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! I I I I I I I I I I I I I I I I I ~97 AUTHOR: TALBOT, R.J., A. MORGAN, S.R. MOORES AND D.H. MATULIONIS DATE: 1987 TITLE: PRELIMINARY STUDIES OF THE INTERACTION BETWEEN ~Puo2 AND CIGARETTE SMOKE IN THE MOUSE LUNG CITATION: INT. J. RADIAT, BIOL., 51(6) 1101-1110 (1987) STUDY DESIGN; These studies were designed to show whether 12 month's exposure to ctqarette smoke enhances the incidence of lung tumours in mice that had previously inhaled Z~PuO2. Female CBA/H mice were 9-11 week old when exposed to Z~gPuO~ and smoking commenced 10 days later. In the first study, 72 mice were divided into three treatment groups at random. One group (TS) received daily smoke exposures, a second group (SS) were sham smoked and the third group were cage controls. TS mice were exposed to mainstream smoke from medium tar cigarettes diluted - 40 fold yielding an airborne concentration of TPM of about 1,2 rag/liter, Mice were exposed for two 30 rain periods, 5 days/week for 3 months. In the second study, 60 mice were given a single 1 h exposure to the aerosol of 239PuO2. At 9 days after exposure, each mouse was whole body counted in a NAI(TI)well crystal. Six mice were killed and the lungs examined. The remaining ~39PuO2 exposed mice were then divided into three treatment groups described for the first study. Smoke ex~sure commenced 10 days after exposure to ~PuO2. At 14, 21 and 49 days after the initial ~3~PuO~ exposure, three mice from each group were killed and lungs analysed for Z~gPuO2. The remaining nine mice were killed after 98 days. RNDINGS/RESULTS: This report presents the results of two preliminary 3-month studies that preceded experiments on tumour induction. The first study showed that mice could tolerate the proposed smoking regime for 3 months, with no sign of ill health. The major difference was a reduce4d growth rate in both smoke and sham exposed mice relative to cage controls. Histopathology and morphometry of lung sections found only slight smoke-induced changes. These included a reduced proportion of alveolar space and an increased number of pulmonary alveolar macrophages (PAM) per unit area. Bronchopulmonary lavage showed that PAM from smoked exposed mice were larger than those from sham-exposed or control mice and the an increased proportion of cells were binucleate. Results from the second study indicated that smoke exposure inhibited the removal of 23~pu from the lung while sham exposure had no effect. Smoke exposure also produced an increase while sham exposure a decrease in lung weights relative to those of cage controls. This was probably a results of their lower growth weight. CONCLUSIONS: These experiments confirmed that the smoking regime used was well tolerated by the mice used, with no deaths in either of the 3 month studies. It was therefore adopted for the longer term (12 month) experiments on the combined effect of 2~PuO~ and then cigarette smoke.