Perinatal exposure to particulate matter 2.5 (PM2.5) is linked to both neurotoxicity and childhood obesity. Given the role of inhibitory control in eating behavior, we propose that early-life PM2.5 disrupts inhibitory control, contributing to obesity as part of a causal pathway. In the PROGRESS cohort (n = 434) in Mexico City, we modeled ambient PM2.5 exposure during pregnancy and the first year of life. Inhibitory control was assessed at age 4 using the Conners Kiddie Continuous Performance Test, and repeated adiposity measures were tracked from ages 4 to 8. We conducted latent profile analysis to identify profiles of inhibitory control and applied multinomial causal mediation analyses to estimate the natural total, direct, and indirect (i.e., mediated) effects of inhibitory control on the prenatal and first-year-of-life PM2.5 exposure with childhood obesity-related outcomes, using separate models for each exposure window. Our analysis show a significant natural indirect effect between first-year postnatal PM2.5 concentrations and greater body mass index (BMI) (β = 1.86 kg/m2, 95%CI: 0.72, 3.19), BMI z-score (β = 0.11, 95%CI: 0.01, 0.25), and percent body fat (β = 3.04%, 95%CI: 1.26,5.04) at 8 years, and BMI change (β = 0.43 kg/m2, 95%CI: 0.14, 0.80) from ages 4 to 8 years mediated through inhibitory control. No evidence of mediation by inhibitory control was found for prenatal PM2.5 predicting obesity-related outcomes. PM2.5 exposure in the first year of life indirectly predicts childhood obesity through a pathway mediated by poorer inhibitory control. This new understanding of the underlying obesogenic mechanisms of air pollution can significantly inform policy and clinical interventions. Perinatal exposure to particulate matter 2.5 (PM2.5) has been shown to have neurotoxic effects and can lead to obesity. This study examined whether changes in inhibitory control, an executive function previously associated with obesity, from prenatal and early postnatal PM2.5 exposure mediate its association with obesity-related outcomes in school-aged children. High exposure early in infancy is linked to altered inhibitory control, which in turn increases the risk of obesity, likely through more impulsive eating behaviors. These findings suggest that reducing early exposure to PM2.5 could support healthier cognitive and metabolic development in children. Lane, Hsu et al. model ambient PM2.5 exposure during pregnancy and the first year of life to examine how perinatal PM2.5 contributes to childhood obesity via a pathway mediated by PM2.5-induced alterations in inhibitory control. They find that PM2.5 exposure in infancy indirectly predicts obesity through its impact on inhibitory control deficits.
Lane et al. (Mon,) studied this question.