Air pollution is made up of several different components including gases, chemical compounds, metals, and tiny particles are known as particulate matter (PM).
Long-term exposure or exposure to high levels of air pollution can be hazardous, leading to health conditions that affect the lungs and heart.
Most research has focused on a component of air pollution known as fine particulate matter (PM2.5) are tiny particles that are 40 times smaller than the width of a human hair.
Studies suggest that tiny air pollution particles (PM2.5) can enter the brain, but at this time it is difficult to say if they play a role in the development of dementia.
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What is Alzheimer’s disease?
Alzheimer’s is the most common type of dementia that causes problems with memory, thinking, and behavior. Alzheimer’s disease accounts for 60 percent to 80 percent of the cases.
Symptoms usually develop slowly and get worse over time, becoming severe enough to interfere with daily tasks.
Alzheimer’s is not just a disease of old age approximately 200,000 Americans under the age of 65 have younger-onset Alzheimer’s disease (also known as early-onset Alzheimer’s).
Around 1.6 million of the Indian population suffers from Alzheimer’s and this number is set to triple by 2050.
Alzheimer’s and Air pollution
Studies conducted on brain tissues (post-mortem) from various animals as well as humans showed signs of neurodegeneration due to chronic exposure to high ambient PM levels, suggesting the potential for neurotoxic consequences of PM-Central Nervous System (CNS) entry. PM mediated damage may be caused by the oxidative stress pathway.
Particulate Matter can Alter and Damage the Blood-Brain Barrier
Studies suggest how PM translocate from their initial pulmonary target site into systemic circulation, and ultimately deposit in other organ systems (e.g., brain).
One such study showed that these ultrafine particles translocate to lungs from the nasal cavity and eventually into the blood .
It is known that PM is covered with bio-contaminants and other organic pollutants that contribute to the free radical activity carried on the particles’ surface.
Contact with such particles can damage these endothelial barriers like CO2:O2 interface, blood brain barrier routes, etc. by the free radical activity and disrupt the tight junctions and facilitate particle translocation .
Young children exposed to ambient air pollution are more susceptible to the underdeveloped and altered blood-brain barriers thus reducing the brain’s capacity to protect itself against potentially dangerous toxicants/ particles.
Children also consume more air and water per unit of body size when compared to adults .
Ultra-fine particles and many toxic contaminants present in polluted air can alter the body’s natural defence barriers. Children are among those most vulnerable to suffering adverse health effects due to exposure to high levels of air pollution.
Inter-relation between Oxidative stress and neuroinflammation in the Alzheimer’s disease
It is well established that neuroinflammation, the elevation of pro-inflammatory cytokines and reactive oxygen species (ROS) in the brain, is a common underlying factor of neurodegenerative diseases.
Studies in human and animal research document that neuroinflammation occurs in response to several inhaled pollutants this hypothesis is termed as ‘The neuroinflammation hypothesis”.
Microglia are the resident innate immune cells in the brain critical to CNS health but when exposed to air pollutants can be reprogrammed into a prominent source of neurotoxic cytokines and reactive oxygen species in the brain .
Reports from small human studies of post mortem brain tissue from individuals residing in a highly polluted Mexico City, when compared to individuals living in less polluted regions, support that neuroinflammation and microglial activation are elevated with ambient outdoor air pollution exposure .
Various animal studies reveal that exposure to diverse forms of ambient outdoor air pollution by inhalation, including Ultra-Fine PM (UFPM) , urban particulate matter , O3 , diesel exhaust, mixed vehicle emissions (combined diesel and gasoline emissions) , and manganese results in elevated pro-inflammatory cytokines and oxidative stress in the brain.
A process that increases in the brain with aging, is involved in many neurodegenerative diseases, caused by air pollution (O3, diesel exhaustion, industrial smoke, etc.) inhalation.
Alzheimer’s disease is a progressive and irreversible neurodegenerative disease manifested as a slowly progressive dementia, which begins with subtle memory loss and progresses to a severe decline in cognitive function and disability.
The brain is an organ rich in fatty acids and consumes high levels of energy and physiological oxygen, with poor antioxidant defence mechanisms. Hence, is particularly vulnerable to oxidative stress.
During the oxidative stress, the reactive oxygen species (ROS) targets various macromolecules (lipids, proteins, DNA, RNA, etc.) and degenerate their structural integrity They induce undesirable oxidation, causing membrane damage, protein modification, DNA damage, and celldeath induced by DNA fragmentation and lipid peroxidation .
This oxidative damage/stress, associated with ROS is believed to be involved in many neurodegenerative diseases including Alzheimer’s disease.
Neuroinflammation can both be a cause, and a consequence, of chronic oxidative stress. Pro-inflammatory cytokines generate copious amounts of reactive oxygen species and reactive nitrogen species, creating an oxidative stress upon ambient neurons.
Conversely, oxidants can stimulate pro-inflammatory gene transcription in glia, leading to various inflammatory reactions.
A direct activation link between inflammation and the pathogenesis of Alzheimer’s disease has been demonstrated
Excessive oxidative stress levels have also been correlated to, increased
- protein carbonylation (addition of carbon monoxide to various proteins),
- nitration (introduction of a nitro group into an organic chemical compound),
- lipid peroxidation (free radicals “steal” electrons from the lipids in cell membranes, resulting in cell damage),
- DNA/RNA oxidative damage,
- hyper phosphorylation and polymerization of tau proteins (found in brain help stabilize neuron structure) thus forming neurofibrillary tangles, and
- the amyloid-beta protein clumps into plaques, both being the primary markers of Alzheimer’s
were revealed in the brain and its bordering tissue samples from patients with AD by post-mortem studies. Increased oxidative stress also damages mitochondrial proteins contributing to the development of AD.
Removal of ROS or prevention of their formation may delay the onset or slow down the progression of the AD through multiple mechanisms including, reduction of oxidative stress-mediated neuronal toxicity.
Therefore, AD prevention or treatment with natural anti-oxidants may be an approach that is capable of targeting a number of different molecular events implicated by oxidative stress.
Neuroinflammation and oxidative stress have been implicated as the co-conspirator in neurodegeneration in the AD. Oxidative stress is the major risk factor for the AD.
In recent years air pollution has been a focus of several studies on cognitive impairment and dementia risk.
There is evidence that tiny air pollution particles can enter the brain, and is responsible for neuroinflammation and oxidative stress leading to neurodegeneration.
Systemic inflammation and oxidative stress are two of the most well-established mechanisms involved in the pathogenesis of dementia as underlying adverse health effects of air pollution.
Although the AD causality is multifactorial, air pollution could increase an individual’s risk of developing AD by accelerating the age-related oxidative changes observed in the brain.
Research has demonstrated an association between exposure to air pollution and cognitive impairment in both young children and older people.
All these studies suggest that there is a strong case for further research into the effect of air pollution on brain health.
Therefore, the control of environmental factors such as air pollution could be a key factor in limiting the predicted increase in the AD cases worldwide.