Air Pollution: Harming Our Nervous Systems

Air pollution is a serious and common public health concern associated with growing morbidity and mortality worldwide. It has been linked to a variety of diseases of the central nervous system (CNS), including stroke, Alzheimer's disease, Parkinson's disease, and neurodevelopmental disorders.

The sources of air pollution can be natural (e.g., volcanic eruptions) or manmade (e.g., industrial activities). It is a serious health problem, especially in rapidly growing countries. Millions of people worldwide are chronically exposed to airborne pollutants in concentrations that are well above legal safety standards.

Air pollution can affect the brain at any age, but the developing brain is particularly vulnerable due to its high neuronal proliferation and differentiation rates, immature metabolism, and imperfect blood-brain barrier. Disturbances in brain development can lead to permanent abnormalities that translate into later life.

The exact mechanisms underlying brain pathology induced by air pollution are not fully understood, but emerging evidence suggests that air pollution-induced neuroinflammation, oxidative stress, microglial activation, cerebrovascular dysfunction, and alterations in the blood-brain barrier contribute to CNS pathology.

Oxidative stress and inflammation: Air pollution can cause oxidative stress and inflammation in the brain, which can lead to neurodevelopmental disorders

Air pollution can cause oxidative stress and inflammation in the brain, which can lead to neurodevelopmental disorders. Oxidative stress refers to an imbalance between the production of reactive oxygen species (ROS) and the body's ability to detoxify reactive intermediates or repair cellular damage caused by ROS. Oxidative stress has been consistently linked to aging-related neurodegenerative diseases. Air pollution can cause an increase in ROS levels, which can result in significant damage to cellular components, including proteins, lipids, and DNA. This can lead to neuroinflammation, which is a common feature of neurodegenerative diseases.

Neuroinflammation is a complex and innate response of neural tissue against harmful stimuli such as pathogens, damaged cells, and other irritants within the central nervous system (CNS). It has been suggested that exposure to airborne pollutants can contribute to neurodegenerative disease processes from early childhood, especially if individuals are chronically exposed to contaminants.

Systemic inflammation: Air pollution can cause systemic inflammation, which can affect the central nervous system

Systemic inflammation arising from the pulmonary or cardiovascular system can affect the central nervous system. Exposure to air pollution can cause systemic inflammation, which can affect the central nervous system. Air pollution can cause oxidative stress and neuroinflammation, which are also common features of neurodegenerative disorders.

Air pollution can cause systemic inflammation, which can affect the central nervous system. The systemic inflammation is accompanied by the production of proinflammatory cytokines such as tumour necrosis factor alpha (TNFα), interleukin-6 (IL-6), and interleukin-1beta (IL-1β). These cytokines can activate cerebral endothelial cells, disrupt the blood-brain barrier (BBB) integrity, or trigger signalling cascades that lead to the activation of mitogen-activated protein (MAP) kinase, and nuclear factor kappa B (NFκB) transcription factor-mediated pathways.

Cerebrovascular dysfunction: Air pollution can cause cerebrovascular dysfunction, which can lead to stroke

Air pollution is a serious and common public health concern, with millions of people worldwide chronically exposed to airborne pollutants. In recent years, air pollution has been associated with diseases of the central nervous system (CNS), including stroke.

Air pollution can cause cerebrovascular dysfunction, which can lead to stroke. The exact mechanisms by which air pollutants affect the nervous system are not yet fully understood, but emerging evidence suggests that air pollution-induced neuroinflammation, oxidative stress, microglial activation, cerebrovascular dysfunction, and alterations in the blood-brain barrier contribute to CNS pathology.

Mechanisms of cerebrovascular dysfunction

Air pollution can affect the cerebrovascular system through various cellular, molecular, and inflammatory pathways. These pathways can either directly damage brain structures or lead to a predisposition to neurological diseases.

Inflammation

Air pollution can activate the innate immune system, leading to neuroinflammation. This, in turn, can cause or exacerbate cerebrovascular dysfunction.

Oxidative stress

Air pollution can induce oxidative stress, which can damage brain structures and lead to cerebrovascular dysfunction.

Microglial activation

Air pollution can activate microglia, the macrophage-like cells of the CNS. Microglial activation can lead to the release of inflammatory mediators, which can further contribute to cerebrovascular dysfunction.

Cerebrovascular damage

Air pollution can directly damage the cerebrovascular system, leading to dysfunction and an increased risk of stroke.

Population-based studies and preventative measures

Population-based and prospective studies are needed to better understand the relationship between air pollution and cerebrovascular disease, especially in regions with high levels of air pollution, such as rapidly industrializing low and middle-income countries.

Preventative measures and strategies to reduce exposure to air pollution are also necessary to mitigate the adverse effects of air pollution on the cerebrovascular system and overall health.

Neuroinflammation: Air pollution can cause neuroinflammation, which can lead to Alzheimer's and Parkinson's disease

Air pollution can cause neuroinflammation, which can lead to Alzheimer's and Parkinson's disease.

Neuroinflammation is a complex and innate response of neural tissue against harmful stimuli such as pathogens, damaged cells, and other irritants within the central nervous system (CNS). It has been found that air pollution can cause neuroinflammation, which can lead to Alzheimer's and Parkinson's disease.

Neuroinflammation is caused by the activation of microglia, the macrophage-like cells of the CNS, which are the principal players in the brain's innate immune response. Microglial activation is the main cellular event during neuroinflammation, as it results in the production and release of a myriad of inflammatory cascade mediators, including Nitric oxide (NO), chemokines, proinflammatory cytokines, ROS, and reactive nitrogen species (RNS) that are deleterious to the CNS.

Neuroinflammation is a common feature of neurodegenerative disorders, including Alzheimer's and Parkinson's disease. Accumulating evidence suggests that exposure to air pollution can trigger these common denominators of neurodegenerative diseases and lead to neuropathology.

Air pollution can cause neuroinflammation through a variety of cellular and molecular mechanisms. Given the complex nature of polluted ambient air, CNS pathology is probably a result of the synergistic interaction of multiple pathways and mechanisms.

Blood-brain barrier disruption: Air pollution can disrupt the blood-brain barrier, which can lead to the accumulation of disease proteins

Blood-brain barrier disruption is one of the ways in which air pollution can affect the nervous system. Air pollution can cause systemic inflammation, which can in turn lead to the activation of inflammatory agents. These inflammatory agents can then lead to or alter the susceptibility for neuroinflammation and neurodegeneration in the central nervous system.

Airborne particulate matter can enter the body through the nose and the lungs, and can eventually enter the circulatory system. Once in the circulatory system, these particles can directly affect vascular endothelium cells by creating local oxidative stress or by causing proinflammatory effects.

The systemic inflammation is accompanied by the production of proinflammatory cytokines such as tumour necrosis factor alpha (TNFα), interleukin-6 (IL-6), and interleukin-1beta (IL-1β). These cytokines can then activate cerebral endothelial cells, disrupt the blood-brain barrier (BBB) integrity, or trigger signalling cascades that lead to the activation of mitogen-activated protein (MAP) kinase, and nuclear factor kappa B (NFκB) transcription factor-mediated pathways.

Disruption of the BBB can be followed by trafficking of mast cells and inflammatory cells expressing CD163, CD68, and HLA-DR to the damaged site.

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