Tobacco and Public Health - TCSC Indonesia

560
TOBACCO AND CARDIOVASCULAR DISEASE
of stroke (Jamrozik et al. 1994) revealed an inverse relationship between current smoking
and major cardiovascular events (Jamrozik et al. 2000b).
Apart from the long-running studies in Framingham (Dawber 1980) and of British
doctors (Doll et al. 1980, 1994) that have already been mentioned, new cohorts continue
to be established in a wide variety of countries. Individual studies take some time
to ‘mature’, although much useful information has already been obtained from the very
large cohorts under follow-up in the Nurses Health Studies (Hu et al. 2000) and Health
Professionals Study (Verhoef 1998) and from men screened for participation in the
Multiple Risk Factor Intervention Trial (MRFIT) (Stamler et al. 1986). In addition,
patients with AMI who participated in the ISIS-2 trial of aspirin and streptokinase
have now been included in one of the largest case–control comparisons ever conducted
for a non-communicable disease (Parish et al. 1995). Once again, the results show a
strong and dose-related increase in risk of major coronary events associated with active
smoking.
A recent, large case–control study of stroke in New Zealand (Bonita et al. 1999)
stands out from all of these studies for two reasons apart from its focus on events in the
cerebral rather than the coronary arteries. The first is that ascertainment of cases was
population-based and therefore less subject to bias related to either the selected nature
of the participants or the fact that, to be included, those suffering an event had to survive
to reach hospital alive. Secondly, it has been one of the first studies deliberately to
exclude passive smokers from the control group, a problem that may have affected
many of the ‘classical’ studies and that, as Bonita et al. demonstrate, serves to underestimate
the effects of active smoking on risk of disease (1999). The difference between
their two sets of estimates, seen in Table 32.6, is sufficiently large to support a recommendation
that exclusion of passive smokers should now be the ‘gold standard’ in such
studies, especially since the spread of smoke-free policies has reached a point where
large proportions of many communities are now able to live, travel, work, and relax in
smoke-free environments if they so choose.
Smoking has long been accepted as a risk factor for both AAA and particularly PAD,
but, as we shall see later, the relative lack of systematic study of these conditions appears
to have contributed to a delay in our learning some important lessons about them.
Consistency
As has already been intimated, that active smoking is an important risk factor for the
development of IHD is now supported by close to fifty years of research that includes
both men and women, both case–control and cohort investigations, and evidence from
a wide variety of geographical settings. Much the same is true of stroke, with one
important proviso to which we will return. The more limited data on PAD and AAA
demonstrate the same features, although both of these tend to be disproportionately
diseases of men, the former possibly because men took up smoking much sooner than
women, the latter at least partly because of a genetic component.