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The effects on humans of lead acetate exposure may involve the cranial nerves, since vertigo and sensory neuronal deafness have been reported in lead workers; however, there exist only a few reports concerning the dose effects of lead acetate both on the cochlea and the eighth cranial nerve. The effects of lead acetate on the cochlea and the eighth nerve were investigated systematically using cochlear microphonics (CM), whole-nerve action potential (AP), and endocochlear potential (EP) in guinea pigs (male albino Hartley). Guinea pigs were injected with 2 ml of a 1% solution of lead acetate (20 mg) once a week for 1-5 weeks. The threshold of whole-nerve AP (N1) was elevated by injection of lead acetate, even 40 mg, and whole-nerve AP (N1) output voltage decreased after injection of 100 mg of lead acetate. On the other hand, no change was observed in CM after lead acetate injection (100 mg) or in EP after lead acetate exposure (40 mg). The blood concentrations of lead acetate were as follows (mean): control, 4.5 micrograms/dl; Expt 1, 80 micrograms/dl; Expt 2, 126 micrograms/dl; Expt 3, 142 micrograms/dl. We conclude that dysfunction of the eighth nerve is induced by high-dose lead exposure, but that lead exposure does not induce electrophysiological dysfunction of the organ of Corti and the stria vascularis.

The effects of 10 mg/kg and 5 mg/kg intraperitoneally administered triethyl lead on rats were observed through measurement of the following: changes in body weight, passive aggressiveness, wheel running activity, the performance level of Rota-Rod Treadmill, and emotional responses in the open field. The results obtained were as follows: Weight losses of TEL-treated rats were recorded from 2 days after injection to 20 days after injection. Scores of passive aggressiveness were drastically increased following administration of TEL. Maximum passive aggressiveness was observed 4 days after injection and it continued until 13 days after injection. Wheel running activity was decreased for 2 days after injection. It was observed that TEL-treated rats showed extreme reaction on the wheel running activity test for about 30 days after administration. Endurance on the Rota-Rod Treadmill was significantly reduced in the 10 mg/kg group. The amount of defecation, ambulation and rearing of the treated group as measured by covariance analysis did not differ from that of the controls. The whole time course of intoxication and the precise measurement of neurotoxicity due to TEL could be followed using the techniques of behavioral toxicology.

Small doses (45-180 micrograms/g) of lead acetate were administered to male rats by gavage every day during the first 3 wk of life. A blood concentration of approximately 59 micrograms/100 ml blood produced signs of disturbances in reflex development and some changes in emotional behavior. Larger doses resulted in subtle changes in the neuromotor coordination function. The effect of low levels of lead exposure on the cognitive function in operant conditioning could not clearly be observed. Brain lead concentration tended to be higher than in other tissues examined. At approximately 10 months following cessation of lead acetate administration, the brain lead concentration had decreased to almost the same level found in control rats, and no distinguishable differences were observed between the lead-treated rats and controls in emotional behavior and neuromotor coordination.

The present study was designed to determine the critical concentrations in blood and brain associated with specific behavioural changes during and after exposure to toluene. The effects of a single four hour exposure to toluene on signalled bar press shock avoidance in rats were tested. Rats exposed to 125, 250, and 500 ppm toluene showed a decline in conditioned avoidance responses at 20 minutes exposure compared with the pre-exposure baseline, although they recovered to almost the same level of performance as that before exposure. Exposure to 1000 ppm toluene for about four hours and 2000 ppm for two hours produced a concentration related increase in incorrect responses, acceleration of the reaction time, and decreases in the effective avoidance response rate. Beginning at 4000 ppm toluene exposure, the response rate increased; thereafter, it gradually decreased and finally slight ataxia was observed. After 4000 ppm exposure, all rats showed signs of excitation such as a pronounced increase in response rate. From analysis of the temporal courses of the blood and brain toluene concentrations during and after each exposure, excitative performance decrements were noticed in rats with blood and brain concentrations about 27 micrograms/ml blood and 32 micrograms/g respectively. Anaesthetic performance decrements were seen when the blood toluene concentration increased to 120 micrograms/ml and that of the brain reached about 160 micrograms/g. According to our results, the effects on the central nervous system are considered to be a function of both the exposure concentration and its duration, which are closely related to the increase of brain and blood toluene concentration.