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Published on: July 16, 2009
Behavioral impairment produced by low-level postnatal PCB exposure in monkeys
1Bureau of Chemical Safety, Food Directorate, Ottawa, Ontario, Canada.
Insights
Polychlorinated biphenyls (PCBs) exposure from birth through breast milk in monkeys caused significant behavioral deficits. These findings suggest breast milk may be a critical exposure route for PCB-induced neurodevelopmental impairment.
Area of Science:
- Neuroscience
- Toxicology
- Developmental Psychology
Background:
- Human studies suggest prenatal polychlorinated biphenyl (PCB) exposure, not breast milk, causes behavioral deficits.
- A recent study indicated lower infant psychomotor scores linked to PCB concentration in breast milk.
Purpose of the Study:
- To investigate the impact of early-life exposure to a PCB congener mixture, representative of human breast milk, on primate behavior.
- To determine if PCB exposure via breast milk contributes to behavioral impairment.
Main Methods:
- Monkeys were dosed from birth to 20 weeks with a PCB congener mixture.
- Blood and fat PCB levels were measured and compared to human population ranges.
- Behavioral assessments were conducted on juvenile monkeys (2.5–5.0 years old) using various cognitive tasks.
Main Results:
- PCB-exposed monkeys exhibited significant deficits in spatial delayed alternation, fixed interval, and differential reinforcement of low rate tasks.
- Behavioral impairments included learning retardation, perseverative behavior, and impaired response inhibition.
- No group differences were found in nonspatial and spatial discrimination reversal tasks.
Conclusions:
- Early-life exposure to PCBs through a breast milk-like mixture can induce robust behavioral deficits in primates.
- These findings highlight the potential contribution of breast milk as a significant exposure route for PCB-induced neurobehavioral effects.
- The study provides evidence supporting concerns about PCB contamination in human breast milk and its impact on neurodevelopment.
Abstract:
The preponderance of evidence in humans suggests that polychlorinated biphenyl (PCB)-induced behavioral deficits result from prenatal exposure rather than exposure through breast milk, although a recent study reported lower psychomotor scores during infancy associated with PCB concentration in breast milk. In the current study, monkeys were dosed from birth to 20 weeks of age with a PCB congener mixture representative of the PCBs found in human breast milk. Blood and fat levels of PCB-exposed monkeys at the end of the dosing period were within the range observed in the general human population, while levels in control monkeys were below averages observed in humans in industrialized countries. Behavioral assessment on a series of tasks was performed when monkeys were between 2.5 and 5.0 years of age. Robust deficits were observed on spatial delayed alternation, fixed interval, and differential reinforcement of low rate performance. No group differences were observed for the number of errors on a series of nonspatial and spatial discrimination reversal tasks. Behavioral deficits included retarded learning, perseverative behavior, and inability to inhibit inappropriate responding. These results have implications for the potential contribution of exposure to PCBs through breast milk to behavioral impairment.

