Adams T, Wan E, Wei Y, Wahab R, Castagna F, Wang G, Emin M, Russo C, Homma S, Le Jemtel TH, Jelic S, et al.
Chest. Date of publication 2015 Jul 1;volume 148(1):112-119.
1. Chest. 2015 Jul;148(1):112-119. doi: 10.1378/chest.14-2045.
Secondhand Smoking Is Associated With Vascular Inflammation.
Adams T(1), Wan E(2), Wei Y(3), Wahab R(1), Castagna F(1), Wang G(1), Emin M(1),
Russo C(2), Homma S(2), Le Jemtel TH(4), Jelic S(1).
Author information:
(1)Division of Pulmonary, Allergy, and Critical Care Medicine, Columbia
University College of Physicians and Surgeons, New York, NY.
(2)Division of Cardiology, Columbia University College of Physicians and
Surgeons, New York, NY.
(3)Division of Biostatistics, Columbia University College of Physicians and
Surgeons, New York, NY.
(4)Section of Cardiology, Tulane University School of Medicine, New Orleans, LA.
Comment in
Chest. 2015 Jul;148(1):6-8.
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.
DOI: 10.1378/chest.14-2045
PMCID: PMC4493867
PMID: 25742439 [Indexed for MEDLINE]
