Protecting our children from environmental tobacco smoke: one of our great healthcare challenges.

This year marks the 50th anniversary of the US Surgeon General’s first report on Smoking and Health. This landmark report in 1964 concluded that cigarette smoking is harmful and causes lung and laryngeal cancer. In 1986, the Surgeon General released a further report on the Health Consequences of Involuntary Smoking, providing conclusive evidence that environmental tobacco smoke (ETS) exposure, or passive smoking, causes lung cancer. Half a century later and despite major public health initiatives on tobacco control, tobacco use remains a leading cause of preventable death worldwide. It is estimated that about one-third of adults are regularly exposed to ETS globally. Within the European Union (EU), 14% of non-smokers are exposed to ETS at home, and 30% of working adults are potentially exposed to passive smoking at the workplace. Astonishingly, asmanyas 700millionchildrenworldwide are also exposed to ETS, mostly at home. Furthermore, those who are most likely to smoke are between the ages of 20 and 45, a period that coincides with parenthood. Thus, ETS may represent perhaps the most ubiquitous, hazardous, and potentially preventable adverse environmental exposure for children. Environmental tobacco smoke is composed of sidestream smoke (emitted from the combusting end of a cigarette) and mainstream smoke exhaled by the smoker, with side stream being the main contributor. At least 4000 chemicals have been identified in sidestream smoke, of which 250 are known to be harmful, including 40–60 carcinogenic compounds. Sidestream smoke is qualitatively similar to mainstream smoke but, as it is generated at lower burning temperatures and is unfiltered, the quantity of its chemical constituents is different. Sidestream smoke contains higher quantities of certain carcinogens (e.g. aromatic amines) and it is thought to be 3–4 times more toxic than mainstream smoke per gram of particulate matter. Although sidestream smoke is diluted by room air prior to inhalation, there appears to be no safe level of ETS exposure. In adulthood, an unequivocal causal relationship between ETS and coronary artery disease has been established, conferring a pooled relative risk increase of 25–30% from meta-analyses. There is also persuasive (although less conclusive) evidence that ETS is causally linked to other vascular disease such as stroke, supported by numerous studies which have consistently demonstrated an association between passive smoking and changes in arterial structure and function, using measurements of carotid intima-media thickness (IMT) and brachial flow-mediated dilatation. Putative mechanisms linking ETS with arterial disease include endothelial dysfunction and injury due to oxidative stress, platelet activation and stimulation of the coagulation cascade, enhancement of inflammation, and activation of matrix metalloproteases in atherosclerotic plaques. In children, ETS exposure is associated with more frequent respiratory tract illnesses, decreased lung function, and middle ear disease. In utero, exposure from maternal passive smoking leads to an increased risk of sudden infant death syndrome and reduced birth weights. It has long been recognized that atherosclerosis begins in childhood, and the study by Gall et al. sheds further light that childhood exposure to cardiovascular insults can lead to long-term changes in arterial structure in adulthood. Pooling data from two large and wellconducted longitudinal cohort studies [Cardiovascular Risk in Young Finns Study and Childhood Determinants of Adults Health (CDAH) Study], the authors demonstrate that childhood exposure to smoking by both parents (compared with no exposure) is associated with a thicker carotid IMT in adulthood. Carotid IMT is a wellcharacterized non-invasive marker of atherosclerosis, correlating with burden of coronary atheroma and predictive of future cardiovascular event rates. This difference in carotid IMT was independent of traditional vascular risk factors and smoking status at follow-up. Interestingly, no difference in carotid IMT was found if only one