Olfactory dysfunction, olfactory bulb pathology and urban air pollution

• Published in: Experimental and toxicologic pathology : official journal of the Gesellschaft für Toxikologische Pathologie Vol. 62; no. 1; pp. 91 - 102
• Main Authors: Calderón-Garcidueñas, Lilian, Franco-Lira, Maricela, Henríquez-Roldán, Carlos, Osnaya, Norma, González-Maciel, Angelica, Reynoso-Robles, Rafael, Villarreal-Calderon, Rafael, Herritt, Lou, Brooks, Diane, Keefe, Sheyla, Palacios-Moreno, Juan, Villarreal-Calderon, Rodolfo, Torres-Jardón, Ricardo, Medina-Cortina, Humberto, Delgado-Chávez, Ricardo, Aiello-Mora, Mario, Maronpot, Robert R., Doty, Richard L
• Format: Journal Article
• Language: English
• Published: 17.03.2009
• ISSN: 0940-2993; 1618-1433
• DOI: 10.1016/j.etp.2009.02.117

Mexico City (MC) residents are exposed to severe air pollution and exhibit olfactory bulb inflammation. We compared the olfactory function of individuals living under conditions of extreme air pollution to that of controls from a relatively clean environment and explore associations between olfaction scores, apolipoprotein E (APOE) status, and pollution exposure. The olfactory bulbs (OBs) of 35 MC and 9 controls 20.8 ± 8.5 y were assessed by light and electron microscopy. The University of Pennsylvania Smell Identification Test (UPSIT) was administered to 62 MC / 25 controls 21.2 ±2.7 y. MC subjects had significantly lower UPSIT scores: 34.24 ± 0.42 versus controls 35.76 ± 0.40, p =0.03. Olfaction deficits were present in 35.5% MC and 12% of controls. MC APOE ε 4 carriers failed 2.4 ± 0.54 items in the 10-item smell identification scale from the UPSIT related to Alzheimer's disease, while APOE 2/3 and 3/3 subjects failed 1.36 ± 0.16 items, p = 0.01. MC residents exhibited OB endothelial hyperplasia, neuronal accumulation of particles (2/35), and immunoreactivity to beta amyloid βA 42 (29/35) and/or α-synuclein (4/35) in neurons, glial cells and/or blood vessels. Ultrafine particles were present in OBs endothelial cytoplasm and basement membranes. Control OBs were unremarkable. Air pollution exposure is associated with olfactory dysfunction and OB pathology, APOE 4 may confer greater susceptibility to such abnormalities, and ultrafine particles could play a key role in the OB pathology. This study contributes to our understanding of the influences of air pollution on olfaction and its potential contribution to neurodegeneration.