Abstract:
Introduction:
- Lung cancer has a well-established strong causal association with smoking, as 80-90% of lung cancers occur in smokers.
- Other associations, such as exposure to radon, asbestos, and secondhand smoke suggest that inhaled toxins is the predominant causative pathway.
- The risk of lung cancer has been found to be inversely associated with fruit intake in current and former smokers.5
- There is disagreement in the literature about the association between beta-carotene and vitamin A and lung cancer.
- Additionally, alcohol consumption is associated with increased risk of breast, colorectal, esophageal, head & neck, and liver cancer.
- The Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial is a large population-based randomized trial of approximately 155,000 participants.
- This study utilizes the extensive, prospectively collected PLCO data to further assess specific components of diet that represent potential risk factors for LCINS
Methods:
Data collection:
- The PLCO de-identified dataset was obtained via the online Cancer Data Access System (CDAS). Data was collected through 2015.
- For the PLCO study, a total of 154,887 women and men aged 55 to 74 were enrolled between 1993 and 2001.
- Study participants were randomized into two arms:
- Screening-arm participants received a series of up to six annual screening examinations for prostate, lung, colorectal, and ovarian cancer.
- Participants in the usual care arm received routine health care from their health care providers.
- All participants completed a baseline self-report questionnaire (BQ).
- Screening-arm participants also completed a dietary questionnaire (DQX).
- A dietary history questionnaire (DHQ) was administered to all participants in 1998.
- All participants were administered the supplemental questionnaire (SQX) in 2006.
Statistical analysis:
- Descriptive statistics: Mean (SD) for continuous variables and count (percentage) for categorical variables compared between smokers, never-smokers, and within never-smokers with and without lung cancer.
- Inferential statistics: Used Cox proportional hazards regression models to identify significant risk factors for LCINS incidence.
- Time from completion of questionnaires to study end used in survival model, with different follow-up times for collected risk factors.
- Multivariable models constructed separately for each questionnaire, using risk factors significant in univariate analysis.
- Final models built by removing variables using backwards selection at a significance level of 0.20; significance considered at 0.05. Analysis conducted using R version 4.0.2.
Results:
- Out of 154,887 participants, 62,295 (40.2%) were never-smokers.
- The incidence of LCINS was 0.4%, one-tenth the 4% incidence of lung cancer noted in smokers.
- There was no evidence to suggest a different risk of developing LCINS based on:
- Drinking status
- Fruit consumption
- Beta-carotene usage
- Vitamin A usage
Conclusion:
- Our study based on a large prospective database demonstrates that no modifiable dietary factors included in DQX or DHQ are associated with a higher likelihood of developing LCINS.
- No statistically significant correlation was noted with drinking status, fruit consumption, beta-carotene usage, or vitamin A usage.
- LCINS is a distinct disease with unique genomic and epidemiologic features and requires further research, especially into the role of environmental exposures.
