Dietary phytoestrogen intake and lung cancer risk: an analysis of the Prostate, Lung, Colorectal and Ovarian (PLCO) cancer screening trial.
- Division of Hematology and Medical Oncology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
- Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA.
- Department of Surgery, Cleveland Clinic Foundation, Cleveland, OH, USA.
- Department of Medicine, Icahn School of Medicine at Mount Sinai Queens, New York, NY, USA.
- Department of Family, Population and Preventive Medicine, Stony Brook University, Stony Brook, NY, USA.
Phytoestrogens (PEs) have estrogen-like activity and were found to lower incidences of several hormone-dependent cancers. Emerging evidence suggests that estrogen may play a role in lung cancer carcinogenesis. We aim to evaluate dietary PE intake and lung cancer risk using data from the Prostate, Lung, Colorectal, and Ovarian cancer screening trial. A total of 1,706 lung cancer cases were identified. The association between lung cancer risk and PE intake (in quartiles) was calculated using the Cox proportional hazard models adjusting for potential confounders. Stratified analyses by smoking status, sex, and histology were also performed. The highest quartile of total PE intake was associated with a reduced risk of lung cancer compared to the lowest quartile (HR=0.85, 95%CI: 0.73-0.99 for > 1,030 μg/day vs < 290 μg/day) (P trend=0.56). Similar patterns were observed among ever smokers (HR=0.84, 95%CI: 0.71-0.98), non-small cell histology (HR=0.84, 95CI: 0.72-0.99), male (HR=0.84, 95%CI: 0.69-1.03) and female (HR=0.80, 95%CI: 0.64-0.99 for 510-1,030 μg/day, HR=0.84, 95%CI: 0.67-1.06 for > 1,030 μg/day vs < 290 μg/day) subjects with no significant linear trend observed. Despite a lower consumption compared to the Asian population, increased PE intake still appears to decrease lung cancer risk in a Caucasian-dominant population. Future studies are needed to replicate these results in independent cohorts and shed a light on the potential mechanism of the protective effect of PEs on lung carcinogenesis and the interaction between PEs, smoking, and endogenous estrogens.