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Association of Maternal Air Pollution Exposure and Infant Lung Function Is Modified by Genetic Propensity to
Dwan Vilcins1, Wen Ray Lee1, Cindy Pham2,3
1Child Health Research Centre, The University of Queensland, South Brisbane, QLD 4101, Australia.
Insights
Prenatal exposure to nitrogen dioxide (NO2) air pollution was linked to reduced infant lung function in babies with a genetic predisposition to oxidative stress (OS). This study highlights a specific genetic risk factor for air pollution
Area of Science:
- Environmental Health
- Pediatric Respiratory Medicine
- Genetics and Epigenetics
Background:
- Air pollution poses significant risks to respiratory health, particularly in developing fetuses.
- Children are uniquely vulnerable to prenatal air pollution exposure due to ongoing organ development.
- Oxidative stress (OS) and inflammation are key biological pathways affected by air pollution.
Purpose of the Study:
- To investigate the impact of maternal exposure to ambient air pollution during pregnancy on infant oxidative stress, inflammation, and lung function.
- To determine if genetic predisposition to oxidative stress modifies the effects of prenatal air pollution on infant respiratory health.
Main Methods:
- Utilized data from the Barwon Infant Study (n=314) to assess prenatal exposure to NO2 and PM2.5.
- Measured infant lung function at 4 weeks using multiple-breath washout.
- Assessed prenatal biomarkers of OS and inflammation (GlycA, OS biomarkers) and calculated a genetic pathway score for OS (gPFSox).
Main Results:
- No association was found between maternal air pollution exposure and infant lung function, or prenatal OS/inflammation markers.
- Infants with a genetic propensity for OS exposed prenatally to NO2 showed significantly lower functional residual capacity (FRC) and higher lung clearance index (LCI).
Conclusions:
- Prenatal exposure to ambient nitrogen dioxide (NO2) is associated with impaired infant lung function (lower FRC, higher LCI) in those with a genetic susceptibility to oxidative stress.
- Maternal and cord blood inflammation and OS biomarkers were not linked to prenatal air pollution exposure.
Background And Objective:
The association between air pollution and poor respiratory health outcomes is well established. Children are particularly at risk from air pollution, especially during the prenatal period as their organs and systems are still undergoing crucial development. This study investigated maternal exposure to air pollution during pregnancy and oxidative stress (OS), inflammation, and infant lung function at 4 weeks of age.
Methods:
Data from the Barwon Infant Study were available for 314 infants. The exposure to NO2 and PM2.5 were estimated. Infant lung function (4 weeks) was measured by multiple-breath washout. Glycoprotein acetyls (GlycA) (36 weeks prenatal), cord blood, and OS biomarkers were measured in maternal urine (28 weeks). A genetic pathway score for OS (gPFSox) was calculated. Linear regression was used and potential modification by the OS genotype was tested.
Results:
There was no relationship between maternal exposure to air pollution and infant lung function, or with GlycA or OS during pregnancy. We found an association in children with a genetic propensity to OS between NO2 and a lower functional residual capacity (FRC) (β = -5.3 mls, 95% CI (-9.3, -1.3), p = 0.01) and lung clearance index (LCI) score (β = 0.46 turnovers, (95% CI 0.10, 0.82), p = 0.01).
Conclusion:
High prenatal exposure to ambient NO2 is associated with a lower FRC and a higher LCI score in infants with a genetic propensity to oxidative stress. There was no relationship between maternal exposure to air pollution with maternal and cord blood inflammation or OS biomarkers.
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