Air pollution refers to the presence of harmful contaminants in the atmosphere, such as dust, fumes, gases, mists, odors, smoke, or vapors, that pose a risk to human health. Inhaling these pollutants can cause damage to various organs, including the lungs, heart, and brain. Short-term exposure can impair lung function, increase the likelihood of respiratory infections, and worsen asthma. Long-term exposure raises the risk of developing chronic noncommunicable diseases, including stroke, heart disease, chronic obstructive pulmonary disease (COPD), and certain cancers.¹

Children, older adults, and pregnant women are particularly vulnerable to air pollution-related health issues. Additionally, factors such as genetics, comorbidities, nutrition, and sociodemographic characteristics can influence an individual’s susceptibility to the harmful effects of air pollution.¹ 

While the general health risks of air pollution are well-established, emerging research has highlighted the  impact on the development of neurological diseases such as dementia and Parkinson’s disease. These chronic conditions, which primarily affect older adults, have been linked to long-term exposure to air pollutants. As more research is conducted on the links between air pollution and health problems, more attention is being brought to the dangers of air pollution and its long-term effects on human health.

Sources of Air Pollution

Particle matter (PM) is defined as the combination of solid particles and liquid drops in the air. PM particles are classified into two categories: PM10 and PM2.5. PM10 particles are typically 10 micrometers or less; PM2.5 particles are typically 2.5 micrometers or smaller. PM10 particulate matter can travel into the lungs and pass through the bloodstream. PM2.5 is the most dangerous form of fine particles as these can easily be inhaled, increasing the risk for serious health complications.² 

Fine particles are too small to be seen individually, but at high pollution levels, they can make the air look thick and hazy. Sources of particle pollution include motor vehicles, factories, power plants, burning wood, and wildfires. Coarse particles can include wind-blown dust, ash, and pollen, while fine particles are often a by-product of burning wood or fossil fuels and may contain toxic compounds, salts, and metals.³ Fine particles can also contain carbon monoxide, ozone, nitrogen dioxide, and sulphur dioxide.¹

Health Conditions Associated with Air Pollution

Fine particulate matter is particularly dangerous, as these tiny particles can penetrate deep into the lungs, enter the bloodstream, and travel to other organs, potentially causing systemic damage, inflammation and carcinogenicity.¹ High levels of particle pollution can cause illness, hospitalization, and premature death. Research suggests that PM2.5 is responsible for nearly 48,000 premature deaths in the US each year.⁴ Current research has elicited growing concerns regarding the harmful effects of air pollution on brain and central nervous system disorders, such as dementia and Parkinson’s disease (PD).⁵ 

Dementia. Fine particulate matter is linked to an increased risk of dementia, as it can affect cognitive function through neuroinflammation caused by systemic inflammation or oxidative stress following lung irritation. The smallest particles, often coated with neurotoxic chemicals, can enter the brain via the olfactory bulb or cross the blood-brain barrier.⁶ 

A study looking at the relationship between air pollution and dementia in the US studied 27,857 individuals, aged 50 years or older and free of dementia at the start of the study, between 1998 and 2016. Over a mean follow-up of 10.2 years, 15 percent of participants developed dementia. Higher levels of total PM2.5 were linked to increased rates of new dementia cases PM2.5 from various sources with the most pollution stemming from farming, automobiles, and wildfires. While traffic and coal combustion were also associated with dementia risk, these results were more sensitive to adjustments for fine particles from other sources. The researchers estimated that nearly 188,000 new dementia cases each year in the US are attributable to total fine particle exposure. Compared to those without dementia, participants who developed the condition were more likely to be non-White, have lower education and wealth, and reside in areas with higher ambient fine particle levels.⁶ 

Building on the growing body of research linking air pollution to dementia, another study conducted by the Emory Goizueta Alzheimer’s Disease Research Center, further investigated this connection by analyzing postmortem brain tissue. The goal of this study was to determine whether changes in DNA methylation (DNAm) in the brain’s prefrontal cortex significantly affected neuropathological markers associated with Alzheimer’s disease due to exposure to traffic-related PM2.5. In total, 159 eligible donors were included in the study. The eligibility criteria included having a residential address in Georgia, being 55 years or older at the time of death, date of death after 1999, and no missing data on factors such as race, sex, and education. The average age at death of the participants was 76.6 years and 56 percent of the participants were male. Overall, most of the participants were White (89.3%), 78.7 percent had completed college, and were living in wealthy neighborhoods.⁷ 

The donor brains were examined to determine the amount of beta-amyloid (Aβ plaques) and neurofibrillary tangles (NFTs), which are present in the brains of patients with dementia.^7,8 PM2.5 particles from the 20 counties within the metropolitan area of Atlanta, Georgia, were calculated yearly from 2002 to 2019 with two air quality models. Researchers removed deoxyribonucleic acid (DNA) from each of the donor brains, and analyzed a total of 167 prefrontal cortex samples, including six duplicates. The researchers looked at extended PM2.5 exposure 1, 3, and 5 years prior to death to determine the association between PM2.5 exposure and increased neuropathology markers, indicative of dementia. Overall, the researchers discovered that the differential DNAm located in the prefrontal cortex tissues were strongly associated with long-term exposure to traffic-related PM2.5 as a result of dementia.⁷ 

Parkinson’s disease (PD). Research indicates that air pollution may contribute to the risk of PD through systemic inflammation, oxidative stress, and direct toxicity upon entering the brain. Small particulate pollutants can travel to the brain through the olfactory system, creating a direct anatomical link from the nose to the brain. These particles may also reach the brain through the autonomic nervous system or the bloodstream.⁹ Research has indicated that pollutants and PM2.5 can be harmful to the human brain, both directly and indirectly when crossing through the blood-brain barrier, which can also lead to neuroinflammation and abnormal protein aggregation which in turn damages the olfactory bulb and frontal cortex, leading to the development of PD.⁵ 

Although research has established a connection between air pollutants and Parkinson’s disease, some studies investigating this link, particularly regarding traffic-related pollution, have shown conflicting results. For example, studies conducted in Taiwan and Denmark found a higher risk of Parkinson’s disease associated with long-term exposure to traffic-related air pollution, as indicated by modeled carbon monoxide (CO) levels, while other research found no such link with measured CO.^9–13 Similarly, other studies have connected fine particulate matter to an increased risk of developing PD^14–20 while others found no associations.^21–26 The conflicting results may be partly due to the complexities of studying the impact of air pollution on PD risk, such as the time lag between the onset of the disease and diagnosis.^9,27,28

A separate study conducted in Olmsted County, Minnesota, examined the relationship between air pollution, specifically PM2.5 exposure, and the risk of developing the akinetic-rigid subtype of Parkinson’s disease—²⁹ which involves minor, slow movements, and inflexibility, and tremors.³⁰ This study included a total of 346 participants, 62.4 percent of whom were male, with a median age of 72 years. These participants were matched for age and sex with 4,813 controls. Researchers analyzed the risk of the akinetic-rigid subtype, evaluating the risks of all-cause mortality and dyskinesia—²⁹ involuntary, writhing movements of the face, arms, legs, and trunk, which are a common side effect from medications used to treat Parkinson’s disease—³¹ adjusting for factors such as age, sex, race, ethnicity, and residential area. Follow-ups were discontinued either at the last medical visit or upon death. This study discovered that exposure to PM2.5 was associated with an increased risk of developing PD, particularly the akinetic-rigid form of the disease, with the overall risk increasing as PM2.5 levels grew. Overall, the greatest risk for PD attributed to air pollution was found to be within central cities of metropolitan areas in Olmsted County, Minnesota, for the top quintile, in comparison to the bottom quintile. Overall, researchers discovered a 36-percent increased risk of developing the akinetic-rigid form of PD. Among PD patients only, higher PM2.5 and NO₂ exposure was linked to an increased risk of dyskinesia. Overall, researchers discovered no link between PM2.5 and all-cause mortality in PD participants.²⁹ 

A separate study looked at 22,187 individuals living in Finland between 1996 to 2015 with seven matched controls per participant based on age, sex, and hospital district. The average age among the participants was 70.6 years, with most participants being male (55%). Compared to the controls, the patients with PD had higher social classes and worked in agriculture. Comorbidity diseases such as asthma, COPD, smoking-related cancers, and traumatic brain injuries were comparable among the cases and controls. The overall exposure amounts for residential areas were estimated throughout the study period. The researchers also considered how many addresses the participants had during the 16-year study period and how long they lived at each of their listed address(es). This data was then evaluated over a total of four exposure periods. The primary focus of this study was on exposure to air pollution between six and 16 years prior to the diagnosis date of PD. Other models also looked at exposure between the following periods: 10 to 16 years, 6 to 10 years, and up to five years prior to PD diagnosis. The exposure levels for both groups were similar during the six to 16 years prior to diagnosis with exposure levels and the subsequent components remaining equal. Among the cases and controls, the results remained consistent with fairly strong correlations between PM10 and PM2.5 and the types of air pollutants studied. The amount of pollutants steadily decreased throughout the study period from 1996 to 2015, a reflection of the overall decrease in emissions of pollutants within Europe during the same period.³² 

Conclusion

Air pollution, particularly fine particulate matter (PM2.5), presents a significant threat to human health, with both short-term and long-term exposure linked to a range of chronic diseases. Emerging research has highlighted the growing concern over air pollution’s role in the development and progression of neurodegenerative diseases such as dementia and Parkinson’s disease. Studies have highlighted that long-term exposure to traffic-related pollutants, particularly PM2.5, is associated with an increased risk of cognitive decline and movement disorders, such as Parkinson’s disease, especially among older adults. As discussed, some studies have not made concrete connections between the effects of air pollution and human health; however, the growing amount of evidence presented highlights the need to raise awareness and to mitigate air pollution.  

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