Racial/ethnic differences in acute and longer-term posttraumatic symptoms following traumatic injury or illness.

BACKGROUND: Racial/ethnic differences in mental health outcomes after a traumatic event have been reported. Less is known about factors that explain these differences. We examined whether pre-, peri-, and post-trauma risk factors explained racial/ethnic differences in acute and longer-term posttraumatic stress disorder (PTSD), depression, and anxiety symptoms in patients hospitalized following traumatic injury or illness. METHODS: PTSD, depression, and anxiety symptoms were assessed during hospitalization and 2 and 6 months later among 1310 adult patients (6.95% Asian, 14.96% Latinx, 23.66% Black, 4.58% multiracial, and 49.85% White). Individual growth curve models examined racial/ethnic differences in PTSD, depression, and anxiety symptoms at each time point and in their rate of change over time, and whether pre-, peri-, and post-trauma risk factors explained these differences. RESULTS: Latinx, Black, and multiracial patients had higher acute PTSD symptoms than White patients, which remained higher 2 and 6 months post-hospitalization for Black and multiracial patients. PTSD symptoms were also found to improve faster among Latinx than White patients. Risk factors accounted for most racial/ethnic differences, although Latinx patients showed lower 6-month PTSD symptoms and Black patients lower acute and 2-month depression and anxiety symptoms after accounting for risk factors. Everyday discrimination, financial stress, past mental health problems, and social constraints were related to these differences. CONCLUSION: Racial/ethnic differences in risk factors explained most differences in acute and longer-term PTSD, depression, and anxiety symptoms. Understanding how these risk factors relate to posttraumatic symptoms could help reduce disparities by facilitating early identification of patients at risk for mental health problems.

Associations between prenatal organophosphate pesticide exposure and placental gene networks.

BACKGROUND: Exposure to organophosphate (OP) pesticides during pregnancy has been linked to deficiencies of neurobehavioral development in childhood; however, the molecular mechanisms underlying this association remain elusive. The placenta plays a crucial role in protecting the fetus from environmental insults and safeguarding proper fetal development including neurodevelopment. The aim of our study is to evaluate changes in the placental transcriptome associated with prenatal OP exposure. METHODS: Pregnant farm workers from two agricultural districts in northern Thailand were recruited for the Study of Asian Women and Offspring's Development and Environmental Exposures (SAWASDEE) from 2017 to 2019. For 254 participants, we measured maternal urinary concentrations of six nonspecific dialkyl phosphates (DAP) metabolites in early, middle, and late pregnancy. In parallel, we profiled the term placental transcriptome from the same participants using RNA-Sequencing and performed Weighted Gene co-expression Network Analysis (WGCNA). Generalized linear regression modeling was used to examine associations of urinary OP metabolites and placental co-expression module eigenvalues. RESULTS: We identified 21 gene co-expression modules in the placenta. From the six DAP metabolites assayed, diethylphosphate (DEP) and diethylthiophosphate (DETP) were detected in more than 70% of the urine samples. Significant associations between DEP at multiple time points and two specific placental gene modules were observed. The 'black' module, enriched in genes involved in epithelial-to-mesenchymal transition (EMT) and hypoxia, was negatively associated with DEP in early (p = 0.034), and late pregnancies (p = 0.016). The 'lightgreen' module, enriched in genes involved in myogenesis and EMT, was negatively associated with DEP in late pregnancy (p = 0.010). We observed 2 hub genes (CELSR1 and PYCR1) of the 'black' module to be negatively associated with DEP in early and late pregnancies. CONCLUSIONS: Our results suggest that prenatal OP exposure may disrupt placental gene networks in a time-dependent manner. Such transcriptomic effects may lead to down-stream changes in placental function that ultimately affect the developing fetus.