Harari Raul, Julvez Jordi, Murata Katsuyuki, Barr Dana, Bellinger David C, Debes Frodi, Grandjean Philippe
Corporación para el Desarrollo de la Producción y el Medio Ambiente Laboral, Quito, Ecuador.
Environ Health Perspect. 2010 Jun;118(6):890-6. doi: 10.1289/ehp.0901582. Epub 2010 Feb 25.
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.
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.
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.
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.
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.
产前接触农药所导致的长期神经毒性风险尚不清楚，但先前一项针对厄瓜多尔学龄儿童的试点研究表明，血压和视觉空间处理能力可能较为脆弱。
在厄瓜多尔北部，花卉种植密集且依赖女性就业，我们开展了一项深入的横断面研究，以评估6至8岁儿童的神经行为功能。
我们使用一套扩展的神经行为测试对当地公立学校两个年级的87名儿童进行了检查。通过产妇访谈获取了索引孕期期间农药接触的信息。从有机磷代谢物的尿排泄和红细胞乙酰胆碱酯酶活性评估儿童当前的农药接触情况。
在84名符合条件的参与者中，35名在孕期通过母亲的职业接触接触到了农药，23名通过父亲的工作间接接触。22名儿童无论产前接触状况如何，当前都有可检测到的接触。只有那些在母亲温室工作中产前接触农药的儿童在进行协变量调整（包括发育迟缓及社会经济变量）后显示出持续的缺陷。与接触相关的缺陷在运动速度（手指敲击任务）、运动协调（圣安娜形状板）、视觉空间表现（斯坦福-比奈临摹测试）和视觉记忆（斯坦福-比奈临摹回忆测试）方面最为明显。这些关联相当于发育延迟1.5至2年。产前农药接触还与收缩压平均升高3.6 mmHg以及体重指数轻微下降1.1 kg/m² 显著相关。纳入试点数据强化了这些结果。
这些发现支持了这样一种观点，即产前接触农药——在未对母亲产生不良健康后果的水平下——可对儿童大脑发育造成持久的不良影响。因此，农药接触可能促成了发育性神经毒性的“无声流行”。
