PCBs, DDE, and child development at 18 and 24 months
1Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709.
Insights
Perinatal exposure to polychlorinated biphenyls (PCBs) may delay child motor development. This study found lower psychomotor scores in infants with high transplacental PCB exposure, detectable up to 24 months.
Area of Science:
- Environmental Health
- Developmental Pediatrics
- Toxicology
Background:
- Background exposure to environmental pollutants like polychlorinated biphenyls (PCBs) and dichlorodiphenyldichloroethene (DDE) is common.
- Understanding the impact of these exposures on early child development is crucial for public health.
Purpose of the Study:
- To investigate the effects of perinatal exposure to background levels of PCBs and DDE on child development up to two years of age.
- To assess the impact of exposure routes, including transplacental and breast milk pathways.
Main Methods:
- A cohort of children was followed to age two years.
- Bayley Scales of Infant Development were administered at 18 and 24 months.
- Transplacental and cumulative breast milk exposures to PCBs and DDE were estimated via sample analysis.
Main Results:
- Children in the highest percentile of transplacental PCB exposure showed significantly lower psychomotor scores at 24 months (4-9 points).
- No consistent effects were observed from PCB exposure via breast milk or from DDE exposure.
- The motor maturation delay linked to transplacental PCBs was evident at 24 months.
Conclusions:
- Transplacental exposure to PCBs is associated with a slight delay in motor maturation in children, persisting to 24 months.
- Exposure to PCBs via breast milk did not show a clear effect by age two, but later effects cannot be ruled out.
- DDE exposure did not demonstrate a significant impact on child development in this cohort.
Abstract:
To determine whether perinatal exposure to "background" levels of polychlorinated biphenyls (PCBs) or dichlorodiphenyldichloroethene (DDE) affected child development, we followed a cohort of children through the age of 2 years; 676 were tested at 18 months and 670 at 24 months with the Bayley Scales. Transplacental and cumulative exposures from breast milk to both chemicals were estimated for each child from analyses of breast milk and other samples. Bayley testing was done without knowing the chemical levels. At 18 and 24 months, adjusted scores on the psychomotor scales were 4 to 9 points lower among children in the top fifth percentile of transplacental PCB exposure, significantly so at 24 months. There were no consistent effects apparent from exposure to PCBs through breast milk, nor from DDE exposure. We conclude that there is a small delay in motor maturation attributable to transplacental exposure to PCBs that is still detectable at 24 months. There is no evidence of an effect from the larger but later exposure through breast milk, although effects may emerge as the children age.
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