Nine Beagle dogs were exposed to aerosols of <tex-math>${}^{90}{\rm Y}$</tex-math> in fused clay and examined serially using pulmonary function, clinical, and radiographic evaluations to better describe the pathogenesis of pulmonary damage resulting from the inhalation of beta-emitting radionuclides. The inhalation exposure resulted in initial lung burdens (ILB) of 390 to 920 μCi <tex-math>${}^{90}{\rm Y}/{\rm kg}$</tex-math> body weight and cumulative doses to the lung of 4900 to 12,000 rads. The evaluation of pulmonary function included measurements of ventilation, lung mechanics, gas exchange, and parameters obtained under the stresses of treadmill exercise and added external respiratory dead space. Functional alterations appeared in all exposed dogs at approximately 8 wk postinhalation exposure and the severity and rapidity of progression of dysfunction was related to dose. Early functional impairments included defects in the distribution of ventilation and in alveolar-capillary gas exchange. Later, tissue alterations increased the energy cost of breathing and created a major disturbance in the matching of ventilation and perfusion. Dogs receiving an ILB of approximately 400 μCi/kg demonstrated an early, transient, subclinical functional impairment that subsequently either resolved or failed to progress. Both treadmill and dead space testing were found useful in detecting subclinical and subradiographic lung damage.

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