Tobacco and Public Health - TCSC Indonesia

Introduction
Chapter 23
Tobacco use and risk of oral cancer
Tongzhang Zheng, Peter Boyle, Bing Zhang,
Yawei Zhang, Patricia H. Owens, Qing Lan
and John Wise
Epidemiological studies from various populations have consistently shown that tobacco
smoking (including filter- and non-filter cigarettes, cigars, and pipe tobacco) increases
oral cancer risk. In sum, these results indicate that: ever-smokers experience an
increased risk; current smokers have a higher risk than ex-smokers; those who started
smoking at younger ages have a higher risk than those that started at later ages;
risk increases with amount of cigarettes smoked per day, duration of smoking, and
lifetime pack-years of smoking; smokers of filter cigarettes have lower risk than
smokers of unfiltered cigarettes. Epidemiological studies have also shown that other
factors may also contribute to the effect of smoking on oral cancer risk. For example,
alcohol consumption dramatically increases the effect of tobacco smoking on the
risk of oral cancer. Similarly, xenobiotic metabolizing enzymes, involved in the metabolism
of tobacco carcinogens, have a significant impact on the relationship between
tobacco smoking and oral cancer risk. Overall, based on very conservative estimates,
about 46% of the cancers of the oral cavity and pharynx in men and 11% in women
are attributable to smoking worldwide, with considerable variation by location (Parkin
et al. 2000).
In this review, we will summarize the results from major epidemiological studies
investigating the association between oral cancer and tobacco product use, including
cigarette smoking, pipe tobacco and cigar smoking, and smokeless tobacco use (snuff
dipping and chewing tobacco). In most of the epidemiological studies, ‘oral cancer’
includes cancer of the tongue (CD9 141), mouth (ICD9 143–145), and pharynx
(ICD146, 148, 149), with a few including larynx (ICD9 161). Cancer of the lip
(ICD9 140), salivary glands (ICD9 142), and nasopharynx (ICD9 147) were not
included in most of the epidemiological studies of oral cancer, and therefore, cancers
of these sites will not be discussed in this review. These cancer sites also appear to have
quite different etiological profiles and very distinct natural histories as reviewed by
Boyle et al. (1995).