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ORAL 23 - Prevention and Cancer Risk (ID 121)
- Event: WCLC 2015
- Type: Oral Session
- Track: Prevention and Tobacco Control
- Presentations: 1
ORAL23.07 - Interactions Between Smoking and the Dietary Inflammatory Index in Relation to Lung Cancer in the Prostate Lung Colorectal and Ovarian Trial (ID 1220)
10:45 - 12:15 | Author(s): J. Houston
Chronic inflammation can influence the process of lung carcinogenesis. Dietary factors can modulate inflammation and may modify the effect of tobacco smoke. In this study, we aim to investigate the association between the inflammatory potential of usual diet, as assessed by the novel Dietary Inflammatory Index (DII), and lung cancer and to assess the interactions between the DII and tobacco use.
Existing data from the Prostate Lung Colorectal and Ovarian Cancer (PLCO) screening trial was used to test the hypothesis that DII influences lung cancer and modifies the effect of tobacco smoke. PLCO participants were enrolled between 1993 and 2001 and randomized to a control arm or screening arm for four target cancers. Data were collected on cancer diagnoses and deaths from all causes that occurred through December 31, 2009. The baseline DII score for each subject was calculated from self-reports via food frequency questionnaires. A proportional hazards model was used to assess the association between the DII and DII-smoking interaction in relation to the probability of developing lung cancer. To investigate the association between DII and lung cancer prognosis, we explored the distribution of the lung cancer stage by the DII quintiles
Of 110,317 participants who met our eligibility criteria, 1850 (1.68%) developed lung cancer. The median follow-up time was 8.38 years. The association between DII and C-reactive protein was significant (beta coefficient of Quintile5 vs. Quntile1 =0.45, p-value<0.01). Results from the proportional hazards model show that those at the higher DII quintiles were at higher risk of lung cancer. The risk of lung cancer among Participants at the 5[th] quintile was 1.28 times higher the risk among these at 1[st] quintile (HR~Q5vsQ1~ = 1.28, 95 % CI 1.09–1.51, and P~trend~ <0.03, after controlling for possible confounders (demographics, smoking, family history, intervention and others) . An interaction was observed between DII score and tobacco smoke in relation to lung cancer (p-value for the interaction =0.01). Among current and former smokers combined HR~Q5vs.Q1~ was 2.00, 95 % CI 1.6-2.36 ( P~trend~ <0.001) compared to 0.82, 95 % CI 0.48-1.41 among never smokers. Table 1 shows the distribution of the lung cancer stage. Cases with worse prognosis were more likely to be in the higher DII quintile. Figure 1
Overall, more pro-inflammatory diets are associated with increased risk of lung cancer, particularly for former and current smokers, suggesting that dietary-mediated inflammation plays an important role in lung carcinogenesis
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