Although the majority of deaths resulting from exposure to sulfur must
ard (HD) have been due to pulmonary dysfunction, there are no detailed
accounts of the pathogenesis or HD-induced lesions in the respiratory
tract. Accordingly, we investigated the early changes within the trac
hea and lungs of rats following inhalation exposure to HD. Anesthetize
d rats were exposed by intratracheal intubation to vaporized HD (0.35
mg in 100 mu l absolute ethanol) or ethanol alone for 50 min. Animals
were euthanatized at 0, 1, 4, 6, 12, 18, and 24 h postexposure (PE), a
nd their respiratory tracts were prepared for histological and ultrast
ructural examination. In rats exposed to HD, multifocal, petechial hem
orrhages were grossly evident on the pleural surface of the lung at 6
h PE. Atelectasis and edema of the accessory lobe occurred at 12-18 h
PE. Histologically, lesions in the respiratory tract were confined pri
marily to the trachea, bronchi and larger bronchioles. In HD-exposed r
ats, there was a progressive depletion of the bronchiolar-associated l
ymphoid tissue (BALT), with necrosis of the lymphoid cells as early as
12 h PE. Necrosis and sloughing of tile tracheal and bronchial epithe
lia at 6-12 h PE was followed by the formation of fibrinous pseudomemb
ranes within the bronchi. Necrosis and separation of airway epithelia
occurred at the mucosal/submucosal interface. Pseudomembranes formed a
lmost exclusively in deepithelialized areas overlying the BALT. Cartil
aginous lesions, characterized by necrosis of individual chondrocytes,
were evident at 12 h PE. Pulmonary edema and occasional alveolar hemo
rrhage occurred from 18 to 24 h PE. Small bronchioles and alveoli were
relatively unaffected and only a few inflammatory cells were observed
at any time.