[Source: Thorax, full page: (LINK). Abstract, edited.]
Timing of secondhand smoke, pet, dampness or mould exposure and lung function in adolescence
Edith B Milanzi 1, Gerard H Koppelman 2,3, Henriette A Smit 4, Alet H Wijga 5, Judith M Vonk 2,6, Bert Brunekreef 1,4, Ulrike Gehring 1
Author affiliations: 1 Institute for Risk Assessment Sciences (IRAS), Utrecht University, Utrecht, The Netherlands; 2 Groningen Research Institute for Asthma and COPD (GRIAC), University Medical Center Groningen, Groningen, The Netherlands; 3 Department of Pediatric Pulmonology and Pediatric Allergology, Beatrix Children’s Hospital, University Medical Center Groningen, Groningen, The Netherlands; 4 Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, The Netherlands; 5 Centre for Nutrition, Prevention and Health Services, National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands; 6 Department of Epidemiology, University Medical Center Groningen, University of Groningen, Groningen, Netherlands
Correspondence to Dr Ulrike Gehring, Institute for Risk Assessment Sciences (IRAS), Utrecht University, Utrecht 3508TD, The Netherlands; U.Gehring@uu.nl
The relevance of timing of exposure in the associations of secondhand tobacco smoke (SHS), pets, and dampness or mould exposure with lung function is unclear. We investigated the relevance of timing of these exposures for lung function in adolescence.
We used data from participants of the Dutch Prevention and Incidence of Asthma and Mite Allergy (PIAMA) cohort with spirometric measurements at ages 12 and 16 years (n=552). Data on residential exposure to SHS, pets, and dampness or mould were obtained by repeated parental questionnaires. We characterised timing of exposure through longitudinal patterns using latent class growth modelling and assessed associations of these patterns with FEV1 and FVC at ages 12 and 16 and FEV1 and FVC growth between ages 12 and 16 using linear regression models.
Childhood SHS exposure was associated with reduced FEV1 growth/year (95% CI) (−0.34% (−0.64% to −0.04%)). Late childhood and early life pet exposure was associated with increased FEV1 growth (0.41% (0.14% to 0.67%)) and reduced FVC growth (−0.28% (−0.53% to −0.03%)), respectively, compared with very low exposure. Early life dampness or mould exposure was associated with reduced lung function growth. All time windows of SHS exposure tended to be associated with lower attained lung function and pet exposure tended to be associated with higher FEV1.
SHS exposure during childhood could lead to reduced lung function growth and lower attained lung function in adolescence. While pet exposure in late childhood may not adversely affect lung function, early childhood pet exposure may slow down FVC growth in adolescence.
BB and HAS were responsible for the conception and design of the PIAMA study. GHK, AHW, HAS and UG secured funding for the present study. EBM and UG designed the study and had full access to the data. EBM carried out the statistical analysis and wrote the initial draft of the manuscript. All authors (1) provided substantial contributions to the conception or design of the work, or the acquisition, analysis or interpretation of the data for the work, (2) revised the manuscript critically for important intellectual content and (3) approved the final version for submission.
The research leading to these results has received funding from Dutch Lung Foundation (Project no. 4.1.14.001). In addition, the PIAMA study has received funding from the Netherlands Organization for Health Research and Development, the Netherlands Organization for Scientific Research, the Netherlands Asthma Fund, the Netherlands Ministry of Spatial Planning, Housing, and the Environment, and the Netherlands Ministry of Health, Welfare, and Sport (PIAMA).
The funders did not play any role in the design of the study, data collection, analysis and interpretation of data, and in writing the manuscript.
GHK received grants from the Dutch Lung Foundation, grants from Ubbo Emmius Foundation, grants from Teva The Netherlands and grants from Stichting Astma Bestrijding, outside the submitted work. UG reports receiving grants from the Dutch Lung Foundation during the conduct of this study.
Patient consent for publication
Parental/guardian consent obtained.
Ethical approval was obtained from participating institutes (ethical approval nos.: Rotterdam, MEC 132.636/1994/39 and 137.326/1994/130; Groningen, MEC 94/08/92; Utrecht, MEC-TNO 95/50).
Provenance and peer review
Not commissioned; externally peer reviewed.
Data availability statement
Data are available on reasonable request.
Copyright information: © Author(s) (or their employer(s)) 2019. No commercial re-use. See rights and permissions. Published by BMJ.
Keywords: Environmental pollution; Pulmonology; Pediatrics.