The effect of limited beryllium additions on a Ni-Cr alloy.
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Fischer 344 rats were exposed for 1 hr to an aerosol of BeO generated at a temperature of 560 degrees C. An initial lung burden of 500 +/- 4.1 ng Be was achieved. Animals were killed at 2.5 hr, and 2, 12, and 21 days postexposure. Bronchopulmonary lavage fluids were analyzed biochemically for enzymes, protein, lipids, and sialic acid, and cytologically to determine the composition of the free alveolar cell population. Nonspecific phagocytosis of yeast was measured in adherent macrophages. There were increases in all the biochemical parameters by 2 days postexposure, which peaked by Day 5 and then began to return to control levels. The cytological response on Days 2 and 5 was characterized by polymorphonuclear leucocyte infiltration and a depression in macrophage number and phagocytic activity. By Day 12, increased numbers of newly recruited macrophages with supranormal phagocytic activity populated the lung. During the same period, there was a reduction in lavage protein and lipid levels, perhaps due to a restoration of normal clearance mechanisms. Tissue morphological changes correlated well with the cytological and biochemical alterations.
The acute response in the lung of mice and rats exposed to an aerosol of BeSO4 was characterized by cell kinetics and histopathology. Animals were exposed for 1 hour in a nose-only chamber to a 13 microgram/liter chamber concentration of BeSO4 or to H2SO4 as control aerosol, and killed thereafter over a period of 21 days. Lung cell kinetics were evaluated as the labeling index (LI), defined as the percentage of cells labeled with tritiated thymidine. The labeled cells were also differentiated as to type. In rats, the LI showed a peak response on Day 8 following exposure, while the LI of mice showed a maximum response at Day 5. In rats, the proliferative response involved type II alveolar epithelial cells, interstitial and capillary endothelial cells. Histopathology showed type II alveolar cell hyperplasia and vacuolization of their cytoplasm, a thickened interstitium with infiltrates of interstitial macrophages and segmental leukocytes; a prominent feature was alveolar macrophages with ragged membranes. Three weeks after exposure, the interstitial response was largely resolved. In mice, the proliferative response was mainly found in the alveolar macrophage population and the interstitial and endothelial cells. Histopathological changes were similar to those found in rats, although less severe.
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In a study designed to assess the potential sensitizing and granulomagenic capacities of selected metallic salts, rabbits were inoculated intradermally with zirconium aluminum glycinate (ZAG), sodium zirconium lactate (NZL), aluminum chlorhydrate (ACH), BeSO 4, and ovalbumin (OVA) by single and multiple injections. Animals immunized with BeSO4 and with OVA developed delayed skin reactivity as well as antigen-specific alveolar macrophage migration inhibition. Neither single nor multiple injections of ZAG or ACH resulted in clear-cut positive skin reactivity, macrophage migration inhibitory factor (MIF) production, or lymphocyte stimulation. Rabbits inoculated with multiple injections of NZL (500 microng) showed some marginally positive macrophage migration inhibition and skin reactivity. Histologically, ZAG and ACH were found to induce well-organized foreign-body granulomas after intradermal injection in both normal and inoculated rabbits. NZL and BeSO4 also induced skin granulomas, but these were less organized and distinct. Cell viability and ultrastructural studies indicated that BeSO4 was highly toxic for isolated alveolar macrophages in vitro at concentrations above 10 microng/ml, but NZL and ZAG did not exert such an effect at these dose levels. BeSO4 also depressed lymphocyte stimulation in sensitized animals which demonstrated delayed skin reactivity and macrophage migration inhibition.
Animals exposed to an aerosol of BeSO4 showed a significant reduction in mortality with iron treatment. Rats were exposed for 2 h in a nose-only inhalation chamber for 14 days to an aerosol of 2.59 micrograms/Be/l. The cumulative mortality of animals concurrently treated with iron salt was significantly reduced (P less than 0.05) compared to animals which had not received iron treatment.
A very low concentration of (7)Be in air at Thessaloniki, Northern Greece (40 degrees 38'N, 22 degrees 58'E) was recorded on November 9, 2003 following a strong event of solar wind that occurred on October 29, 2003.