Olsen A O, Dillner J, Skrondal A, Magnus P
Department of Population Health Sciences, National Institute of Public Health, Oslo, Norway.
Epidemiology. 1998 May;9(3):346-9.
To study the combined effect of smoking and human papillomavirus (HPV) type 16 infection in high-grade cervical intraepithelial neoplasia, we analyzed data from a Norwegian population-based case-control study including 90 patients and 216 controls, 20-44 years of age. We assessed HPV-16 status both by polymerase chain reaction detecting virus DNA and by enzyme-linked immunosorbent assay detecting antibodies against virus capsid. Smoking was associated with cervical intraepithelial neoplasia grade II-III in HPV-16-positive individuals. Using the jointly unexposed (HPV-16 DNA-negative never-smokers) as the reference group, we determined the risk of cervical intraepithelial neoplasia grade II-III in HPV-16 DNA-positive never-smokers and HPV-16 DNA-positive ever-smokers (odds ratio = 15.7; 95% confidence limits = 3.2, 76.5, and odds ratio = 65.9; 95% confidence limits = 22.3, 194.3, respectively). The estimated proportion of cases among HPV-16-positive smokers that is attributable to the interaction between the two causes is 74%, based on HPV-16 DNA positivity.
为研究吸烟与人乳头瘤病毒16型（HPV-16）感染在高级别宫颈上皮内瘤变中的联合作用，我们分析了一项挪威基于人群的病例对照研究的数据，该研究纳入了90例患者和216名对照，年龄在20至44岁之间。我们通过聚合酶链反应检测病毒DNA以及通过酶联免疫吸附测定检测针对病毒衣壳的抗体来评估HPV-16状态。在HPV-16阳性个体中，吸烟与宫颈上皮内瘤变II - III级相关。以联合未暴露组（HPV-16 DNA阴性从不吸烟者）作为参照组，我们确定了HPV-16 DNA阳性从不吸烟者和HPV-16 DNA阳性曾经吸烟者发生宫颈上皮内瘤变II - III级的风险（比值比分别为15.7；95%置信区间为3.2, 76.5和比值比为65.9；95%置信区间为22.3, 194.3）。基于HPV-16 DNA阳性，在HPV-16阳性吸烟者中，由这两种病因之间相互作用导致的病例估计比例为74%。
