Is Exposure to Air Pollution a Risk Factor for Alzheimer's and Parkinson's Diseases?

Lilian Calderón-Garcidueñas, M.D., Ph.D.
University of Montana and Instituto Nacional de Pediatria, Mexico
NIEHS Grant R21ES013293

New research findings from NIEHS-supported researchers at the University of Montana reveal that exposure to air pollution at a young age may predispose people to develop Alzheimer's or Parkinson's disease. The researchers studied the brains of young people who died suddenly from causes unrelated to neurological conditions. Study subjects came from heavily polluted Mexico City or from two relatively unpolluted cities in Mexico.

The primary purpose of the research was to investigate key inflammatory genes and receptors based on previous research findings demonstrating that neuroinflammatory processes lead to a chain of events that result in neurodegeneration. The highly air pollution exposed subjects exhibited increased activity of cyclooxygenase-2, interleukin-1, and CD14 in several areas of the brain, disruption of the blood-brain barrier, oxidative stress, and other evidence of inflammatory processes. The researchers also found evidence of particulate matter in the olfactory bulbs.

The researchers conclude that exposure to air pollution causes neuroinflammation and the accumulation of amyloid and synuclein proteins in brain tissue. Subjects with a genetic susceptibility for Alzheimer's disease (APOE carriers) might have a higher risk of developing Alzheimer's disease if they live in a highly polluted environment. Further research is needed to confirm these results, but they represent evidence that exposure to highly polluted air at young ages may pre-dispose people to debilitating neurodegenerative diseases.

Citation: Calderón-Garcidueñas L, Solt AC, Henríquez-Roldán C, Torres-Jardón R, Nuse B, Herritt L, Villarreal-Calderón R, Osnaya N, Stone I, García R, Brooks DM, González-Maciel A, Reynoso-Robles R, Delgado-Chávez R, Reed W. Long-Term Air Pollution Exposure Is Associated with Neuroinflammation, an Altered Innate Immune Response, Disruption of the Blood-Brain-Barrier, Ultrafine Particulate Deposition, and Accumulation of Amyloid {beta}-42 and {alpha}-Synuclein in Children and Young Adults. Toxicol Pathol. 2008 Mar 18; Epub ahead of print.