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Tobacco and Public Health - TCSC Indonesia

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TONGZHANG ZHENG ET AL. 411<br />

the control group selected represents the population that produced the cases. Indeed,<br />

in some of the hospital-based case–control studies, the control group considered<br />

included cancers thought to be unrelated to smoking <strong>and</strong> drinking, <strong>and</strong> some with<br />

benign neoplastic or non-neoplastic lesions, which may be smoking related. If it turns<br />

out that these diseases were actually associated with tobacco smoking, then, the true<br />

relationship between tobacco smoking <strong>and</strong> oral cancer risk would be underestimated.<br />

Since most of these studies showed a strong association between cigarette smoking <strong>and</strong><br />

oral cancer risk, underestimation is less of a concern. But the variation of disease in<br />

controls in different studies is still important to note as when considered together with<br />

the relatively small sample size in some of the studies, it may explain in large part, the<br />

significant variation in the magnitude of the reported association between tobacco<br />

smoking <strong>and</strong> oral cancer risk.<br />

In 1984, Elwood et al.reported an alcohol-adjusted OR of 2.8 (95% CI 1.3–6.0) for<br />

smoking 50 or more cigarettes per day when compared to never smokers. Additional<br />

adjustment for 4 other factors reduced the OR to 2.1 (95% CI 0.9–4.8). A weak association<br />

observed in this study could be due to the fact that controls were composed of<br />

various cancer patients (including cancer of the prostate, colo-rectum, skin, breast, etc.).<br />

In a case–control study of oral cancer in Brazil, Franco et al. (1989) reported that<br />

tobacco smoking was, by any measure, the strongest risk factor for oral cancer in this<br />

population. The adjusted ORs for ever vs. never smokers were 6.3 (95% CI 2.4–16.3),<br />

5.5 (95% CI 1.2–24.8), 13.9 (95% CI 4.4–44.2), <strong>and</strong> 7.0 (95% CI 2.7–18.7) for industrial<br />

br<strong>and</strong> cigarettes, cigars, pipe, <strong>and</strong> h<strong>and</strong>-rolled cigarettes, respectively. The OR for the<br />

heaviest vs. the lowest consumption categories (>100 vs. 49 pack-years when compared to non-smokers. In<br />

females, the corresponding values were 1.5 (95% CI 0.4–5.1) <strong>and</strong> 12.0 (95% CI<br />

3.8–38.0), respectively. Site-specific analysis for males also showed a significant<br />

increase with increasing pack-years of cigarette smoking for cancer of the larynx<br />

(P trend < 0.01), tongue (P trend < 0.01), <strong>and</strong> floor of mouth (P trend = 0.02), but not for<br />

orohypopharynx (P trend = 0.13), <strong>and</strong> other oral cavity (P trend = 0.15). A significant risk<br />

reduction was observed after 15 or more years of smoking cessation.<br />

Zheng et al. (1990) conducted a case–control study of oral cancer in Beijing, China,<br />

including 404 histologically confirmed incident cases <strong>and</strong> an equal number of hospitalbased<br />

controls. The study reported an alcohol-adjusted OR of 2.4 (95% CI 1.5–4.0) for<br />

male smokers when compared to never smokers. Three measures of level of exposure—<br />

cigarette equivalents smoked per day, years smoked, <strong>and</strong> lifetime pack-years of<br />

smoking—all showed highly significant exposure–response relationships (P trend < 0.001).

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