A substantial body of epidemiological and laboratory data indicates that, unlike the case with lung cancer, the risk of acute myocardial infarction and coronary heart disease associated with exposure to tobacco smoke is non-linear at low doses, increasing rapidly with relatively small doses such as those received from secondhand smoke or actively smoking one or two cigarettes a day.3,4,5
At higher levels of exposure from active smoking (for instance, five to 20 cigarettes a day), the risk of coronary heart disease increases more slowly and in a more linear way.2,8,9
Consistent with the epidemiological findings both for active smoking at lower numbers of cigarettes a day and for exposure to secondhand smoke, laboratory data suggest that even small exposures significantly and rapidly increase platelet aggregation and induce other arterial and haemodynamic changes.5-7,16,18,19
An acute myocardial infarction is commonly precipitated by the activation and aggregation of platelets and the resulting formation of a thrombus or clot that obstructs the arterial blood supply to part of the heart.4,5
Other mechanisms that increase the overall risk of acute myocardial infarction and coronary heart disease, such as reduced high density lipoprotein cholesterol and increased carboxyhaemoglobin concentrations, have been shown to have a more linear dose-response relation with exposure to tobacco smoke.5
Secondhand smoke has a small effect on several of these other mechanisms, but the risk they impart is much more substantial for the dose of toxins delivered by active smoking (for example, from smoking five or more cigarettes a day).
Law and Wald have produced a conceptual model that integrates epidemiological risk data for ischemic heart disease or coronary heart disease for active exposure and exposure to secondhand smoke ().5
In this model, it is estimated that a large proportion, and particularly the more acute aspects, of the risks from exposure to the toxins in tobacco smoke come close to peaking at relatively low levels of exposure, increasing little with exposure to higher levels of active smoking.5
Research has identified the likely mechanisms, including thrombosis, endothelial dysfunction, and inflammation, by which smoking causes acute cardiovascular events.3-7,16,18,19
Figure 1 Dose-response association between exposure to tobacco smoke toxins and ischaemic heart disease (adapted from Law and Wald5)
A recent epidemiological study found that, compared with unexposed non-smokers, non-smokers exposed to secondhand smoke had higher blood chemistry values related to these types of mechanisms—including white blood cells, C reactive protein, homocysteine, fibrinogen, and oxidised low density lipoprotein cholesterol concentrations—and that the values for these biomarkers of inflammation were similar to those observed in active smokers.20
Additionally, laboratory data suggest that even 30 minutes of exposure to a typical dose of secondhand smoke induces changes in arterial endothelial function in exposed non-smokers of a magnitude similar to those measured in active smokers.21
Finally, data on smokers indicate that the risks of sudden death and acute myocardial infarction decline within days or months after smoking cessation.2-3,5,22
Hence, these data and reviews of the laboratory findings on mechanisms3-7,16,18,19
indicate that short term reductions in acute myocardial infarction events after reductions in exposure to low doses of toxins in tobacco smoke are biologically plausible.