TY - JOUR
T1 - In-utero exposure to indoor air pollution or tobacco smoke and cognitive development in a South African birth cohort study
AU - Christensen, Grace M.
AU - Rowcliffe, Claire
AU - Chen, Junyu
AU - Vanker, Aneesa
AU - Koen, Nastassja
AU - Jones, Meaghan J.
AU - Gladish, Nicole
AU - Hoffman, Nadia
AU - Donald, Kirsten A.
AU - Wedderburn, Catherine J.
AU - Kobor, Michael S.
AU - Zar, Heather J.
AU - Stein, Dan J.
AU - Hüls, Anke
N1 - Publisher Copyright:
© 2022 The Authors
PY - 2022/8/15
Y1 - 2022/8/15
N2 - 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.
AB - 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.
KW - Air pollution
KW - Environmental epidemiology
KW - Epigenomics
KW - Neurodevelopment
KW - Particulate matter
UR - http://www.scopus.com/inward/record.url?scp=85129119138&partnerID=8YFLogxK
U2 - 10.1016/j.scitotenv.2022.155394
DO - 10.1016/j.scitotenv.2022.155394
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C2 - 35460774
AN - SCOPUS:85129119138
SN - 0048-9697
VL - 834
JO - Science of the Total Environment
JF - Science of the Total Environment
M1 - 155394
ER -
