Tobacco and Public Health - TCSC Indonesia

438
SMOKING AND STOMACH CANCER (B)
Several surveys have shown that H. pylori infection status is not associated with the
smoking habit. Limburg et al. (2001) examined association between seropositivity
for H. pylori with different risk factors in Linxian prospective study. The proportion
of seropositive individuals was similar in non-smokers (58%) and in smokers
(61%). Moreover, the prevalence of CagA seropositive individuals was higher in
non-smokers (32%), than in smokers (24%). Another study in China looked at association
between prevalence of H. pylori infection and smoking, drinking, and diet.
Prevalence of H. pylori positivity was higher among never smokers, relative risk
for ever smoking being 0.9 (0.7–1.0). In highest category of smokers of more than
14 235 pack-years OR was 0.8 (0.6–1.1) (Brown et al. 2002). Similar evidence is
observed in Europe. Prevalence of seropositive subjects is similar among never
(50.9%), former (48.7%), and current smokers (45.1%). In fact, among never smokers
proportion of H. pylori seropositives is somewhat higher than among current smokers
(OR = 0.8, CI 0.7–0.9) (The EUROGAST study group 1993). In only one study
conducted in north England smoking of more than 35 cigarettes/day turned to be
associated with higher risk of H. pylori positivity. However, it should be noted that the
proportion of subjects infected were identical in all lower smoking intensity categories.
Overall there is no association between H. pylori infection status and smoking
(Moaygedy et al. 2002).
Zaridze et al. (2000) computed the interaction between H. pylori seropositivity and
smoking in relation to the risk of stomach cancer. H. pylori infection did not affect
smoking-associated risk of stomach cancer. However, relative risk of stomach cancer
was higher among H. pylori positive men. Similar results were obtained by Siman et al.
(2001). The results of these analyses suggest that smoking potentiates the effect of
H. pylori infection on the risk of stomach cancer.
The relative risk of gastric cancer associated with smoking is most probably underestimated
in hospital-based case–control studies, due to substantial proportion of
patient with smoking-related diseases in control groups. Of special concern are the
studies in which prevalence of smoking was higher in controls than in cases and in
which controls with smoking-associated diseases were recruited (Jedrichowski et al.
1986; Lee et al. 1990; Boeing et al. 1991; Agudo et al. 1992).
According to one widely accepted model of gastric carcinogenesis development
of cancer in stomach is preceded by several stages, including chronic atrophic
gastritis, intestinal metaplasia, and dysplasia. Relative risk of developing these
lesions have been shown to be associated with smoking. Risk of both metaplasia (P =
0.03) and dysplasia (P < 0.001) increased significantly with increasing tobacco
consumption, but the magnitude of association was much stronger for dysplasia. The
odds ratio for dysplasia among heavy smokers (> 20 cigarettes/day) compared with
lifelong non-smokers exceeded 2 and was statistically significant (OR = 2.2, 95% CI
1.5–3.3). The risks of metaplasia and dysplasia also increased with increasing duration
of smoking. P values for trend were 0.02 and < 0.001 for metaplasia and dysplasia,