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Arterial Endothelial Dysfunction Related to Passive Smoking Is Potentially Reversible in Healthy Young Adults

Olli T. Raitakari, MD, PhD; Mark R. Adams, MB, BS, PhD, FRACP; Robyn J. McCredie, BSc; Kaye A. Griffiths, DMU; and David S. Celermajer, MB, BS, PhD, FRACP
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From Royal Prince Alfred Hospital, The Heart Research Institute, and University of Sydney, Sydney, Australia; and University of Turku, Turku, Finland.

Ann Intern Med. 1999;130(7):578-581. doi:10.7326/0003-4819-130-7-199904060-00017
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Background: Passive smoking is associated with early arterial damage, but the potential for reversibility of this damage is unknown.

Objective: To assess the reversibility of arterial endothelial dysfunction, a key marker of early atherosclerosis.

Design: Cross-sectional study.

Setting: Academic medical center.

Participants: 60 healthy persons 15 to 39 years of age: 20 with no exposure to active or passive smoking, 20 nonsmoking passive smokers (exposure to environmental tobacco smoke for ≥ 1 hour per day for ≥ 2 years), and 20 former passive smokers.

Measurements: Arterial endothelial function measured by noninvasive ultrasonography.

Results: Endothelium-dependent dilatation was significantly better in former passive smokers (5.1% ± 4.1% [range, −1.2% to 15.6%]) than in current passive smokers (2.3% ± 2.1% [range, −0.2% to 6.7%]) (P = 0.01), although both groups were significantly impaired compared with nonsmoking controls (8.9% ± 3.2% [range, 2.1% to 16.7%]) (P ≤ 0.01 for both comparisons).

Conclusions: In healthy young adults, arterial endothelial dysfunction related to passive smoking seems to be partially reversible.


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Flow-mediated, endothelium-dependent dilatation in 20 nonsmokers, 20 former passive smokers, and 20 passive smokers.

For each study group, the box represents the interquartile range (between the 25th and 75th percentiles), with the median value shown as a horizontal bar within each box. The bars outside each box show the range of 95% of values.

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