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Original research
Female reproductive histories and the risk of chronic obstructive pulmonary disease
  1. Chen Liang1,
  2. Hsin-Fang Chung1,
  3. Annette Dobson1,
  4. Sven Sandin2,
  5. Elisabete Weiderpass3,
  6. Gita D Mishra1
  1. 1 School of Public Health, The University of Queensland, Brisbane, Queensland, Australia
  2. 2 Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden
  3. 3 International Agency for Research on Cancer, World Health Organization, Lyon, France
  1. Correspondence to Professor Gita D Mishra, School of Public Health, The University of Queensland, Brisbane, QLD 4006, Australia; g.mishra{at}uq.edu.au

Abstract

Background Female reproductive factors may influence the development of chronic obstructive pulmonary disease (COPD) through the female hormonal environment, but studies on this topic are limited. This study aimed to assess whether age at menarche, number of children, infertility, miscarriage, stillbirth and age at natural menopause were associated with the risk of COPD.

Methods Women from three cohorts with data on reproductive factors, COPD and covariates were included. Cause specific Cox regression models were adjusted for birth year, race, educational level, body mass index and pack years of smoking, stratified by asthma, and incorporating interaction between birth year and time. Between cohort differences and within cohort correlations were taken into account.

Results Overall, 2 83 070 women were included and 10 737 (3.8%) developed COPD after a median follow-up of 11 (IQR 10–12) years. Analyses revealed a U shaped association between age at menarche and COPD (≤11 vs 13: HR 1.17, 95% CI 1.11 to 1.23; ≥16 vs 13: HR 1.24, 95% CI 1.21 to 1.27). Women with three or more children (3 vs 2: HR 1.14, 95% CI 1.12 to 1.17; ≥4 vs 2: HR 1.34, 95% CI 1.28 to 1.40), multiple miscarriages (2 vs 0: HR 1.28, 95% CI 1.24 to 1.32; ≥3 vs 0: HR 1.36, 95% CI 1.30 to 1.43) or stillbirth (1 vs 0: HR 1.38, 95% CI 1.25 to 1.53; ≥2 vs 0: HR 1.67, 95% CI 1.32 to 2.10) were at a higher risk of COPD. Among postmenopausal women, earlier age at natural menopause was associated with an increased risk of COPD (<40 vs 50–51: HR 1.69, 95% CI 1.63 to 1.75; 40–44 vs 50–51: HR 1.42, 95% CI 1.38 to 1.47).

Conclusions Multiple female reproductive factors, including age at menarche, number of children, miscarriage, stillbirth, and age at natural menopause were associated with the risk of COPD.

  • COPD epidemiology

Data availability statement

Data may be obtained from a third party and are not publicly available. Data are not publicly available due to the data transfer agreements or restrictions under license for the current study. The anonymised dataset is governed by a Collaborative Research Agreement among several institutions. Those interested in collaborating on the project can contact the scientific committee at interlace@uq.edu.au.

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Data availability statement

Data may be obtained from a third party and are not publicly available. Data are not publicly available due to the data transfer agreements or restrictions under license for the current study. The anonymised dataset is governed by a Collaborative Research Agreement among several institutions. Those interested in collaborating on the project can contact the scientific committee at interlace@uq.edu.au.

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Footnotes

  • Contributors Manuscript concept, study design, and statistical methods: CL, H-FC, AD, and GDM. Contributing data: AD, SS, EW, and GDM. Analysis, interpretation of the data, and drafting of the manuscript: CL. Critical revision of manuscript for important intellectual content: all authors. GDM accepts full responsibility for the finished work and/or the conduct of the study, had access to the data, and controlled the decision to publish. All authors read and approved the final manuscript.

  • Funding InterLACE project is funded by the Australian National Health and Medical Research Council project grant (APP1027196) and Centres of Research Excellence (APP1153420). GDM is supported by the Australian National Health and Medical Research Council Leadership Fellowship (APP2009577). The findings and views in this paper are not those from the original studies or their respective funding agencies.

  • Disclaimer Where authors are identified as personnel of the International Agency for Research on Cancer / World Health Organization, the authors alone are responsible for the views expressed in this article and they do not necessarily represent the decisions, policy, or views of the International Agency for Research on Cancer / World Health Organization.

  • Competing interests GDM reports grants from the Australian National Health and Medical Research Council.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.

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