Tobacco and Public Health - TCSC Indonesia

carcinoma compared with other combined genotypes, in particular, at a low dose level
of cigarette smoking. These observations are consistent with the suggestion that genetic
variations in the ability to metabolize tobacco smoke carcinogens are most important in
determining cancer risk at low levels of exposure, and may be less relevant at higher
smoking doses where high levels of carcinogen exposure overwhelm polymorphisminduced
differences in enzyme activity and/or expression (London et al. 1995).
It should be pointed out, however, that epidemiological results linking, smoking,
gene and oral cancer risk have been inconsistent. In their recent review of 24 published
studies that evaluated the risk of squamous-cell carcinoma of the head and neck in
relation to GSTM1 and GSTT1 genetic polymorphisms, Geisler and Olshan (2001)
reported that some of the studies reported weak-to-moderate associations and others
finding no elevation in risk for the main effect of the gene. Few studies have directly
evaluated the interaction with tobacco. As pointed out by Geisler and Olshan (2001)
none of the studies conducted to date have been able to assess gene–environment
interaction with precision due to limited statistical power. Lack of accurate and
detailed measurement of exposure in many of the studies may have also contributed to
the inconsistent results. It is obvious that well-designed studies with large sample size
are needed to better understand the relationship between smoking, gene and risk of
oral cancer.
Attributable risk
TONGZHANG ZHENG ET AL. 425
The International Agency for Research on Cancer has classified cancer of the oral cavity,
pharynx, and larynx as tobacco-related cancers. A number of case–control studies have
estimated the proportion of oral cancer cases attributable to tobacco smoking, but the
estimated proportion depends on the validity of the estimation of the prevalence of
smoking in the population and the relative risk from the exposure. A number of factors
may affect the estimation: for example, hospital-based studies with patients as
controls, population-based studies with high refusal rate, or lack of adequate control
for major confounding factors (such as alcohol consumption). Since smoking and
drinking are highly correlated, some studies calculated estimates of the population
attributable risk (PAR) of oral cancer due to smoking and/or drinking rather than due
to smoking alone. In most of the studies, the reported PAR from smoking did not
include the impact from smokeless tobacco use, or even pipe and cigar smoking.
Parkin et al. (2000) have estimated that about 46% of the cancer of the oral cavity
and pharynx in men and 11% of these diseases in women are attributable to smoking
worldwide. Estimates vary for specific countries and are presented below.
In Italy, Merletti et al. (1989) estimated that 72.4% of oral cancer cases in men and
53.9% of the cases in women are attributable to smoke of more than 7 g of tobacco/day.
The study by Negri et al. (1993) reported that, for both sexes, the single factor with the
highest attributable risk was smoking, which in males accounted for 81–87% of oral
cancer cases and in females for 42–47%.