Particulate matter (PM) in air pollution is known to cause problems for our lungs and hearts. However, the damage doesn’t stop there. Airborne PM may also be associated with brain disorders. The harmful effects associated with PM have become an increasingly severe global issue.
Inhalable PM is a mixture of particles suspended in the air, which may be directly released into the air as combusted diesel/gasoline from vehicles, mineral dust, industrial emissions, or generated through chemical reactions of other airborne pollutants, such as nitrogen oxides, heavy metals, and organic compounds. Apart from occupational exposure among construction or printer workers and exposure in disasters and war, the most common sites for PM exposure are roads with heavy traffic.
PM10 are particles up to 10 μm (microns). These include airborne viruses, bacteria, smoke, dust, and mold spores. PM2.5 are particles up to 2.5 μm. These are likely to be particles from power plants, vehicle exhausts, wildfires, and other types of combustion. PM0.1 are particles up to 0.1 μm. This is ultra-fine dust, largely from the same sources as PM2.5 particles, but much finer. They are the most common indoor particles.
PM0.1 particles are the most hazardous to human health since they are so infinitesimal, they can evade the body’s defenses, internal barriers against intrusive foreign matter, and even the immune system’s sentinel cells. Recent research suggests PM0.1 particles are sources of oxidative stress and cardiovascular toxicity.
How Does PM Enter the Brain?
PM can enter the brain through the olfactory system, the Blood-brain barrier (BBB) from the systemic circulation, or to a lesser extent, the trigeminal or facial nerves.
The olfactory system provides a nose-to-brain route for inhaled particles. In the olfactory epithelium the primary olfactory neurons contact with the environment and project to the olfactory bulb via axons. Foreign substances, such as airborne nanosized inorganic particles, may enter the brain via olfactory nerves in a retrograde manner.
The nasal cavity is innervated by the maxillary division of the trigeminal nerve that projects to the spinal trigeminal nucleus. The trigeminal nerve could serve as a transportation route for nasal aerosols.
PM may induce neurotoxicity, oxidative stress, neuroinflammation, and impairs BBB: potential pathogenic effects of PM on neurodegeneration and cognitive impairment.
Recent epidemiological studies reported that PM exposure was correlated with an increased risk of the onset of dementia and Alzheimer’s disease (AD), the most common neurodegenerative disease that is featured with cognitive impairment. PM, especially PM2.5, is correlated with the decline of cognitive performance in people of various age groups who are chronically exposed to high levels of PM2.5.
Chronic exposure to PM2.5 impaired motor development in infants and retarded the development of working memory in school children in Spain. Indeed, the correlation between PM exposure and the cognitive decline in adults, especially in those older than 50 years of age, was prominent as revealed by a series of studies including thousands of participants from the United States, Europe and China. These cognitive impairments included working memory deficits and episodic memory loss, the hallmark symptoms of preclinical AD, and mild cognitive impairment, which is the intermediate state between normal cognitive aging and dementia.
PM may induce neurodegenerative pathology. Along with cognitive decline, neuropathological changes were also found in the brains of adults living in heavily polluted urban areas. Neuroinflammation and oxidative stress are central mediators that form a vicious cycle leading to the adverse effects in the brain caused by exposure to PM.
Exposure to PM induces prominent cognitive decline in humans and laboratory animals due to structural changes and atrophy in the gray and white matter. Oxidative stress is one of the most common detrimental factors in the brain and plays a central role in the neurotoxicity caused by PM. The pro-inflammatory effects of PM may mediate the indirect neurotoxicity.
Damage to the BBB
The BBB is created by the endothelial cells that form the walls of the capillaries. Tight junctions are formed at the margins of endothelial cells which seal the aqueous paracellular diffusional pathway between these cells. The integrated tight junctions form a physical barrier to the brain that helps shield the CNS from neurotoxic substances circulating in the blood. The disruption of tight junctions contributes to the increased permeability of the BBB and subsequently results in an imbalance in the CNS homeostasis and worsened disease progression. A key component of the effects of air pollution in the brain is the breakdown of epithelial and endothelial barriers, especially the BBB, because airborne pollutants induce neuroinflammation leading to the robust production of antibodies against the integral proteins in the tight junctions of the BBB.
Autophagy is a general term for the degradation of intracellular substances through lysosomes after cells are stimulated. Moderate autophagy in the early stage of the body has a protective effect, while over-activated autophagy will aggravate the damage to the body's function. PM2.5 exposure increases the level of autophagy in the brain.
Brain Nerve Damage
The damage of PM2.5 -induced cranial nerves is mainly manifested in neurological and psychiatric diseases caused by neurotoxic effects, such as Alzheimer's disease, Parkinson's disease, cognitive impairment, depression, anxiety, and autism.
The gut microbiota is the normal microbiota present in the gut. It is closely linked to human metabolism, gut homeostasis, immune development, and brain development processes and behavior. A stable and diverse intestinal flora is optimal for maintaining health. Alterations or dysbiosis of the gut microbiota can trigger a variety of diseases, such as inflammatory bowel disease, celiac disease, metabolic syndrome, diabetes, autism, anxiety, depression, and neurodegenerative diseases.
The link between gut flora and the physiological functions of the brain is described as the “gut–microbe–brain”. It has been shown that disruption or interruption of any of the communication pathways between these microbes and the brain may trigger an inflammatory response in the organism. Pathogenic microbes release metabolites and molecules that trigger cytokines in the host and cause inflammation in the central nervous system, greatly contributing to the development and progression of brain disease. PM2.5 can enter the gastrointestinal tract either directly or indirectly. Some studies have shown that exposure to PM through inhalation can alter the composition of the gut microbiota across the gastrointestinal tract, increasing the permeability of the intestinal barrier and increasing the chances of pathogens, such as bacteria, crossing the intestinal mucosa and entering the circulatory system. PM2.5 exposure can induce the secretion of inflammatory cytokines from intestinal epithelial cells through the damaged intestinal barrier from the peripheral system to the central nervous system, leading to neuroinflammation. Recent evidence has demonstrated a relationship between microbiome changes and the pathophysiology of AD.
Tips to Reduce Air Pollution
Limit driving by using public transportation, biking, and walking. Conserve energy, remember to turn off lights, computers, and electric appliances when not in use, run dishwashers and clothes washers only when full and use energy efficient light bulbs. Seal containers of household cleaners, workshop chemicals and solvents to prevent volatile organic compounds from evaporating into the air.
To reduce your home’s indoor air pollution: cleaning and dusting should be thorough, get rid of odors; don’t mask them, remove, or reduce allergens, open windows and doors to increase airflow to give your house better ventilation, make sure your gas stove is well-ventilated, remove carpeting, if possible, keep trash covered, remove shoes at the door and make your house smoke-free.