Table 3 shows the estimates of association between cigarette smoking variables and Barrett’s esophagus, compared with both GERD controls and population-based controls. Subjects with Barrett’s esophagus were significantly more likely to have ever-smoked cigarettes than both the population controls (OR = 1.67) and the GERD controls (OR = 1.61), although the GERD study-specific estimates appeared to be less heterogeneous (I2 = 11%, 95% uncertainty interval: 0–81%) than estimates from population-based control models (I2 = 82%, 95% uncertainty interval: 54–93%). Increasing pack-years of cigarette smoking was associated with
an increasing OR for Barrett’s esophagus compared with both ABT-263 in vivo control groups ( Table 3, Figure 1), although the risk relationship was not strictly linear in the categories used for assessment; the ORs for Barrett’s esophagus were approximately check details 1.5 for both <15 and 15 to 29 pack-years of smoking exposure groups, and approximately 2 for each of the higher exposure groups (ie, 30–44 and ≥45 pack-years of smoking) compared with each of the control groups and using never smokers as the referent. The spline models, shown in Figure 2, are somewhat more indicative of a linear relationship—at least until approximately 20 pack-years of smoking—and this did not
change when never-smokers were excluded. Conversely, the P value for trend for pack-years of smoking was statistically Docetaxel ic50 significant only when never smokers were included for analysis ( Table 3). Lastly, the additional cigarette smoking variables of duration, intensity, age of initiation,
and duration of cessation were not associated with Barrett’s esophagus after adjustment for total exposure ( Table 3). As shown in Figure 1, there were moderate-to-high levels of heterogeneity that were predominantly the product of the relatively lower estimates generated by the FINBAR study. When the FINBAR study was excluded, the summary ORs from the fully adjusted models slightly increased and heterogeneity (I2 values) decreased (population-based controls: ORever-smoke = 2.09; 95% CI: 1.54–2.83; I2 = 44%; OR<15 = 1.93; 95% CI: 1.36–2.74; I2 = 30%; OR15–29 = 1.75; 95% CI, 0.93–3.30; I2 = 68%; OR30–44 = 2.49; 95% CI: 1.70–3.65; I2 = 0%; OR≥45 = 2.57; 95% CI: 1.79–3.67; I2 = 0%; GERD controls: ORever-smoke = 1.75; 95% CI: 1.43–2.15; I2= 0%; OR<15 = 1.32; 95% CI: 0.95–1.84; I2 = 38%; OR15–29 = 1.62; 95% CI: 1.09–2.41; I2 = 25%; OR30–44 = 2.87; 95% CI: 1.88–4.38; I2 = 19%; OR≥45 = 2.12; 95% CI: 1.50–3.00; I2 = 0%). The stratified models tested whether the effect of a single exposure in relation to Barrett’s esophagus was modified by another variable. When stratified by sex, the estimates for ever-smoking and categories of pack-years, in relation to Barrett’s esophagus, were slightly higher in men (ORever-smoke = 1.81; 95% CI: 1.43–2.