Tobacco and Public Health - TCSC Indonesia

KONRAD JAMROZIK 569
arterial CVD remain unanswered. Some of these are of considerable significance in
terms of public health, others suggest novel lines of enquiry into the biology of vascular
disease, and yet others potentially have ramifications in both these spheres.
Type of tobacco product
The great bulk of the evidence concerning the impact of smoking on CVD is derived
from studies of users of manufactured cigarettes. When pipes and cigars receded from
the tobacco markets in most developed countries in the 1970s and 1980s, epidemiological
interest in these products also waned, but it has been rekindled by a recent resurgence
in the smoking of cigars. There is little doubt that use of such products is
associated with significant hazard (Hein et al. 1992; Jacobs et al. 1999). Much less
information is available concerning hazards potentially associated with traditional
forms of smoking in other communities.
Changes over time in manufactured cigarettes raise a related set of questions, especially
as it is not clear which component or components of tobacco smoke are responsible
for the increased risk of arterial disease in smokers. In practice, with the
epidemiology at least of IHD also changing rapidly, it would be very difficult to detect
whether changes in the source and blend of tobacco, other additives, cigarette papers
or filters affected the risk of vascular events in smokers. Nevertheless, because manufacturers
attempt to tailor their products to particular markets, divergences between
the patterns of vascular disease in otherwise similar countries might potentially provide
clues as to which aspects of tobacco products or their use are particularly relevant
to the development of atherosclerosis.
On the other hand, there is little uncertainty regarding one question relating to type
of tobacco product and risk of CVD. The evidence already cited suggests that smokers
of cigarettes should not be encouraged to change to other tobacco products in an
attempt to reduce their risk of CVD. Direct support for this inference is available from
a long-term prospective study of ‘switching’. Former smokers of cigarettes who
changed to pipes and cigars experienced a significant reduction in risk compared with
men who continued smoking cigarettes but also a 57% excess risk of dying from one of
IHD, lung cancer, and COPD compared with those who stopped smoking entirely
(Wald and Watt 1997). The explanation almost certainly lies in the fact that former
smokers of cigarettes continue to inhale the smoke when they change to other forms of
tobacco product (Goldman 1977).
Lack of reversibility in AAA and PAD
As already noted, case–control studies from Western Australia suggest that the elevation
in risk of AAA and PAD persists long after the individual stops smoking, in contrast
to the rapid declines in excess risk of IHD and CeVD. Wilmink et al. (1999) reported
a relative risk for AAA of 3.0 (95% CL 1.4–6.4) in ex-smokers, but Blanchard et al. (2000),
who summarized a history of smoking in terms of pack-years, did not draw attention