Background: Inhalation of particles aggravates respiratory symptoms including mucus hypersecretion in patients with chronic airway disease and induces goblet cell hyperplasia (GCH) in experimental animal models. However, the underlying mechanisms remain poorly understood.

This study aimed to (1) determine the deposition and clearance rates of utrafine metallic nickel (Uf-Ni) in rats after a 5 hours single inhalation exposure, and (2) to histopathologically examine the pulmonary lesions induced at dose levels comparable to the Occupational Exposure Limit recommended in Japan (OEL). The exposure concentrations of Uf-Ni for the 3 groups were 0.15 (Low), 1.14 (Medium), and 2.54 (High) mg/m3. Five rats/group were sacrificed at Oh and 1, 3, 7, 14, and 21 days post exposure. The amount of Ni in the lung accumulated dose-dependently. The halftimes for Ni in the lung were estimated as 32 days on average, and were similar to each other regardless of the initial dosage. The histopathologically observed pulmonary lesions induced by a single inhalation of Uf-Ni were, (1) a significant increase in lung weight in the High and Medium groups with time, (2) accumulation of foamy alveolar macrophages (AM), (3) degenerated AM indicating alveolar lipoproteinosis which was aggravated for up to 4 weeks in the High group and (4) acute calcification of the degenerated AM was remarkable. The present results suggest that even a single inhalation of Uf Ni induces potency of lung lesions at dose levels comparable to the OEL (1 mg/m3 as Ni), or the TWA of ACGIH (1.5 mg/m3 for elemental/metal).

Rats continuously exposed to NO2 at 0.04, 0.4, and 4.0 ppm for as long as 27 months were submitted to morphological observation and electronmicroscopic morphometry of the lung. At 4 ppm exposure for 9 months, bronchial epithelium showed typical proliferation, which progressed further at 18 months. At this stage, proliferation of type II alveolar epithelium and edematous extension of interstitial tissue were evident and yielded fibrosis at 27 months. At 0.4 ppm, morphological changes in 18-month specimens were still ambiguous, although a tendency toward epithelial changes, as well as interstitial edema of the alveolar wall, was noticed under the electron microscope. Slight but definite alteration of the epithelium became evident after 27 months. At 0.04 ppm there were no remarkable changes throughout the entire exposure period. The morphometry revealed concentration- and duration-dependent increases in arithmetic mean thickness (AMT) of the alveolar wall. At 4 ppm, increase of AMT started as early as 9 months, became significant at 18 months, and showed a slight decrease at 27 months. This decrease was interpreted as a recovery of alveolar epithelium and decreased amount of septal edema, which in turn led to fibrosis. At 0.4 ppm, a slight increase of AMT started at 18 months and extended significantly in 27 months. A similar but insignificant tendency was found even at 0.04 ppm. The morphological alterations were parallel to the concentration and duration of exposure. These findings suggested that an intensive study should be conducted to confirm whether alterations were due to prolonged exposure and/or due to elevated sensitivity of the aged lung.ImagesFIGURE 1.FIGURE 2.FIGURE 3.FIGURE 4.FIGURE 5.FIGURE 6.FIGURE 7.FIGURE 12. AFIGURE 12. BFIGURE 13.FIGURE 15.

Abstruct:Using an ultrasonic nebulizer, cobalt aerosols (MMAD=0.76ƒÊm, og=2.1) were

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