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      Organophosphate Pesticide Exposure and Neurodevelopment in Young Mexican-American Children

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          Abstract

          Background

          Organophosphate (OP) pesticides are widely used in agriculture and homes. Animal studies suggest that even moderate doses are neurodevelopmental toxicants, but there are few studies in humans.

          Objectives

          We investigated the relationship of prenatal and child OP urinary metabolite levels with children’s neurodevelopment.

          Methods

          Participating children were from a longitudinal birth cohort of primarily Latino farm-worker families in California. We measured six nonspecific dialkylphosphate (DAP) metabolites in maternal and child urine as well as metabolites specific to malathion (MDA) and chlorpyrifos (TCPy) in maternal urine. We examined their association with children’s performance at 6 ( n = 396), 12 ( n = 395), and 24 ( n = 372) months of age on the Bayley Scales of Infant Development [Mental Development (MDI) and Psychomotor Development (PDI) Indices] and mother’s report on the Child Behavior Checklist (CBCL) ( n = 356).

          Results

          Generally, pregnancy DAP levels were negatively associated with MDI, but child measures were positively associated. At 24 months of age, these associations reached statistical significance [per 10-fold increase in prenatal DAPs: β = −3.5 points; 95% confidence interval (CI), −6.6 to −0.5; child DAPs: β = 2.4 points; 95% CI, 0.5 to 4.2]. Neither prenatal nor child DAPs were associated with PDI or CBCL attention problems, but both prenatal and postnatal DAPs were associated with risk of pervasive developmental disorder [per 10-fold increase in prenatal DAPs: odds ratio (OR) = 2.3, p = 0.05; child DAPs OR = 1.7, p = 0.04]. MDA and TCPy were not associated with any outcome.

          Conclusions

          We report adverse associations of prenatal DAPs with mental development and pervasive developmental problems at 24 months of age. Results should be interpreted with caution given the observed positive relationship with postnatal DAPs.

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          Most cited references 36

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            Multiple significance tests: the Bonferroni method.

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              Critical periods of vulnerability for the developing nervous system: evidence from humans and animal models.

               Greg Rice,  S Barone (2000)
              Vulnerable periods during the development of the nervous system are sensitive to environmental insults because they are dependent on the temporal and regional emergence of critical developmental processes (i.e., proliferation, migration, differentiation, synaptogenesis, myelination, and apoptosis). Evidence from numerous sources demonstrates that neural development extends from the embryonic period through adolescence. In general, the sequence of events is comparable among species, although the time scales are considerably different. Developmental exposure of animals or humans to numerous agents (e.g., X-ray irradiation, methylazoxymethanol, ethanol, lead, methyl mercury, or chlorpyrifos) demonstrates that interference with one or more of these developmental processes can lead to developmental neurotoxicity. Different behavioral domains (e.g., sensory, motor, and various cognitive functions) are subserved by different brain areas. Although there are important differences between the rodent and human brain, analogous structures can be identified. Moreover, the ontogeny of specific behaviors can be used to draw inferences regarding the maturation of specific brain structures or neural circuits in rodents and primates, including humans. Furthermore, various clinical disorders in humans (e.g., schizophrenia, dyslexia, epilepsy, and autism) may also be the result of interference with normal ontogeny of developmental processes in the nervous system. Of critical concern is the possibility that developmental exposure to neurotoxicants may result in an acceleration of age-related decline in function. This concern is compounded by the fact that developmental neurotoxicity that results in small effects can have a profound societal impact when amortized across the entire population and across the life span of humans. Images Figure 2 Figure 3 Figure 4 Figure 5 Figure 6 Figure 8 Figure 9 Figure 12 Figure 14 Figure 16 Figure 17
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                Author and article information

                Journal
                Environ Health Perspect
                Environmental Health Perspectives
                National Institute of Environmental Health Sciences
                0091-6765
                May 2007
                4 January 2007
                : 115
                : 5
                : 792-798
                Affiliations
                [1 ] Center for Children’s Environmental Health Research, School of Public Health, University of California, Berkeley, California, USA
                [2 ] National Center for Environmental Health, Centers for Disease Control and Prevention, Atlanta, Georgia, USA
                [3 ] Center for the Health Assessment of Mothers and Children of Salinas, Clinica de Salud del Valle de Salinas, Berkeley, California, USA
                Author notes
                Address correspondence to B. Eskenazi, Center for Children’s Environmental Health Research, School of Public Health, UC Berkeley, 2150 Shattuck Ave., Suite 600, Berkeley, CA 94720-7380 USA. Telephone: (510) 642-3496. Fax: (510) 642-9083 E-mail: eskenazi@ 123456berkeley.edu .

                The authors declare they have no competing financial interests.

                Article
                ehp0115-000792
                10.1289/ehp.9828
                1867968
                17520070
                This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original DOI
                Categories
                Research
                Children's Health

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