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ToxSci Advance Access published online on July 10, 2007
Toxicological Sciences, doi:10.1093/toxsci/kfm172
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Published by Oxford University Press 2007.

Acute Toluene Exposure and Rat Visual Function in Proportion to Momentary Brain Concentration

William K. Boyes*, Mark Bercegeay*, Q. Todd Krantz{dagger}, Elaina M. Kenyon{dagger}, Ambuja S. Bale*, Timothy J. Shafer*, Philip J. Bushnell* and Vernon A. Benignus{ddagger}

* Neurotoxicology Division {dagger} Experimental Toxicology Division {ddagger} Human Studies Division, National Health and Environmental Effects Research Laboratory, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina

Address for correspondence and reprints: William K. Boyes, B105-05, Neurotoxicology Division, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711, Telephone: 919-541-7538, Fax: 919-541-4849, Email: boyes.william{at}epa.gov

Received May 9, 2007; revision received July 3, 2007; accepted July 3, 2007


  Abstract

Acute exposure to toluene was assessed in two experiments to determine the relationship between brain toluene concentration and changes in neurophysiological function. The concentration of toluene in brain tissue at the time of assessment was estimated using a physiologically-based pharmacokinetic (PBPK) model. Brain neurophysiological function was measured using pattern-elicited visual evoked potentials (VEP) recorded from electrodes located over visual cortex of adult male Long-Evans rats. In the first experiment, VEPs were recorded before and during exposure to control air or toluene at 1000 ppm for 4 hr, 2000 ppm for 2 hr, 3000 ppm for 1.3 hr, or 4000 ppm for 1 hr. In the second experiment, VEPs were recorded during and after exposure to clean air or 3000 or 4000 ppm toluene. In both experiments, the response amplitude of the major spectral component of the VEP (F2 at twice the stimulus rate in steady state responses) was reduced by toluene. A logistic function was fit to baseline-adjusted F2 amplitudes from the first experiment that described a significant relationship between brain toluene concentration and VEP amplitude deficits. In the second experiment, 3000 ppm caused equivalent VEP deficits during or after exposure as a function of estimated brain concentration, but 4000 ppm showed a rapid partial adaptation to the acute effects of toluene after exposure. In general, however, the neurophysiological deficits caused by acute toluene exposure could be described by estimates of the momentary concentration of toluene in the brain at the time of VEP evaluation.

Key Words: neurotoxicity; PBPK model; volatile organic compound; organic solvent; visual evoked potential.


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W. K. Boyes, M. Bercegeay, W. M. Oshiro, Q. T. Krantz, E. M. Kenyon, P. J. Bushnell, and V. A. Benignus
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[Abstract] [Full Text] [PDF]


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