The frequency of smoking-induced nasopharyngeal lymphoid hyperplasia i
n heavy smokers and its potential clinical implications are still unkn
own. Precise criteria to differentiate this entity from other types of
nasopharyngeal lymphoid hyperplasia are needed. A prospective clinico
pathological study of smoking-induced nasopharyngeal lymphoid hyperpla
sia was conducted in 17 heavy smokers. Ten nonsmoking patients, five o
f them with chronic sinusitis, three with adult-onset adenoid hypertro
phy, and two children with adenoidal hypertrophy served as a control g
roup. Both in smokers and in nonsmokers, lymphocytic infiltration of t
he mucosa was characterized immunohistochemically as T cells. In smoke
rs, semithin (1 micron) sections revealed deformed and migrating cytot
oxic lymphocytes in the nasopharyngeal mucosa. The lymphocytes were at
tached to epithelial, ciliated, and goblet cells, resulting in cell da
mage. Transmission electron microscopy of biopsies from smokers reveal
ed emperipolesis, characterized by mucosal invasion and epithelial cel
l damage by an unusual population of migrating T lymphocytes that pene
trate them. These findings confirm a direct effect of smoking on the n
asopharyngeal lymphoid tissue, which forms part of the immune system.
It is concluded that the diagnostic evaluation and therapeutic approac
h of heavy smokers with otological and airway symptoms should be based
on thorough endoscopic examination of the nasopharynx. When the diagn
osis is not clear-cut, selective tele-endoscopic biopsy and electron m
icroscopic examination are recommended. This entity should be added to
the list of known clinical manifestations of the smoking habit.