Grace M Christensen1, Claire Rowcliffe1, Junyu Chen1, Aneesa Vanker2, Nastassja Koen3, Meaghan J Jones4, Nicole Gladish5, Nadia Hoffman6, Kirsten A Donald7, Catherine J Wedderburn8, Michael S Kobor5, Heather J Zar9, Dan J Stein3, Anke Hüls10. 1. Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, GA, USA. 2. Department of Paediatrics and Child Health, Red Cross War Memorial Children's Hospital, University of Cape Town, South Africa. 3. Neuroscience Institute, University of Cape Town, Cape Town, South Africa; Department of Psychiatry and Mental Health, University of Cape Town, Cape Town, South Africa; South African Medical Research Council (SAMRC) Unit on Risk and Resilience in Mental Disorders, University of Cape Town, Cape Town, South Africa. 4. Department of Biochemistry and Medical Genetics, University of Manitoba, Children's Hospital Research, Institute of Manitoba, Winnipeg, Canada. 5. Department of Medical Genetics, University of British Columbia, Vancouver, BC, Canada; BC Children's Hospital Research Institute, Vancouver, BC, Canada; Centre for Molecular Medicine and Therapeutics, Vancouver, BC, Canada. 6. Neuroscience Institute, University of Cape Town, Cape Town, South Africa; Department of Psychiatry and Mental Health, University of Cape Town, Cape Town, South Africa. 7. Department of Paediatrics and Child Health, Red Cross War Memorial Children's Hospital, University of Cape Town, South Africa; Neuroscience Institute, University of Cape Town, Cape Town, South Africa. 8. Department of Paediatrics and Child Health, Red Cross War Memorial Children's Hospital, University of Cape Town, South Africa; Neuroscience Institute, University of Cape Town, Cape Town, South Africa; Department of Clinical Research, London School of Hygiene & Tropical Medicine, London, UK. 9. Department of Paediatrics and Child Health, Red Cross War Memorial Children's Hospital, University of Cape Town, South Africa; South African Medical Research Council (SAMRC) Unit on Risk and Resilience in Mental Disorders, University of Cape Town, Cape Town, South Africa. 10. Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, GA, USA; Gangarosa Department of Environmental Health, Rollins School of Public Health, Emory University, USA. Electronic address: anke.huels@emory.edu.
Abstract
BACKGROUND AND AIMS: There is increasing evidence indicating that air pollution exposure is associated with neuronal damage. Since pregnancy is a critical window of vulnerability, air pollution exposure during this period could have adverse effects on neurodevelopment. This study aims 1) to analyze associations of prenatal exposure to indoor air pollution (particulate matter with diameters ≤10 μm, PM10) and tobacco smoke with neurodevelopment and 2) to determine whether these associations are mediated by deviations of epigenetic gestational age from chronological gestational age (ΔGA). METHODS: Data of 734 children from the South African Drakenstein Child Health Study were analyzed. Prenatal PM10 exposure was measured using devices placed in the families' homes. Maternal smoking during pregnancy was determined by maternal urine cotinine measures. The Bayley Scales of Infant and Toddler Development III (BSID-III) was used to measure cognition, language and motor development and adaptive behavior at two years of age. Linear regression models adjusted for maternal age, gestational age, sex of child, ancestry, birth weight/length, and socioeconomic status were used to explore associations between air pollutants and BSID-III scores. A mediation analysis was conducted to analyze if these associations were mediated by ΔGA using DNA methylation measurements from cord blood. RESULTS: An increase of one interquartile range in natural-log transformed PM10 (lnPM10; 1.58 μg/m3) was significantly associated with lower composite scores in cognition, language, and adaptive behavior sub-scores (composite score β-estimate [95%-confidence interval]: -0.950 [-1.821, -0.120]). Maternal smoking was significantly associated with lower adaptive behavior scores (-3.386 [-5.632, -1.139]). Associations were not significantly mediated by ΔGA (e.g., for PM10 and cognition, proportion mediated [p-value]: 4% [0.52]). CONCLUSION: We found an association of prenatal exposure to indoor air pollution (PM10) and tobacco smoke on neurodevelopment at two years of age, particularly cognition, language, and adaptive behavior. Further research is needed to understand underlying biological mediators.
BACKGROUND AND AIMS: There is increasing evidence indicating that air pollution exposure is associated with neuronal damage. Since pregnancy is a critical window of vulnerability, air pollution exposure during this period could have adverse effects on neurodevelopment. This study aims 1) to analyze associations of prenatal exposure to indoor air pollution (particulate matter with diameters ≤10 μm, PM10) and tobacco smoke with neurodevelopment and 2) to determine whether these associations are mediated by deviations of epigenetic gestational age from chronological gestational age (ΔGA). METHODS: Data of 734 children from the South African Drakenstein Child Health Study were analyzed. Prenatal PM10 exposure was measured using devices placed in the families' homes. Maternal smoking during pregnancy was determined by maternal urine cotinine measures. The Bayley Scales of Infant and Toddler Development III (BSID-III) was used to measure cognition, language and motor development and adaptive behavior at two years of age. Linear regression models adjusted for maternal age, gestational age, sex of child, ancestry, birth weight/length, and socioeconomic status were used to explore associations between air pollutants and BSID-III scores. A mediation analysis was conducted to analyze if these associations were mediated by ΔGA using DNA methylation measurements from cord blood. RESULTS: An increase of one interquartile range in natural-log transformed PM10 (lnPM10; 1.58 μg/m3) was significantly associated with lower composite scores in cognition, language, and adaptive behavior sub-scores (composite score β-estimate [95%-confidence interval]: -0.950 [-1.821, -0.120]). Maternal smoking was significantly associated with lower adaptive behavior scores (-3.386 [-5.632, -1.139]). Associations were not significantly mediated by ΔGA (e.g., for PM10 and cognition, proportion mediated [p-value]: 4% [0.52]). CONCLUSION: We found an association of prenatal exposure to indoor air pollution (PM10) and tobacco smoke on neurodevelopment at two years of age, particularly cognition, language, and adaptive behavior. Further research is needed to understand underlying biological mediators.
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