Urban air pollution: Influences on olfactory function and pathology in exposed children and young adults

  • Lilian Calderón-Garcidueñas
  • , Maricela Franco-Lira
  • , Carlos Henríquez-Roldán
  • , Norma Osnaya
  • , Angelica González-Maciel
  • , Rafael Reynoso-Robles
  • , Rafael Villarreal-Calderon
  • , Lou Herritt
  • , Diane Brooks
  • , Sheyla Keefe
  • , Juan Palacios-Moreno
  • , Rodolfo Villarreal-Calderon
  • , Ricardo Torres-Jardón
  • , Humberto Medina-Cortina
  • , Ricardo Delgado-Chávez
  • , Mario Aiello-Mora
  • , Robert R. Maronpot
  • , Richard L. Doty

Research output: Contribution to journalArticlepeer-review

301 Scopus citations

Abstract

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 years 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 years. 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{lunate} 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 βA42 (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.

Original languageEnglish
Pages (from-to)91-102
Number of pages12
JournalExperimental and Toxicologic Pathology
Volume62
Issue number1
DOIs
StatePublished - Jan 2010

Funding

This work supported in part by the National Science Foundation 0346458, the Montana Board of Research and Commercialization Technology 04-06 to Rafael Villarreal-Calderon, NCRR Grant #P20 RR015583, and P30 ES013508. This work was presented in part at the Neurotoxicology 25th Meeting, October 13, 2008, Rochester, NY, USA, by Rodolfo Villarreal-Calderon. R.L. Doty is President and major shareholder in Sensonics, Inc., the manufacturer of the olfactory tests used in this study.

Funder number
0346458
P30ES013508
20 RR015583
04-06

    Keywords

    • APOE
    • Air pollution
    • Alzheimer's disease
    • Amyloid β 42
    • Olfaction
    • Olfactory bulb
    • Parkinson's disease
    • Ultrafine particulate matter
    • α Synuclein

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