Tobacco and Public Health - TCSC Indonesia

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LARYNGEAL CANCER
55 100 in developing countries. More than 90% of cancers of the larynx are squamous
cell carcinomas, and the majority originate from the supraglottic and glottic parts of
the organ.
In most populations, the majority of cases of laryngeal cancer are attributable to
tobacco smoking, alcohol drinking, and the interaction between these two factors (see
below). A protective effect is probably exerted by high intake of fruits and vegetables,
although the evidence regarding specific micronutrients such as carotenoids and
vitamin C is inadequate to draw a conclusion (WCRF 1997). Maté drinking has been
suggested to be a risk factor in studies from Brazil and Uruguay (Austin and Reynolds
1996). Data concerning a possible effect of other food items are not consistent.
Occupational exposure to mists of strong inorganic acids, sulfuric acid in particular, is
an established risk factor for laryngeal cancer (IARC 1992). A possible effect has been
suggested for other occupational exposures, including nickel, asbestos, and ionizing radiation,
but the evidence is not conclusive (Berrino 1993). Laryngeal papillomatosis, a
condition characterized by multiple benign tumours called papillomas, is caused by
infection with human papillomavirus (HPV) types 6 and 11, the same types that cause
genital condylomata acuminata. In children, infection occurs in both genders, during
delivery; in adults, infection is common among men and may occur via orogenital
sexual contact. Papillomatosis patients have an increased risk of laryngeal cancer;
however, studies aimed at assessing the presence of HPV DNA have not yet provided
conclusive evidence for a higher prevalence of infection in cases of laryngeal cancer
than in controls. Herpes simplex virus type 1 is another virus with a possible
causal role in laryngeal cancer (Austin and Reynolds 1996). There is no evidence of
strong genetic factors in laryngeal carcinogenesis; however, polymorphism for
enzymes implicated in the metabolism of alcohol and tobacco, such as alcohol and
aldehyde dehydrogenase, are possible susceptibility factors, with relative risks in the
order of 1.5–2.
Tobacco smoking
A strong association between tobacco smoking and laryngeal cancer has been reported
since the 1950s (Schrek et al. 1950; Doll and Hill 1954; Wynder et al. 1955). This finding
has been replicated in different populations and under different circumstances of
tobacco smoking. As early as 1964, public health and scientific authorities considered
that the causal association between tobacco smoking and laryngeal cancer was clearly
established (USDEHW 1964). Since then, evidence has accumulated on different
aspects of the carcinogenic effect of tobacco smoking on the larynx, based on data
from both cohort and case–control studies. On the one hand, cohort studies, although
they may be considered methodologically superior, are mainly based on mortality data
and have primarily been assembled in areas with a low incidence of laryngeal cancer,
such as the USA, the United Kingdom, Japan, and the Nordic countries, resulting in a
relatively small number of cases, even in the largest cohorts. For example, during the