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UNICEF estimates that over 100 million infants worldwide are exposed to toxic air pollution. We are investigating how this alters vulnerable brain cell development during pregnancy and after birth. 

Challenge

Air pollution is a serious common public health concern increasingly associated with morbidity and mortality and resulting in an estimated 7 million premature deaths per year. Air pollution is a mixture of several components, including particulate matter (PM) derived from traffic, fuel burning and industry. The World Health Organisation identified that over 90% of the population are exposed to levels of PM2.5 that are significantly higher than recommended levels.

Exposure to air pollution is associated with marked increases in cardiovascular and respiratory disease risk and death. The central nervous system is also a proposed target organ for the adverse effects of air pollution with exposure linked to an increased risk of developing neurodegenerative diseases such as Alzheimer's disease. Early-life exposure to PM, either during pregnancy or in infancy has been implicated in conditions of neurological impairment, anxiety and depression-like behaviours in humans and rodent models. Brain development may therefore be vulnerable to the detrimental effects of PM exposure.

Solution

The aim of this project is to examine the cellular mechanisms of brain cell development that are interrupted following exposure to air pollution. To tackle this question, we will use experimental paradigms which span all the way from cell culture, through zebrafish models to human neuroimaging, combining the latter with environmental data gathered in London. We will determine the effects of PM on neuroinflammation and neurocellular stress and have already begun to identify targets within inflammatory and neuronal cells that are vulnerable to exposure to PM.

Impact

This project will identify air pollution-induced neurodevelopmental and behavioural changes in animal models and children, using data obtained from air quality measurements in London. Although we plan to identify points of therapeutic intervention for those affected by chronic air pollution exposure, a wider impact of our data will be to contribute to the growing drive for social and economic change required to improve environmental policy in the UK. A policy change to reduce emissions, through traffic control and greater restrictions on pollutants released by industry, would decrease the risk not only of air pollution-related cardiovascular and respiratory conditions but also those targeting brain injury through the life-course, from neurodevelopment to neurodegeneration.

Partners

Professor Serena Counsell, 

Publications