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Forest Fires, Cars, and Power Plants


Air pollution from amyloid plaques, shows a study conducted by UCSF.

A new study by researchers at UC San Francisco found that older Americans with cognitive impairment are more likely to develop amyloid plaques the greater the air pollution in their neighborhood – a hallmark of Alzheimer Illness. The study complements a body of evidence suggesting that pollution from automobiles, factories, power plants, and forest fires is associated with established risk factors for dementia such as smoking and diabetes.

In the study that appears in JAMA Neurology On November 30, 2020, researchers examined the PET scans of more than 18,000 seniors with an average age of 75 years. Participants had dementia or mild cognitive impairment and lived in zip codes across the country. The researchers found that those in the most polluted areas had a 10 percent increased chance of a PET scan showing amyloid plaques compared to those in the least polluted areas.

When applied to the U.S. population of an estimated 5.8 million people over 65 with Alzheimer’s disease, tens of thousands of cases can be exposed to high levels of exposure to microscopic airborne particles.

“This study provides additional evidence for a growing and convergent literature, ranging from animal models to epidemiological studies, indicating that air pollution is a major risk factor for Alzheimer’s disease and dementia,” said senior author Gil Rabinovici, MD, of UCSF Memory and Aging Center, Department of Neurology and Weill Institute for Neuroscience.

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Amyloid plaques, which are not indicative of all dementia

The 18,178 participants were enrolled in the Imaging Dementia (Evidence for Amyloid Scanning) study, which included Medicare beneficiaries diagnosed with mild cognitive impairment or dementia after extensive evaluation. Later, not all participants were found to have a positive PET scan – 40 percent showed no evidence of plaques on the scan, suggesting non-Alzheimer’s diagnoses such as frontotemporal or vascular dementia, which are not associated with the tell-tale amyloid plaques.

The air pollution in each participant’s neighborhood was estimated using data from the Environmental Protection Agency, which measured ground level ozone and PM2.5, atmospheric particles less than 2.5 microns in diameter. The researchers also divided the sites into quartiles according to the concentration of PM2.5. They found that the likelihood of a positive PET scan increased progressively with increasing levels of pollutants, and predicted a 10 percent difference between the least and most polluted areas.

“Exposure to PM2.5 in our daily lives, even at levels believed to be normal, could help trigger a chronic inflammatory response,” said first author Leonardo Iaccarino, PhD, also from the UCSF Center for Memory and Aging, division for Neurology and the Weill Institute of Neurosciences. “Over time, this could affect brain health in a number of ways, including contributing to amyloid plaque accumulation.”

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The total concentration of PM2.5 would not be considered very high because it has a significant association with amyloid plaques, which is an annual average during the San Francisco study period, Rabinovici added.

“I feel it is very appropriate that the changeable risk factors highlighted by the Lancet Commission on Dementia have been added to air pollution,” he said, referring to the journal’s decision to include air pollution, along with excessive alcohol consumption and traumatic brain injury, on their list of the Risk factors.

The study complements previous large-scale studies linking air pollution to dementia and Parkinson’s disease and adds new evidence by including a cohort with mild cognitive impairment – a common precursor to dementia – and using amyloid plaques as biomarkers for disease . Other studies have linked air pollution to adverse effects on cognitive, behavioral, and psychomotor development in children, including a UCSFUniversity of Washington Study examining the effects on the IQ of the offspring of pregnant women.

Reference: November 30, 2020, JAMA Neurology.

Co-authors: Dr. Renaud La Joie, Dr. Eunice Lee and Dr. Isabel Allen from UCSF; Orit Lesman-Segev, MD, from UCSF and Sheba Medical Center, Israel; Lucy Hanna and Constantine Gatsonis, PhD, from Brown University School of Public Health; Bruce Hillner, MD, from Virginia Commonwealth University; Barry Siegel, MD, from Washington University School of Medicine; Rachel Whitmer, PhD, from Kaiser Permanente, Oakland and UC Davis; Maria Carrillo, PhD, of the Alzheimer’s Association.

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Funding: The IDEAS study was funded by the Alzheimer Association, the American College of Radiology, Avid Radiopharmaceuticals, Inc., GE Healthcare, and Life Molecular Imaging.

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