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Original Research: Tobacco Cessation and Prevention |

Secondhand Smoking Is Associated With Vascular InflammationVascular Inflammation in Secondhand Smoking

Tessa Adams, MD; Elaine Wan, MD; Ying Wei, PhD; Romina Wahab, MD; Francesco Castagna, MD; Gang Wang, PhD; Memet Emin, MD; Cesare Russo, MD; Shunichi Homma, MD; Thierry H. Le Jemtel, MD; Sanja Jelic, MD
Author and Funding Information

From the Division of Pulmonary, Allergy, and Critical Care Medicine (Drs Adams, Wahab, Castagna, Wang, Emin, and Jelic), the Division of Cardiology (Drs Wan, Russo, and Homma), and the Division of Biostatistics (Dr Wei), Columbia University College of Physicians and Surgeons, New York, NY; and the Section of Cardiology (Dr Le Jemtel), Tulane University School of Medicine, New Orleans, LA.

CORRESPONDENCE TO: Sanja Jelic, MD, Columbia University College of Physicians and Surgeons, Division of Pulmonary, Allergy, and Critical Care Medicine, PH8 Center, Room 101, 630 W 168th St, New York, NY 10032; e-mail: sj366@columbia.edu


FOR EDITORIAL COMMENT SEE PAGE 6

FUNDING/SUPPORT: Support for this study was received from the National Institutes of Health/National Heart, Lung, and Blood Institute [Grant R01HL106041 to Dr Jelic].

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2015;148(1):112-119. doi:10.1378/chest.14-2045
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BACKGROUND:  The relative risk for cardiovascular diseases in passive smokers is similar to that of active smokers despite almost a 100-fold lower dose of inhaled cigarette smoke. However, the mechanisms underlying the surprising susceptibility of the vascular tissue to the toxins in secondhand smoke (SHS) have not been directly investigated. The aim of this study was to investigate directly vascular endothelial cell function in passive smokers.

METHODS:  Using a minimally invasive method of endothelial biopsy, we investigated directly the vascular endothelium in 23 healthy passive smokers, 25 healthy active smokers, and 23 healthy control subjects who had never smoked and had no regular exposure to SHS. Endothelial nitric oxide synthase (eNOS) function (expression of basal eNOS and activated eNOS [phosphorylated eNOS at serine1177 (P-eNOS)]) and expression of markers of inflammation (nuclear factor-κB [NF-κB]) and oxidative stress (nitrotyrosine) were assessed in freshly harvested venous endothelial cells by quantitative immunofluorescence.

RESULTS:  Expression of eNOS and P-eNOS was similarly reduced and expression of NF-κB was similarly increased in passive and active smokers compared with control subjects. Expression of nitrotyrosine was greater in active smokers than control subjects and similar in passive and active smokers. Brachial artery flow-mediated dilation was similarly reduced in passive and active smokers compared with control subjects, consistent with reduced endothelial NO bioavailability.

CONCLUSIONS:  Secondhand smoking increases vascular endothelial inflammation and reduces active eNOS to a similar extent as active cigarette smoking, indicating direct toxic effects of SHS on the vasculature.

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