four TSNAs in thirty-two commercially available e-cigarettes. The results demonstrated that the method exhibits excellent linearity and high mass accuracy. The limits of quantification (LOQ) of four TSNAs in e-cigarettes were 0.0010 –0.0165 (e-liquids) and 0.0032–0.0554 (aerosols) ng·g−1. The limits of detection (LOD) of four TSNAs in e-cigarettes were 0.0011–0.0165 (e-liquids) and 0.0033–0.0537 (aerosols) ng·20 puffs−1. The recovery of four TSNAs ranged from 73.06 % to 109.95 %. The e-liquids contained: 0–33.970 (NNN), 0.063–15.654 (NNK), 0–10.033 (NAT), and 0–0.251 (NAB) ng·g−1. The aerosols contained: 0–60.662 (NNN), 0.021–9.435 (NNK), 0.202– 29.866 (NAT), and 0–2.841 (NAB) ng·20 puffs−1. The correlation analysis results have shown that there was no significant correlation between the concentrations of four TSNAs and nicotine in e-cigarettes. The concentrations of four TSNAs in e-liquid containing tobacco extract were significantly higher than that in e-liquid without tobacco extract, suggested that the main source of TSNAs was tobacco extract. This method is fast, simple, highly sensitive, and has low detection limits. The approach taken can provide data support for the actual supervision of e-cigarettes, and evaluation of safety components, contributing to effective quality evaluation systems.

Sex-specific alterations in pulmonary metabolic, xenobiotic and lipid signalling pathways after e-cigarette aerosol exposure during adolescence in mice

BackgroundE-cigarette use is now prevalent among adolescents and young adults, raising concerns over potential adverse long-term health effects. Although it is hypothesised that e-cigarettes promote inflammation, studies have yielded conflicting...

Perception of Health Risks of Electronic Cigarette Use Among College Students: Examining the Roles of Sex, Field of Study, Vaping Device Type, and Their Associations.

Electronic cigarettes are marketed as a safer alternative to regular (combustible) cigarettes, based on the claim that there is no tobacco burning and fewer toxic chemicals in their vapor. However, recent evidence challenges the notion that e-cigarette aerosols are benign. Heating of compounds in e-liquids to high temperatures can lead to the release of toxic compounds in e-cigarette aerosols. However, users and the public may not be aware of these unique harms, impacting their perception of harm from using e-cigarettes. This research explored the perceptions of harm of e-cigarettes compared to regular cigarettes among 418 college students, aged 18-34, by employing a Qualtrics based smartphone survey. The findings revealed a vaping prevalence of 16.7% among our study population, indicating e-cigarette use among college aged young adults is at concerning levels. Perceptions of harm varied significantly by vaping status, sex, and field of study. Non-e-cigarette users and female students were less likely to perceive e-cigarettes as less harmful than regular cigarettes. Among e-cigarette users (vapers), male vapers and users of pod-type devices, such as JUUL and disposables, were more inclined to view e-cigarettes as less harmful. Among vapers, students in non-health-related fields were significantly more likely to perceive e-cigarettes as less harmful than regular cigarettes, underscoring the impact of educational background on health risk awareness. In conclusion, this study provides crucial insights into the varied perceptions of e-cigarettes among young adults. The results emphasize the need for targeted public health interventions and educational efforts to address this growing public health concern.

90. E-cigarette vapor extracts impact spine fusion capacity through osteogenic and chondrogenic differentiation of bone mesenchymal and periosteal derived stem cells

90. E-cigarette vapor extracts impact spine fusion capacity through osteogenic and chondrogenic differentiation of bone mesenchymal and periosteal derived stem cells

Composition of e-cigarette aerosols: A review and risk assessment of selected compounds.

The potential harms and benefits of e-cigarettes, or electronic nicotine delivery systems (ENDS), have received significant attention from public health and regulatory communities. Such products may provide a reduced risk means of nicotine delivery for combustible cigarette smokers while being inappropriately appealing to nicotine naive youth. Numerous authors have examined the chemical complexity of aerosols from various open- and closed-system ENDS. This body of literature is reviewed here, with the risks of ENDS aerosol exposure among users evaluated with a margin of exposure (MoE) approach for two non-carcinogens (methylglyoxal, butyraldehyde) and a cancer risk analysis for the carcinogen N-nitrosonornicotine (NNN). We identified 96 relevant papers, including 17, 13, and 5 reporting data for methylglyoxal, butyraldehyde, and NNN, respectively. Using low-end (minimum aerosol concentration, low ENDS use) and high-end (maximum aerosol concentration, high ENDS use) assumptions, estimated doses for methylglyoxal (1.78 × 10-3-135 μg/kg-bw/day) and butyraldehyde (1.9 × 10-4-66.54 μg/kg-bw/day) corresponded to MoEs of 227-17,200,000 and 271-280,000,000, respectively, using identified points of departure (PoDs). Doses of 9.90 × 10-6-1.99 × 10-4μg/kg-bw/day NNN corresponded to 1.4-28 surplus cancers per 100,000 ENDS users, relative to a NNN-attributable surplus of 7440 per 100,000 cigarette smokers. It was concluded that methylglyoxal and butyraldehyde in ENDS aerosols, while not innocuous, did not present a significant risk of irritant effects among ENDS users. The carcinogenic risks of NNN in ENDS aerosols were reduced, but not eliminated, relative to concentrations reported in combustible cigarette smoke.

E-cigarette vapor extract alters human eosinophil gene expression in an effect mediated by propylene glycol, glycerin, and nicotine.

E-cigarette use has become widespread, and its effects on airway inflammation and disease are not fully delineated. E-cigarette vapor extract (EVE) profoundly affects neutrophil function. We hypothesized that EVE also alters eosinophil function and thus could impact allergic airway disease. We employed RNA sequencing to measure the ex vivo effect of EVE components on human eosinophil transcription. Blood eosinophils from 9 nonvaping subjects without asthma were isolated by negative selection. Cells were incubated for 48 h with EVE consisting of glycerin, propylene glycol, and nicotine (EVE+), EVE without nicotine ("EVE-"), air-exposed media termed extract buffer (EB), or untreated media. Bulk RNA sequencing was performed. Transcriptomic analysis revealed that the EB, EVE-, and EVE+ conditions showed highly variable gene expression with respect to no treatment and each other. Differential gene expression analysis comparing a combination of EVE+, EVE-, and EB revealed 3,030 differentially expressed genes (DEGs) with an adjusted P value <0.05 and log2 fold change >0.5 or <0.5. There were 645 DEGs between EB and EVE-, 1,713 between EB and EVE+, and 404 between EVE- and EVE+. Gene set enrichment analysis demonstrated that DEGs between both EVE+ and EVE- and the EB control were positively enriched for heme metabolism and apoptosis and negatively enriched tumor necrosis factor α signaling, interferon γ signaling, and inflammatory response. Thus, EVE significantly alters eosinophil metabolic and inflammatory pathways, mediated by propylene glycol and glycerin, with both enhancing and unique effects of nicotine. This study motivates further research into the pathogenic effects of vaping on airway eosinophils and allergic airways disease.

Structured adaptive boosting trees for detection of multicellular aggregates in fluorescence intravital microscopy

Fluorescence intravital microscopy captures large data sets of dynamic multicellular interactions within various organs such as the lungs, liver, and brain of living subjects. In medical imaging, edge detection is used to accurately identify and delineate important structures and boundaries inside the images. To improve edge sharpness, edge detection frequently requires the inclusion of low-level features. Herein, a machine learning approach is needed to automate the edge detection of multicellular aggregates of distinctly labeled blood cells within the microcirculation. In this work, the Structured Adaptive Boosting Trees algorithm (AdaBoost.S) is proposed as a contribution to overcome some of the edge detection challenges related to medical images. Algorithm design is based on the observation that edges over an image mask often exhibit special structures and are interdependent. Such structures can be predicted using the features extracted from a bigger image patch that covers the image edge mask. The proposed AdaBoost.S is applied to detect multicellular aggregates within blood vessels from the fluorescence lung intravital images of mice exposed to e-cigarette vapor. The predictive capabilities of this approach for detecting platelet-neutrophil aggregates within the lung blood vessels are evaluated against three conventional machine learning algorithms: Random Forest, XGBoost and Decision Tree. AdaBoost.S exhibits a mean recall, F-score, and precision of 0.81, 0.79, and 0.78, respectively. Compared to all three existing algorithms, AdaBoost.S has statistically better performance for recall and F-score. Although AdaBoost.S does not outperform Random Forest in precision, it remains superior to the XGBoost and Decision Tree algorithms. The proposed AdaBoost.S is widely applicable to analysis of other fluorescence intravital microscopy applications including cancer, infection, and cardiovascular disease.

The Untapped Biomarker Potential of MicroRNAs for Health Risk-Benefit Analysis of Vaping vs. Smoking.

Despite the popularity of electronic cigarettes (e-cigs) among adolescent never-smokers and adult smokers seeking a less pernicious substitute for tobacco cigarettes, the long-term health impact of vaping is largely unknown. Like cigarette smoke, e-cig vapor contains harmful and potentially harmful compounds, although in fewer numbers and at substantially lower concentrations. Many of the same constituents of e-cig vapor and cigarette smoke induce epigenetic changes that can lead to the dysregulation of disease-related genes. MicroRNAs (MiRNAs) are key regulators of gene expression in health and disease states. Extensive research has shown that miRNAs play a prominent role in the regulation of genes involved in the pathogenesis of smoking-related diseases. However, the use of miRNAs for investigating the disease-causing potential of vaping has not been fully explored. This review article provides an overview of e-cigs as a highly consequential electronic nicotine delivery system, describes trends in e-cig use among adolescents and adults, and discusses the ongoing debate on the public health impact of vaping. Highlighting the significance of miRNAs in cell biology and disease, it summarizes the published and ongoing research on miRNAs in relation to gene regulation and disease pathogenesis in e-cig users and in vitro experimental settings. It identifies gaps in knowledge and priorities for future research while underscoring the need for empirical evidence that can inform the regulation of tobacco products to protect youth and promote public health.

Aerosolized e-liquid base constituents induce cytotoxicity and genotoxicity in oral keratinocytes.

Electronic cigarette (e-cigarette) use among adults in the United States continues to rise. Particularly concerning is the impact of e-cigarette aerosol inhalation on the oral mucosa. Aerosols are derived from a heated e-liquid base of propylene glycol/glycerin (PG/G) often mixed with nicotine and chemical flavors. Of note, harmful and potentially harmful constituents (HPHCs), including metals and volatile organic compounds, have been detected in e-cigarette aerosols. It remains unknown, however, whether aerosols exclusively derived from e-liquid PG/G are detrimental to oral keratinocytes. The present study analyzed toxicological outcomes in normal oral keratinocytes exposed to model nicotine-free, unflavored PG/G e-liquid aerosols. Cell viability/cytotoxicity, genotoxicity, and immunoblotting assays were conducted in NOKSI, a gingiva-derived oral keratinocyte cell line, following exposure to model e-liquid aerosols or non-aerosolized controls. The HPHC acrolein, reported to form DNA adducts in the buccal mucosa from e-cigarette users, was also used in similar assays. PG/G e-liquid aerosol extracts significantly enhanced cytotoxic and DNA damaging responses in NOKSI cells when compared to non-aerosolized e-liquid treatment. Acrolein treatment led to similar results. The aerosolization process of PG/G e-liquid is a critical determinant of marked cytotoxic and genotoxic stimuli in oral keratinocytes.

Exploring the Utility of Long Non-Coding RNAs for Assessing the Health Consequences of Vaping.

Electronic cigarette (e-cig) use, otherwise known as "vaping", is widespread among adolescent never-smokers and adult smokers seeking a less-harmful alternative to combustible tobacco products. To date, however, the long-term health consequences of vaping are largely unknown. Many toxicants and carcinogens present in e-cig vapor and tobacco smoke exert their biological effects through epigenetic changes that can cause dysregulation of disease-related genes. Long non-coding RNAs (lncRNAs) have emerged as prime regulators of gene expression in health and disease states. A large body of research has shown that lncRNAs regulate genes involved in the pathogenesis of smoking-associated diseases; however, the utility of lncRNAs for assessing the disease-causing potential of vaping remains to be fully determined. A limited but growing number of studies has shown that lncRNAs mediate dysregulation of disease-related genes in cells and tissues of vapers as well as cells treated in vitro with e-cig aerosol extract. This review article provides an overview of the evolution of e-cig technology, trends in use, and controversies on the safety, efficacy, and health risks or potential benefits of vaping relative to smoking. While highlighting the importance of lncRNAs in cell biology and disease, it summarizes the current and ongoing research on the modulatory effects of lncRNAs on gene regulation and disease pathogenesis in e-cig users and in vitro experimental settings. The gaps in knowledge are identified, priorities for future research are highlighted, and the importance of empirical data for tobacco products regulation and public health is underscored.

Method Development and Validation of an Aerosol Sampling Technique for the Analysis of Nicotine in Electronic Cigarette Aerosols.

Because of the increasing popularity of e-cigarettes, monitoring the e-cigarette market has become important for national health authorities to guarantee safety and quality. In the EU, the Tobacco Products Directive requires emission studies for e-cigarette products. The absence of industry guidelines for studying these emissions and the lack of proper validation in the literature led us to develop and validate a method using the total error approach for the determination of nicotine in e-cigarette aerosols. A commercial vaping device was used to generate aerosols, which were then collected on Cambridge filter pads and measured for nicotine concentration by UHPLC-DAD after extraction. The method was successfully validated by generating accuracy profiles, which show that the β-expectation tolerance intervals remained below the acceptance limits of ±20%. Within-run repeatability and intermediate precision were considered acceptable since the highest RSD value obtained was below 5%. The method was applied to 15 commercial e-liquids. A complete validation of a method for the analysis of e-cigarette emissions is presented, including several parameters that impact the accuracy and reproducibility. Similar systematic approaches for method development and validation could be used for other e-cigarette emission analysis methods to ensure the reliability of the measurements.

Chronic Exposure to Both Electronic and Conventional Cigarettes Alters Ileum and Colon Turnover, Immune Function, and Barrier Integrity in Mice.

Although the effects of cigarette smoke (CS) on the development of several intestinal diseases is well documented, the impact of e-cigarette aerosol (e-cig) on digestive health is largely unknown. To compare the effects of e-cig and CS on mouse ileum and colon, animals were chronically exposed for 6 months by nose-only inhalation to e-cig at 18 or 30 W power, or to 3R4F CS. Results showed that e-cig exposure decreased colon cell proliferation. Several other proliferative defects were observed in response to both e-cig and CS exposure, including up- and down-regulation of cyclin D1 protein levels in the ileum and colon, respectively. E-cig and CS exposure reduced myeloperoxidase activity in the ileum. In the colon, both exposures disrupted gene expression of cytokines and T cell transcription factors. For tight junction genes, ZO-1- and occludin-protein expression levels were reduced in the ileum and colon, respectively, by e-cig and CS exposure. The 16S sequencing of microbiota showed specific mild dysbiosis, according to the type of exposure. Overall, e-cig exposure led to altered proliferation, inflammation, and barrier function in both the ileum and colon, and therefore may be a gut hazard on par with conventional CS.

Examining the Oxidation States of Metals in Aerosols Emitted by Electronic Cigarettes.

Electronic cigarettes (ECs) emit many toxic substances, including metals, that can pose a threat to users and the environment. The toxicity of the emitted metals depends on their oxidation states. Hence, this study examines the oxidation states of metals observed in EC aerosols. X-ray photoelectron spectroscopy analysis of the filters that collected EC aerosols identified the oxidation states of five primary metals (based on surface sample analysis), including chromium(III) (close to 100%) under low power setting while a noticeable amount of chromium(VI) (15%) at higher power settings of the EC, and copper(II) (100%), zinc(II) (100%), nickel(II) (100%), lead(II) (65%), and lead(IV) (35%) regardless of power settings. This observation indicates that the increased temperature due to higher power settings could alter the oxidation states of certain metals. We noted that many metals were in their lesser toxic states; however, inhaling these metals may still pose health risks.

Secondhand Nicotine Absorption From E-Cigarette Vapor vs Tobacco Smoke in Children

ImportanceWith the prevalence of e-cigarette use (vaping) increasing worldwide, there are concerns about children’s exposure to secondhand vapor.ObjectiveTo compare nicotine absorption among children who are (1) exposed to secondhand tobacco smoke only or (2) exposed to secondhand vapor only with (3) those exposed to neither.Design, Setting, and ParticipantsThe US Continuous National Health and Nutrition Examination Survey (NHANES) is a repeat cross-sectional survey. Participants are interviewed in their homes and, several days after, visit a mobile examination center to provide biological specimens. This study uses data from a nationally representative sample of US households from 2017 to 2020. Participants were children aged 3 to 11 years with serum cotinine levels incompatible with current firsthand nicotine use (ie, <15 μg/L). The final analysis was conducted on January 9, 2024.ExposuresReported exposure to secondhand smoke or vapor indoors in the past 7 days (only secondhand smoke, only secondhand vapor, or neither). Covariates included age, sex, ethnicity, family income, body weight, and height.Main Outcomes and MeasuresThe primary outcome was serum cotinine concentration, an objective biomarker of nicotine absorption. Geometric mean cotinine levels and 95% CIs were calculated using log-normal tobit regression, accounting for the complex survey design and weights.ResultsThe mean (SD) age of the 1777 children surveyed was 7.4 (2.6) years, 882 (49.6%) were female, and 531 (29.9%) had family incomes below the poverty level. Nicotine absorption, as indexed by serum cotinine level, was highest among children only exposed to secondhand smoke (0.494 μg/L μg/L; 95% CI, 0.386-0.633 μg/L), followed by those exposed only to secondhand vapor (0.081 μg/L; 95% CI, 0.048-0.137 μg/L), equating to 83.6% (95% CI, 71.5%-90.5%; P < .001) lower nicotine absorption. Among children with no reported secondhand exposure, the geometric mean cotinine level was 0.016 μg/L (95% CI, 0.013-0.021 μg/L), or 96.7% (95% CI, 95.6%-97.6%; P < .001) lower than for those with exposure to secondhand smoke. Results were similar after covariate adjustment.Conclusions and RelevanceIn this cross-sectional study of US children, nicotine absorption was much lower in children who were exposed to secondhand vapor vs secondhand smoke, but higher than in those exposed to neither. These findings suggest that switching from smoking to vaping indoors may substantially reduce, but not eliminate, children’s secondhand exposure to nicotine and other noxious substances.

Cytotoxic impact of nicotine products on periodontal ligament cells

ObjectivesThe primary objective of this in vitro experiment was an assessment of proliferative capacity, metabolic activity, and potential cellular detriment of human periodontal ligament cells (hPDL) exposed to cigarette smoke (CS), electronic cigarette vapor (eCV), and heated tobacco product aerosol (HTP), or air (control).Materials and methodsUsing a CAD/CAM-designed exposition chamber, hPDL were exposed to CS, eCV, HTP, or air (control) based on the Health Canada Intense Smoking Regime. Cell proliferation, metabolic activity, and cellular detriment were assessed at various time points.ResultsCompared to the control, hPDL exposed to CS exhibited significantly decreased cell numbers at all time points. HTP exposure led to reduced cell numbers 48 h and 72 h post-exposure, while eCV-exposed cells showed no significant decrease. The metabolic activity of eCV-treated hPDL was slightly reduced at 7 h but recovered at 24 h and 48 h. In contrast, CS-treated cells exhibited significantly decreased metabolic activity at 24 h and 48 h, and HTP-exposed cells showed a significant decrease after 48 h. Flow cytometry indicated both apoptotic and necrotic cell death following CS exposure, with necrotic cell death being more pronounced.ConclusionseCV and HTP demonstrated comparatively reduced detrimental effects on hPDL compared to CS.Clinical relevance: The findings suggest that conventional cigarette smoke poses a substantial risk to periodontal health by significantly impairing cell proliferation and metabolic activity. However, alternatives such as eCV and HTP may offer a comparatively reduced risk.

Acute exposure to dihydroxyacetone promotes genotoxicity and chromosomal instability in lung, cardiac, and liver cell models.

Inhalation exposures to dihydroxyacetone (DHA) occur through spray tanning and e-cigarette aerosols. Several studies in skin models have demonstrated that millimolar doses of DHA are cytotoxic, yet the genotoxicity was unclear. We examined the genotoxicity of DHA in cell models relevant to inhalation exposures. Human bronchial epithelial cells BEAS-2B, lung carcinoma cells A549, cardiomyocyte Ac16, and hepatocellular carcinoma HepG3 were exposed to DHA, and low millimolar doses of DHA were cytotoxic. IC90 DHA doses induced cell cycle arrest in all cells except the Ac16. We examined DHA's genotoxicity using strand break markers, DNA adduct detection by Repair Assisted Damage Detection (RADD), metaphase spreads, and a forward mutation assay for mutagenesis. Similar to results for skin, DHA did not induce significant levels of strand breaks. However, RADD revealed DNA adducts were induced 24 h after DHA exposure, with BEAS-2B and Ac16 showing oxidative lesions and A549 and HepG3 showing crosslink-type lesions. Yet, only low levels of reactive oxygen species or advanced glycation end products were detected after DHA exposure. Metaphase spreads revealed significant increases in chromosomal aberrations in the BEAS-2B and HepG3 with corresponding changes in ploidy. Finally, we confirmed the mutagenesis observed using the supF reporter plasmid. DHA increased the mutation frequency, consistent with methylmethane sulfonate, a mutagen and clastogen. These data demonstrate DHA is a clastogen, inducing cell-specific genotoxicity and chromosomal instability. The specific genotoxicity measured in the BEAS-2B in this study suggests that inhalation exposures pose health risks to vapers, requiring further investigation.

Coverage of Indoor Smoking and Vaping Restrictions in the U.S., 1990–2021

Secondhand smoke exposure increases the risk of premature death and disease in children and non-smoking adults. As a result, many US states and local jurisdictions have enacted comprehensive indoor smoking restrictions (ISR). Indoor vaping restrictions (IVR) have also been adopted to protect against exposure to secondhand e-cigarette aerosol. This study aimed to quantify state and national US coverage of policies restricting indoor cigarette and e-cigarette use over time. Data from the American Nonsmokers Rights' Foundation on US ISR from 1990 to 2021 and IVR from 2006 to 2021 were analyzed. Combining these data with 2015 US Census population estimates, the percentage of state and national residents covered by partial and comprehensive restrictions in bars, restaurants, and workplaces, were calculated (analysis in 2023-2024) over time. Between 1990-2021, national coverage of comprehensive ISR increased for bars (0% to 67.3%), restaurants (0% to 78.2%), and workplaces (0% to 77.5%). Partial ISR coverage decreased for bars (14.8% to 13.9%), restaurants (40.2% to 15.4%) and workplaces (40.2% to 22.5%). From 2006 to 2021, comprehensive IVR coverage increased for bars (0% to 43.5%), restaurants (0% to 51.5%), and workplaces (0% to 53.2%). Despite these increases in coverage, by the end of 2021, <50% of the population was protected by comprehensive ISR for bars, restaurants, and workplaces in 19, 12, and 14 states, respectively. The percentage of the US population protected by ISR and IVR has increased over time. However, gaps in coverage remain, which may contribute to disparities in tobacco-related disease and death.

Different Lengths of Gestational Exposure to Secondhand Smoke or e-Cigarette Vapor Induce the Development of Placental Disease Symptoms.

Exposure to cigarette smoke is known to induce disease during pregnancy. Recent evidence showed that exposure to secondhand smoke (SHS) negatively impacts fetal and placental weights, leading to the development of intrauterine growth restriction (IUGR). Electronic cigarettes (eCigs) represent a phenomenon that has recently emerged, and their use is also steadily rising. Even so, the effects of SHS or eCigs during gestation remain limited. In the present study, we wanted to characterize the effects of SHS or eCig exposure at two different important gestational points during mouse pregnancy. C57/Bl6 mice were exposed to SHS or eCigs via a nose-only delivery system for 4 days (from 14.5 to 17.5 gestational days (dGA) or for 6 days (from 12.5 dGA to 17.5 dGA)). At the time of necropsy (18.5 dGA), placental and fetal weights were recorded, maternal blood pressure was determined, and a dipstick test to measure proteinuria was performed. Placental tissues were collected, and inflammatory molecules in the placenta were identified. Treatment with SHS showed the following: (1) a significant decrease in placental and fetal weights following four days of exposure, (2) higher systolic and diastolic blood pressure following six days of exposure, and (3) increased proteinuria after six days of exposure. Treatment with eCigs showed the following: (1) a significant decrease in placental weight and fetal weight following four or six days of exposure, (2) higher systolic and diastolic blood pressure following six days of exposure, and (3) increased proteinuria after six days of exposure. We also observed different inflammatory markers associated with the development of IUGR or PE. We conclude that the detrimental effects of SHS or eCig treatment coincide with the length of maternal exposure. These results could be beneficial in understanding the long-term effects of SHS or eCig exposure in the development of placental diseases.

Dual Exposure to E-Cigarette Vapour and Cigarette Smoke Results in Poorer Airway Cell, Monocyte, and Macrophage Function Than Single Exposure.

E-cigarette users predominantly also continue to smoke cigarettes. These Dual Users either consume e-cigarettes in locations where smoking is not allowed, but vaping is, or to reduce their consumption of cigarettes, believing it will lead to harm reduction. Whilst it is known that e-cigarette vapour is chemically less complex than cigarette smoke, it has a distinct chemical profile, and very little is known about the health impacts of exposure to both chemical profiles vs. either alone. We simultaneously exposed cells in vitro to non-toxic levels of e-cigarette vapour extract (EVE) and cigarette smoke extract (CSE) to determine their effects on 16HBE14o- airway epithelial cell metabolism and inflammatory response, as well as immune cell (THP-1 cells and monocyte-derived macrophages (MDM) from healthy volunteers) migration, phagocytosis, and inflammatory response. We observed increased toxicity, reduced metabolism (a marker of proliferation) in airway epithelial cells, and reduced monocyte migration, macrophage phagocytosis, and altered chemokine production after exposure to either CSE or EVE. These cellular responses were greater after dual exposure to CSE and EVE. The airway epithelial cells from smokers showed reduced metabolism after EVE (the Switcher model) and dual CSE and EVE exposure. When EVE and CSE were allowed to interact, the chemicals were found to be altered, and new chemicals were also found compared to the CSE and EVE profiles. Dual exposure to e-cigarette vapour and cigarette smoke led to worse functional outcomes in cells compared to either single exposure alone, adding to limited data that dual use may be more dangerous than smoking only.