Full Report - Food, Nutrition, and the Prevention of Cancer

4.7.4.2 Specific
Classification. Different types of tea, coffee, and soft drinks
are consumed in different cultures. The ways in which tea
and coffee are prepared and drunk also vary. For coffee, this
includes the degree of roasting, the methods of brewing
(which determine the strength and composition), and the
different substances added. Similarly, tea may be consumed
with or without milk and in different strengths. Associations
seen in one population but not another may reflect some
aspect of the drink as consumed in that population rather
than the drinks themselves. In some studies, fruit juices and
bottled waters are included in the definition of soft drinks.
Measurement. Fluid intake is best estimated from urine
collection, but this is rarely done. Instead, estimates are
usually made from food frequency questionnaires.
Confounding. In interpreting the results of epidemiological
studies of all types of drink, confounding by other habits
should be considered. For example, heavy consumers of soft
drinks, tea, or coffee may also be smokers and drinkers of
alcohol.
People who are physically active often consume more liquid
than those who are not. Physical activity is therefore a confounder
of the relationship between the volume of fluid drunk
and cancer risk, but may not be adequately adjusted for.
Reporting bias. Soft and cola drinks are often identified as
unhealthy, and studies that depend on self-reporting may
disproportionately underestimate consumption.
4.7.5 Evidence and judgements
The full systematic literature review (SLR) is contained on
the CD included with this Report.
4.7.5.1 Water
The evidence was too sparse or inconsistent to draw any conclusion
about the relationship between water quantity and
cancer risk.
4.7.5.1.1 Water-borne contaminants: arsenic
Ecological studies based on known arsenic concentrations in
water may be interpreted more robustly than for many other
dietary exposures.
Lung
Two cohort studies, 12-17 2 case-control studies 18 19 and 12
ecological studies 20-30 investigated arsenic in drinking water
and lung cancer.
Both cohort studies showed statistically significant
increased risk of lung cancer for the highest intake group
compared to the lowest. 12-17 Although meta-analysis was not
possible, both studies reported that a dose-response relationship
was apparent. One study (in Taiwan) based in a
population with endemic black foot disease, a manifestation
of arsenicosis, reported an effect estimate of 3.29 (95% confidence
interval (CI) 1.60–6.78) for average arsenic level in
152
P ART 2 • EVIDENCE AND JUDGEMENTS
well water. 13 The other study reported a quantified effect
estimate, which was 3.66 (95% CI 1.81–7.03), but this study
(based in Japan) did not adjust for smoking. 17
Both case-control studies showed increased risk of lung
cancer for the highest intake group compared to the lowest, 18
19 19 which was statistically significant in one. The other study
did not report confidence intervals. Effect estimates were
3.0118 and 8.9 (95% CI 4.0–19.6). 19
Ecological studies were made in populations from
Argentina, 27 Belgium, 21 Chile, 29 China, 23 Switzerland, 20 and
Taiwan, 22-26 30 as well as worldwide. 28 Eight studies showed
increased risk of lung cancer with increasing levels of arsenic
in drinking water, 21-25 27 29 30 which was statistically signifi-
cant in four. 24 27 29 30 Two studies showed decreased risk,
20 26
which was statistically significant in one. 26 One study reported
different inconsistent results for men and women (correlation
coefficients of -0.51 for men and 0.07 for women). 28
One study showed that measures to lower arsenic levels in
drinking water by using tap water rather than well water
were associated with a fall in lung cancer rates in a region
of Taiwan with endemic black foot disease. 25
The general mechanisms through which arsenic could
plausibly cause cancer are outlined below. In addition, soluble
arsenic in drinking water induces lung cancers in animal
models and causes chronic lung disease. 5
The evidence is ample and consistent, both from
cohort and case-control as well as ecological studies.
There is a dose-response relationship and the effect
size is relatively large. There is robust evidence for
mechanisms. The evidence that arsenic is a cause of
lung cancer is convincing.
Skin
Two cohort studies, 31 32 5 case-control studies, 33-37 1 crosssectional
study, 38 20 22 24 27 29 30 39-43
and 11 ecological studies
investigated arsenic in drinking water and skin cancer.
Both cohort studies showed non-significant increased risk
with increasing levels of arsenic in the water31 32 ; however,
for one study the increased risk was apparent in women but
not in men. 32 Effect estimates were 1.82 (95% CI 0.5–4.66)
for women and 0.83 (95% CI 0.17–2.43) for men in Utah, 32
and 1.21 (95% CI 1.00–1.47) per 100 µg/l. 31
Two case-control studies measured arsenic levels in toeand
fingernails. 36 37 Such measures are less subject to error
and bias than some other methods to assess actual exposure
to a carcinogen. One study reported a significant increased
risk for melanoma with a risk estimate of 1.65 (95% CI
1.27–2.14) per 100 ng/g36 ; the other study reported non-significant
increased risk 1.02 (95% CI 0.90–1.17) per 100 ng/g
for basal cell carcinoma and 1.12 (95% CI 0.95–1.32) for
squamous cell carcinoma. 37
Two case-control studies that reported on dietary arsenic
showed increased risk with increased intake, 33 35 which was
statistically significant in one. 33 One study reported a nonsignificant
decreased risk. 34
The cross-sectional study showed a statistically significant
increased risk, with a partially adjusted effect estimate of
5.04 (95% CI 1.07–23.8) for > 0.71 versus 0 parts per mil-