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Risk assessments often must consider exposures that vary over time or for which the exposure duration of concern differs from the available data, and a variety of extrapolation procedures have been devised accordingly. The present experiments explore the relationship(s) between exposure concentration (C) and time (t) to investigate procedures for assessing the risks of short-term solvent exposures. The first hypothesis tested was that the product of C x t would produce a constant health effect (Haber's rule). The second hypothesis tested was that exposure conditions produce effects in proportion to the tissue concentrations created. Awake, adult, male Long-Evans (LE) rats were exposed to trichloroethylene (TCE) vapor in a head-only exposure chamber while pattern onset/offset visual evoked potentials (VEPs) were recorded. Exposure conditions were designed to provide C x t products of 0 ppm/h (0 ppm for 4 h) or 4000 ppm/h created through four exposure scenarios: 1000 ppm for 4 h; 2000 ppm for 2 h; 3000 ppm for 1.3 h; or 4000 ppm for 1h (n = 9-10/concentration). The amplitude of the VEP frequency double component (F2) was decreased significantly by exposure; this decrease was related to C but not to t or to the C x t product, indicating that Haber's rule did not hold. The mean amplitude (+/- SEM in muV) of the F2 component in the control and treatment groups measured 4.4 +/- 0.5 (0 ppm/4 h), 3.1 +/- 0.5 (1000 ppm/4 h), 3.1 +/- 0.4 (2000 ppm/2 h), 2.3 +/- 0.3 (3000 ppm/1.3 h), and 1.9 +/- 0.4 (4000 ppm/1 h). A physiologically based pharmacokinetic (PBPK) model was used to estimate the concentrations of TCE in the brain achieved during each exposure condition. The F2 amplitude of the VEP decreased monotonically as a function of the estimated peak brain concentration but was not related to the area under the curve (AUC) of the brain TCE concentration. In comparison to estimates from the PBPK model, extrapolations based on Haber's rule yielded approximately a 6-fold error in estimated exposure duration when extrapolating across only a 4-fold change in exposure concentration. These results indicate that the use of a linear form of Haber's rule will not predict accurately the risks of acute exposure to TCE, nor will an estimate of AUC of brain TCE. However, an estimate of the brain TCE concentration at the time of VEP testing predicted the effects of TCE across exposure concentrations and durations.

The negative peak occurring approximately 160 ms after stimulation (peak N160) of flash evoked potentials (FEPs) of rats changes with repeated testing. Habituation, sensitization, and arousal have all been invoked to explain these changes, but few studies have directly tested these explanations. We examined within-session changes in peak N160 amplitude with repeated testing, and the modulatory effects of stimulus intensity and auditory white noise. Peak N160 amplitude increased with daily testing (between-session changes), and was larger at greater stimulus intensities. In contrast, peak N160 amplitude underwent within-session increases on early days and within-session decreases on later days. The within-session changes were not affected by stimulus intensity. In rats previously tested in a quiet environment, exposure to acoustic white noise increased motor activity and transiently decreased peak N160 amplitude, which then increased and subsequently decreased with continued photic and acoustic stimulation. Repeated testing in the presence of noise did not alter the within-session changes in peak N160 amplitude. Heart rate showed both within- and between-session decreases, but was unaffected by noise. The data suggest that the within-session changes in peak N160 amplitude may reflect a habituation-like response to the test environment.

A frequent problem in the radiofrequency (RF) irradiation of experimental animals in health effects studies is the temporal variation of the specific absorption rate (SAR) with animal movement. An RF power controller that regulates the energy absorption rate has been designed for use with transmission line exposure systems that utilize the power difference method to monitor the SAR. The controller operates by altering the incident power to the exposure cell in order to compensate for the change in RF energy absorption rate that is due to animal motion. A circuit diagram is presented as well as experimental data under three conditions of exposure. The controller is effective in maintaining the mean value of energy absorption rate at the setpoint value even for the case of a highly active animal.

1. 1. Colonic and tail skin temperature of the unrestrained Fischer rat were measured immediately after a 90 min exposure to 600MHz radiofrequency radiation in a waveguide-type system. Ambient temperature (Ta) was maintained at either 20, 28 or 35°C. The specific absorption rate (SAR) in dimensions of W/kg was controlled at a constant level through a feedback control circuit. 2. 2. The SAR needed to elevate colonie and tail skin temperature decreased with increasing Ta. For example, a 0.5°C elevation in colonic temperature occurred at SARs of 4.3, 0.9 and 0.5 W/kg when Ta was maintained at 20, 28 and 35°C, respectively. 3. 3. Data from the present study were combined with data from earlier studies to assess the impact of varying Ta on the thermogenic effect of RF radiation in different species. In species ranging in mass from 0.02 to 3.2 kg, a double logarithmic plot of body mass versus SAR needed to elevate colonie temperature by 0.5°C was linear and inverse with a high goodness of fit (r2 = − 0.94). 4. 4. The highly correlated allometric relationship shows that, as body mass decreases, the relative impact of 7, on the thermogenic effect of RF radiation increases.

The permeability of the blood-brain barrier to high-and low-molecular-weight compounds has been measured as a function of continuous-wave (CW) and pulsed-microwave radiation. Adult rats, anesthetized with pentobarbital and injected intravenously with a mixture of [14C] sucrose and [3H] inulin, were exposed for 30 min at a specific absorption rate of 0.1 W/kg to 1.7-GHz CW and pulsed (0.5-microseconds pulse width, 1,000 pps) microwaves. After exposure, the brain was perfused and sectioned into nine regions, and the radioactivity in each region was counted. During identical exposure conditions, temperatures of rats were measured in eight of the brain regions by a thermistor probe that did not perturb the field. No change in uptake of either tracer was found in any of the eight regions as compared with those of sham-exposed animals.