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Cancer Causes & Control

, Volume 26, Issue 1, pp 11–24 | Cite as

Risk factors shared by COPD and lung cancer and mediation effect of COPD: two center case–control studies

  • Lei Yang
  • Xiaoxiao Lu
  • Jieqiong Deng
  • Yumin Zhou
  • Dongsheng Huang
  • Fuman Qiu
  • Xiaorong Yang
  • Rongrong Yang
  • Wenxiang Fang
  • Pixin Ran
  • Nanshan Zhong
  • Yifeng Zhou
  • Shenying Fang
  • Jiachun LuEmail author
Original paper

Abstract

Purpose

To reveal the shared risk factors for chronic obstructive pulmonary disease (COPD) and lung cancer, and to analyze the mediation effect of COPD during lung carcinogenesis.

Methods

We conducted four independent case–control studies included 1,511 COPD patients and 1,677 normal lung function controls and 1,559 lung cancer cases and 1,679 cancer-free controls during 2002–2011 in southern and eastern Chinese.

Results

Eight factors were observed to be consistently associated with both diseases risk, including pre-existing tuberculosis, smoking, passive smoking, occupational exposure to metallic toxicant, poor housing ventilation, biomass burning, cured meat consumption, and seldom vegetables/fruits consumption. Furthermore, smoking and biomass burning conferred significantly higher risk effects on lung cancer in individuals with pre-existing COPD than those without. COPD also had significant mediation effects during lung carcinogenesis caused by smoking, passive smoking, and biomass burning, which explained about 12.0 % of effect, 3.8 % of effect, and 6.1 % of effect of these factors on lung tumorigenesis in turn.

Conclusion

Our study mapped a shared spectrum of etiological factors for both COPD and lung cancer in Chinese, and COPD acts as a mediator during lung cancer development. These observations should be in consideration for the prevention of both diseases.

Keywords

COPD Lung cancer Case–control study Risk factor Mediation effect 

Notes

Acknowledgments

This study was supported by the National Natural Scientific Foundation of China Grants 30671813, 30872178, 81072366, 81273149, 81473040 (J. Lu), and partly by 81001278, 81171895, 81472630 (Y. Zhou); 81402753 (L. Yang), 81102159 (L. Zhang), 81102061 (Q. Jiang), 30972540 (B. Liu); and Guangdong Provincial High Level Experts Grants 2010-79 (J. Lu). We thank Dr. Zhanhong Xie, Dr. Wanmin Zeng and Dr. Ling Liu for their assistances in recruiting the subjects; Dr. Lisha Zhang for their laboratory assistances.

Conflict of interest

No conflict of interest exists for any author.

Supplementary material

10552_2014_475_MOESM1_ESM.doc (68 kb)
Supplementary material 1 (DOC 68 kb)

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Copyright information

© Springer International Publishing Switzerland 2014

Authors and Affiliations

  • Lei Yang
    • 1
  • Xiaoxiao Lu
    • 1
    • 2
  • Jieqiong Deng
    • 3
  • Yumin Zhou
    • 4
  • Dongsheng Huang
    • 5
  • Fuman Qiu
    • 1
  • Xiaorong Yang
    • 1
  • Rongrong Yang
    • 1
  • Wenxiang Fang
    • 1
  • Pixin Ran
    • 4
  • Nanshan Zhong
    • 4
  • Yifeng Zhou
    • 3
  • Shenying Fang
    • 6
  • Jiachun Lu
    • 1
    Email author
  1. 1.The State Key Lab of Respiratory Disease, The Institute for Chemical Carcinogenesis, Collaborative Innovation Center for Environmental ToxicityGuangzhou Medical UniversityGuangzhouChina
  2. 2.School of Arts and SciencesColby-Sawyer CollegeNew LondonUSA
  3. 3.Soochow University Laboratory of Cancer Molecular GeneticsMedical College of Soochow UniversitySuzhouChina
  4. 4.The State Key Lab of Respiratory Disease, Guangzhou Institute of Respiratory Diseases, The First Affiliated HospitalGuangzhou Medical UniversityGuangzhouChina
  5. 5.Department of Respiratory MedicineGuangzhou Chest HospitalGuangzhouChina
  6. 6.Department of EpidemiologyThe University of Texas MD Anderson Cancer CenterHoustonUSA

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