Dataset Information

Effects of mango and mint pod-based e-cigarette aerosol inhalation on inflammatory states of the brain, lung, heart, and colon in mice.

ABSTRACT: While health effects of conventional tobacco are well defined, data on vaping devices, including one of the most popular e-cigarettes which have high nicotine levels, are less established. Prior acute e-cigarette studies have demonstrated inflammatory and cardiopulmonary physiology changes while chronic studies have demonstrated extra-pulmonary effects, including neurotransmitter alterations in reward pathways. In this study we investigated the impact of inhalation of aerosols produced from pod-based, flavored e-cigarettes (JUUL) aerosols three times daily for 3 months on inflammatory markers in the brain, lung, heart, and colon. JUUL aerosol exposure induced upregulation of cytokine and chemokine gene expression and increased HMGB1 and RAGE in the nucleus accumbens in the central nervous system. Inflammatory gene expression increased in the colon, while gene expression was more broadly altered by e-cigarette aerosol inhalation in the lung. Cardiopulmonary inflammatory responses to acute lung injury with lipopolysaccharide were exacerbated in the heart. Flavor-specific findings were detected across these studies. Our findings suggest that daily e-cigarette use may cause neuroinflammation, which may contribute to behavioral changes and mood disorders. In addition, e-cigarette use may cause gut inflammation, which has been tied to poor systemic health, and cardiac inflammation, which leads to cardiovascular disease.

SUBMITTER: Moshensky A

PROVIDER: S-EPMC9005188 | biostudies-literature | 2022 Apr

REPOSITORIES: biostudies-literature

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Effects of mango and mint pod-based e-cigarette aerosol inhalation on inflammatory states of the brain, lung, heart, and colon in mice.

Moshensky Alex A Brand Cameron S CS Alhaddad Hasan H Shin John J Masso-Silva Jorge A JA Advani Ira I Gunge Deepti D Sharma Aditi A Mehta Sagar S Jahan Arya A Nilaad Sedtavut S Olay Jarod J Gu Wanjun W Simonson Tatum T Almarghalani Daniyah D Pham Josephine J Perera Samantha S Park Kenneth K Al-Kolla Rita R Moon Hoyoung H Das Soumita S Byun Min Kwang MK Shah Zahoor Z Sari Youssef Y Heller Brown Joan J Crotty Alexander Laura E LE

eLife 20220412

While health effects of conventional tobacco are well defined, data on vaping devices, including one of the most popular e-cigarettes which have high nicotine levels, are less established. Prior acute e-cigarette studies have demonstrated inflammatory and cardiopulmonary physiology changes while chronic studies have demonstrated extra-pulmonary effects, including neurotransmitter alterations in reward pathways. In this study we investigated the impact of inhalation of aerosols produced from pod- ...[more]

PMID: 35411847

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Project description:Background Previous studies showed that nicotinized electronic cigarettes (hereafter, e-cigarettes) elicit systemic oxidative stress and inflammation. However, the effect of the aerosol alone on endothelial function is not fully understood. Purpose To quantify surrogate markers of endothelial function in nonsmokers after inhalation of aerosol from nicotine-free e-cigarettes. Materials and Methods In this prospective study (from May to September 2018), nonsmokers underwent 3.0-T MRI before and after inhaling nicotine-free e-cigarette aerosol. Peripheral vascular reactivity to cuff-induced ischemia was quantified by temporally resolving blood flow velocity and oxygenation (SvO2) in superficial femoral artery and vein, respectively, along with artery luminal flow-mediated dilation. Precuff occlusion, resistivity index, baseline blood flow velocity, and SvO2 were evaluated. During reactive hyperemia, blood flow velocity yielded peak velocity, time to peak, and acceleration rate (hyperemic index); SvO2 yielded washout time of oxygen-depleted blood, rate of resaturation, and maximum SvO2 increase (overshoot). Cerebrovascular reactivity was assessed in the superior sagittal sinus, evaluating the breath-hold index. Central arterial stiffness was measured via aortic pulse wave velocity. Differences before versus after e-cigarette vaping were tested with Hotelling T2 test. Results Thirty-one healthy never-smokers (mean age, 24.3 years ± 4.3; 14 women) were evaluated. After e-cigarette vaping, resistivity index was higher (0.03 of 1.30 [2.3%]; P < .05), luminal flow-mediated dilation severely blunted (-3.2% of 9.4% [-34%]; P < .001), along with reduced peak velocity (-9.9 of 56.6 cm/sec [-17.5%]; P < .001), hyperemic index (-3.9 of 15.1 cm/sec2 [-25.8%]; P < .001), and delayed time to peak (2.1 of 7.1 sec [29.6%]; P = .005); baseline SvO2 was lower (-13 of 65 %HbO2 [-20%]; P < .001) and overshoot higher (10 of 19 %HbO2 [52.6%]; P < .001); and aortic pulse wave velocity marginally increased (0.19 of 6.05 m/sec [3%]; P = .05). Remaining parameters did not change after aerosol inhalation. Conclusion Inhaling nicotine-free electronic cigarette aerosol transiently impacted endothelial function in healthy nonsmokers. Further studies are needed to address the potentially adverse long-term effects on vascular health. © RSNA, 2019 Online supplemental material is available for this article.

Project description:Since poor air quality affects human health in the short and long term, much research has been performed on indoor and outdoor aerosol exposure; however, there is a lack of specific data on the exposure and health risks of inhalable aerosols that contain bioaerosol in different environments of human life. To investigate the potential exposure to inhalable aerosols (in the monitoring of particulate matter (PM) based on R modeling, variations of PM depend on the ventilation system and bioaerosols based on size distribution) in various environments, the special viability and culturability of bioaerosols and their deposition doses in the respiratory system were evaluated. We conducted exposure assessments on inhalable aerosols in various indoor environments (childcare facilities, schools, commercial buildings, elderly and homes). The fractions of PM (PM10, PM4 and PM2.5) were investigated and, for the bioaerosol, the viability, culturability, inhalation daily dose and the deposited dose of the aerosol in the respiratory system were calculated to evaluate the human health effects. For two years, the distribution of the indoor PM concentration was high in all PM fractions in schools and commercial buildings, and low in the elderly and at homes. For airborne bacteria, the highest concentrations were shown in the childcare facility during the four seasons, while airborne fungi showed high concentrations in the buildings during the spring and summer, which showed significant differences from other investigated environments (between the buildings and elderly and homes: p < 0.05). The viability and culturability for the bioaerosol showed no significant difference in all environments, and the correlation between inhalable PM and bioaerosol obtained from the six-stage impactor showed that the coefficient of determination (R2) between coarse particles (PM10-2.5, the size of stage 2-3) and cultivable airborne bacteria ranged from 0.70 (elderly and homes) to 0.84 (school) during the summer season.

Project description:IntroductionEmerging heated tobacco products (HTPs) were designed to reduce exposure to toxicants from cigarette smoke (CS) by avoiding burning tobacco and instead heating tobacco. We studied the effects of short-term inhalation of aerosols emitted from HTP called IQOS, on lung damage and immune-cell recruitment to the lungs in mice.MethodsNumerous markers of lung damage and inflammation including albumin and lung immune-cell infiltrates, proinflammatory cytokines, and chemokines were quantified in lungs and bronchoalveolar (BAL) fluid from IQOS, CS, or air-exposed (negative control) mice.ResultsImportantly, as a surrogate marker of lung epithelial-cell damage, we detected significantly increased levels of albumin in the BAL fluid of both HTP- and CS-exposed mice compared with negative controls. Total numbers of leukocytes infiltrating the lungs were equivalent following both IQOS aerosols and CS inhalation and significantly increased compared with air-exposed controls. We also observed significantly increased numbers of CD4+IL-17A+ T cells, a marker of a T-cell immune response, in both groups compared with air controls; however, numbers were the highest following CS exposure. Finally, the numbers of CD4+RORγt+ T cells, an inflammatory T-cell subtype expressing the transcription factor that is essential for promoting differentiation into proinflammatory Th17 cells, were significantly augmented in both groups compared with air-exposed controls. Levels of several cytokines in BAL were significantly elevated, reflecting a proinflammatory milieu.ConclusionsOur study demonstrates that short-term inhalation of aerosols from IQOS generates damage and proinflammatory changes in the lung that are substantially similar to that elicited by CS exposure.ImplicationsExposure of mice to IQOS, one of the candidate modified-risk tobacco products, induces inflammatory immune-cell accumulation in the lungs and augments the levels of proinflammatory cytokines and chemokines in the BAL fluid. Such an exacerbated pulmonary proinflammatory microenvironment is associated with lung epithelial-cell damage in IQOS-exposed mice, suggesting a potential association with the impairment of lung function.

Dataset Information

Effects of mango and mint pod-based e-cigarette aerosol inhalation on inflammatory states of the brain, lung, heart, and colon in mice.

Publications

Effects of mango and mint pod-based e-cigarette aerosol inhalation on inflammatory states of the brain, lung, heart, and colon in mice.

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