smoke exposure
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Author(s):  
Weeberb J. Requia ◽  
Stefania Papatheodorou ◽  
Petros Koutrakis ◽  
Rajarshi Mukherjee ◽  
Henrique L. Roig

2022 ◽  
Vol 158 ◽  
pp. 106993
Author(s):  
Anthony P. Brown ◽  
Lucy Cai ◽  
Benjamin I. Laufer ◽  
Lisa A. Miller ◽  
Janine M. LaSalle ◽  
...  

2021 ◽  
pp. 153857442110630
Author(s):  
Amir F. Azarbal ◽  
Tana Repella ◽  
Eric Carlson ◽  
Elise C. Manalo ◽  
Braden Palanuk ◽  
...  

Objective Tobacco smoke exposure is a major risk factor for aortic aneurysm development. However, the initial aortic response to tobacco smoke, preceding aneurysm formation, is not well understood. We sought to create a model to determine the effect of solubilized tobacco smoke (STS) on the thoracic and abdominal aorta of mice as well as on cultured human aortic smooth muscle cells (HASMCs). Methods Tobacco smoke was solubilized and delivered to mice via implanted osmotic minipumps. Twenty male C57BL/6 mice received STS or vehicle infusion. The descending thoracic, suprarenal abdominal, and infrarenal abdominal segments of the aorta were assessed for elastic lamellar damage, smooth muscle cell phenotype, and infiltration of inflammatory cells. Cultured HASMCs grown in media containing STS were compared to cells grown in standard media in order to verify our in vivo findings. Results Tobacco smoke solution caused significantly more breaks in the elastic lamellae of the thoracic and abdominal aorta compared to control solution ( P< .0001) without inciting an inflammatory infiltrate. Elastin breaks occurred more frequently in the abdominal aorta than the thoracic aorta ( P < .01). Exposure to STS-induced aortic microdissections and downregulation of α-smooth muscle actin (α-SMA) by vascular smooth muscle cells (VSMCs). Treatment of cultured HASMCs with STS confirmed the decrease in α-SMA expression. Conclusion Delivery of STS via osmotic minipumps appears to be a promising model for investigating the early aortic response to tobacco smoke exposure. The initial effect of tobacco smoke exposure on the aorta is elastic lamellar damage and downregulation of (α-SMA) expression by VSMCs. Elastic lamellar damage occurs more frequently in the abdominal aorta than the thoracic aorta and does not seem to be mediated by the presence of macrophages or other inflammatory cells.


2021 ◽  
Vol 9 ◽  
Author(s):  
E. Melinda Mahabee-Gittens ◽  
Penelope J. E. Quintana ◽  
Eunha Hoh ◽  
Ashley L. Merianos ◽  
Lara Stone ◽  
...  

2021 ◽  
pp. 2101581
Author(s):  
Niroop Kaza ◽  
Vivian Y. Lin ◽  
Denise Stanford ◽  
Shah S. Hussain ◽  
Emily Falk Libby ◽  
...  

Rationale.The majority of chronic obstructive pulmonary disease (COPD) patients have chronic bronchitis, for which specific therapies are unavailable. Acquired cystic fibrosis transmembrane conductance regulator (CFTR) dysfunction is observed in chronic bronchitis, but has not been proven in a controlled animal model with airway disease. Furthermore, the potential of CFTR as a therapeutic target has not been tested in vivo, given limitations to rodent models of COPD. Ferrets exhibit cystic fibrosis-related lung pathology when CFTR is absent and COPD with bronchitis following cigarette smoke exposure.Objectives.To evaluate CFTR dysfunction induced by smoking and test its pharmacologic reversal by a novel CFTR potentiator, GLPG2196, in a ferret model of COPD with chronic bronchitis.Methods.Ferrets were exposed for six months to cigarette smoke to induce COPD and chronic bronchitis and then treated with eneral GLPG2196 once daily for one month. Electrophysiologic measurements of ion transport and CFTR function, assessment of mucociliary function by one-micron optical coherence tomography imaging and particle tracking microrhelogy, microcomputed tomography imaging, histopathological analysis, and quantification of CFTR protein and mRNA expression were used to evaluate mechanistic and pathophysiological changes.Measurements and Main Results.Following cigarette smoke exposure, ferrets exhibited CFTR dysfunction, increased mucus viscosity, delayed mucociliary clearance, airway wall thickening, and airway epithelial hypertrophy. In COPD ferrets, GLPG2196 treatment reversed CFTR dysfunction, increased mucus transport by decreasing mucus viscosity, and reduced brochial wall thickening and airway epithelial hypertrophy.Conclusions.The pharmacologic reversal of acquired CFTR dysfunction is beneficial against pathologic features of chronic bronchitis in a COPD ferret model.


Molecules ◽  
2021 ◽  
Vol 26 (24) ◽  
pp. 7540
Author(s):  
Kerry Wilkinson ◽  
Renata Ristic ◽  
Imogen McNamara ◽  
Beth Loveys ◽  
WenWen Jiang ◽  
...  

It has been well established that bushfire/wildfire smoke can taint grapes (and therefore wine), depending on the timing and duration of exposure, but the risk of smoke contamination from stubble burning (a practice employed by some grain growers to prepare farmland for sowing) has not yet been established. This study exposed excised bunches of grapes to smoke from combustion of barley straw and pea stubble windrows to investigate the potential for stubble burning to elicit smoke taint. Increased levels of volatile phenols (i.e., chemical markers of smoke taint) were detected in grapes exposed to barley straw smoke (relative to control grapes), with smoke density and the duration of smoke exposure influencing grape volatile phenols. However, the sensory panel did not perceive wine made from grapes exposed to low-density smoke to be tainted, despite the presence of low levels of syringol providing compositional evidence of smoke exposure. During the pea stubble burn, grapes positioned amongst the burning windrows or on the edge of the pea paddock were exposed to smoke for ~15–20 and 30–45 min, respectively, but this only resulted in 1 µg/kg differences in the cresol and/or syringol concentrations of smoke-affected grapes (and 1 µg/L differences for wine), relative to controls. A small, but significant increase in the intensity of smoke aroma and burnt rubber flavor of wine made from the grapes positioned amongst the burning pea stubble windrows provided the only sensory evidence of any smoke taint. As such, had vineyards been located immediately downwind from the pea stubble burn, it is unlikely that there would have been any smoke contamination of unharvested grapes.


Nature ◽  
2021 ◽  
Author(s):  
Leviel Fluhr ◽  
Uria Mor ◽  
Aleksandra A. Kolodziejczyk ◽  
Mally Dori-Bachash ◽  
Avner Leshem ◽  
...  

Author(s):  
Masayuki Teramoto ◽  
Hiroyasu Iso ◽  
Kenji Wakai ◽  
Akiko Tamakoshi

Abstract We examined whether secondhand smoke exposure during childhood was associated with cancer mortality in adulthood among never smokers. In the Japan Collaborative Cohort Study, we analyzed data from 45,722 Japanese lifetime non-smokers who were aged 40–79 years with no history of cancer at the baseline (1988–1990) and completed a lifestyle questionnaire including the number of family members who smoked at home during their childhood (0/1/2/3+ members). The Cox proportional hazards model and competing risk regression were used to calculate the multivariable hazard ratios (HRs) and subdistribution hazard ratios (SHRs) with 95% confidence intervals (CIs) of all and site-specific cancer mortality, according to the number of smoking family members during the participant’s childhood after adjusting for potential confounding factors. During the median follow-up of 19.2 years, a total of 2,356 deaths from cancer were documented. Secondhand smoke exposure was positively associated with the risk of mortality from pancreatic cancer in adulthood; the multivariable HR of 3+ smoking family members was 2.32 (95% CI: 1.14, 4.72), compared with 0 members. The associations were not evident for the risks of total or other types of smoking-related cancers. In conclusion, secondhand smoke exposure during childhood was associated with an increased risk of mortality from pancreatic cancer in adulthood.


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