LAUSR

E xposure to environmental tobacco smoke, also called passive smoking and secondhand smoke (SHS), is the process of breathing other people’s smoke. SHS is a complex mixture of gases and particles and includes sidestream smoke given off from burning cigarettes, cigars, and pipe tobacco, and mainstream smoke exhaled by the smoker [1,2]. Many SHS chemicals are present in higher concentrations in sidestream smoke than in the mainstream smoke that the smoker inhales, with nearly 85% of the smoke in a room, resulting from sidestream smoke [1]. SHS is a public health problem given that there are usually at least as many passive as active smokers. It has been estimated that exposure to SHS affects onequarter–one-third of the population, accounting for 1% of worldwide mortality and 0.7% of the worldwide burden of disease in disability-adjusted life years in 2004 [3]. One of the main long-term outcomes related to SHS is cardiovascular disease (CVD), in particular, coronary heart disease and stroke [1–4]. Among others, an atherosclerotic mechanism mediating the association has been invoked [1]. Cardiovascular risk factors are thus of interest in this association as they might add biological plausibility to the SHS/ CVD association, and they may also be preventable outcomes of passive smoking. However, little is known about the relationship between passive smoking and major cardiovascular risk factors. The few previous studies on the relationship between passive smoking and blood pressure (BP) or hypertension found a positive association [5–9]; however, the evidence has strong methodological limitations (e.g. using a crosssectional study design). Interestingly, passive smoking has also been found to be associated with masked hypertension [10], although this study was again cross-sectional and limited to subjects self-referred to an out-patient hypertensive clinic. Likewise, a few studies on the relationship