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Original Research

Current asthma contributes as much as smoking to chronic bronchitis in middle age: a prospective population-based study

, , , , , , , , , & show all
Pages 1911-1920 | Published online: 16 Aug 2016
 

Abstract

Background and objective

Personal smoking is widely regarded to be the primary cause of chronic bronchitis (CB) in adults, but with limited knowledge of contributions by other factors, including current asthma. We aimed to estimate the independent and relative contributions to adult CB from other potential influences spanning childhood to middle age.

Methods

The population-based Tasmanian Longitudinal Health Study cohort, people born in 1961, completed respiratory questionnaires and spirometry in 1968 (n=8,583). Thirty-seven years later, in 2004, two-thirds responded to a detailed postal survey (n=5,729), from which the presence of CB was established in middle age. A subsample (n=1,389) underwent postbronchodilator spirometry between 2006 and 2008 for the assessment of chronic airflow limitation, from which nonobstructive and obstructive CB were defined. Multivariable and multinomial logistic regression models were used to estimate relevant associations.

Results

The prevalence of CB in middle age was 6.1% (95% confidence interval [CI]: 5.5, 6.8). Current asthma and/or wheezy breathing in middle age was independently associated with adult CB (odds ratio [OR]: 6.2 [95% CI: 4.6, 8.4]), and this estimate was significantly higher than for current smokers of at least 20 pack-years (OR: 3.0 [95% CI: 2.1, 4.3]). Current asthma and smoking in middle age were similarly associated with obstructive CB, in contrast to the association between allergy and nonobstructive CB. Childhood predictors included allergic history (OR: 1.3 [95% CI: 1.1, 1.7]), current asthma (OR: 1.8 [95% CI: 1.3, 2.7]), “episodic” childhood asthma (OR: 2.3 [95% CI: 1.4, 3.9]), and parental bronchitis symptoms (OR: 2.5 [95% CI: 1.6, 4.1]).

Conclusion

The strong independent association between current asthma and CB in middle age suggests that this condition may be even more influential than personal smoking in a general population. The independent associations of childhood allergy and asthma, though not childhood bronchitis, as clinical predictors of adult CB raise the possibility of some of this burden having originated in childhood.

View correction statement:
Current asthma contributes as much as smoking to chronic bronchitis in middle age: a prospective population-based study [Corrigendum]

Acknowledgments

We acknowledge the TAHS study participants and previous investigators, Drs Heather Gibson, Bryan Gandevia, Harold Silverstone, and Norelle Lickiss. We thank the TAHS investigators who are not coauthors of this manuscript, Prof Mark Jenkins, Assoc Prof Stephen Morrison, Dr Iain Feather, and Dr Adrian Lowe, for their assistance including obtaining funds and data collection. We also acknowledge all the respiratory scientists who collected data in the lung function laboratories of Tasmania, Victoria, Queensland, and New South Wales; the research interviewers and data entry operators; and the organizational roles of Ms Cathryn Wharton and Dr Desiree Mészáros. Finally, we thank the Archives Office of Tasmania for providing data from the 1968 and 1974 TAHS questionnaires and copies of the school medical records.

This study was supported by the National Health and Medical Research Council of Australia, research grant 299901; The University of Melbourne; Clifford Craig Medical Research Trust of Tasmania; the Victorian, Queensland & Tasmanian Asthma Foundations; The Royal Hobart Hospital; Helen MacPherson Smith Trust; GlaxoSmithKline; and JLH. SCD, MCM, AJL, EHW, JAB, and JLH are supported by the NHMRC of Australia. JLP is supported by the Center for Air quality and health Research evaluation (CAR), which is also funded by the NHMRC of Australia.

Author contributions

SCD and JLP confirm they are equal first authors and equal legal and equitable owners of the paper and fully capable of granting the Exclusive License to Dove Medical Press Limited and entering into the agreement to publish this manuscript as an open access paper. EHW and MCM should be considered as equal senior authors. Study concept and design: SCD, EHW, MJA, DPJ, GGG, JLH; Acquisition of data: SCD, EHW, MJA, MCM, PST, DPJ; Analysis and interpretation of data: JLP, SCD, MJA, EHW, JAB, CJL; Drafting of the manuscript: JLP, SCD, MJA, EHW, MCM, JAB, CJL; Critical revision of the manuscript for important intellectual content: all authors; Statistical analysis: JLP, SCD; Obtained funding: SCD, EHW, MJA, DPJ, JLH; Administrative, technical and material support: SCD; Study supervision: SCD, EHW, MCM, DPJ, MJA.

Disclosure

EHW and DPJ have received honoraria from GlaxoSmithKline for giving lectures; MJA has received investigator initiated grants for unrelated research from Pfizer and Boehringer-Ingelheim, a consultancy from AstraZeneca and conference support from Boehringer-Ingelheim and Sanofi. The funding agencies had no direct role in the conduct of the study, the collection, management, statistical analysis, and interpretation of the data, preparation, or approval of the manuscript. The authors report no other conflicts of interest in this work.