Rice D C, Hayward S
Toxicology Research Division, Bureau of Chemical Safety, Food Directorate Health Protection Branch, Health Canada, Ottawa, Ontario.
Neurotoxicol Teratol. 1999 Jan-Feb;21(1):47-58. doi: 10.1016/s0892-0362(98)00032-4.
Behavioral impairment as a consequence of PCB exposure beginning in utero has been reported in both humans and animals. The present study assessed the behavioral consequences of postnatal exposure to PCBs. Male monkeys (Macaca fascicularis) were dosed from birth to 20 weeks of age with 7.5 microg/kg/day of a PCB mixture representative of the PCBs typically found in human breast milk (eight monkeys) or vehicle (four monkeys). Blood PCB levels at 20 weeks of age were 0.30-0.37 ppb for control and 1.84-2.84 ppb for treated monkeys, and fat levels were 50-198 and 1694-3560 ppb for the two groups, respectively. Beginning at about 5.0 years of age, monkeys performed under concurrent schedules of reinforcement in which separate random intervals were in effect on two buttons independently. After steady-state performance was reached, the relative reinforcement ratio on the buttons was changed a total of four times, and performance both during transition and steady state was examined. There was no evidence for treatment-related differences in performance across the series of changes in schedule contingencies. The negative results failed to support the hypothesis that performance on an intermittent schedule, combined with the requirement for shifting response strategy, would prove particularly sensitive to postnatal PCB exposure. Following the concurrent schedules, monkeys were tested under a progressive ratio (PR) schedule preceded by a training procedure consisting of a within-session series of increasing fixed ratios. PCB-treated monkeys emitted more responses than controls over the first few sessions of the PR, which may be indicative of retarded acquisition of their steady-state PR performance. These results extend previous studies in these monkeys on the characterization of PCB-induced behavioral deficits.
已有报道称,子宫内开始接触多氯联苯会导致人类和动物出现行为障碍。本研究评估了出生后接触多氯联苯的行为后果。雄性食蟹猴从出生到20周龄,每天接受7.5微克/千克的多氯联苯混合物剂量,该混合物代表了人类母乳中通常发现的多氯联苯(8只猴子),或接受赋形剂处理(4只猴子)。20周龄时,对照组猴子的血液多氯联苯水平为0.30 - 0.37 ppb,处理组猴子为1.84 - 2.84 ppb;两组的脂肪水平分别为50 - 198 ppb和1694 - 3560 ppb。从大约5.0岁开始,猴子在并发强化程序下进行操作,其中两个按钮分别独立设置随机间隔。达到稳态表现后,按钮上的相对强化比率总共改变了四次,并检查了过渡期间和稳态期间的表现。在一系列计划突发事件变化中,没有证据表明处理相关的表现存在差异。这些负面结果未能支持以下假设:间歇计划下的表现,加上转换反应策略的要求,会被证明对出生后接触多氯联苯特别敏感。在并发程序之后,猴子在累进比率(PR)程序下接受测试,之前有一个训练程序,包括一系列在会话内增加固定比率的操作。在PR的前几个会话中,多氯联苯处理的猴子比对照组发出更多反应,这可能表明它们的稳态PR表现的习得延迟。这些结果扩展了之前对这些猴子进行的关于多氯联苯诱导行为缺陷特征的研究。