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There is growing, but inconsistent evidence suggesting oestrogen may play a key role in lung cancer development, especially among never‐smoking women for whom lung cancer risk factors remain largely elusive. Using the China Kadoorie Biobank, a large‐scale prospective cohort with 302 510 women aged 30 to 79 years recruited from 10 regions in China during 2004 to 2008, we assessed the risk of lung cancer death among self‐reported never‐smoking women who were cancer‐free at baseline, in relation to age at menarche, age at menopause, time since menopause, prior use of oral contraceptives (OCP), number of livebirths, breastfeeding and age at first livebirth. Women were followed up to December 31, 2016 with linkage to mortality data. Hazard ratios (HR) and 95% confidence intervals (CI) were estimated using Cox regression, adjusting for key confounders including several socio‐demographic, environmental and lifestyle factors. Among 287 408 never‐smoking women, 814 died from lung cancer with a median follow‐up of 10.3 years. Women who had used OCP within 15 years prior to baseline had a significantly higher hazard of lung cancer death compared with never‐users: HR = 1.85 (95% CI: 1.14‐3.00) and risk increased by 6% with each additional year of use: HR = 1.06 (1.01‐1.10). Among parous women, the hazard of lung cancer death increased by 13% with each single livebirth: HR = 1.13 (1.05‐1.23); and among post‐menopausal women, the risk increased by 2% with each year since menopause: HR = 1.02 (1.01‐1.04). These results suggest that reproductive factors which were proxies for lower endogenous oestrogen level, for example, longer duration of OCP use, could play a role in lung cancer development. [ABSTRACT FROM AUTHOR]

Background Household air pollution (HAP) has been classified as a major risk factor for lung cancer (LC) among never-smokers, however, evidence is largely from case-control studies. Using the prospective cohort China Kadoorie Biobank (CKB), we investigated the association of HAP with LC death among never-smokers. Methods The CKB, a large-scale cohort study, recruited 512,715 adults aged 30–79 years from ten regions in China during 2004-2008. Self-reported never-smoking participants were followed up to 31/12/2016 with linkage to mortality data. Total duration of HAP exposure was calculated from self-reported solid fuel use in domestic cooking and slow-burning stoves in participants' three most recent residences, and self-reported coal-smoky home in winter during their lifetime. Hazard ratios (HR) and 95% confidence intervals (CI) of LC death associated with HAP exposure were estimated using Cox regression, adjusting for key confounders including several demographic, environmental and lifestyle factors. Results There were 979 LC deaths among 323,794 never-smokers without prior cancer during a median follow-up of 10.2 years. There was a log-linear positive association between HAP exposure and LC death (p-trend=0.0034), with 4% increased risk per 5-year longer exposure (HR = 1.04; 95% CI 1.01-1.06); and participants with 40.1-50.0 years of exposure had the highest risk compared to the never-exposed (HR = 1.53; 95% CI 1.13-2.07). Conclusions This study provides new prospective evidence that HAP exposure is associated with LC death among Chinese never-smokers, and strengthens the previous evidence largely based on case-control studies. Key messages This study supports HAP as an important risk factor for LC development among never-smokers. [ABSTRACT FROM AUTHOR]

Rationale: Household air pollution and secondhand tobacco smoke are known carcinogens for lung cancer, but large-scale estimates of the relationship with lung cancer mortality are lacking. Objectives: Using the large-scale cohort China Kadoorie Biobank, we prospectively investigated associations between these two risk factors and lung cancer death among never-smokers. Methods: The Biobank recruited 512,715 adults aged 30-79 years from 10 regions in China during 2004-2008. Self-reported never-smoking participants were followed up to December 31, 2016, with linkage to mortality data. Total duration of exposure to household air pollution was calculated from self-reported domestic solid fuel use. Exposure to secondhand tobacco smoke was ascertained using exposure at home and/or other places. Hazard ratios and 95% confidence intervals for associations between these two exposures and lung cancer death were estimated using Cox regression, adjusting for key confounders. Measurements and Main Results: There were 979 lung cancer deaths among 323,794 never-smoking participants without a previous cancer diagnosis during 10.2 years of follow-up. There was a log-linear positive association between exposure to household air pollution and lung cancer death, with a 4% increased risk per 5-year increment of exposure (hazard ratio = 1.04; 95% confidence interval = 1.01-1.06; P trend = 0.0034), and participants with 40.1-50.0 years of exposure had the highest risk compared with the never-exposed (hazard ratio = 1.53; 95% confidence interval = 1.13-2.07). The association was largely consistent across various subgroups. No significant association was found between secondhand smoke and lung cancer death. Conclusions: This cohort study provides new prospective evidence suggesting that domestic solid fuel use is associated with lung cancer death among never-smokers.