Exposure to PM_2.5 causes genetic changes in fetal rat cerebral cortex and hippocampus

<jats:title>ABSTRACT</jats:title><jats:p>PM<jats:sub>2.5</jats:sub> travels along the respiratory tract and enters systemic blood circulation. Studies have shown that PM<jats:sub>2.5</jats:sub> increases the incidence of various diseases not only in adults but also in newborn infants. It causes chronic inflammation in pregnant women and retards fetal development. In this study, pregnant rats were exposed to PM<jats:sub>2.5</jats:sub> for extended periods of time and it was found that PM<jats:sub>2.5</jats:sub> exposure increased immune cells in mother rats. In addition, cytokines and free radicals rapidly accumulated in the amniotic fluid and indirectly affected the fetuses. The authors collected cerebral cortex and hippocampus samples at E18 and analyzed changes of miRNA levels. Expression levels of cortical miR‐6315, miR‐3588, and miR‐466b‐5p were upregulated, and positively correlated with the genes <jats:italic>Pkn2</jats:italic> (astrocyte migration), <jats:italic>Gorab</jats:italic> (neuritogenesis), and <jats:italic>Mobp</jats:italic> (allergic encephalomyelitis). In contrast, PM<jats:sub>2.5</jats:sub> decreased expression of miR‐338‐5p and let‐7e‐5p, both related to mental development. Further, PM<jats:sub>2.5</jats:sub> exposure increased miR‐3560 and let‐7b‐5p in the hippocampus, two proteins that regulate genes <jats:italic>Oxct1</jats:italic> and <jats:italic>Lin28b</jats:italic> that control ketogenesis and glycosylation, and neural cell differentiation, respectively. miR‐99b‐5p, miR‐92b‐5p, and miR‐99a‐5p were decreased, leading to reduced expression of <jats:italic>Kbtbd8</jats:italic> and <jats:italic>Adam11</jats:italic> which reduced cell mitosis, migration, and differentiation, and inhibited learning abilities and motor coordination of the fetus. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1412–1425, 2017.</jats:p>