The air people breathe every day could leave subtle signs in the brain long before memory problems appear.
New research has linked exposure to traffic-related and other outdoor pollution with differences in brain tissue in areas that are often damaged by Alzheimer’s disease.
The study comes from researchers at the USC Mark and Mary Stevens Neuroimaging and Informatics Institute, part of the Keck School of Medicine of USC. It was published in NeuroToxicology.
Scientists have long known that dirty air can harm the lungs and cardiovascular system. In recent years, evidence has also raised concerns that pollution may affect the brain and possibly contribute to dementia risk.
One reason is that very small pollution particles can enter deep into the lungs and trigger inflammation throughout the body. Researchers are investigating whether these responses can affect blood vessels and nerve cells in the brain over many years.
The new research examined 1,484 adults without dementia or a previous stroke. The scientists estimated how much air pollution each person had been exposed to near their home during the three years before an MRI brain scan.
They studied PM2.5 and nitrogen dioxide, two pollutants common in towns and cities. PM2.5 refers to microscopic particles produced by sources including vehicle exhaust, fires and power plants, while nitrogen dioxide is a gas produced largely when fuels are burned.
The MRI scans allowed researchers to measure the cortex, the brain’s outer layer. Although only a few millimeters thick, the cortex contains huge numbers of nerve cells and plays a central role in memory, language, attention and decision-making.
The cortex naturally becomes thinner as people age. Faster or unusual thinning in certain areas can also occur with brain diseases, including Alzheimer’s.
The researchers concentrated on four regions known to be vulnerable to Alzheimer’s disease. They then examined the rest of the cortex to see whether pollution was connected with more widespread differences.
Among 1,097 older women, whose average age was about 78, higher exposure to both PM2.5 and nitrogen dioxide was associated with thinner tissue in the Alzheimer’s-sensitive regions. PM2.5 was also associated with thinning in 23 of the 34 brain regions examined.
To put the size of the association into perspective, the researchers compared it with normal age-related thinning. Each extra microgram per cubic meter of PM2.5 corresponded statistically to about 13 months of aging in the Alzheimer’s-sensitive regions.
For nitrogen dioxide, each additional part per billion was comparable to about three months of aging. These figures describe statistical similarities and should not be interpreted as a precise clock showing how much pollution ages an individual brain.
The researchers expected the second group to show a similar pattern, but it did not. Among 387 men who were around 62 years old on average, greater pollution exposure was associated with thicker cortex in the same vulnerable regions.
This surprising result does not necessarily mean pollution benefited the younger men. Scientists increasingly recognize that thicker tissue can sometimes appear during an early stage of injury or disease.
For example, inflammation may cause temporary swelling. Changes in the size of brain cells or early biological reactions to abnormal protein buildup might also increase measured thickness before damaged tissue eventually becomes thinner.
The study could not test those possibilities because it did not directly measure inflammation or the Alzheimer’s-related proteins amyloid and tau. The researchers therefore cannot say what caused the greater thickness.
Age patterns among the men provided a possible clue. The connection between PM2.5 exposure and thicker cortex became progressively weaker between roughly ages 55 and 64, then shifted toward thinning after about age 65.
However, the association after age 65 was not statistically significant. It could therefore have occurred by chance, and the apparent transition needs to be confirmed in a much larger study.
One possibility is that the brain reacts to pollution in stages. Earlier exposure could produce inflammation or other changes that temporarily increase thickness, while years of accumulated injury could eventually result in loss of brain tissue.
But the study cannot establish that sequence. The younger participants were men and the older participants were women, meaning researchers cannot separate the effects of age from possible differences related to sex or other characteristics of the two study populations.
Another limitation is that each participant essentially provided a snapshot. The researchers did not repeatedly scan the same people as they moved from middle age into older age, so they could not watch the cortex become thicker and then thinner.
Nor does the research prove that any participant’s pollution exposure caused Alzheimer’s disease. Everyone in the study was free of dementia at the time considered, and many factors including genetics, education, smoking, cardiovascular health and other environmental exposures can affect brain aging.
Even with these limitations, the study is important because it shows that pollution is associated with measurable brain differences before dementia is present. It also warns against assuming that one simple brain measurement, such as greater cortical thickness, always means better health.
Arthur W. Toga, director of the Stevens Neuroimaging and Informatics Institute, noted that air pollution is potentially changeable at the community level. Unlike age or inherited genes, pollution exposure can be reduced through public policy, cleaner technology and changes in transportation and energy systems.
The next step is to follow comparable groups of men and women over many years. Repeated MRI scans, memory testing and measurements of amyloid, tau and inflammation could reveal whether pollution-related thickening really comes before thinning and whether either pattern predicts dementia.
The study therefore raises an important possibility rather than delivering a final answr. If future research confirms that long-term pollution contributes to a chain of brain changes leading toward Alzheimer’s, cleaner air could become part of a much broader strategy for protecting brain health as populations age.
If you care about brain health, please read studies about vitamin D deficiency linked to Alzheimer’s and vascular dementia, and blood pressure problem at night may increase Alzheimer’s risk.
For more information about brain health, please see recent studies about antioxidants that could help reduce dementia risk, and epilepsy drug may help treat Alzheimer’s disease.
Source: Keck School of Medicine of USC.
