Acute exposure to environmental tobacco smoke (ETS) is considered to adversely influence atherogenesis. The aim of this article was to assess whether brachial ultrasonography in subjects with endothelial dysfunction after ETS exposure is associated with atherosclerotic lesions. Never smoker healthy volunteers (n = 18) and subjects with a previous myocardial infarction (MI; n = 10) were studied. Healthy volunteers were 12 men (66%) and 6 women (34%) with a mean age of 34 +/- 9 years. Post-MI subjects were men with a mean age of 53.8 +/- 4.8 years. After assessing endothelial function (by brachial ultrasonography) at rest, study subjects underwent brachial ultrasonography twice: in a smoke-free environment and then in the same environment polluted by cigarette combustion (35 ppm carbon monoxide concentration). Carboxyhemoglobin concentration was measured before and after ETS exposure. Baseline brachial-artery diameter, diameter during reactive hyperemia, and diameter after sublingual nitroglycerin (GTN) administration (endothelium-independent vasodilator) were measured at rest and in both smoke-free and smoking environments. Each study subject acted as their own control. No comparison was made between the two groups. A strong correlation between ETS exposure and endothelial dysfunction was observed in both groups. Post-MI subjects also showed endothelium-independent vasodilation worsening, which is usually due to arterial wall alterations. After ETS exposure, mean flow-mediated vasodilation after GTN was significantly (P < .01) reduced only in post-MI subjects (P < .01). Carboxyhemoglobin concentration increased in both groups (P < .01). ETS exposure may be an effective test to identify endothelial dysfunction and arterial wall alterations by using brachial ultrasonography.