Raul Harari1, Jordi Julvez2, Katsuyuki Murata3, Dana Barr4, David C. Bellinger2,5, Frodi Debes6, Philippe Grandjean2,6
1Corporación para el Desarrollo de la Producción y el Medio Ambiente Laboral, Quito, Ecuador; 2Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA; 3Division of Environmental Health Sciences, Akita University, Akita, Japan; 4National Center for Environmental Health, Centers for Disease Control and Prevention, Atlanta, Georgia, USA; 5Department of Neurology, Children’s Hospital, Boston, Massachusetts, USA; 6Department of Environmental Medicine, University of Southern Denmark, Odense, Denmark
Background: The long-term neurotoxicity risks caused by prenatal exposures to pesticides are unclear, but a previous pilot study of Ecuadorian school children suggested that blood pressure and visuospatial processing may be vulnerable.
Objectives: In northern Ecuador, where floriculture is intensive and relies on female employment, we carried out an intensive cross-sectional study to assess children’s neurobehavioral functions at 6–8 years of age.
Methods: We examined all 87 children attending two grades in the local public school with an expanded battery of neurobehavioral tests. Information on pesticide exposure during the index pregnancy was obtained from maternal interview. The children’s current pesticide exposure was assessed from the urinary excretion of organophosphate metabolites and erythrocyte acetylcholine esterase activity.
Results: Of 84 eligible participants, 35 were exposed to pesticides during pregnancy via maternal occupational exposure, and 23 had indirect exposure from paternal work. Twenty-two children had detectable current exposure irrespective of their prenatal exposure status. Only children with pre-natal exposure from maternal greenhouse work showed consistent deficits after covariate adjustment, which included stunting and socioeconomic variables. Exposure-related deficits were the strongest for motor speed (Finger Tapping Task), motor coordination (Santa Ana Form Board), visuospatial performance (Stanford-Binet Copying Test), and visual memory (Stanford-Binet Copying Recall Test). These associations corresponded to a developmental delay of 1.5–2 years. Prenatal pesticide exposure was also significantly associated with an average increase of 3.6 mmHg in systolic blood pressure and a slight decrease in body mass index of 1.1 kg/m2. Inclusion of the pilot data strengthened these results.
Conclusions: These findings support the notion that prenatal exposure to pesticides—at levels not producing adverse health outcomes in the mother—can cause lasting adverse effects on brain development in children. Pesticide exposure therefore may contribute to a “silent pandemic” of developmental neurotoxicity.