Secondhand smoke exposure induces acutely airway acidification and oxidative stress

Κostikas, Κonstantinos; Minas, Markos; Nikolaou, Eftychia; Papaioannou, Andriana Ι.; Liakos, Panagiotis; Gougoura, Sofia; Gourgoulianis, Konstantinos; Dinas, Petros C.; Metsios, Giorgos S.; Jamurtas, Athanasios Z.; Flouris, Andreas D.; Koutedakis, Yiannis

doi:10.1016/j.rmed.2012.10.017

Cited by 24 publications

(19 citation statements)

References 38 publications

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“…Previous studies have not reported consistent associations between ETS exposure and oxidative stress biomarkers measured in EBC. After a 1h experimental exposure to ETS, healthy young adults had significantly higher levels of H 2 O 2 in EBC (Kostikas et al, 2013). In another study, healthy children who had one or two parents who were smokers did not have significantly higher levels of H 2 O 2 in EBC when compared to children who were not exposed to ETS (Doniec et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

“…Spatial variability and temporality have been shown to be significant predictors of BC concentrations in NYC, stressing the importance of understanding local exposure patterns (Clougherty et al, 2013). Therefore, we sought to characterize the association between short-term domestic measures of BC, and additionally PM 2.5 and environmental tobacco smoke (ETS), another known pollutant associated with oxidative stress (Kostikas et al, 2013; Noakes et al, 2007) and 8-isoprostane measured in EBC as a surrogate marker of oxidative stress in a cohort of children living in NYC. We hypothesized that increased levels of all three of these measures of pollutant exposure would be associated with increased levels of 8-isoprostane in EBC.…”

Section: Introductionmentioning

confidence: 99%

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Domestic airborne black carbon levels and 8-isoprostane in exhaled breath condensate among children in New York City

Rosa

Yan

Chillrud

et al. 2014

Environmental Research

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Background Exposure to airborne black carbon (BC) has been associated with asthma development, respiratory symptoms and decrements in lung function. However, the mechanism through which BC may lead to respiratory symptoms has not been completely elucidated. Oxidative stress has been suggested as a potential mechanism through which BC might lead to adverse health outcomes. Exhaled breath condensate (EBC) allows for the non-invasive collection of airway lining fluid containing biomarkers of oxidative stress like 8-isoprostane, a stable by-product of lipid peroxidation. Therefore, we sought to characterize the association between domestic airborne BC concentrations and 8-isoprostane in EBC. Materials and methods Seven- and eight-year-old children participated in an asthma case–control study in New York City. During home visits, air samples and EBC were collected. Seven day averages of domestic levels of particulate matter <2.5 µm (PM2.5), BC and environmental tobacco smoke (ETS) were measured. Urea and 8-isoprostane were measured by liquid chromatography tandem mass spectrometry (LC/MS/MS) in EBC. Results In univariate models, PM2.5 and BC, but not ETS, were significantly associated with increases in 8-isoprostane in the EBC (β = 0.006 and β = 0.106 respectively, p < 0.05 for both). These associations remained statistically significant for both PM2.5 and BC after adjustment for covariates. In a co-pollutant model including PM2.5, BC and ETS, only BC remained a statistically significant predictor of 8-isoprostane (p < 0.05). Conclusions Our findings suggest the BC fraction of PM might contain exposure relevant to increased oxidative stress in the airways.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Domestic airborne black carbon levels and 8-isoprostane in exhaled breath condensate among children in New York City

Rosa

Yan

Chillrud

et al. 2014

Environmental Research

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“…In the 15 non-smokers, percentage flow-mediated vasodilation decreased and plasma 8-isoprostane increased significantly to concentrations comparable to those of the active smokers. Kostikas et al undertook a randomised controlled cross-over trial in which they exposed 18 never smokers to bar/restaurant levels of ETS for one hour [18]. Following exposure, H 2 O 2 in the exhaled breath condensate increased and remained significantly higher four hours after exposure.…”

Section: Discussionmentioning

confidence: 99%

Association between Exposure to Environmental Tobacco Smoke and Biomarkers of Oxidative Stress Among Patients Hospitalised with Acute Myocardial Infarction

et al. 2013

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ObjectiveTo determine whether exposure to environmental tobacco smoke was associated with oxidative stress among patients hospitalised for acute myocardial infarction.DesignAn existing cohort study of 1,261 patients hospitalised for acute myocardial infarction.SettingNine acute hospitals in Scotland.ParticipantsSixty never smokers who had been exposed to environmental tobacco smoke (admission serum cotinine ≥3.0 ng/mL) were compared with 60 never smokers who had not (admission serum cotinine ≤0.1 ng/mL).InterventionNone.Main outcome measuresThree biomarkers of oxidative stress (protein carbonyl, malondialdehyde (MDA) and oxidised low-density lipoprotein (ox-LDL)) were measured on admission blood samples and adjusted for potential confounders.ResultsAfter adjusting for baseline differences in age, sex and socioeconomic status, exposure to environmental tobacco smoke was associated with serum concentrations of both protein carbonyl (beta coefficient 7.96, 95% CI 0.76, 15.17, p = 0.031) and MDA (beta coefficient 10.57, 95% CI 4.32, 16.81, p = 0.001) but not ox-LDL (beta coefficient 2.14, 95% CI −8.94, 13.21, p = 0.703).ConclusionsExposure to environmental tobacco smoke was associated with increased oxidative stress. Further studies are requires to explore the role of oxidative stress in the association between environmental tobacco smoke and myocardial infarction.

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“…This study was part of a 103 larger study and the procedures followed are described in detail elsewhere (Flouris et al, 2013). 104…”

Section: Study Design and Procedures 99mentioning

confidence: 99%

“…The specific e-cigarette and liquid was selected for the study due 114 to the fact that this liquid was the only one in Greece that had been previously analyzed by an 115 independent publicly-funded Research Institute and consisted of >60% propylene glycol, <10% nicotine, 116 <5% linalool, <5% tobacco essence and <1% methyl vanilyn (Leondiadis, 2009) Non-smokers underwent a control session (PS CON ), a passive tobacco cigarette smoking session (PS TOB ) 124 and a passive e-cigarette smoking session (PS E-CIG ). Blood samples were collected prior to, immediately 125 after, as well as one hour after the smoking sessions, as previously described (Flouris et al, 2013). 126…”

Section: Active Smokers 106mentioning

confidence: 99%

Antioxidant responses following active and passive smoking of tobacco and electronic cigarettes

Poulianiti

Karatzaferi

Flouris

et al. 2016

Toxicology Mechanisms and Methods

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Context: It has been indicated that acute active and passive tobacco cigarette smoking may cause 22 changes on redox status balance that may result in significant pathologies. However, no study has 23 evaluated the effects of active and passive e-cigarette smoking on redox status of consumers. 24Objective: To examine the acute effects of active and passive e-cigarette and tobacco cigarette smoking 25 on selected redox status markers. 26Methods: Using a randomized single-blind crossover design, 30 participants (15 smokers and 15 non-27 smokers) were exposed to three different experimental conditions. Smokers underwent a control 28 session, an active tobacco cigarette smoking session (smoked 2 cigarettes within 30-min) and an active 29 e-cigarette smoking session (smoked a pre-determined number of puffs within 30-min using a liquid 30 with 11 ng/ml nicotine). Similarly, non-smokers underwent a control session, a passive tobacco 31 cigarette smoking session (exposure of 1 hour to 23±1 ppm of CO in a 60 m 3 environmental chamber) 32 and a passive e-cigarette smoking session (exposure of 1 hour to air enriched with pre-determined 33 number of puffs in a 60 m 3 environmental chamber). Total antioxidant capacity (TAC), catalase activity 34 (CAT) and reduced glutathione (GSH) were assessed in participants' blood prior to, immediately after, 35 and 1-hour post-exposure. Results: TAC, CAT and GSH remained similar to baseline levels immediately 36 after and 1-hour-post exposure (p>0.05) in all trials. Conclusions: Tobacco and e-cigarette smoking 37 exposure do not acutely alter the response of the antioxidant system, neither under active nor passive 38 smoking conditions. Overall, there is not distinction between tobacco an e-cigarette active and passive 39 smoking effects on specific redox status indices. 40

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Secondhand smoke exposure induces acutely airway acidification and oxidative stress

Cited by 24 publications

References 38 publications

Domestic airborne black carbon levels and 8-isoprostane in exhaled breath condensate among children in New York City

Domestic airborne black carbon levels and 8-isoprostane in exhaled breath condensate among children in New York City

Association between Exposure to Environmental Tobacco Smoke and Biomarkers of Oxidative Stress Among Patients Hospitalised with Acute Myocardial Infarction

Antioxidant responses following active and passive smoking of tobacco and electronic cigarettes

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