Particulate matter exposure and its consequences on hippocampal neurogenesis and cognitive function in experimental models

Abstract

Exposure to air pollution is thought to cause millions of deaths globally each year. According to the Who 2018, approximately 7 million deaths annually are caused predominantly by noncommunicable diseases due to air pollution. Exposure to air particulate matter 2.5 (PM2.5) has been strongly associated with increased mortality and has significant effects on brain health. Air pollution, particularly ultrafine particulate matter, has emerged as a serious environmental concern with profound implications for human health. Studies in animal models have indicated that exposure to these pollutants during gestational development impacts prenatal and postnatal brain development. In particular, air pollution has been increasingly identified as a potential causative factor, as it affects neurogenesis in the brain's hippocampal region. The hippocampus is highly vulnerable to PM exposure, and any alteration in the structure or function of this region leads to various neurodevelopmental defects and neurodegenerative disorders via oxidative stress, microglial activation, neuronal death, and differential expression of genes. The neurogenesis process involves several steps, such as proliferation, differentiation, migration, synaptogenesis, and neuritogenesis. If any step of the neurogenesis process is hampered by environmental exposure or other factors, it can lead to neurodevelopmental defects, neurodegenerative disorders, and cognitive decline. One significant contributor to these alterations is air pollution, which ranks as the leading environmental risk factor worldwide. Some of the most common effects include oxidative stress, neuroinflammation, depressive behavior, altered cognitive processes, and microglial activation. This review explores how prenatal and postnatal PM exposure affects the hippocampal regions of the brain and the defects associated with exposure.