In our present study we examined the pathology of the nasal mucociliary system after x-ray irradiation in an animal model namely the rabbit. A reduced ciliary activity was observed immediately after the irradiation and did not show any recovery during our observation. No ciliary activity was seen in the nasal mucosa 8 weeks after the irradiation. Morphologically, hypersecretion of goblet cells was observed immediately after irradiation. Cytoplasmic vacuolation and nuclear pyknosis of ciliated cells started after irradiation, and sloughing of ciliated cells was observed for up to 3 weeks. Epithelial metaplasia started from 4 weeks, and no cilia were seen in the nasal mucosa and the surface of the epithelium was covered with flat squamous cells. Our present study shows that x-ray irradiation has serious influence on the function and structure of the nasal mucociliary system and that recovery from degeneration due to x-ray irradiation cannot be expected within several weeks.

The recovery process of pathological changes in the respiratory mucosa following exposure to styrene were experimentally studied to improve the understanding of the respiratory toxicity of styrene. Thirty male SD rats were exposed to 150 ppm or 1000 ppm of styrene for 4 h a day over 3 weeks (5 days a week). They were killed for examination at 1 day or 12 weeks after completion of the exposure sequence. Bilateral mucosal samples from the nasal septum and the trachea of the animals were examined for ciliary activity and subjected to electron microscopy. Complete functional and morphological recovery of the nasal and tracheal mucosa was observed at the 12th week post-exposure to 150 ppm of styrene. After exposure to 1000 ppm of styrene, almost normal function and morphology of the tracheal mucosa was found at the 12th week post-exposure, but the nasal mucosa continued to show decreased ciliary activity and an affected morphology.

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A variety of atmospheric pollutants are known to depress mucociliary function in the respiratory system. Since the mucociliary function in the middle ear is similar, and the middle ear may be invaded by atmospheric pollutants, we decided to investigate the possible contribution of sulfur dioxide to middle ear effusion. Guinea pigs were exposed for 24 hours to 300 ppm of sulfur dioxide or air. Immediately after exposure, ciliary activity and epithelial structure were examined close to the tympanic orifice (proximal site) and more distal to it (distal site). In the animals exposed to sulfur dioxide, no effusion was found in the tympanic cavity. Ciliary activity was reduced only in the distal site. Electron microscopy demonstrated hypersecretion in the proximal site and severe pathologic changes in the distal site. Although the normally functioning cilia in the proximal site may prevent retention of surplus secretions in the ear, sulfur dioxide may promote middle ear effusion when combined with other detrimental factors, because it stimulates mucus secretion in the proximal site and impairs ciliary function in the distal site.

Single field, fixed irradiation of bilateral tympanic cavities using 200-kV x-rays was administered to five guinea pigs. The irradiation dose was 30 Gy. They were killed immediately after irradiation, and bilateral middle ear mucosa was examined for ciliary activity and epithelial structure. Significant deterioration of the ciliary activity in the middle ear mucosa was observed, proximal as well as distal to the eustachian tube. Electron microscopy showed various changes in the irradiated middle ear mucosa. The most conspicuous findings were hyperreactivity in secretion, vacuolation of ciliated cells, and stomal edema.