Cognitive impairment, depressive-like behaviors and hippocampal microglia activation following exposure to air pollution nanoparticles.

Air pollution particulate matter (PM) is a world risk factor that the effects of long-term exposure to these factors in terms of damage to cardiovascular and pulmonary function are well known, but little is known comparatively about the effects of PM on emotional and cognitive processes. Exposure to PM can adversely affect the central nervous system (CNS) by inflammatory pathways and activation of reactive oxygen species (ROS) associated with urban air pollution PM. Therefore, we investigated whether prolonged exposure to diesel exhaust particles (DEPs) affects hippocampal inflammatory cytokines and emotional and cognition responses. Male mice were exposed to DEPs for 6 and 12 weeks. DEP-exposed mice indicated more disorders in depressive-like responses and spatial memory and learning than in control groups. Pro-inflammatory cytokine expression in tge hippocampus was increased among mice exposed to DEPs. The number of activated microglia increased in the dentate gyrus (DG) and CA1 regions of the hippocampus in DEP-exposed mice. These results show that chronic exposure to DEPs can alter neurobehavioral and impair cognition. Generally, these findings reaffirm the importance of protecting from exposure to ambient PM2.5 and also advance our understanding of the toxic actions of air pollution nanoparticles.

Prenatal exposure to diesel exhaust particles causes anxiety, spatial memory disorders with alters expression of hippocampal pro-inflammatory cytokines and NMDA receptor subunits in adult male mice offspring.

Air pollution by Diesel exhaust (DE) consists of gaseous compounds and diesel exhaust particles (DEPs). Previous studies show associations between prenatal exposure to diesel exhaust affects the central nervous system (CNS). However, there was not reported that these effects were caused by gaseous compounds, diesel exhaust particles, or both. A limited number of studies in rodent models have shown that exposure to DEPs can result in CNS. Here, we explored the effects of prenatal exposure to DEPs on anxiety and learning and memory in NMRI mice male offspring. Three groups of pregnant mice were exposed to 350-400 µg DEPs/m3 for 2, 4 and 6 h daily in a closed system room. We examined anxiety and learning and memory in 8-to-9-week-old male offspring using the Elevated plus maze and Morris water maze (MWM) test. Hippocampi were isolated after the behavioral tests and measured pro-inflammatory cytokines and N-methyl-D-aspartate (NMDA) receptor expression by quantitative RT-PCR analysis. Mice exposed to DEPs in utero showed deficits in the Elevated plus maze and Morris water maze test. In addition, DEPs exposed mice exhibited decreased hippocampal NR2A and NR3B expression. Taken together, our data suggest that maternal DEP exposure is associated with anxiety, disrupts learning and memory and reduction hippocampal NR2A and NR3B expression in male offspring.