Mount st. Helens ash from the 18 may 1980 eruption: chemical, physical, mineralogical, and biological properties.

Samples of ash from the 18 May 1980 eruption of Mount St. Helens were collected from several locations in eastern Washington and Montana. The ash was subjected to a variety of analyses to determine its chemical, physical, mineralogical, and biological characteristics. Chemically, the ash samples were of dacitic composition. Particle size data showed bimodal distributions and differed considerably with location. However, all samples contained comparable amounts of particles less than 3.5 micrometers in diameter (respirable fraction). Mineralogically, the samples ranged from almost totally glassy to almost totally crystalline. Crystalline samples were dominated by plagioclase feldspar (andesine) and orthopyroxene (hypersthene), with smaller amounts of titanomagnetite and hornblende. All but one of the samples contained from less than 1 percent to 3 percent free crystalline silica (quartz, trydimite, or cristobalite) in both the bulk samples and 1 to 2 percent in the fractions smaller than 3.5 micrometers. The long-lived natural radionuclide content of the ash was comparable to that of crustal material; however, relatively large concentrations of short-lived radon daughters were present and polonium-210 content was inversely correlated with particle size. In vitro biological tests showed the ash to be nontoxic to alveolar macrophages, which are an important part of the lungs' natural clearance mechanism. On the basis of a substantial body of data that has shown a correlation between macrophage cytotoxicity and fibrogenicity of minerals, the ash is not predicted to be highly fibrogenic.

A particulate isotopic standard of plutonium in an aluminosilicate matrix.

Plutonium isotopic microstandard particles have been produced for mass spectrometer calibration. The particles may also be useful as an elemental standard for calibration of electron and ion microprobe instruments. The standard consists of spherical, micrometer-size aluminosilicate particles loaded with plutonium of known isotopic distribution. The morphology, elemental composition, and plutonium isotopic composition of the particles have been characterized.

Toxicology of high-fired beryllium oxide inhaled by rodents. II. Metabolism and early effects.

Several groups of male and female rats and hamsters were exposed by inhalation to an aerosol of BeO particles calcined at 1000 C. Initial alveolar depositions ranged from 12 mug to 160mug Be. The alveolar retention half-life for BeO was approximately six months. Only the pulmonary lymph nodes accumulated detectable amounts of translocated BeO. Early alterations were seen in the alveolar macrophages, which were subsequently converted to histiocytic cells that accumulated in subpleural and peribronchiolar granulomatous lesions within eight months after the exposure. The alveolar clearance of a test aerosol, radioactive plutonium dioxide (239PuO2), was decreased to 60% of the normal rate when the radioactive material was given at 1, 30, or 60 days after exposure to BeO. These results demonstrate the important function of the alveolar macrophage in Be-induced granulomatous disease, as well as the rapid impairment of alveolar macrophage function by phagocytized BeO.

The flow-past chamber: an improved nose-only exposure system for rodents.

We have designed a nose-only inhalation exposure chamber in which fresh aerosol is flowed past each exposure port and exhaled air is immediately exhausted. This allows all animals in the chamber to be exposed to the same aerosol concentration. In tests comparing initial lung burdens (ILB) of animals exposed in a standard chamber with those of animals exposed in the flow-past chamber, coefficients of variation in ILBs were significantly smaller for the latter.

Asbestos cement dust inhalation by hamsters.

Two groups of 96 male Syrian golden hamsters were exposed to respirable asbestos cement aerosol at concentrations of approximately 1 and approximately 10 micrograms/liter, respectively, 3 hours/day, 5 days/week. Average fiber counts ranged from 5 to about 120 fibers/cm3. Each group was randomly divided into six subgroups of 16 animals. The first subgroup was sacrificed after 3 months of exposure, the second after 6 months, and the third after 15 months. The fourth subgroup was withdrawn from exposure after 3 months, observed for an additional 3 months, and then sacrificed. The fifth and sixth subgroups were withdrawn after 3 and 6 months of exposure, respectively, and maintained for observation up to the 15-month exposure point of the third subgroup at which time all surviving animals were sacrificed. All other experimental procedures were similar to those delineated in a previous publication describing the development of an animal model, techniques, and an exposure system for asbestos cement dust inhalation (A. P. Wehner, G. E. Dagle, and W. C. Cannon, 1978, Environ. Res. 16, 393-407). The asbestos cement exposures had no significant effect on body weight and mortality of the animals. Higher aerosol concentration and longer exposure times increased the number of macrophages and ferruginous bodies found in the lungs of the exposed animals. Recovery periods had no effect on the incidence of macrophages and ferruginous bodies. The incidence of very slight to slight fibrosis in the animals sacrificed after 15 months of exposure shows a significant (P less than 0.01) trend when the untreated control group and the 1 and 10 microgram/liter dose level groups are compared, indicating a dose-response relationship. Development of minimal fibrosis continued in animals withdrawn from exposure. No primary carcinomas of the lung and respiratory tract and no mesotheliomas were found.

Pulmonary function in elastase-treated guinea pigs and rats exposed to ammonium sulfate or ammonium nitrate aerosols.

Three weeks following intratracheal instillations of elastase dissolved in saline, or saline alone, guinea pigs and rats were exposed for 5 or 20 days, 6 hr/day, 5 days/week to filtered room air, 1 mg/m3 ammonium sulfate [NH4)2SO4) or 1 mg/m3 ammonium nitrate (NH4NO3) aerosols. Pulmonary function evaluations conducted in guinea pigs showed no detrimental effects of (NH4)2SO4 or NH4NO3 exposure and very little effect of elastase treatment. Lung function changes in elastase-treated rats were consistent with a condition of experimentally induced pulmonary emphysema. Rats exposed to NH4NO3 aerosols showed no consistent exposure-related changes. Compared with air-exposed animals, rats exposed to (NH4)2SO4 aerosols had increased values of residual volume and functional residual capacity and decreased slope of single-breath N2 washout curves. We conclude that elastase treatment had no significant effect on lung function changes resulting from inhalation of (NH4)2SO4 aerosols. Lung function was more affected by (NH4)2SO4 exposure than by NH4NO3 exposure, and lung function changes were more pronounced in rats than in guinea pigs.

Reproductive toxicology of inhaled styrene oxide in rats and rabbits.

Experiments were performed to evaluate reproductive and developmental toxicology in rats and rabbits exposed to styrene oxide by inhalation. Female rats were exposed to 100 or 300 ppm styrene oxide or to filtered air for 7 h/day, 5 days/week for 3 weeks. Extensive mortality occurred in rats that received prolonged exposure to 100 ppm styrene oxide while 300 ppm was rapidly lethal. As a result exposures were terminated in this latter group and the group was eliminated from further study. The rats of the 0 and 100 ppm groups were then mated and exposed to 0 or 100 ppm styrene oxide daily through 18 days of gestation (dg). Female rabbits were artificially inseminated and exposed for 7 h daily to 0, 15, or 50 ppm styrene oxide through 24 dg. Both of these lower concentrations used for exposure of the rabbits produced mortality of does. The rats were killed at 20 dg and the rabbits at 30 dg. Pregnant animals were examined for toxic changes including altered tissue weights and histopathologic effects. Litters were evaluated using several measures of embryotoxicity, and live fetuses were examined for external, visceral, and skeletal malformations. Exposure during gestation appeared to increase preimplantation loss in rats, and tended to increase the incidence of resorptions in rabbits. In both species, fetal weights and crown-rump lengths were reduced by gestational exposure. The incidences of ossification defects of the sternebrae aned occipital bones were increased by gestational exposure of rats to styrene oxide. These results indicate that inhalation exposures at these concentrations produce reproductive and development toxicity, as well as maternal toxicity.

Effects of sulfur dioxide or ammonium sulfate exposure, alone or combined, for 4 or 8 months on normal and elastase-impaired rats.

Normal and lung-impaired rats were compared after exposure to SO2 and/or (NH4)2SO4 for 4 or 8 months, or for 8 months plus 3 months recovery. Young adult male Sprague-Dawley rats were pretreated intratracheally with either physiologic saline (normal lungs) or porcine pancreatic elastase (impaired lungs). Rats from each pretreatment group were exposed to filtered air (control), to SO2 (1 ppm) or (NH4)2SO4 (0.5 mg/m3), or to combined SO2 + (NH4)2SO4 for 5 hr/day, 5 days/week. Morphologic, physiologic, and immunologic criteria were evaluated. At 4 months cellular immunologic responsiveness was not impaired, but physiologic changes were detected. Morphologic changes were apparent in all time periods. Elastase-induced changes included greater lung volumes, emphysema, and alveolar interstitial fibrosis. Pollutant effects included bronchiolar epithelial hyperplasia and changes in alveolar mean chord length (MCL). Relative to controls, bronchiolar epithelial hyperplasia and MCL increased in saline/pollutant groups, but decreased in elastase/pollutant rats at 4 months. The pretreatment/pollutant interaction was not observed at 8 months. Elastase effects persisted throughout the recovery period. Pollutant effects were more transitory, although alveolar septal fibrosis was greater in saline/(NH4)2SO4 rats at 8 months. Pulmonary function changes associated with elastase included increases in residual volume, functional residual capacity, and the residual volume/total lung capacity ratios. The alveolar plateau of single-breath washout (N2 slope) was significantly steeper in elastase-treated rats but less steep in animals exposed to SO2 or to (NH4)2SO4 than in those exposed to air only.

Effects of ammonium sulfate aerosol exposure on lung structure of normal and elastase-impaired rats and guinea pigs.

Rats and guinea pigs, pretreated with intratracheally administered elastase or saline, were exposed to 1.03 mg/m3 (NH4)2SO4; MMAD, 0.42 micron. Identically treated controls were sham exposed. Measurements and evaluation of structural changes were conducted using morphometric techniques on SEM photographs and by applying subjective ratings. Pathology studies were conducted by light and electron microscopy. All examination methods confirmed elastase-induced emphysema, which was aggravated by (NH4)2SO4 exposure in the rat. Ammonium sulfate exposure of saline-treated animals produced measurable degrees of enlargement of alveoli, and alveolar ducts and sacs. Electron microscopy revealed increased interstitial collagen in affected lung areas of elastase-treated, (NH4)2SO4-exposed animals. Alveolar-pore size was significantly increased in elastase-treated animals (control and exposed) but not in saline-treated, exposed animals. The data suggest a possible difference between elastase and (NH4)2SO4 in the mechanisms responsible for the increased diameter of alveolar structures. Hypertrophy and hyperplasia of nonciliated epithelial cells of the small airways and of the Type II alveolar cells were observed in otherwise untreated guinea pigs exposed to (NH4)2SO4 but not in elastase-treated guinea pigs, nor in any of the rats.

Effects of ammonium nitrate aerosol exposure on lung structure of normal and elastase-impaired rats and guinea pigs.

Groups of rats and guinea pigs with normal lungs and others with elastase-induced emphysema were exposed to NH4NO3 aerosols of 0.60 mass median aerodynamic diameter at 1 mg/m3 for 6 hr/day, 5 days/week, for 4 weeks. Morphologic and morphometric studies were performed on lungs perfused with cacodylate-buffered 2% glutaraldehyde under 20 cm H2O pressure at necropsy. The tissues were studied for pathologic change by light and electron microscopy; emphysema was evaluated by subgross and microscopic methods, including changes in mean alveolar chord length using scanning electron microscopy techniques. Elastase produced emphysema to a degree quantifiable by all criteria studied; however, it apparently obscured the effects of nitrate inhalation. The NH4NO3 exposure (compared to air alone) tended to increase values for pulmonary parameters in normal animals of both species and to decrease them in elastase-treated animals. The NH4NO3 exposure increased values for lung volume in rats, percentage area affected in elastase-treated rats, and chord length beta in normal animals of both species. The responses to NH4NO3 were slight (P less than 0.10) and were not accompanied by any detectable changes in alveolar structure. Therefore, the effects of NH4NO3 at this exposure level and duration, are regarded as biologically insignificant for rats and guinea pigs.