Taborelli Martina, Montella Maurizio, Libra Massimo, Tedeschi Rosamaria, Crispo Anna, Grimaldi Maria, Dal Maso Luigino, Serraino Diego, Polesel Jerry
Unit of Cancer Epidemiology, CRO Aviano National Cancer Institute, via Franco Gallini 2, 33081, Aviano, PN, Italy.
Unit of Epidemiology, National Cancer Institute "G. Pascale" Foundation, via Marino Semmola, 80131, Naples, Italy.
BMC Cancer. 2017 Jun 16;17(1):421. doi: 10.1186/s12885-017-3414-2.
Previous studies have provided limited support to the association between tobacco smoking and lymphomas with weak evidence of a dose-response relationship.
We investigated the relationship between tobacco smoking and risk of non-Hodgkin lymphomas (NHL) and Hodgkin lymphomas (HL) through logistic regression spline models. Data were derived from an Italian hospital-based case-control study (1999-2014), which enrolled 571 NHLs, 188 HLs, and 1004 cancer-free controls. Smoking habits and other lifestyle factors were assessed through a validated questionnaire. Odds ratios (OR) and 95% confidence intervals (CI) were estimated by logistic regression, adjusting for potential confounders.
Compared to never smokers, people smoking ≥15 cigarettes/day showed increased risks of both NHL (OR = 1.42, 95% CI: 1.02, 1.97) and HL (OR = 2.47, 95% CI: 1.25, 4.87); the risk was particularly elevated for follicular NHL (OR = 2.43; 95% CI:1.31-4.51) and mixed cellularity HL (OR = 5.60, 95% CI: 1.31, 23.97). No excess risk emerged for former smokers or people smoking <15 cigarettes/day. Spline analyses showed a positive dose-response relationship with significant increases in NHL and HL risks starting from 15 and 21 cigarettes/day, respectively, with the most evident effects for follicular NHL and mixed cellularity HL. Smoking duration was significantly associated with the HL risk only (OR = 2.15, 95% CI: 1.16, 3.99).
These findings support a role of tobacco smoking in the etiology of both NHL and HL, providing evidence of a direct association of risk with smoking intensity.
以往的研究对吸烟与淋巴瘤之间的关联支持有限，剂量反应关系的证据薄弱。
我们通过逻辑回归样条模型研究吸烟与非霍奇金淋巴瘤（NHL）和霍奇金淋巴瘤（HL）风险之间的关系。数据来自一项基于意大利医院的病例对照研究（1999 - 2014年），该研究纳入了571例NHL患者、188例HL患者和1004名无癌对照者。通过一份经过验证的问卷评估吸烟习惯和其他生活方式因素。通过逻辑回归估计比值比（OR）和95%置信区间（CI），并对潜在混杂因素进行调整。
与从不吸烟者相比，每天吸烟≥15支的人患NHL（OR = 1.42，95% CI：1.02，1.97）和HL（OR = 2.47，95% CI：1.25，4.87）的风险增加；滤泡性NHL（OR = 2.43；95% CI：1.31 - 4.51）和混合细胞性HL（OR = 5.60，95% CI：1.31，23.97）的风险尤其升高。既往吸烟者或每天吸烟<15支的人未出现额外风险。样条分析显示存在正剂量反应关系，分别从每天15支和21支香烟开始，NHL和HL风险显著增加，对滤泡性NHL和混合细胞性HL的影响最为明显。吸烟持续时间仅与HL风险显著相关（OR = 2.15，95% CI：1.16，3.99）。
这些发现支持吸烟在NHL和HL病因学中的作用，为风险与吸烟强度的直接关联提供了证据。
