Lung clearance and translocation of 239Pu and 244Cm in rats following inhalation individually or as a mixed oxide.

Wistar rats were exposed via inhalation to aerosols of 239PuO2, 244Cm oxide or a mixed Pu-Cm oxide with an activity ratio of about 1:1. Activity in lung and several extrapulmonary tissues were examined up to 120 d after exposure to determine whether calcining Pu and Cm together affected lung clearance or translocation to other sites in the body for either nuclide. Initial deposition was about 1,200 Bq (32 nCi) for 239PuO2, 4,200 Bq (115 nCi) for 244Cm, and 2,400 Bq (65 nCi) total alpha for the mixed oxide. The kinetics of single nuclides were as expected, with Pu oxide confined mainly to lung at all times and cleared with a half-time of 42 d. Curium was translocated rapidly to liver, with a peak activity of about 10% of the initial alveolar deposition at 7-14 d. Skeleton activity increased gradually, amounting to 12-15% of initial deposition near the end of the study. Lung clearance of Cm was more rapid than for Pu, with about 13% of Pu and less than 5% of Cm remaining at the end of the experiment. Both Pu and Cm remained in the lung somewhat longer when administered as a mixed oxide than the respective nuclides administered singly, and virtually all activity in the body was confined to the lung. Translocation of Cm to extrapulmonary tissues was almost entirely prevented by incorporation into the PuO2 matrix. Therefore, calcining the two radionuclides together in an aerosol altered the kinetics of both following inhalation in rats, but most dramatically for 244Cm. The resulting change in radionuclide distribution for the lung and the body following such a mixed inhalation exposure would presumably alter the long-term health effects compared to those seen with the pure compounds.

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.

Pulmonary toxicity of inhaled coal liquid aerosols (boiling range 230-450 degrees C).

The biological activity of materials produced in the direct liquefaction of coal is being assessed by a variety of test systems. In this study, the pulmonary toxicity of process solvent (PS) from the solvent refined coal-I (SRC-I) process was determined by histamine aerosol challenge tests and pulmonary function and morphologic evaluations. Guinea pigs inhaled aerosols of PS (boiling range, 230 to 450 degrees C) for 6 hr/day, 5 day/week, for up to 12 days in three different experiments. In the first experiment, 8-week-old animals inhaled 0 (controls), 0.15, or 0.60 mg/liter PS aerosols with a mass median aerodynamic diameter (MMAD) of 1.3 micrometer. Exposure to 0.15 mg/liter PS for 12 days resulted in depressed weight gain and marked hypersensitivity to inhaled histamine compared with sham-exposed control animals. Four of five animals exposed to 0.6 mg/liter PS died of respiratory failure during exposure. During the second experiment, 14-week-old animals inhaled 0 (controls) or 0.19 mg/liter PS (MMAD, 1.3 microns) for 1, 3, or 12 days. Hypersensitivity to aerosolized histamine occurred only after 12 days exposure to PS aerosols. At that time, morphologic lung evaluations showed mild to moderate pneumonitis and accumulation of exudate in bronchioles of PS-exposed animals. In the third experiment, pulmonary function evaluations were conducted on 4-week-old animals exposed to 0 (controls) or 0.19 mg/liter PS for 8 days. Functional changes measured in these animals (compared to controls) included increased gas trapping at low lung volumes, decreased quasi-static compliance, and decreased diffusion capacity of the lung for carbon monoxide. These studies showed that measurable changes in lung function were produced in guinea pigs after 8 to 12 days exposure to 0.15 or 0.19 mg/liter PS and that exposure to PS affected weight gain only in younger animals (4 and 8 weeks old) but not in 14-week-old animals.