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

Abstract

Air pollution is a serious environmental health problem closely related to the occurrence of central nervous system diseases. Exposure to particulate matter with an aerodynamic diameter less than or equal to 2.5 µm (PM2.5) during pregnancy may affect the growth and development of infants. The present study was to investigate the effects of maternal exposure to PM2.5 during pregnancy on brain development in mice offspring. Pregnant mice were randomly divided into experimental groups of low-, medium-, or high-dosages of PM2.5, a mock-treated group which was treated with the same amount of phosphate buffer solution (PBS), and acontrol group which was untreated. The ethology of offspring mice on postnatal days 1, 7, 14, 21, and 30, along with neuronal development and apoptosis in the cerebral cortex were investigated. Compared with the control, neuronal mitochondrial cristae fracture, changed autophagy characteristics, significantly increased terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) positive cell rate, and mRNA levels of apoptosis-related caspase-8 and caspase-9 were found in cerebral cortex of mice offspring from the treatment groups, with mRNA levels of Bcl-2 and ratio of Bcl-2 to Bax decreased. Treatment groups also demonstrated enhanced protein expressions of apoptosis-related cleaved caspase-3, cleaved caspase-8 and cleaved caspase-9, along with declined proliferating cell nuclear antigen (PCNA), Bcl-2, and ratio of Bcl-2 to Bax. Open field experiments and tail suspension experiments showed that exposure to high dosage of PM2.5 resulted in decreased spontaneous activities but increased static accumulation time in mice offspring, indicating anxiety, depression, and social behavioral changes. Our results suggested that maternal exposure to PM2.5 during pregnancy might interfere with cerebral cortex development in mice offspring by affecting cell apoptosis.

Effects of early postnatal exposure to fine particulate matter on emotional and cognitive development and structural synaptic plasticity in immature and mature rats

“…Kulas et al () found that prenatal exposure to PM2.5 in mice led to elevated SYP expression and unchanged PSD95 expression in the hippocampus of male offspring. Zhang et al () reported that prenatal PM2.5 exposure in mice decreased postsynaptic densities of membranes and the number of synaptic vesicles in the cerebral cortex of offspring, and an in vitro study suggested that PM2.5 exposure reduced PSD95 expression in cortical neurons (Chen, Li, & Sang, ). These results suggested that PM2.5 exposure during early life might change synaptic structural plasticity.…”

Adverse organogenesis and predisposed long-term metabolic syndrome from prenatal exposure to fine particulate matter

“…Also, increased susceptibility of offspring to experimentally induced heart failure was identified after female mice were exposed to diesel exhaust PM before conception as well as during gestation and early postnatal life (13). In addition, exposure of gestating mice to PM 2.5 during pregnancy impaired development of the cerebral cortex and induced anxiety, depression, and social behavioral changes in offspring (14). Prenatal exposure to diesel exhaust particles between embryonic days 9 and 17 induced neuroinflammation and predisposed offspring to diet-induced obesity in adulthood (15).…”

“…including oxidative stress, inflammation, vascular dysfunction, and increased susceptibility to metabolic syndrome including obesity and diabetes (11)(12)(13)(14)(15)(16)(17). In addition, a recent study revealed that in utero ultrafine PM exposure leads to offspring pulmonary immunosuppression in offspring (10).…”

Maternal exposure to fine particulate matter during pregnancy induces progressive senescence of hematopoietic stem cells under preferential impairment of the bone marrow microenvironment and aids development of myeloproliferative disease

“…However, little is known about the mechanisms underlying the effects of PM 2.5 on stem progenitor cells, particularly hematopoietic stem progenitor cells (HSPCs). There is growing evidence that maternal exposure to PM 2.5 during pregnancy can harm both the embryo and progeny [4][5][6]. The embryo and fetus are more susceptible to external stress than the adult.…”

“…The embryo and fetus are more susceptible to external stress than the adult. Although there is growing evidence regarding the detrimental risks to the embryo and offspring that have been maternally exposed to PM 2.5 during pregnancy [4][5][6], little is known about the effects of maternal PM 2.5 exposure to stem cells, which begin to emerge, activate, and mature during embryo development.…”