What is it about?

Air pollution is rampant in many large cities worldwide, affecting human health. While its effects on our respiratory and cardiovascular systems have been sufficiently established, research also links it to impaired cognitive development, especially in children. This paper reviews studies that assess the effects of air pollution on brain development in mice and in children. Mice studies have found that air pollutants triggered the formation of harmful free radicals that cause oxidative stress, neuron damage, neuroinflammation, and neurodegeneration. Diesel exhaust particles and smoking have been also been linked to the development of Alzheimer’s disease and Parkinsonism in mice. The developmental effects seen in animals are similar to those observed in children. What’s more, children are more exposed to the elements and may lack the discretion to avoid being in a potentially hazardous environment. All these factors leave children more vulnerable to harm from pollutants and could affect the healthy development of the blood-brain barrier. Exposure to pollutants triggers the release of chemicals called ‘cytokines’, which cause inflammation, damage, and loss of brain tissue in various areas of the brain. It also leads to the loss of ‘myelin’ (the tissue that protects nerves) in brain cells, leading to impaired cognitive function.

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Why is it important?

The paper hopes to spark an interest in public health and further research on the topic of air pollution from a neural development perspective. There is a need for policies and public health targets that reduce the effect of air pollution on brain development, especially in urban areas. Key takeaway Air pollution affects the integrity of the blood-brain barrier in children, leading to stunted brain and cognitive development. This needs to be ad-dressed from a public health perspective.

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This page is a summary of: How air pollution alters brain development: the role of neuroinflammation, Translational Neuroscience, January 2016, De Gruyter, DOI: 10.1515/tnsci-2016-0005.
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