Ontology highlight
ABSTRACT: Methods
Participants were 526 mother-child pairs, born ≥37 weeks. Cotinine was measured at ~27 weeks gestation. Whole pregnancy and trimester-specific O3 and PM2.5 were estimated via. inverse-distance weighted interpolation from stationary monitors. Neonatal adiposity (fat mass percentage) was measured via. air displacement plethysmography. Child weight and length/height were abstracted from medical records. Interaction was assessed by introducing cotinine (<31.5 vs. ≥31.5 ng/mL [indicating active smoking]), O3/PM2.5 (low [tertiles 1-2] vs. high [tertile 3]), and their product term in linear regression models for birth weight and neonatal adiposity and mixed-effects models for BMI trajectories.Results
The rate of BMI growth among offspring jointly exposed to maternal smoking and high PM2.5 (between 8.1 and 12.7 μg/m3) in the third trimester was more rapid than would be expected due to the individual exposures alone (0.8 kg/m2 per square root year; 95% CI = 0.1, 1.5; P for interaction = 0.03). We did not detect interactions between maternal smoking and O3 or PM2.5 at any other time on birth weight, neonatal adiposity, or BMI trajectories.Conclusions
Although PM2.5 was generally below the EPA annual air quality standards of 12.0 μg/m3, exposure during the third trimester may influence BMI trajectories when combined with maternal smoking.
SUBMITTER: Moore BF
PROVIDER: S-EPMC8196098 | biostudies-literature |
REPOSITORIES: biostudies-literature