4.2 Cardiovascular disease and passive smoking

Research findings from Australia and overseas have confirmed an association between exposure to environmental tobacco smoke and the development of cardiovascular disease.(17,18,19,20)

Three reviews of the available epidemiological studies measuring ETS exposure and the incidence of cardiovascular disease have concluded that passive smoking increases the risk of heart disease.(18,19,20) The American Heart Association's Council on Cardiopulmonary and Critical Care has concluded that 'environmental tobacco smoke is a major preventable cause of cardiovascular disease and death'.(21) Glantz and Parmley(18) estimate that heart disease caused by passive smoking is the third leading preventable cause of death in the United States, ranking behind active smoking and alcohol abuse, and that non-smokers living with smokers show an increased risk of ischaemic heart disease or myocardial infarction of around 30%. A clear dose-response relationship is evident.

The authors conclude that it is likely that disease mechanisms are similar in non-smokers to those causing heart disease in active smokers, but that exposure to passive smoking also causes biochemical and enzyme changes, which could promote disease progression in non-smokers.(18) (Mechanisms by which active smoking causes heart disease are discussed in Chapter 3, Section 1). All three reviews conclude that passive smoking causes ten or more times the burden of illness through heart disease than it does from lung cancer.

A New South Wales study has shown that exposure to environmental tobacco smoke at home more than doubles the risk of myocardial infarction or coronary death among non-smoking women.(20) This study has also observed that exposure to ETS increases fibrinogen concentrations in non-smokers. An increased level of fibrinogen, a blood clotting factor, in turn promotes development of thrombosis (blood clotting), which suggests that passive smoking may increase the risk of cardiac death by at least some of the same mechanisms as active smoking.(20)

A joint study undertaken by researchers in London and Sydney examined damage to arteries from passive smoking in healthy people aged 15 to 30. They found that people as young as 15 had signs of the first stages of damage to their arteries as a result of long-term exposure to tobacco smoke. The researchers also found that effect was dose-related, that is, the greater the exposure to environmental tobacco smoke, the greater the effect on the arteries' dilation.(22)

A recent meta-analysis of 19 studies determined that environmental tobacco smoke caused a 23% increased risk of ischaemic heart disease.(22a) This risk seems high, however a small exposure to tobacco smoke has a large effect on heart disease. The research shows that this is probably due to the body's blood clotting system being very sensitive to small amounts of tobacco smoke.

 


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