Introduction Adult spirometry following community-acquired childhood pneumonia has variably been reported as showing obstructive or non-obstructive deficits. We analysed associations between doctor-diagnosed childhood pneumonia/pleurisy and more comprehensive lung function in a middle-aged general population cohort born in 1961.
Methods Data were from the prospective population-based Tasmanian Longitudinal Health Study cohort. Analysed lung function was from ages 7 years (prebronchodilator spirometry only, n=7097), 45 years (postbronchodilator spirometry, carbon monoxide transfer factor and static lung volumes, n=1220) and 53 years (postbronchodilator spirometry and transfer factor, n=2485). Parent-recalled histories of doctor-diagnosed childhood pneumonia and/or pleurisy were recorded at age 7. Multivariable linear and logistic regression were used.
Results At age 7, compared with no episodes, childhood pneumonia/pleurisy-ever was associated with reduced FEV1:FVC for only those with current asthma (beta-coefficient or change in z-score=−0.20 SD, 95% CI −0.38 to –0.02, p=0.028, p interaction=0.036). At age 45, for all participants, childhood pneumonia/pleurisy-ever was associated with a restrictive pattern: OR 3.02 (1.5 to 6.0), p=0.002 for spirometric restriction (FVC less than the lower limit of normal plus FEV1:FVC greater than the lower limit of normal); total lung capacity z-score −0.26 SD (95% CI −0.38 to –0.13), p<0.001; functional residual capacity −0.16 SD (−0.34 to –0.08), p=0.001; and residual volume −0.18 SD (−0.31 to –0.05), p=0.008. Reduced lung volumes were accompanied by increased carbon monoxide transfer coefficient at both time points (z-score +0.29 SD (0.11 to 0.49), p=0.001 and +0.17 SD (0.04 to 0.29), p=0.008, respectively).
Discussion For this community-based population, doctor-diagnosed childhood pneumonia and/or pleurisy were associated with obstructed lung function at age 7 for children who had current asthma symptoms, but with evidence of ‘smaller lungs’ when in middle age.
- clinical epidemiology
- respiratory infection
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EHW and SCD are joint senior authors.
EHW and SCD contributed equally.
Presented at Part of this work was presented by oral presentation at the regional Thoracic Society of Australia and New Zealand (TSANZ) and thematic poster at the American Thoracic Society Conference, San Diego, 2014.
Funding This study was supported by the National Health and Medical Research Council (NHMRC) of Australia (research grants 299901 and 1021275); the University of Melbourne; Clifford Craig Foundation; the Victorian, Queensland and Tasmanian Asthma Foundations; Royal Hobart Hospital; Helen MacPherson Smith Trust; GlaxoSmithKline; and John L Hopper. JLP, CL, AL, EHW and SD are funded through the NHMRC of Australia. JLP was also in part supported by Lung Foundation Australia (LFA). ABC is funded by an NHMRC Practitioner Fellowship (APP1154302) and Children’s Hospital Foundation (Queensland, grant 50286). 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.
Competing interests CFM has directed speaker fees to her institution from Menarini and AstraZeneca. MJA has received investigator-initiated grants for unrelated research from Pfizer and Boehringer Ingelheim, and an unrelated consultancy from Sanofi. BRT has received speaker fees from Mundipharma Australia and AstraZeneca. ABC has received other fees from GlaxoSmithKline. JLP has received a travel grant from Boehringer Ingelheim.
Patient consent for publication Not required.
Ethics approval This study was approved by separate human ethics review committees at all participating institutions, principally The University of Melbourne (040375) and the University of Tasmania (H0012710). Written informed consent was obtained from all participants.
Provenance and peer review Not commissioned; externally peer reviewed.
Data availability statement Data may be obtained from a third party and are not publicly available.