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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 -42 and -Synuclein in Children and

^* To whom correspondence should be addressed. E-mail: lilian.calderon-garciduenas{at}umontana.edu.

	Abstract

Air pollution is a serious environmental problem. We investigated whether residency in cities with high air pollution is associated with neuroinflammation/neurodegeneration in healthy children and young adults who died suddenly. We measured mRNA cyclooxygenase-2, interleukin-1, and CD14 in target brain regions from low (n = 12) or highly exposed residents (n = 35) aged 25.1 ± 1.5 years. Upregulation of cyclooxygenase-2, interleukin-1, and CD14 in olfactory bulb, frontal cortex, substantia nigrae and vagus nerves; disruption of the blood-brain barrier; endothelial activation, oxidative stress, and inflammatory cell trafficking were seen in highly exposed subjects. Amyloid 42 (A42) immunoreactivity was observed in 58.8% of apolipoprotein E (APOE) 3/3 < 25 y, and 100% of the APOE 4 subjects, whereas -synuclein was seen in 23.5% of < 25 y subjects. Particulate material (PM) was seen in olfactory bulb neurons, and PM < 100 nm were observed in intraluminal erythrocytes from lung, frontal, and trigeminal ganglia capillaries.

Exposure to air pollution causes neuroinflammation, an altered brain innate immune response, and accumulation of A42 and -synuclein starting in childhood. Exposure to air pollution should be considered a risk factor for Alzheimer’s and Parkinson’s diseases, and carriers of the APOE 4 allele could have a higher risk of developing Alzheimer’s disease if they reside in a polluted environment.

First published on March 18, 2008, doi:10.1177/0192623307313011

Toxicologic Pathology 2008;36:289.

A more recent version of this article appeared on February 1, 2008


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