Prenatal DDT exposure and child adiposity at age 12: The CHAMACOS study

Marcella Warner1, Morgan Ye1, Kim Harley1

  • 1Center for Environmental Research and Children's Health (CERCH), School of Public Health, University of California, Berkeley, CA, USA.

Environmental Research
|September 17, 2017
PubMed

Insights

Prenatal exposure to dichlorodiphenyltrichloroethane (DDT) and dichlorodiphenylethylene (DDE) was linked to increased childhood obesity risk in boys. This supports the chemical obesogen hypothesis, suggesting environmental factors influence later-life health outcomes.

Area of Science:

  • Environmental Health
  • Pediatric Endocrinology
  • Toxicology

Background:

  • The chemical obesogen hypothesis posits that certain environmental chemicals can disrupt normal metabolic processes, leading to obesity.
  • Dichlorodiphenyltrichloroethane (DDT) and its metabolite dichlorodiphenylethylene (DDE) are persistent organic pollutants with known endocrine-disrupting properties.

Purpose of the Study:

  • To investigate the association between prenatal exposure to DDT and DDE and child adiposity at age 12.
  • To explore potential sex-specific effects of in utero organochlorine pesticide exposure on childhood obesity.

Main Methods:

  • Utilized data from the Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS) birth cohort study.
  • Measured DDT and DDE concentrations in maternal serum during pregnancy and assessed child body mass index (BMI) z-scores at age 12.
  • Classified children as overweight or obese based on CDC growth charts (BMI z-score ≥ 85th percentile).

Main Results:

  • Prenatal DDT and DDE exposure was significantly associated with increased adiposity measures in boys, but not in girls.
  • A 10-fold increase in prenatal DDT and DDE concentrations correlated with higher BMI z-scores in boys.
  • Observed sex differences in the association between prenatal organochlorine exposure and adiposity persisted after accounting for pubertal status.

Conclusions:

  • Findings support the chemical obesogen hypothesis, indicating that in utero exposure to DDT and DDE may elevate obesity risk in males.
  • Highlights the potential for early-life environmental exposures to influence long-term metabolic health and disease risk.
  • Suggests a need for further research into sex-specific vulnerabilities to environmental obesogens.
Abstract