As an integrated physical activity and nutrition intervention, the IWP has shown its strength in addressing some of the lifestyle behaviors for CVD prevention in this at-risk target population.

No abstract

Behavioral and biochemical effects of low-level whole-body inhalation exposure to the chemical warfare nerve agent cyclosarin (GF) were evaluated. Sprague-Dawley rats were first trained on a variable-interval, 56-s (VI56) schedule of food reinforcement. The VI56 schedule specifies that a single lever press, following an average interval of 56 s, produces food reinforcement (i.e., a single food pellet). Subjects were then exposed to GF vapor at concentrations of 1.6-5.2 mg/m3, or air control, for 60 min. Following exposures, performance on the VI56 and acquisition and maintenance of a radial-arm maze (RAM) spatial memory task were evaluated during 55 test sessions over approximately 11 wk. GF exposures produced miosis in all subjects and other mild clinical signs of toxicity at the highest concentration. Convulsions were not observed in any subjects. GF exposures produced concentration-dependent decreases in acetylcholinesterase and butyrylcholinesterase activity. Additionally, blood assays revealed concentration-dependent levels of regenerated GF, thus verifying systemic exposure. The largest concentration of GF disrupted performance on the VI56 task. The deficit, however, resolved by the third postexposure test session. All subjects acquired, and maintained, performance on the RAM task, and no significant differences were seen as a result of GF exposure. No delayed effects from exposures were observed. These results demonstrate that, in rats, inhalation exposure to GF at levels below those producing convulsions and other severe clinical signs of toxicity may produce performance deficits on learned behaviors, but the deficits appear to not be persistent.

To investigate cognitive and general performance effects of low-level exposure to an organophosphorus chemical warfare agents (CWA), we evaluated behavior in rats inhalation-exposed (whole body, 60 min duration) to GB (1.7 mg/m3 -4.0 mg/m3 X 1; 4.0 mg/m3 x 3) and GF (1.6-5.2 mg/m 3 X 1). Before exposure, rats were trained on a variable-interval 56 sec schedule of reinforcement (VI56), which served as a general index of behavioral performance. Beginning 48 hours after inhalation exposure, testing on the VI56 continued and acquisition of a four-of-eight, radial-arm maze task began. Performance on the maze task provided a measure of acquisition of a new task having a substantial cognitive component (i.e., spatial memory). Evaluations using both procedures were conducted during 55 sessions occurring during approximately 11 weeks following exposure. Performance deficits were observed, as a decrease in response rate, on the VI56 procedure following the highest concentrations tested of GB and GF. The deficits, however, were small and resolved relatively quickly. Small differences in the initial phases of acquisition on the maze task were observed in that some CWA-exposed rats tended to take longer to solve the maze and to make more errors. All rats, however, learned and maintained proficiency on the task. No deficits were observed to have a delayed onset. These results demonstrate that, in rats, low-level, largely asymptomatic, inhalation exposure to CWA can produce small performance deficits, but the deficits are not persistent.