Calibration of position and angular data from a magnetic tracking device.

This paper describes a method for calibrating data from a magnetic tracking device. Position and orientation data were collected in a 1. 6x0.8x1.4m(3) volume using a Polhemus Fastrak((R)) in conjunction with both a long-range and standard transmitter. Position and orientation data were calibrated using a locally linear model based on the position of the measurement. After calibration, the average position and angular errors were less than 1.8cm and 1.2 degrees up to 1.8m from the transmitter for the long-range transmitter. For the standard transmitter, even after calibration, errors increased sharply when the sensor was more than 1.2m from the transmitter. Up to that distance, post-calibration errors were less than 1.2cm and 1. 2 degrees, while up to 1.8m they were below 5cm and 4 degrees. These errors could be further reduced by noise filtering. However, use of the standard transmitter is not recommended at distance greater than 1.2m due to orientation-based effects. It was concluded that for the volume investigated, tracking devices could provide similar three-dimensional accuracy to video systems.

Evaluation of a long-range transmitter for use with a magnetic tracking device in motion analysis.

The suitability of a long-range transmitter was evaluated for use with a Polhemus Fastrak magnetic tracking device in kinesiologic studies. Performance was judged by comparing positional and rotational accuracy to a standard transmitter. Data were obtained at distances of up to 2.7 and 5.0 m for the standard and long-range transmitters, respectively. Use of the long-range transmitter improved system performance allowing reproducible measurements at a greater distance. However, it is necessary to calibrate the system in each new test environment as there can be significant distortion of the magnetic field.

Cancer risk assessment with intermittent exposure.

Applications of methods for carcinogenic risk assessment often focus on estimating lifetime cancer risk. With intermittent or time-dependent exposures, lifetime risk is often approximated on the basis of a lifetime average daily dose (LADD). In this article, we show that there exists a lifetime equivalent constant dose (LECD) which leads to the same lifetime risk as the actual time-dependent exposure pattern. The ratio C = LECD/LADD then provides a measure of accuracy of risk estimates based on the LADD, as well as a basis for correcting such estimates. Theoretical results derived under the classical multistage model and the two-stage birth-death-mutation model suggest that the maximum value of C, which represents the factor by which the LADD may lead to underestimates of risk, will often lie in the range of 2- to 5-fold. The practical application of these results is illustrated in the case of astronauts subjected to relatively short-term exposure to volatile organics in a closed space station environment, and in the case of the ingestion of pesticide residues in food where consumption patterns vary with age.

Carcinogenic risk assessment with time-dependent exposure patterns.

Previous applications of carcinogenic risk assessment using mathematical models of carcinogenesis have focused largely on the case where the level of exposure remains constant over time. In many situations, however, the dose of the carcinogen varies with time. In this paper, we discuss both the classical Armitage-Doll multistage model and the Moolgavkar-Venzon-Knudson two-stage birth-death-mutation model with time-dependent dosing regimens. Bounds on the degree of underestimation of risk that can occur through the use of a simple time-weighted average dose are derived by means of comparison with an equivalent constant dose corresponding to the actual risk under the time-dependent dosing regimen.

Tissue distribution and elimination of trichlorobenzenes in the rat.

The tissue distribution and excretion of three trichlorobenzene isomers (TCB) were investigated in the rat. Single doses of TCBs were administered orally to groups of 5 fasted rats at 10 mg/kg body weight. Serial sacrifices were carried out and the radioactivity contents were determined in tissues and blood. For all three TCB isomers, radioactivity appeared in the blood and tissues at 0.5 h, and peaked around 2-4 h after dosing. Fat, skin, and liver had high concentrations of the parent compound while kidney and muscle had high levels of metabolites. Elimination of TCB from tissues and blood can best be described by a two-compartmental open pharmacokinetic model. The terminal half-lives were 145, 93 and 68 h for 1,2,3-, 1,2,4 and 1,3,5-TCB isomer respectively. Ninety-five percent of the administered 1,2,3- and 89% of the 1,3,5-isomers were eliminated within 48 h in the urine and feces with the former being the major route.