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

Background: 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.