Dataset Information

Brief exposure to secondhand smoke reversibly impairs endothelial vasodilatory function.

ABSTRACT:

Introduction

We sought to determine the effects of brief exposures to low concentrations of tobacco secondhand smoke (SHS) on arterial flow-mediated dilation (FMD, a nitric oxide-dependent measure of vascular endothelial function), in a controlled animal model never before exposed to smoke. In humans, SHS exposure for 30 min impairs FMD. It is important to gain a better understanding of the acute effects of exposure to SHS at low concentrations and for brief periods of time.

Methods

We measured changes in FMD in rats exposed to a range of real-world levels of SHS for durations of 30 min, 10 min, 1 min, and 4 breaths (roughly 15 s).

Results

We observed a dose-response relationship between SHS particle concentration over 30 min and post-exposure impairment of FMD, which was linear through the range typically encountered in smoky restaurants and then saturated at higher concentrations. One min of exposure to SHS at moderate concentrations was sufficient to impair FMD.

Conclusions

Brief SHS exposure at real-world levels reversibly impairs FMD. Even 1 min of SHS exposure can cause reduction of endothelial function.

SUBMITTER: Pinnamaneni K

PROVIDER: S-EPMC3977486 | biostudies-literature | 2014 May

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Brief exposure to secondhand smoke reversibly impairs endothelial vasodilatory function.

Pinnamaneni Kranthi K Sievers Richard E RE Sharma Rikki R Selchau Amanda M AM Gutierrez Gustavo G Nordsieck Eric J EJ Su Robert R An Songtao S Chen Qiumei Q Wang Xiaoyin X Derakhshandeh Ronak R Aschbacher Kirstin K Heiss Christian C Glantz Stanton A SA Schick Suzaynn F SF Springer Matthew L ML

Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco 20131203 5

<h4>Introduction</h4>We sought to determine the effects of brief exposures to low concentrations of tobacco secondhand smoke (SHS) on arterial flow-mediated dilation (FMD, a nitric oxide-dependent measure of vascular endothelial function), in a controlled animal model never before exposed to smoke. In humans, SHS exposure for 30 min impairs FMD. It is important to gain a better understanding of the acute effects of exposure to SHS at low concentrations and for brief periods of time.<h4>Methods</ ...[more]

PMID: 24302638

Similar Datasets

Project description:BackgroundAirports may represent significant sources of secondhand smoke (SHS) exposure for both travelers and employees. While previously common smoking rooms have largely disappeared from US airports, smoking continues to occur outdoors at terminal entrances. SHS may be especially high at arrival areas, since they oftentimes are partially enclosed by overhead departures, creating stagnant microenvironments. This study assessed particulate matter <2.5 microns in diameter (PM2.5), a common surrogate for SHS, at airport terminal locations to evaluate both outdoor exposure risk and possible indoor drift of SHS from outdoor sources.MethodsA convenience sample of nine airport terminal arrival areas in the US state of Florida was surveyed between February and July 2018. PM2.5 levels were assessed outdoors and indoors at terminal entrances and at control areas far into terminal interiors. We also examined the impact of smoking location on SHS exposure by correlating cigarette and passing vehicle counts with PM2.5 levels at terminals with contrasting proximity of designated smoking locations to terminal entrances.ResultsAlthough outdoor PM2.5 levels (mean 17.9, SD 6.1 µg/m3) were significantly higher than indoors (p < 0.001), there was no difference between indoor areas directly inside terminal entrances and areas much further interior (mean 8.8, SD 2.6 vs mean 8.5, SD 3.0 µg/m3, p=0.49). However, when smoking areas were in close proximity to terminal entrances, the number of lit cigarettes and vehicular traffic per minute predicted 70% of the variance of PM2.5 levels (p < 0.001), which was attributable mostly to the cigarette number (β = 0.83; 95% CI (0.55 to 1.11); p < 0.001). This effect was not observed at smoking areas further away.ConclusionPM2.5 data did not suggest indoor drift from outside smoking. Nevertheless, absolute exposure outdoors was high and correlated with the location of designated smoking areas. Further studies are needed to examine the effect of microclimate formation on exposure risk.

Project description:BackgroundProlonged past exposure to secondhand tobacco smoke (SHS) in never-smokers is associated with abnormal lung function and reduced diffusing capacity suggestive of an associated lung tissue injury and damage. The mechanisms by which past SHS exposure may contribute to lung tissue damage are unknown. Elastin is a major constituent of extracellular matrix in lung parenchyma.ObjectiveTo determine whether past exposure to SHS is associated with ongoing lung tissue damage as indicated by elevated elastin degradation products that are linked to lung function.MethodsWe measured the plasma levels of elastin degradation markers (EDM) from 193 never-smoking flight attendants with a history of remote SHS exposure in aircraft cabins and 103 nonsmoking flight attendants or sea-level control participants without such history of cabin SHS exposure and examined those levels versus their lung function with adjustment for covariates. The cabin SHS exposure was estimated based on airline employment history and years of the smoking ban enactment.ResultsThe median [interquartile range] plasma EDM level for all participants was 0.30 [0.24-0.36] ng/mL with a total range of 0.16-0.65 ng/mL. Plasma EDM levels were elevated in those with a history of exposure to cabin SHS compared to those not exposed (0.33±0.08 versus 0.26±0.06 ng/mL; age- and sex-adjusted P<0.001). In those with a history of cabin SHS exposure, higher EDM levels were associated with a lower diffusing capacity (parameter estimate [PE] 95% [confidence interval(CI)]=4.2 [0.4-8.0] %predicted decrease per 0.1 ng/mL increase in EDM; P=0.030). Furthermore, EDM levels were inversely associated with forced expiratory volume in 1 second (FEV1), FEV1 to forced vital capacity (FVC) ratio , and forced expiratory flow rate between 25% and 75% ( FEF25%-75%) (PE [95%CI]=5.8 [2.1-9.4], 4.0 [2.2-5.7], and 12.5 [5.8-19.2] %predicted decrease per 0.1 ng/mL increase in EDM, respectively; P<0.001). Plasma EDM mediated a substantial fraction of the association of SHS with FEV1, FVC, and FEF25%-75% (P<0.05).ConclusionsLong after past exposure to SHS, there is ongoing elastin degradation beyond what is expected from the aging process, which likely contributes to lower lung function and a reduced pulmonary capillary bed as seen in chronic obstructive pulmonary disease (COPD).

Dataset Information

Brief exposure to secondhand smoke reversibly impairs endothelial vasodilatory function.

Introduction

Methods

Results

Conclusions

Publications

Brief exposure to secondhand smoke reversibly impairs endothelial vasodilatory function.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets