Background: Interleukin 1B (IL1B) is involved in pulmonary inflammation induced by environmental or occupational toxins. Chronic inflammation has been implicated in the development of lung cancer.
Methods: We evaluated the role of IL1B (rs1143634, 3954C>T) in a case-control study comprised of 462 lung cancer cases and 379 controls in a Japanese population. Logistic regression was used to assess the adjusted odds ratios (OR) and 95% confidence intervals (95% CI).
Results and discussion: Individuals with a history of smoking and at least one T allele (adjusted OR = 5.45, 95% CI = 2.75-4.42, p < 0.01) presented a higher risk of lung cancer than those with the CC genotype (adjusted OR = 2.86, 95% CI = 2.02-4.05, p < 0.01) as compared with never smokers with the CC genotype (reference). The adjusted attributable proportion because of interaction between the IL1B rs1143634 genotypes and smoking was estimated to be 0.45 (95% CI = 0.08-0.83, p = 0.02), indicating that 45% of the excess risk for lung cancer in ever smokers with at least one T allele was due to additive interaction. Subjects with excessive alcohol intake and at least one T allele had a significantly higher risk (OR = 2.48, 95% CI =1.36-4.54, p < 0.01) than drinkers with appropriate intake and the CC genotype. There was no interaction between the polymorphism and alcohol intake.
Conclusions: Our findings indicate the possible association of the T allele carriers of the IL1B rs1143634 polymorphism with higher risk of lung cancer especially among smokers. Additional studies are warranted to confirm the IL1B rs1143634-smoking interaction suggested in this study.