Tobacco and Public Health - TCSC Indonesia

studies have demonstrated a positive correlation between DNA adduct levels and patient
smoking status. Jones et al. (1993) have shown that the mean adduct levels in isolated oral
tissue DNA from smokers were significantly higher than in non-smokers, and adduct
levels in ex-smokers (1–12 years since cessation) were similar to those in nonsmokers.
Studies have suggested that the p53 tumor suppressor gene is a likely target for
tobacco carcinogens (Jones 1998; Ralhan et al. 1998; Saranath et al. 1999; Hsieh et al.
2001). p53 tumor suppressor gene mutations are the most frequently found genetic
errors in oral cancer (Jones 1998). Brennan et al. (1995) have shown that p53 mutation
were more common in tumors from patients who were exposed to both tobacco and
alcohol than in tumors from patients who were not exposed to these risk factors.
As discussed previously, genetic polymorphism of drug-metabolizing enzymes may
affect the susceptibility to oral cancer from exposure to tobacco carcinogens.
Conclusion
In 1986 an IARC Working Party concluded that there was sufficient evidence that
tobacco was carcinogenic to humans and that the occurrence of malignant tumors of
the upper digestive tract was causally related to the smoking of different forms of
tobacco. IARC has also concluded that there is sufficient evidence that oral use of snuff
of the types commonly used in North America and western Europe is carcinogenic to
humans, and there was sufficient evidence that the habit of chewing betel quid containing
tobacco was carcinogenic in humans (IARC 1985). More recent epidemiological
studies and experimental studies further support these conclusions. There is convincing
evidence that a large attributable risk can be ascribed to the joint habits of cigarette
smoking and alcohol consumption.
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