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Toxicologic Pathology
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Articles

Smoking-associated Squamous Metaplasia in Olfactory Mucosa of Patients with Chronic Rhinosinusitis

Karen K. Yee1, Edmund A. Pribitkin1,2, Beverly J. Cowart1, Aldona A. Vainius1, Christopher T. Klock1, David Rosen2, Chang-Gyu Hahn3 and Nancy E. Rawson1

1 Monell Chemical Senses Center, Philadelphia, Pennsylvania
2 Otolaryngology-Head and Neck Surgery, Thomas Jefferson University, Philadelphia, Pennsylvania
3 Department of Psychiatry, University of Pennsylvania, Philadelphia, Pennsylvania

Correspondence: Address correspondence to: Karen K. Yee, Monell Chemical Senses Center, 3500 Market St., Philadelphia PA 19104-3308; e-mail:karenyee{at}monell.org.

Few studies have examined the induction of squamous metaplasia in human olfactory nasal tissue caused by tobacco use and the implications it may have for olfaction, particularly when there are pre-existing insults, such as chronic rhinosinusitis (CRS). Quantitative histopathological analyses were performed on Alcian blue- and H&E-stained sections of nasal biopsies taken from the upper aspect of the middle turbinate of CRS patients. Chronic rhinosinusitis patients who were current smokers had a predominance of squamous metaplasia in the olfactory sensory epithelium, whereas CRS patients who were nonsmokers and were not exposed to secondhand cigarette smoke had a prevalence of goblet cell hyperplasia. In spite of this difference, the groups did not differ significantly in olfactory threshold sensitivity. The impact of primary cigarette smoke on olfaction and a possible role of squamous metaplasia in preserving olfactory neurogenesis are discussed.

Key Words: morphology • olfactory epithelium • tobacco smoke

Abbreviations: CRS, chronic rhinosinusitis • CT, computed tomography • OM, olfactory mucosa • OMP, olfactory marker protein • OSNs, olfactory sensory neurons • PEA, phenylethyl alcohol

This version was published on August 1, 2009

Toxicologic Pathology, Vol. 37, No. 5, 594-598 (2009)
DOI: 10.1177/0192623309338055


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