Tobacco and Public Health - TCSC Indonesia

Table 32.8 Application of Bradford Hill criteria to the evidence on passive smoking and
arterial disease
KONRAD JAMROZIK 567
Criterion Manifestation of arterial disease
Ischaemic Cerebrovascular Abdominal Peripheral
heart disease disease aortic aneurysm arterial disease
Strength � � � �
dose–response ✓ ✓ � �
Consistency
time ✓ ✓ � �
place ✓ ✓ � �
person ✓ � � �
epidemiological ✓ � � �
method
Temporal sequence ✓ � � �
Reversibility
individual � � � �
population � � � �
Specificity � � � �
Biological plausibility ✓ ✓ ✓ ✓
✓ = Evidence available and supports criterion.
� = Available evidence does not support criterion.
� = Evidence either not available or inconclusive.
The epidemiological evidence implicating passive smoking as a cause of IHD
continues to mount (Ciruzzi et al. 1998; McElduff et al. 1998b; Thun et al. 1999;
Irabarren et al. 2001; Rosenlund et al. 2001), with new meta-analyses appearing at
frequent intervals (He et al. 1999), and the data on stroke are also growing (Bonita
et al. 1999). However, as may be seen from Table 32.8, little attention has been afforded
to the role of passive smoking in the genesis of AAA and PAD, and the question of
whether the risk of any of the arterial diseases falls when a non-smoking individual
stops being passively exposed to tobacco smoke has not been studied systematically.
Although the elevation in risk of IHD associated with passive smoking is modest,
both coronary disease and exposure to tobacco smoke are so common among nonsmokers
that the aggregate number of additional cases of heart attack potentially
attributable to passive smoking is very large indeed (Wells 1994). The sceptics, some of
whom openly acknowledge support from the tobacco industry, regularly advance arguments
about misclassification of continuing smokers as ex-smokers, publication bias
(LeVois and Layard 1995)—the tendency for studies showing no association not to be
submitted or accepted for publication—and confounding—systematic differences in
the lifestyles of non-smokers who are and are not passive smokers that render the
former more prone to development of IHD—as possible explanations for pattern of
positive findings in the available literature. These objections are theoretical and largely