Abstract
Introduction Indoor air pollution and maternal smoking during pregnancy are associated with respiratory symptoms in infants, but little is known about the direct association with lung function or interactions with genetic risk factors. We examined associations of indoor particulate matter of diameter ≤10 µm (PM10) exposure and maternal smoking with infant lung function and the role of gene-environment interactions.
Methods Data from the Drakenstein Child Health Study, a South African birth cohort, were analysed (N=270). Lung function was measured at 6 weeks and 1 year of age and lower respiratory tract illness (LRTI) episodes were documented. We measured prenatal and postnatal PM10 exposures using devices placed in homes and prenatal tobacco smoke exposure using maternal urine cotinine levels. Genetic risk scores (GRS) determined from associations with childhood-onset asthma (COA) in the UK Biobank were used to investigate effect modifications.
Results Pre- and postnatal exposure to PM10 as well as maternal smoking during pregnancy were associated with reduced lung function at 6 weeks and 1 year as well as LRTI in the first year. Due to a significant interaction between the GRS and prenatal exposure to PM10, infants carrying more COA-risk alleles were more susceptible to PM10-associated reduced lung function (p-interaction=0.007). This interaction was stronger in infants with black African ancestry (p-interaction=0.001) and non-existent in children with mixed ancestry (p-interaction=0.876).
Conclusions PM10 and maternal smoking exposures were associated with reduced lung function, with a higher susceptibility for infants with an adverse genetic predisposition for asthma that also depended on the infant's ancestry.
Footnotes
This manuscript has recently been accepted for publication in the European Respiratory Journal. It is published here in its accepted form prior to copyediting and typesetting by our production team. After these production processes are complete and the authors have approved the resulting proofs, the article will move to the latest issue of the ERJ online. Please open or download the PDF to view this article.
Conflict of interest: Dr. Huels has nothing to disclose.
Conflict of interest: Dr. Vanker reports grants from Bill & Melinda Gates Foundation (OPP1017641, grants from Discovery Foundation, grants from South African Thoracic Society AstraZeneca Respiratory Fellowship, grants from National Research Fund, South Africa, grants from CIDRI Clinical Fellowship, grants from Medical Research Council, South Africa, during the conduct of the study.
Conflict of interest: Dr. Gray has nothing to disclose.
Conflict of interest: Dr. Koen has nothing to disclose.
Conflict of interest: Dr. MacIsaac has nothing to disclose.
Conflict of interest: Dr. Lin has nothing to disclose.
Conflict of interest: Dr. Ramadori has nothing to disclose.
Conflict of interest: Dr. Sly has nothing to disclose.
Conflict of interest: Dr. Stein reports personal fees from Lundbeck, personal fees from Biocodex, personal fees from Sun, outside the submitted work.
Conflict of interest: Dr. Kobor has nothing to disclose.
Conflict of interest: Dr. Zar reports grants from Bill and Melinda Gates Foundation, grants from NIH, grants from Wellcome Trust, grants from SA MRC, grants from National Research Foundation SA, grants from South African Thoracic Society, during the conduct of the study.
- Received September 18, 2019.
- Accepted December 21, 2019.
- Copyright ©ERS 2020
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