Combined and sequential exposure to prenatal second hand smoke and postnatal maternal distress is associated with cingulo-opercular global efficiency and attention problems in school-age children.

BACKGROUND: Prenatal exposure to secondhand (environmental) tobacco smoke (SHS) is associated with adverse neurodevelopmental outcomes, including altered functional activation of cognitive control brain circuitry and increased attention problems in children. Exposure to SHS is more common among Black youth who are also disproportionately exposed to socioeconomic disadvantage and concomitant maternal distress. We examine the combined effects of exposure to prenatal SHS and postnatal maternal distress on the global efficiency (GE) of the brain's cingulo-opercular (CO) and fronto-parietal control (FP) networks in childhood, as well as associated attention problems. METHODS: Thirty-two children of non-smoking mothers followed in a prospective longitudinal birth cohort at the Columbia Center for Children's Environmental Health (CCCEH) completed magnetic resonance imaging (MRI) at ages 7-9 years old. GE scores were extracted from general connectivity data collected while children completed the Simon Spatial Incompatibility functional magnetic resonance imaging (fMRI) task. Prenatal SHS was measured using maternal urinary cotinine from the third trimester; postnatal maternal distress was assessed at child age 5 using the Psychiatric Epidemiology Research Interview (PERI-D). The Child Behavior Checklist (CBCL) measured Attention and Attention Deficit Hyperactivity Disorder (ADHD) problems at ages 7-9. Linear regressions examined the interaction between prenatal SHS and postnatal maternal distress on the GE of the CO or FP networks, as well as associations between exposure-related network alterations and attention problems. All models controlled for age, sex, maternal education at prenatal visit, race/ethnicity, global brain correlation, and mean head motion. RESULTS: The prenatal SHS by postnatal maternal distress interaction term associated with the GE of the CO network (ß = 0.673, Bu = 0.042, t(22) = 2.427, p = .024, D = 1.42, 95% CI [0.006, 0.079], but not the FP network (ß = 0.138, Bu = 0.006, t(22) = 0.434, p = .668, 95% CI [-0.022, 0.033]). Higher GE of the CO network was associated with more attention problems (ß = 0.472, Bu = 43.076, t(23) = 2.780, p = .011, D = 1.74, n = 31, 95% CI [11.024, 75.128], n = 31) and ADHD risk (ß = 0.436, Bu = 21.961, t(29) = 2.567, p = .018, D = 1.81, 95% CI [4.219, 39.703], n = 30). CONCLUSIONS: These preliminary findings suggest that sequential prenatal SHS exposure and postnatal maternal distress could alter the efficiency of the CO network and increase risk for downstream attention problems and ADHD. These findings are consistent with prior studies showing that prenatal SHS exposure is associated with altered function of brain regions that support cognitive control and with ADHD problems. Our model also identifies postnatal maternal distress as a significant moderator of this association. These data highlight the combined neurotoxic effects of exposure to prenatal SHS and postnatal maternal distress. Critically, such exposures are disproportionately distributed among youth from minoritized groups, pointing to potential pathways to known mental health disparities.

Effects of prenatal polycyclic aromatic hydrocarbons and childhood material hardship on reading achievement in school-age children: A preliminary study.

Background: Children from socioeconomically disadvantaged backgrounds are at elevated risk for reading problems. They are also likely to live in neighborhoods with high levels of air pollution and to experience material hardship. Despite these risk factors, the links between prenatal chemical exposures, socioeconomic adversities, and reading problems in youth from disadvantaged backgrounds remain understudied. Here we examine associations between prenatal exposure to polycyclic aromatic hydrocarbons (PAH), a common air pollutant, and reading skills, and determine if this relationship is exacerbated by material hardship among Black and/or Latinx children who have been followed as part of a longitudinal urban birth cohort. Methods: Mothers and their children, who were participants in a prospective birth cohort followed by the Columbia Center for Children's Environmental Health, were recruited for the current study. Personal prenatal PAH exposure was measured during the third-trimester of pregnancy using a personal air monitoring backpack. Mothers reported their level of material hardship when their child was age 5 and children completed measures of pseudoword and word reading [Woodcock Johnson III Tests of Achievement (WJ-III) Basic Reading Index] at age 7. We used multiple linear regression to examine the effects of the interaction between prenatal PAH and material hardship on Basic Reading Index, controlling for ethnicity/race, sex, birthweight, presence of a smoker in the home (prenatal), and maternal education (prenatal) (N = 53). Results: A prenatal PAH × material hardship interaction significantly associated with WJ-III Basic Reading Index scores at age 7 (ß = -0.347, t(44) = -2.197, p = 0.033). Exploratory analyses suggested that this effect was driven by untimed pseudoword decoding (WJ-III Word Attack: ß = -0.391, t(44) = -2.550, p = 0.014). Conclusion: Environmental chemical exposures can be particularly toxic during the prenatal period when the fetal brain undergoes rapid development, making it uniquely vulnerable to chemical perturbations. These data highlight the interactive effects of environmental neurotoxicants and unmet basic needs on children's acquisition of reading skill, specifically phonemic processing. Such findings identify potentially modifiable environmental risk factors implicated in reading problems in children from economically disadvantaged backgrounds.