Regular exposure to environmental tobacco smoke is associated with early arterial injury and an increased risk of coronary disease in nonsmokers. The reversibility of these harmful cardiovascular effects would encourage the development of healthier environments. Raitakari and associates compared endothelial responses in three matched groups of healthy young adults: nonsmokers, passive smokers and former passive smokers.

Sixty healthy young adults were studied, comprising a control group of 20 lifelong non-smokers, a group of 20 nonsmokers who had been exposed to environmental tobacco smoke for at least one hour per day for two or more years (with this exposure ceasing at least one year before the study began) and a group of 20 nonsmokers who were currently exposed to environmental tobacco smoke. During the study visit, brachial arterial reactivity and flow were measured ultrasonographically at rest, during reactive hyperemia and after sublingual administration of nitroglycerin. Vessel diameter was measured in each study subject by two independent observers who were blinded as to the participant's smoking status. This measurement technique has demonstrated accuracy for detection of small changes in arterial diameter.

Endothelial-dependent dilatation was significantly better in the former passive smokers than in the current passive smokers, although compared with nonsmoking control subjects, both groups were impaired. In the former passive smoking group, endothelial function was most severely impaired in participants whose last exposure to environmental tobacco smoke was two years before the study or less, compared with those in whom exposure ended two or more years before the study visit.

The authors conclude that endothelial function, a marker of arterial health, is significantly better in young adults who do not have regular exposure to environmental tobacco smoke, with maximal improvement at two years after cessation of passive smoking. Neither group with exposure to tobacco smoke had normal function, suggesting only partial reversibility of the arterial damage associated with passive smoking. The observed partial recovery of the arteries' ability to produce nitric oxide after cessation of passive smoking may indicate disease reversibility. Whether clinical benefit may be obtained by withdrawing from exposure to passive smoke requires further study, but the current data support avoidance of smoke-filled environments.