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

Abstract

PM travels along the respiratory tract and enters systemic blood circulation. Studies have shown that PM 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 for extended periods of time and it was found that PM 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 Pkn2 (astrocyte migration), Gorab (neuritogenesis), and Mobp (allergic encephalomyelitis). In contrast, PM decreased expression of miR-338-5p and let-7e-5p, both related to mental development. Further, PM exposure increased miR-3560 and let-7b-5p in the hippocampus, two proteins that regulate genes Oxct1 and Lin28b 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 Kbtbd8 and Adam11 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.

Maternal Exposure to PM2.5 during Pregnancy Induces Impaired Development of Cerebral Cortex in Mice Offspring

“…According to the American Environmental Protection Administration (EPA) (2015), the major air pollutants include NO x , SO 2 , O 3 , PM 2.5 , and PM 10 . PM 2.5 refers to fine particles with an aerodynamic diameter less than or equal to 2.5 μm [ 1 ]. It consists of complex constituents including heavy metals and toxic organic pollutants, and there are several investigations concerning the effects of exposure to air pollutants on admission rates, mortality rates and prognosis of respiratory diseases, cardiovascular disease, and stroke [ 2 , 3 , 4 , 5 , 6 ].…”

Particle toxicology and health - where are we?

“…Neonatal mice exposed to secondary organic particles demonstrated a decrease in social behaviour with down-regulation of estrogen receptor-β and oxytocin receptor in the hypothalamus [173]. Ming-Wei Chao et al reported an increase in reactive oxygen species and several cytokines in the amniotic fluid, and changes in microRNA expression profile in the cerebral cortex and hippocampus of foetal brains in rats following exposure to PM 2.5 [174].…”

Gestational Exposure to Particulate Matter 2.5 (PM2.5) Leads to Spatial Memory Dysfunction and Neurodevelopmental Impairment in Hippocampus of Mice Offspring

“…One of the biological mechanisms by which air pollutants may affect brain is through neuroinflammation (Allen et al, 2013). Exposure to PM 2.5 causes chronic inflammation in pregnant women, along with retarded fetal development and genetic changes in fetal hippocampus (Chao et al, 2017). Our results showed that the exposure led to activation of microglia and astrocytes, along with enhanced GFAP-labeled astrocytes and Iba1-labeled microglia in CA1, CA3, and DG regions, suggesting the activation of neuroglial cells in these hippocampal regions.…”

“…Air pollutants are complex mixtures containing particles, gasses, adsorbed metals and organic pollutants. PM 2.5 (aerodynamic diameters equal to or less than 2.5 μm) acts as a major type of air pollutants and can absorb large quantities of heavy metals and toxic organic pollutants (Chao et al, 2017). Environmental exposure to PM 2.5 results in about 42 million deaths, accounting for approximately 7.6% of the total number of deaths worldwide (Cohen et al, 2017).…”