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(Hypertension. 2008;51:1468.)
© 2008 American Heart Association, Inc.

Editorial Commentaries

Environmental Smoke Exposure

A Complex Cardiovascular Challenge

Martin Hausberg; Virend K. Somers

From the Department of Internal Medicine D (M.H.), University of Muenster Hospitals and Clinics, Muenster, Germany; and the Division of Cardiovascular Diseases (V.K.S.), Department of Internal Medicine, Mayo Clinic, Rochester, Minn.

Correspondence to Virend K. Somers, Division of Cardiovascular Diseases, Department of Internal Medicine, Mayo Clinic, 200 First St SW, Rochester, MN 55905. E-mail somers.virend@mayo.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Passive smoking, or environmental tobacco smoke (ETS) exposure, is a significant public health concern. It is widespread and has been implicated in excess cardiovascular mortality.¹ In the United States, as many as 50 000 cardiovascular deaths per year may be attributable to passive smoking.

The mechanisms by which passive smoking may increase cardiovascular risk are becoming increasingly clear,^1,2 with added insights offered by an intriguing study appearing in this issue of Hypertension.³ Using an elegant experimental design, Argacha et al³ assessed the vascular effects of ETS exposure in humans. They hypothesized, first, that vascular effects of ETS are in part secondary to increased plasma nicotine levels after ETS exposure and, second, that the vascular effects of passive smoking are sustained even after stopping the smoke exposure. To test these hypotheses, they placed subjects in a ventilation hood and exposed them randomly for 1 hour to sidestream tobacco smoke, sidestream nontobacco smoke (from herbal cigarettes), and normal air. Moreover, subjects received nicotine and placebo tablets in random order.

The investigators observed that sidestream tobacco smoke, but not air or nontobacco smoke, increased the augmentation index and heart rate, an effect that persisted even after the end of tobacco smoke exposure. There were no effects on central or peripheral blood pressure. The changes in the augmentation index correlated with the increase in plasma nicotine during ETS exposure, and similar increases in the augmentation index could be induced by nicotine but not placebo tablets. Moreover, sidestream tobacco smoke induced a reduction in . . . [Full Text of this Article]

Related Article:

Acute Effects of Passive Smoking on Peripheral Vascular Function

Jean-François Argacha, Dionysios Adamopoulos, Marko Gujic, David Fontaine, Nadia Amyai, Guy Berkenboom, and Philippe van de Borne
Hypertension 2008 51: 1506-1511. [Abstract] [Full Text] [PDF]