[目的]评价COX-2 765基因多态性与环境因素在食管癌的发生过程中是否存在交互作用。[方法]采用病例对照研究,病例组食管癌202例,对照组236名正常人。应用Taqman探针法检测COX-2 765位点单核苷酸多态性;运用相乘模型计算COX-2 765基因型与环境因素间的交互作用。[结果]病例组COX-2 765位点C等位基因频率为15.8%,对照组为3.0%,两组差异有统计学意义(χ2=44.489,P<0.001)。携带COX-2 765 GC基因型的个体患食管癌的风险比COX-2 765 GG基因型增加(HR=7.354,95%CI:3.972~13.617)。COX-2 765基因位点与反酸、住所周围有无工厂、住所周围有无空气污染、住所周围有无水污染、10年前水源和被动吸烟等因素的相乘模型交互作用有统计学意义(P<0.05)。[结论]COX-2 765 C等位基因可能为食管癌的遗传危险因素,且COX-2 765基因型与反酸、住所周围有无工厂、住所周围有无空气污染、住所周围有无水污染、10年前水源和被动吸烟存在相乘模型交互作用。 [Objective] To evaluate whether there is an interaction between COX-2 765 gene polymorphism and environmental factors in the pathogenesis of esophageal cancer. [Methods] A case-control study was conducted in 202 cases of esophageal cancer and 236 normal controls in the control group. The single nucleotide polymorphism of COX-2 765 locus was detected by Taqman probe method. The interaction between COX-2 765 genotype and environmental factors was calculated by multiplication model. [Results] The frequency of C allele at COX-2 765 locus was 15.8% in the case group and 3.0% in the control group. There was significant difference between the two groups (χ2 = 44.489, P <0.001). Individuals with the COX-2 765 GC genotype had a higher risk of esophageal cancer than the COX-2 765 GG genotype (HR = 7.354, 95% CI: 3.972 to 13.617). COX-2 765 locus and acid reflux, presence of factories around the residence, air pollution around the residence and water pollution around the residence. The interaction between water source and passive smoking ten years ago was statistically significant (P <0.05). [Conclusion] The COX-2 765 C allele may be the genetic risk factor for esophageal cancer. COX-2 765 genotype and acid reflux, whether there are factories around the residence, air pollution around the residence, water pollution around the residence There was a multiplicative model interaction between water sources and passive smoking 10 years ago.