Joint effects of ambient air pollution and maternal smoking on neonatal adiposity and childhood BMI trajectories in the Healthy Start study

Coexposure to air pollution and tobacco smoke may influence early-life growth, but few studies have investigated their joint effects. We examined the interaction between fetal exposure to maternal smoking and ozone (O(3)) or fine particulate matter (PM(2.5)) on birth weight, neonatal adiposity, and body mass index (BMI) trajectories through age 3 years. METHODS: Participants were 526 mother-child pairs, born ≥37 weeks. Cotinine was measured at ~27 weeks gestation. Whole pregnancy and trimester-specific O(3) and PM(2.5) 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]), O(3)/PM(2.5) (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 PM(2.5) (between 8.1 and 12.7 μg/m(3)) in the third trimester was more rapid than would be expected due to the individual exposures alone (0.8 kg/m(2) per square root year; 95% CI = 0.1, 1.5; P for interaction = 0.03). We did not detect interactions between maternal smoking and O(3) or PM(2.5) at any other time on birth weight, neonatal adiposity, or BMI trajectories. CONCLUSIONS: Although PM(2.5) was generally below the EPA annual air quality standards of 12.0 μg/m(3), exposure during the third trimester may influence BMI trajectories when combined with maternal smoking.