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Tobacco and Public Health - TCSC Indonesia

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390<br />

SMOKING AND CANCER OF THE OESOPHAGUS<br />

Ille-et-Vilaine, OC is a rare disease in non-smoking moderate drinkers. Further studies<br />

have confirmed that the risk of OC in heavy smokers <strong>and</strong> drinkers, compared to nonor<br />

light smokers <strong>and</strong> drinkers, is of that order of magnitude (Segal et al. 1988; Zambon<br />

et al. 2000).<br />

Tuyns <strong>and</strong> colleagues further noted that the risks appeared to follow a multiplicative<br />

model, i.e. the risk for subjects simultaneously exposed to both alcohol <strong>and</strong> tobacco is<br />

the product of the risks of those exposed to only one factor. Breslow <strong>and</strong> Day (1980)<br />

have modeled in detail the relation between alcohol <strong>and</strong> tobacco consumption <strong>and</strong> risk<br />

of cancer of the oesophagus, using the Ille-et-Vilaine data. Also in many other studies,<br />

a multiplicative model appeared to describe the joint ORs for alcohol <strong>and</strong> tobacco<br />

satisfactorily (Zambon et al. 2000). Moreover, smoking may interact in a multiplicative<br />

way also with other risk factors, e.g. dietary factors.<br />

Although oesophageal cancer is less frequent in women than in men in many<br />

countries, <strong>and</strong> most of the studies were based only or prevalently on men, smoking <strong>and</strong><br />

drinking are also risk factors for women (Gallus et al. 2001).<br />

<strong>Tobacco</strong> in alcohol non-drinkers. The few studies that investigated the effect of smoking<br />

in alcohol non-drinkers were generally based on small numbers of cases. Nevertheless,<br />

they have consistently reported that smoking is a risk factor for OC also in absence of<br />

alcohol consumption (Tuyns 1983; La Vecchia <strong>and</strong> Negri 1989; Tavani et al. 1996).<br />

These studies included both never <strong>and</strong> former drinkers. In a case–control study<br />

conducted in Hong Kong among never drinkers, smoking was still a risk factor for OC,<br />

<strong>and</strong> the OR for heavy smokers was increased 10-fold compared to never smokers<br />

(Cheng et al. 1995).<br />

Smoking <strong>and</strong> drinking cessation. Several studies have shown that the risk is lower in<br />

ex-smokers than in current smokers, <strong>and</strong> declines steeply with time since stopping smoking<br />

(Brown et al. 1988; Yu et al. 1988; La Vecchia et al. 1990; Castellsagué et al. 1999a).<br />

A study conducted in Italy <strong>and</strong> Switzerl<strong>and</strong> provided convincing evidence that stopping<br />

consumption of both alcohol <strong>and</strong> tobacco leads to a substantial reduction of OC<br />

risk (Bosetti et al. 2000). After 10 or more years since stopping both habits the risk was<br />

only about one-tenth of that of current smokers <strong>and</strong> drinkers (Fig. 22.2). Similar<br />

results were found also in a combined analysis of five case–control studies conducted<br />

in South America (Castellsagué et al. 2000).<br />

Attributable risks. The proportion of cases of OC attributable to smoking, <strong>and</strong> to the<br />

joint effect of alcohol <strong>and</strong> tobacco, varies widely between geographical areas. The<br />

attributable fraction depends not only from the relative risk but also from the frequency<br />

of the exposure in a population. Moreover, as shown above, the effect of smoking is<br />

magnified by alcohol (<strong>and</strong> possibly other risk factors). Thus, even the same amount of<br />

smoking may have a different impact in populations with different exposure to alcohol<br />

or other factors. In North <strong>and</strong> South America <strong>and</strong> Europe, alcohol <strong>and</strong> tobacco explain<br />

the vast majority of cases, particularly in men, where the disease is more frequent than

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