The dose-response relationship between tobacco smoking and the risk of lymphomas: A case-control study

Martina Taborelli, Maurizio Montella, Massimo Libra, Rosamaria Tedeschi, Anna Crispo, Maria Grimaldi, Luigino Dal Maso, Diego Serraino, Jerry Polesel

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Background: Previous studies have provided limited support to the association between tobacco smoking and lymphomas with weak evidence of a dose-response relationship. Methods: 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 hospitalbased 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. Results: 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). Conclusions: 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.

Original languageEnglish
Article number421
JournalBMC Cancer
Volume17
Issue number1
DOIs
Publication statusPublished - 2017

Fingerprint

Hodgkin Disease
Case-Control Studies
Lymphoma
Smoking
Non-Hodgkin's Lymphoma
Odds Ratio
Confidence Intervals
Follicular Lymphoma
Tobacco Products
Logistic Models
Habits
Life Style
Neoplasms

Keywords

  • Case-control study
  • Dose-response relationship
  • Hodgkin lymphoma
  • Non-Hodgkin lymphoma
  • Spline models
  • Tobacco smoking

ASJC Scopus subject areas

  • Oncology
  • Genetics
  • Cancer Research

Cite this

The dose-response relationship between tobacco smoking and the risk of lymphomas : A case-control study. / Taborelli, Martina; Montella, Maurizio; Libra, Massimo; Tedeschi, Rosamaria; Crispo, Anna; Grimaldi, Maria; Maso, Luigino Dal; Serraino, Diego; Polesel, Jerry.

In: BMC Cancer, Vol. 17, No. 1, 421, 2017.

Research output: Contribution to journalArticle

Taborelli, Martina ; Montella, Maurizio ; Libra, Massimo ; Tedeschi, Rosamaria ; Crispo, Anna ; Grimaldi, Maria ; Maso, Luigino Dal ; Serraino, Diego ; Polesel, Jerry. / The dose-response relationship between tobacco smoking and the risk of lymphomas : A case-control study. In: BMC Cancer. 2017 ; Vol. 17, No. 1.
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abstract = "Background: Previous studies have provided limited support to the association between tobacco smoking and lymphomas with weak evidence of a dose-response relationship. Methods: 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 hospitalbased 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. Results: 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). Conclusions: 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.",
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AU - Crispo, Anna

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AB - Background: Previous studies have provided limited support to the association between tobacco smoking and lymphomas with weak evidence of a dose-response relationship. Methods: 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 hospitalbased 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. Results: 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). Conclusions: 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.

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