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Determinants of early-life lung function in African infants
  1. Diane Gray1,
  2. Lauren Willemse1,
  3. Ane Visagie1,
  4. Dorottya Czövek2,
  5. Polite Nduru3,
  6. Aneesa Vanker1,
  7. Dan J Stein4,
  8. Nastassja Koen4,
  9. Peter D Sly2,
  10. Zoltán Hantos2,5,6,
  11. Graham L Hall7,8,
  12. Heather J Zar1
  1. 1Department of Paediatrics and Child Health, Red Cross War Memorial Children's Hospital and MRC Unit on Child and Adolescent Health, University of Cape Town, Cape Town, South Africa
  2. 2Children's Lung, Environment and Asthma Research, Child Health Research Centre, University of Queensland, Brisbane, Queensland, Australia
  3. 3Division of Epidemiology and Biostatistics, Department of Public Health and Family Medicine, University of Cape Town, Cape Town, South Africa
  4. 4Department of Psychiatry and MRC Unit on Anxiety and Stress Disorder, University of Cape Town, Cape Town, South Africa
  5. 5Department of Medical Physics and Informatics, University of Szeged, Szeged, Hungary
  6. 6Department of Pulmonology, University of Szeged, Szeged, Hungary
  7. 7Telethon Kids Institute, Australia Centre for Child Health Research, University of Western Australia, Perth, Western Australia, Australia
  8. 8Faculty of Health Sciences, School of Physiotherapy and Exercise Science, Curtin University, Perth, Western Australia, Australia
  1. Correspondence to Dr Diane Gray, Department of Paediatrics and Child Health, Red Cross War Memorial Children's Hospital, Klipfontein Road, Cape Town 7700, South Africa; Diane.Gray{at}


Background Low lung function in early life is associated with later respiratory illness. There is limited data on lung function in African infants despite a high prevalence of respiratory disease.

Aim To assess the determinants of early lung function in African infants.

Method Infants enrolled in a South African birth cohort, the Drakenstein child health study, had lung function measured at 6–10 weeks of age. Measurements, made with the infant breathing via a facemask during natural sleep, included tidal breathing, sulfur hexafluoride multiple breath washout and the forced oscillation technique. Information on antenatal and early postnatal exposures was collected using questionnaires and urine cotinine. Household benzene exposure was measured antenatally.

Results Successful tests were obtained in 645/675 (95%) infants, median (IQR) age of 51 (46–58) days. Infant size, age and male gender were associated with larger tidal volume. Infants whose mothers smoked had lower tidal volumes (−1.6 mL (95% CI −3.0 to −0.1), p=0.04) and higher lung clearance index (0.1 turnovers (95% CI 0.01 to 0.3), p=0.03) compared with infants unexposed to tobacco smoke. Infants exposed to alcohol in utero or household benzene had lower time to peak tidal expiratory flow over total expiratory time ratios, 10% (95% CI −15.4% to −3.7%), p=0.002) and 3.0% (95% CI −5.2% to −0.7%, p=0.01) lower respectively compared with unexposed infants. HIV-exposed infants had higher tidal volumes (1.7 mL (95% CI 0.06 to 3.3) p=0.04) compared with infants whose mothers were HIV negative.

Conclusion We identified several factors including infant size, sex, maternal smoking, maternal alcohol, maternal HIV and household benzene associated with altered early lung function, many of which are factors amenable to public health interventions. Long-term study of lung function and respiratory disease in these children is a priority to develop strategies to strengthen child health.

  • Paediatric Lung Disaese
  • Respiratory Measurement
  • Tobacco and the lung
  • Clinical Epidemiology

This is an Open Access article distributed in accordance with the terms of the Creative Commons Attribution (CC BY 4.0) license, which permits others to distribute, remix, adapt and build upon this work, for commercial use, provided the original work is properly cited. See:

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  • GLH and HJZ contributed equally as senior authors.

  • Contributors DG, GLH and HJZ conceived the study; DG, PDS, ZH, AV, DJS, GLH and HJZ contributed to the study design; LW, AA, AV and NK recruited patients and collected data; DG, LW and AA recorded measurement data; DG, DC and PN processed the recordings and analysed the data; DG, GLH and HJZ drafted the manuscript; all authors have seen and approved the submitted manuscript.

  • Funding This study was supported by grants from the Wellcome Trust (No. 098479/z/12/z), Bill and Melinda Gates Foundation (OPP1017641), Worldwide University Network Research Mobility Award, University of Cape Town equipment grant, the Hungarian Scientific Research Fund (No. 105403) and Thrasher Foundation (No. 9207). GLH is funded by the National Health and Medical Research Foundation of Australia (No. 1025550). PDS is funded by the National Health and Medical Research Foundation of Australia (No. 1002035). ZH was supported by a travel grant from MGC Diagnostics. HJZ and DJS are supported by the South African Medical Research Council.

  • Competing interests None.

  • Ethics approval Faculty of Health Sciences Research Ethics Committee, University of Cape Town.

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

  • Data sharing statement All data generated during the project are kept in the Drakenstein Child Health Study Data repository which is password protected and anonymised. Data are freely available to the study investigators. Data deposited into Drakenstein Child Health Study Data Repository will be maintained for a minimum of 20 years. There are no security, licensing or ethical issues related to the included data, and all data used in the project have been generated directly as a result of the project, without any pre-existing data being used.

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