Early life exposure to air pollution impacts neuronal and glial cell function leading to impaired neurodevelopment

Abstract

The World Health Organisation recently listed air pollution as the most significant threat to human health. Air pollution comprises particulate matter (PM), metals, black carbon and gases such as ozone (O 3 ), nitrogen dioxide (NO 2 ) and carbon monoxide (CO). In addition to respiratory and cardiovascular disease, PM exposure is linked with increased risk of neurodegeneration as well as neurodevelopmental impairments.Critically, studies suggest that PM crosses the placenta, making direct in utero exposure a reality. Rodent models reveal that neuroinflammation, neurotransmitter imbalance and oxidative stress are triggered following gestational/early life exposure to PM, and may be exacerbated by concomitant mitochondrial dysfunction. Gestational PM exposure (potentiated by mitochondrial impairment in the metabolically active neonatal brain) not only impacts neurodevelopment but may sensitise the brain to subsequent cognitive impairment. Having reviewed this field, we conclude that strategies are urgently required to reduce exposure to PM during this sensitive developmental period.

Differential Effects of Urban Particulate Matter on BV2 Microglial-Like and C17.2 Neural Stem/Precursor Cells

“…Activation of microglia following exposure to air pollution is a recognized outcome in both cell studies and animal models (reviewed in [26]). Indeed, microglia activation by PM can be direct (inhaled nasally, bypassing the BBB) or through systemic inflammation (via the respiratory system [46]).…”

“…However, we found that in measures of cytotoxicity, ROS gen- eration and proinflammatory response were greater in BV2 cells than in C17.2 cells following exposure to UPM. Activation of microglia following exposure to air pollution is a recognized outcome in both cell studies and animal models (reviewed in [26]). Indeed, microglia activation by PM can be direct (inhaled nasally, bypassing the BBB) or through systemic inflammation (via the respiratory system [46]).…”

“…The cellular effects of exposure to PM include oxidative stress and neuroinflammation, which can negatively impact the highly regulated process of neurodevelopment [25,26]. Glial cell activation occurs in response to PM exposure of all sizes and types, increasing the production of proinflammatory cytokines and reactive oxygen species (ROS [27][28][29]).…”

Preventing cognitive impairment by reducing air pollution

“…7 Fifth, in addition to the old age, early life (during pregancy and early childhood) is another sensitive period of cognitive impairment, and it remains to be determined whether air pollution abatement in early life could result in longterm improvement of cognitive function. 8 Air pollution has been considered the single largest environmental threat for human health, and the disease burden related to air pollution has been estimated to be on a par with other common behavioural risk factors in predicting future health. 9 The work by Yao and colleagues 3 strengthens the scientific evidence for a link between air pollution and cognitive decline.…”

Air pollution and individuals’ mental well-being in the adult population in United Kingdom: A spatial-temporal longitudinal study and the moderating effect of ethnicity

“…For example, particulate matter of small diameter such as PM1 or PM2.5 might initiate oxidative stress and lead to the formation of inflammatory cytokines that infiltrate the blood-brain barrier causing neurodegeneration and neuroinflammation [ 11 ]. Specifically, exposure to ambient PM2.5 results in depressive responses and increased hippocampal pro-inflammatory cytokines [ 11 ], while exposure to PM1 leads to increased inflammation and reactive oxygen species (ROS) generation and impacts learning and memory [ 12 ]. In this context, traffic related air pollution (e.g., particulate matter and NO 2 ) have been linked by observational research to increased rates of mental health problems including: autism spectrum disorders [ 13 ], schizophrenia [ 14 ], dementia [ 15 ], psychotic experiences [ 16 , 17 ], cognitive disabilities [ 18 ], anxiety and major depressive disorders [ 19 ].…”