world cancer report - iarc

Fig. 2.13 Some advertising of alcohol (such as this poster from Malaysia) is
directed specifically towards women. The liquor concerned is advertised as
containing herbs traditionally taken by Chinese women after delivery of their
baby. D. Jernigan
this issue is inconclusive at present.
Similarly, there is no clear evidence as to
whether the key factor in alcohol carcinogenesis
is level of alcohol intake, or
whether the pattern of drinking (e.g. regular
intake of moderate quantities, typically
at meals, versus intermittent intake of
large quantities (“binge drinking”) also
plays a role.
Alcohol drinking is estimated to be
involved in the etiology of 3% of all cancers
(that is, 4% in men, 2% in women,
Table 2.6). In women, approximately half
of the neoplasms attributed to alcohol
drinking are breast cancers. However, the
actual burden of cancers attributable to
alcohol consumption may be greater than
these estimates, given that alcohol drinking
may be a causative factor in cancers
other than those presented, as well as the
likely underestimation of the risk.
Mechanism of carcinogenesis and relevant
model systems
The mechanism(s) of cancer causation by
alcoholic beverages is not known. Ethanol
has not been established as being carcinogenic
to experimental animals. The
compound does not appear to react with
DNA in mammalian tissue. Among
hypotheses proposed to explain the
increased cancer risk are (i) a carcinogenic
effect of chemicals other than
ethanol present in alcoholic beverages
(such as N-nitrosamines); (ii) a solvent
action which facilitates absorption of
other carcinogens (e.g. those in tobacco
smoke); (iii) a carcinogenic role for
acetaldehyde, the major metabolite of
ethanol (Fig. 2.12). This last hypothesis is
supported by evidence that acetaldehyde
is carcinogenic in experimental animals,
as well as by results of recent studies in
populations exhibiting polymorphisms in
genes encoding enzymes which are
involved in the metabolism of alcohol.
Genetic polymorphisms lead to variations
in the level of activity of these enzymes
between individuals (Genetic susceptibility,
p71) such that varying quantities of
acetaldehyde are found from the same
intake of ethanol. Studies in Japan, where
such polymorphisms are frequent, have
shown an increased risk of cancer in subjects
with a genetic profile that is associated
with higher acetaldehyde levels following
alcohol drinking [6]. Results from
Western populations, however, are less
clear-cut.
Apart from being associated with an
increased risk of several types of cancer,
overconsumption of alcohol causes alcoholism
(alcohol addiction), alcohol psychosis,
chronic pancreatitis, liver cirrhosis,
hypertension, haemorrhagic stroke
and low birth weight in babies born to
alcoholic mothers. Furthermore, inebriation
associated with alcohol drinking is
responsible for a high proportion of all
accidents and injuries (15-40%, according
Fig. 2.14 Multiplicative increase in relative risk of laryngeal cancer as a consequence
of both alcohol drinking and active smoking (colour coding approximates
progressive doubling of risk as exposure increases). A.J. Tuyns et al.
(1988) Int J Cancer, 41:483-91.
to the type of injury) and, in particular,
traffic accidents. In global terms, immoderate
consumption of alcohol is responsible
for 1.5% of all deaths and 3.5% of disability-adjusted
years of life lost (Table
2.5) [7]. In contrast, the regular consumption
of a single alcoholic beverage per day
has been clearly associated with a
decreased risk of ischaemic heart disease
[8]. This effect is likely to be due to an
alcohol-induced increase in high-density
Fig. 2.15 An advertisement in the Tamil language
targeted at Indian labourers in Malaysia.
Alcohol drinking 31