An intercomparison of whole-body counters at participating region III nuclear power plants.

Seventeen Region III nuclear stations originated and participated in an intercomparison study of their whole body counting procedures using the same calibration standard. The first phase of the study involved transporting a phantom containing four reactor-produced radionuclides and 40K to each plant. The plant staff were asked to follow all procedures applicable for a human subject including routine and investigative counts, if necessary, and to provide a printout of the results to the project investigators. The results from each plant were normalized for intercomparison by calculating the ratio of the reported activity to the actual activity after correcting for the appropriate amount of decay to the time of the count. Five plants reported 60Co values outside 1 standard deviation (SD) of the mean for 60Co and one plant did not detect the presence of 60Co. According to previously established procedures, these six plants were revisited after a period of time in which internal recalibration and corrective actions could be made. Four of the six plants had results which were still outside 1 SD of the mean for the original study. A final report in coded form to protect plant anonymity was provided to those stations to guide them in making further improvements, if they chose to do so.

Effects of chlorphentermine and nitrogen dioxide on murine alveolar macrophages.

Male Swiss-Webster mice were treated daily for 14 days with either 120 mg/kg chlorphentermine (CP) to produce pulmonary lipidosis or an equal volume of water. Animals in each treatment group were then exposed by whole-body inhalation to either air or NO2 for 48 h. Immediately following exposure, alveolar macrophages (MPs) were collected from each animal by bronchoalveolar lavage. Assays performed on adherent viable MPs showed some changes in metabolic reduction, phagocytosis, and killing activity. 5'-Nucleotidase activity and yeast phagocytosis and killing assays suggested that CP elicited an increase in phagocytosis over control levels. Although the percentage metabolic reduction and microbicidal killing activities following CP were not increased when compared to controls, absolute reduction and killing (percentage values times total MPs) were significantly increased. These increased functions seemed to be highly dependent on the large increase in the total number of MPs induced by CP. It is possible that the large accumulation of MPs in the airways of the lipidotic lung may help protect the alveolar epithelium from NO2 by quenching free radicals produced during NO2-induced lipid peroxidation.

The effect of chlorphentermine pretreatment on the toxicity of nitrogen dioxide in mice.

Chlorphentermine HCl (CP) was used to induce preexisting alveolar alterations resembling a pulmonary lipidosis in mice to study these effects on the severity and duration of nitrogen dioxide (NO2) toxicity. Results indicated that a daily dose of 120 mg/kg for 14 days produced consistent histopathologic changes characterized by an accumulation of large foamy macrophages. Male Swiss-Webster mice were divided into a control and three treatment groups. Group 1 received 120 mg/kg CP po daily for 2 weeks followed by exposure to air for 48 hr. Group 2 received 20 ppm NO2 for 48 hr via whole-body inhalation, and group 3 received 120 mg/kg CP daily for 2 weeks followed by 20 ppm NO2 for 48 hr. The fourth group served as a nontreated control and received water in place of CP and air in place of NO2. All groups were compared by morphologic evaluation of pulmonary tissues at the light and electron microscopic levels at Days 0, 1, 3, 5, and 7 after the 48-hr exposure to air or NO2. In a second experiment using the same treatment groups, thin-section light microscopy was used to count the number of type I and type II cells and macrophages. NO2 exposure alone caused deaths in 20.8 and 18.5% of the mice in the two studies, but no deaths were seen in the combination groups from both experiments. Histopathologic evaluation showed a typical cellular response to the NO2 exposure, but differences were noted between the two groups receiving NO2 on this treatment. There was increased type II cell hyperplasia and terminal bronchiolitis on Days 0 and 1 but less on Days 3 to 7 in the combination group compared to the NO2 alone group. CP treatment prior to NO2 exposure caused less terminal bronchiolar epithelial hyperplasia and less pulmonary edema than was seen in the NO2 along group. The CP treatment appeared to protect against the lethal effects of NO2 at the concentration and time of exposure used and altered the cellular repair mechanism that occurs in response to NO2 toxicity. CP treatment prior to NO2 exposure caused significantly less loss of type I cells and less increase in type II cells due to NO2 damage. The combination treatment also caused an increase in macrophages greater than that seen in either individual treatment, and this number remained increased through 5 days post-NO2 exposure, whereas the NO2 alone caused a steady increase in macrophages following the exposure until Day 3.(ABSTRACT TRUNCATED AT 400 WORDS)

Radionuclide content of and 222Rn emanation from building materials made from phosphate industry waste products.

The radionuclide content and 222Rn emanation coefficients of selected construction materials were determined. The materials were analyzed for 226Ra, 228Ra and 40K by gamma-ray spectrometry. Mineral wool insulation, which is made from Tennessee phosphate slag, and commonly used insulation, which is made from blast furnace slag, had similar concentrations of these radionuclides. Concrete blocks made with phosphate slag had enhanced 226Ra and 228Ra contents when compared to ordinary concrete block. The mineral wool insulation materials which were examined had emanation coefficients that were a few (2-6) times 10(-3). All other materials had emanation coefficients that ranged from 6 X 10(-4) to 4 X 10(-2).

Method for quantitative operant response measurement during inhalation exposure.

A method for pharmacologic and toxicologic investigation of operant responses during inhalation exposure has been developed. The method was tested with rats. Toluene was utilized as a reference chemical. Toluene has been reported to cause significant increases in response rates of animals responding under operant schedules. A fixed interval schedule (F1-120 sec) was used. A significant increase in response rate was observed. Thus, the results indicated that the method was reliable and allowed operant schedule data to be obtained. The significance of this method lies in its versatility to allow an integrative study of operant response, inhalation kinetics, and pharmacologic action. Potential practical applications of the method include studies of the actions of drugs and chemicals administered via inhalation exposure.

Effects of toluene inhalation on brain biogenic amines in the rat.

The effects of toluene exposure on the biogenic amine concentrations in the central nervous system were investigated in the rat. Toluene was administered via inhalation to groups of rats at concentrations of 0, l00, 300, or 1000 ppm. After an 8-h continuous exposure, animals were sacrificed and whole brain concentrations of dopamine (DA), norepinephrine (NE), and 5-hydroxytryptamine (5-HT) were determined. The data indicated a significant increase in whole brain concentrations of DA following the 100-ppm exposure. A regional analysis of DA, NE, and 5-HT concentrations in rats exposed to 1000 ppm of toluene for 8-h indicated a significant increase in DA concentration in the striatum. A significant increase in NE concentrations was detected in the medulla and midbrain while 5-HT concentrations were significantly increase in the cerebellum, medulla, and striatum. The results indicate that toluene action results in elevated concentrations of behaviorally significant neuro-transmitters.

The pharmacokinetics of inhaled chlorobenzene in the rat.

Male rats were exposed for 8 hr/day to 100, 400, or 700 ppm of [14C]chlorobenzene vapor for either 1 or 5 days for the purpose of examining the dose dependency of parameters indicative of the toxicity process and the effect of repeated exposure. 14C burdens in the blood, liver, kidneys, lungs, and fat were measured at 0, 16, and 48 hr after exposure. The labeled material excreted in the urine and expired air was collected for 48 hr. Analysis was performed on both the rats and total amounts eliminated. The mercapturic acid percentage of the urinary metabolites excreted in the first 24 hr was measured. The 14C burdens of all tissues increased in proportion to increased exposure concentrations, except for adipose tissue burdens, which increased more than 30-fold between 100 and 700 ppm. Respiratory elimination of 14C also increased disproportionately. The urinary metabolite profile was altered, with a dose-dependent decreased in the mercapturic acid percentage from 68% at 100 ppm to 51% at 700 ppm. Changes due to multiple versus single exposures were higher tissue burdens 48 hr after exposure, less total excretion of label, a lesser percentage of the total excreted through respiration, and a change in the rate of respiratory excretion. The dose-dependent changes are postulated to be due to saturation of the metabolic elimination of chlorobenzene. The effect of multiple exposure is apparently some stimulation of metabolism.

Deterioration of stannous ion in radiopharmaceutical kits during storage.

The deterioration of stannous ion (Sn++) in inhouse-prepared and commercial radiopharmaceutical kits was studied. Sn++ content of three types of nonlyophilized, deoxygenated, aqueous inhouse-prepared kits [diethylenetriamine pentaacetic acid (DTPA), pyrophosphate and glucoheptonate] and of three commercially prepared kits (two lyophilized pyrophosphate kits and one diphosphonate in sealed glass ampul kit) was measured by differential pulse polarography. Inhouse-prepared kits were assayed initially and after storage for 6, 12, 24 and 48 days at 24, 5 and -18 C. Commercial kits were assayed initially and after storage for 12, 24 and 48 days at 5 and 24 C. Of the inhouse-prepared kits, Sn++ stability when stored for 48 days at 5 and 24 C. Freezer storage should be used, when possible, to insure maximum stability of Sn++ in inhouse-prepared, nonlyophilized ratiopharmaceutical kits. The commercial procedures of lyophilization and of sealing the reagent in a sealed glass ampul prolong Sn++ stability.

Fetal effects of cadmium in pregnant rats on normal and zinc deficient diets.

This investigation has shown that not only the extent of fetal resoprtion and malformation but also the types of malformation seen in rats depend upon the strain used and day of gestation. Furthermore, the effects of zinc deficiency and cadmium administration on the fetus can be at least additive, as was seen for malformations. For fetal resorption, zinc deficiency potentiated the action of cadmium.