Pesticide exposure and stunting as independent predictors of neurobehavioral deficits in Ecuadorian school children.
OBJECTIVE
To examine possible effects on blood pressure, neurological function, and neurobehavioral tests in school-aged children with and without prenatal pesticide exposure in an area where stunting is common.


METHODS
In a community of Northern Ecuador with intensive floriculture and a high female employment rate, we invited 79 children attending the 2 lowest grades of a public school for clinical examinations. In addition to a thorough physical examination, we administered simple reaction time, Santa Ana dexterity test, Stanford-Binet copying, and Wechsler Intelligence Scale for Children-Revised Digit Spans forward. Maternal interview included detailed assessment of occupational history to determine pesticide exposure during pregnancy. Recent and current pesticide exposure was assessed by erythrocyte acetylcholine esterase activity and urinary excretion of organophosphate metabolites.


RESULTS
All eligible children participated in the study, but 7 children were excluded from data analysis due to other disease or age >9 years. A total of 31 of the remaining 72 children were classified as stunted based on their height for age. Maternal occupational history revealed that 37 children had been exposed to pesticides during development. After confounder adjustment, prenatal pesticide exposure was associated with a higher systolic blood pressure than in the controls. On neurological examination, 14 exposed children and 9 controls showed > or =1 abnormalities. Of 5 neurobehavioral tests, the Stanford-Binet copying test showed a lower drawing score for copying designs in exposed children than in controls. Stunting was associated with a lower score on this test only, and both risk factors remained statistically significant in a multiple regression analysis with adjustment for demographic and social confounders. Increased excretion of dimethyl and diethyl metabolites of organophosphates was associated with increased reaction time and no other outcomes.


CONCLUSIONS
Prenatal pesticide exposure may cause lasting neurotoxic damage and add to the adverse effects of malnutrition in developing countries. The effects differ from those due to acute pesticide exposure.
Grandjean
Philippe
P
Institute of Public Health, University of Southern Denmark, Odense, Denmark. pgrand@hsph.harvard.edu
Harari
Raul
R
Barr
Dana B
DB
Debes
Frodi
F
D001794:Blood Pressure; D002648:Child; D002657:Child Development; D004484:Ecuador; D005260:Female; D006130:Growth Disorders / Q000139:chemically induced*; D006801:Humans; D007360:Intelligence; D008297:Male; D009483:Neuropsychological Tests; D016273:Occupational Exposure; D010575:Pesticides / Q000009:adverse effects*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D011597:Psychomotor Performance
D010575:Pesticides