INFLUENCE OF INHALED CADMIUM OXIDE ON ALVEOLAR CLEARANCE OF PU02 PARTICLES

Investigators: C. L. Sanders and A. W. Conklin

Cadmium oxide inhaled 24 hr or 1 wk previously, reduced the alveolar clearance rate of inhaled 239pu02 particles.

A previous study demonstrated the impair­ of the 40% cleared is phagocytized by alveolar ment of alveolar macrophage function by macrophages prior to clearance from the phagocytized beryllium oxide particles. In ciliated bronchiolar regions. Instillation that study, the alveolar clearance of 239PU02 of CdO, either 24 hr after 239Pu02 or simul­ was decreased to 60% of the normal rate when taneously with 239pu02, did not si~nificantly 239PU02 was inhaled at 1, 30 or 60 days alter the alveolar clearance of 23 Pu. after inhalation of beryllium oxide (Sanders, However, instillation of 239pu02 24 hr or et al., Arch. Environ. Health 30: 546, 1 wk after CdO instillation significantly 1975). Cadmium, a highly toxicmetal, is reduced the alveolar clearance of 239pU to present in effluents of fossil fuel combus­ about half that seen without CdO treatment tion. Lung-deposited cadmium oxide, (in (Table 17). contrast to highly insoluble beryllium oxide) is very soluble in the lung and accu­ TABLE 17. Influence of Cadmium Oxide on the Alveolar mulates in liver and kidney (Annual Report, Clearance of Intratracheally instilled 239PU02' Each value 1978). Inhaled cadmium oxide causes pul­ monary edema due to membrane damage of Type I (:t S.D.) is a mean of values for five rats. alveolar epithelium (Annual Report, 1977). % of Instilled 239PU in Lung Our objective in this study was to examine Treatment 30 Days After Instillation the influence of cadmium oxide on the alveolar 239PU, Only 60 ± 9.1 clearance of a highly insoluble test particle, 239pu02' 239PU2 CdO 54 ± 6.6 Simultaneously Five groups of five rats each were exposed to 239PU02 (calcined at 750°C for 2 hr) CdO 24 hr and/or cadmium oxide. The metal oxides were After mpUO, 56 ± 21 given to young adult, female, Wistar rats in 1.0 ml 0.9% NaCl by intratracheal instilla­ CdO 24 hr tion; amounts instilled were 20 Vg cadmium Before mpuO, 78 ± 6.3 oxide (MMD, 1-2 vm) and/or 10 nCi 239pu02 (AMAD, 2 ~m). The five treatments were CdO 1 wk as foll ows: Before 23gpuO, 81 ± 4.4 1) 239Pu02 given alone, 2} 239PU02 given simultaneously with CdO, It is theorized that cadmium ions inter­ fered with the phagocytosis of 239PU02 3) CdO given 24 hr prior to 239pu02, particles by alveolar macrophages (thus 4) CdO given 24 hr after 239pu02' and reducing macrophage-related clearance) since simultaneous administration of CdO 5} CdO given 1 wk prior to 239PU02' with PU02 did not decrease clearance. Rats were placed in individual metabolism Presumably, wit~ simultaneous instillations cages and excreta were collected for 30 days. of both metals, PU02 phagocytosis was largely The sum of 239pu in excreta and whole body at completed before sufficient CdO solubiliza­ 30 days after instillation was defined as the tion occurred to depress phagocytosis. instilled 239pU dose. The study is being repeated with Fischer About 60% of instilled 239pU remained in rats. Similar studies are planned with the lung 30 days after instillation. Pre­ other toxic metals, such as vanadium and vious studies have shown that the majority antimony. 117