A simplified compartment model indicated that fat styrene content might be used as an index of the whole body styrene burden. Intermittent exposure of adult male rats to 300 ppm 5 d a week, 6 h daily for 1 to 11 weeks showed an initial steady increase in the fat styrene content up to the 4th week and an exponential decrease thereafter. This phenomenon might have resulted from the enhancement of styrene oxidation due to the prolonged exposure. The effect of the increased oxidation on the body styrene burden is theoretically doubled after 9.1 weeks of exposure. Neurochemical effects after that time might have resulted from an increased binding of styrene oxide in the cellular macromolecules, e.g., to their sulfhydryl groups. The activity of the metabolite towards the cellular constituents could very well explain the increased proteolysis possibly caused by lysosomal labilization. The present data also lend support to the theory of the importance of metabolic activation to styrene and other solvent toxicity.

Key terms accumulation; inhalation exposure; long-term exposure; long-term inhalation exposure; metabolic activation; neurochemical effect; rat; styrene; styrene monomer; styreno oxid