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Tobacco and Public Health - TCSC Indonesia

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556<br />

TOBACCO AND CARDIOVASCULAR DISEASE<br />

Table 32.2 Application of Bradford Hill criteria to the evidence on ACTIVE smoking <strong>and</strong><br />

arterial disease<br />

Criterion Manifestation of arterial disease<br />

Ischaemic Cerebrovascular Abdominal Peripheral<br />

heart disease disease aortic aneurysm arterial disease<br />

Strength ✓ ✓ ✓ ✓<br />

dose–response ✓ ✓ ✓ ✓<br />

Consistency<br />

time ✓ ✓ ✓ ✓<br />

place ✓ ✓ ✓ ✓<br />

person ✓ ✓ ✓ ✓<br />

epidemiological method ✓ ✓ � ✓<br />

Temporal sequence ✓ ✓ � ✓<br />

Reversibility<br />

individual ✓ ✓ � �<br />

population ✓ � � �<br />

Specificity � � � �<br />

Biological plausibility ✓ ✓ ✓ ✓<br />

✓ = Evidence available <strong>and</strong> supports criterion.<br />

� = Available evidence does not support criterion.<br />

� = Evidence either not available or inconclusive.<br />

of secular trends in these diseases in whole communities, <strong>and</strong> the role that changes in<br />

smoking habits play in initiating <strong>and</strong> maintaining those trends, is even more difficult.<br />

Secondly, as the foregoing discussion makes clear, smoking is just one of several major,<br />

independent, <strong>and</strong> potentially modifiable risk factors for development of CVD, which<br />

has direct implications for Bradford Hill’s criterion of specificity. Thirdly, if both cigarettes<br />

<strong>and</strong> patterns of their use change simultaneously, it may be close to impossible<br />

to discern, at least retrospectively, how much, if any, each change contributed to a<br />

population’s experience of CVD.<br />

But all of this is to run before we can walk. Let us first consider the individual criteria<br />

proposed by Bradford Hill <strong>and</strong> how they apply to the data on active smoking. Table 32.2<br />

summarizes such a survey.<br />

Strength <strong>and</strong> dose–response<br />

As may be seen from Table 32.2, active smoking of cigarettes is a strong risk factor for<br />

disease in each of the four principal arterial territories, <strong>and</strong> shows an obvious<br />

dose–response in each. The dose–response relationships shown in Tables 32.3 <strong>and</strong> 32.4<br />

are representative of those seen internationally, <strong>and</strong> those for IHD in Perth are further<br />

supported by data from cohort studies conducted in the same population (see Table 32.5).<br />

Unexpectedly, follow-up of healthy subjects recruited to the earlier case–control study

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