New research reveals that air pollution, especially PM2.5, may contribute to cerebral atrophy but does not seem to impair cognitive function. Urbanization affects the strength of this link.
Study: Association of ambient air pollution with cognitive functioning and markers of structural brain damage: The Maastricht study. Image Credit: fran_kie / Shutterstock
In a recent study published in the journal Environment International, researchers investigated the potential relationship of exposure to various types of air pollutants with brain structure and cognitive function among middle-aged and older adults. They found that high exposure to fine particulate matter of diameter less than 2.5 micrometers (PM2.5) was associated with lower gray matter and higher cerebrospinal fluid volumes, indicating cerebral atrophy, with stronger effects in men for white matter volume.
However, these associations became non-significant after adjusting for urbanization. They found no significant association with cognitive function or most brain markers, although curvilinear associations between PM2.5 and brain volumes were observed, with mid- to high-range exposure linked to greater cerebral atrophy.
Background
Dementia is a progressive condition characterized by a decline in cognitive functions such as memory, attention, and planning, most commonly caused by Alzheimer's disease and cerebrovascular issues.
The global incidence of dementia is expected to rise threefold by 2050, straining healthcare systems and increasing caregiving burdens. While modifiable lifestyle and cardiovascular factors are known to contribute to dementia risk, shared environmental factors like air pollution are also emerging as significant contributors.
Air pollution, especially PM2.5, has been linked to neuroinflammation and cognitive decline, potentially affecting brain structure by reducing grey matter and causing other forms of cerebral atrophy. Recent studies show that air pollution might increase dementia risk more than other factors such as hypertension or diabetes, but most research has focused on individual pollutants and linear associations.
Further investigation, particularly using brain imaging alongside cognitive assessments, is needed to understand the non-linear impacts of air pollution on brain health and cognitive decline. Therefore, researchers in the present study examined the relationship between ambient air pollution, cognitive performance, and brain structure in older adults while accounting for demographic and modifiable dementia risk factors.
About the study
Researchers obtained data from the Maastricht study, a population-based cohort focused on the etiology and complications of type 2 diabetes (T2DM) among adults aged 40-75 years in the southern Netherlands. Participants were recruited via media and registries, and those with missing data were excluded. A total of 4,002 adults were included. The mean age was 59.2 years, and 49.2% of them were men.
Ambient air pollution exposure was assessed using the Geoscience and Health Cohort Consortium (GECCO) data using local and national models for pollutants like PM2.5, PM10, soot, and NO2, mapped to the postal addresses of participants.
Cognitive functioning was evaluated through standardized neuropsychological tests, while magnetic resonance imaging (MRI) scans were used to assess structural brain markers such as grey matter (GM), white matter (WM), and cerebrospinal fluid (CSF) volume.
Dementia risk factors were summarized using the Lifestyle for Brain Health (LIBRA) score. Socioeconomic position was evaluated through education, occupation, and household income. Statistical analysis involved the use of t-tests, chi-square tests, multiple linear regression, binary logistic regression, likelihood ratio tests, and sensitivity analysis.
Results and discussion
Elevated PM2.5 exposures were noted across the study region, with minimal variation in exposure levels. Excluded participants were older, had lower SEP, higher T2DM prevalence, and were more often male. They were exposed to higher levels of air pollution with higher LIBRA scores, smaller GM and WM volumes, larger CSF and WMH volumes, and lower cognitive performance in overall cognition, memory, processing speed, and executive function.
The study found no significant linear associations between exposure to air pollution (PM2.5, PM10, NO2, and soot) and cognitive function, cognitive domains, or brain volumetric markers (GM, WM, CSF, WM hyperintensity). However, curvilinear relationships were found between PM2.5 and GM/CSF volumes.
Mid- to high-range PM2.5 exposure (12.14–15.48 μg/m3) was linked to lower GM and higher CSF volumes (indicating cerebral atrophy), while lower exposures (10.08–12.14 μg/m3) were linked to higher GM volumes. Adjusting for urbanization removed these significant spline associations.
Gender was found to moderate the associations between air pollution and WM/CSF volumes, with stronger effects seen in men, particularly for PM2.5, PM10, and NO2. However, no significant interactions were found for T2DM status, age, LIBRA score, socioeconomic position score, or degree of urbanization.
The study is strengthened by its large population-based sample, midlife age range, detailed cognitive and MRI assessments, integration of air pollution data with individual dementia risk factors, and stable regional environmental data for deeper analysis.
However, the study is limited by a limited exposure variation, potential misclassification of air pollution exposure, inability to account for long-term or indoor pollution, and possible selection bias towards healthier participants, reducing generalizability and diluting associations with brain MRI and cognitive outcomes.
Conclusion
In conclusion, the study found that mid- to high-range exposure to PM2.5 is linked to increased CSF volumes, indicating reduced brain tissue volume or atrophy, but showed no association with cognitive functioning. Although these associations were observed, adjusting for urbanization weakened the findings.
Further research across diverse populations is necessary to confirm these results, but reducing air pollution remains a potential target for public health policy aimed at safeguarding brain health.