Prenatal particulate matter exposure and mitochondrial dysfunction at the maternal-fetal interface: Effect modification by maternal lifetime trauma and child sex.

摘要: Abstract Background Prenatal ambient fine particulate matter (PM2.5) and maternal chronic psychosocial stress have independently been linked to changes in mithochondrial DNA copy number (mtDNAcn), a marker of mitochondrial response dysfunction. Further, overlapping research shows sex-specific effects PM2.5 on developmental outcomes. Interactions among PM2.5, stress, child sex not examined this context. Methods We associations exposure prenatal lifetime traumatic stressors, mtDNAcn at birth sociodemographically diverse pregnancy cohort (N = 167). Mothers' daily over gestation was estimated using satellite-based spatio-temporally resolved prediction model. Lifetime stressors ascertained the Life Stressor Checklist-Revised; categorized as high vs. low based median split. Quantitative real-time polymerase chain reaction (qPCR) used determine placenta cord blood leukocytes. Bayesian Distributed Lag Interaction regression models (BDLIMs) were statistically model visualize timing-dependent pattern with explore effect modification by trauma sex. Results Increased across associated decreased (cumulative estimate = − 0.78; 95%CI − 1.41, − 0.16). Higher reduced (β = − 0.33; − 0.63, − 0.02). Among women reporting trauma, increased late (30–38 weeks gestation) significantly placenta; no significant association found group. BDLIMs identified 3-way interaction between Specifically, 25 40 weeks placental boys mothers trauma. In contrast, same window girls Similar interactive observed blood. Conclusions These results indicate that joint influence maternal-fetal interface manner. Additional studies will assist understanding if patterns reflect distinct pathophysiological processes addition