Ka. Brenneman et al., Olfactory neuron loss in adult male CD rats following subchronic inhalation exposure to hydrogen sulfide, TOX PATHOL, 28(2), 2000, pp. 326-333
Dysosmia and anosmia are reported to occur following human exposure to hydr
ogen sulfide (H2S) gas. The clinical association between H2S exposure and o
lfactory dysfunction in humans necessitates evaluation of the nasal cavity
and olfactory system in experimental animals used to study H2S toxicity. Th
e purpose of this study was to subchronically expose 10-week-old male CD ra
ts to relatively low concentrations of H2S and to histologically evaluate t
he nasal cavity fur exposure-related lesions. Rats (n = 12/group) were expo
sed via inhalation to 0, 10, 30, or 80 ppm H2S 6 h/d and 7 d/wk for 10 week
s. Following exposure to 30 and 80 ppm H2S, a significant increase in nasal
lesions limited to the olfactory mucosa was observed. The lesions, which c
onsisted of olfactory neuron loss and basal cell hyperplasia, were multifoc
al, bilaterally symmetrical, and had a characteristic rostrocaudal distribu
tion pattern. Regions of the nasal cavity affected included the dorsal medi
al meatus and the dorsal and medial portions of the ethmoid recess. The no
observed adverse effect level fur olfactory lesions in this study was 10 pp
m. For perspective, the American Conference of Governmental Industrial Hygi
enists threshold limit value (TLV) recommendation for H2S is currently 10 p
pm (proposed revision: 5 ppm), so the concentrations employed in the presen
t study were 3 and 8 times the TLV. These findings suggest that subchronic
inhalation exposure to a relatively low level of H2S (30 ppm) can result in
olfactory toxicity in rats. However, because of differences in the breathi
ng style and nasal anatomy of rats and humans, additional research is requi
red to determine the significance of these results for human health risk as
sessment.