There are three major epithelial types in the nasal mucosa, in addition to numerous accessory structures, some of which are species specific. Without careful and consistent processing of the nose tissue, histopathologic assessment of lesions in the nasal cavity may be compromised. While formalin fixation may be used for routine review of the nasal cavity, Bouin's fixation provides better histologic detail and fewer artifacts. Decalcification is not recommended for nasal tissues to be examined by transmission electron microscopy because of the detrimental effect of decalcifying solutions on sensory cells. Three levels of the nasal cavity may be used for routine histologic review of the nasal cavity, but four or five levels may be more appropriate for certain studies.
Rodents are commonly used for inhalation toxicology studies, but until recently the nasal passages have often been overlooked or only superficially examined. The rodent nose is a complex organ in which toxicant-induced lesions may vary, depending on the test compound. A working knowledge of rodent nasal anatomy and histology is essential for the proper evaluation of these responses. Lack of a systematic approach for examining rodent nasal tissue has led to a paucity of information regarding nonneoplastic lesions in the rodent nose. Therefore, slides from the National Toxicology Program (NTP) and the Chemical Industry Institute of Toxicology (CIIT) were examined, and the literature was reviewed to assemble the spectrum of nonneoplastic rodent nasal pathology. Presented are lesions associated with the various types of epithelia lining the rodent nasal cavity plus lesions involving accessory nasal structures. Even though there are anatomic and physiologic differences between the rodent and human nose, both rats and mice provide valuable animal models for the study of nasal epithelial toxicity, following administration of chemical compounds.
There are three major epithelial types in the nasal mucosa, in addition to numerous accessory structures, some of which are species specific. Without careful and consistent processing of the nose tissue, histopathologic assessment of lesions in the nasal cavity may be compromised. While formalin fixation may be used for routine review of the nasal cavity, Bouin's fixation provides better histologic detail and fewer artifacts. Decalcification is not recommended for nasal tissues to be examined by transmission electron microscopy because of the detrimental effect of decalcifying solutions on sensory cells. Three levels of the nasal cavity may be used for routine histologic review of the nasal cavity, but four or five levels may be more appropriate for certain studies.
The accidental release of methyl isocyanate (MIC) in Bhopal, India, was reportedly responsible for the deaths of more than 2,000 people. To study the pathology of acute inhalation exposure to MIC, the tissues of male and female Fischer 344 rats were evaluated immediately after a single 2-hr exposure to 0, 3, 10, or 30 ppm MIC, and through day 91. Early gross pathologic changes in the 30 ppm-exposed rats included a reddish white encrustation around the mouth and nose, a small thymus, and distension of the gastrointestinal tract with gas. Lungs (middle and median lobes) showed consolidation and hemorrhage and failed to deflate when the chest cavity was opened. Microscopic changes in the upper respiratory tract 3 hr after exposure included marked erosion and separation of olfactory and respiratory epithelia from the basement membrane with accumulation of serofibrinous fluid. On day 1, acute inflammation and fibrinopurulent exudate partially blocked the nasal passages. Epithelial cells had sloughed from the nasopharynx, trachea, bronchi, and major bronchioles, leaving the basement membrane covered with fibrin and exudate. Granulomatous inflammation and intraluminal fibrosis of the airways were observed by day 3, with increased intraluminal fibrosis by day 7. Lower airways became blocked by exfoliated cells, mucous plugs, and/or intraluminal fibrosis. Damage to the lung parenchyma, even at lethal concentrations, was limited to moderate inflammation. Intraluminal fibrosis, mild bronchitis and bronchiolitis, and mucous plugs persisted throughout the 91-day study. These changes could account for evidence of obstructive lung disease detected in pulmonary function studies in companion studies. Evidence of direct injury to nonrespiratory tissues was not found; pulmonary injury and associated respiratory obstruction appeared sufficient to cause both early and delayed deaths.
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