Reproductive factors play role in lung carcinogenesis

Longer fertility span and late menopause appear to contribute to an increased risk of developing lung adenocarcinoma among nonsmoking women, as suggested in a study.

The study drew data from the Japan Public Health Center-based Prospective Study and included 42,615 never-smoking women. There were 400 incident lung cancer cases, 305 of which were adenocarcinoma, documented over a median of 21 years.

In Cox proportional hazards models, the risk of incident lung adenocarcinoma was about 1.5-times higher among women with a shorter fertility span (≥36 years vs ≤32 years; hazard ratio [HR], 1.48, 95 percent confidence interval [CI], 1.07–2.06; p_trend=0.01). This association was not seen for lung cancer and nonadenocarcinoma.

Furthermore, women who went through menopause at an older age (≥50 years) were at greater risk of lung adenocarcinoma compared with those whose menopause occurred at ≤47 years (HR, 1.41, 95 percent CI, 1.01–1.96; p_trend=0.04). A similar risk increase was noted among women with natural menopause (HR, 1.99, 95 percent CI, 1.02–3.88) or surgical menopause (HR, 2.75, 95 percent CI, 1.33–5.67) relative to premenopausal women.

Meanwhile, breastfeeding had a protective effect on the risk of nonadenocarcinoma (HR, 0.51, 95 percent CI, 0.28–0.92).

Lung cancer showed no significant association with parity, age at first birth, exogenous hormone use, or length of menstrual cycle.

The findings indicate the potential utility of fertility span and age at menopause in developing risk prediction models for lung adenocarcinoma among nonsmoking women. More studies that include oestrogen and progesterone biomarkers are needed to establish the role of endogenous hormones in lung carcinogenesis.