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Total Environment Assessment of Stressors Associated with Cognitive Development - A Meta Analysis
Citation:
Ruiz, J., J. Quackenboss, AND N. Tulve. Total Environment Assessment of Stressors Associated with Cognitive Development - A Meta Analysis. ISES Annual Meeting, Henderson, NV, Henderson, NV, October 18 - 22, 2015.
Impact/Purpose:
The National Exposure Research Laboratory (NERL) Human Exposure and Atmospheric Sciences Division (HEASD) conducts research in support of EPA mission to protect human health and the environment. HEASD research program supports Goal 1 (Clean Air) and Goal 4 (Healthy People) of EPA strategic plan. More specifically, our division conducts research to characterize the movement of pollutants from the source to contact with humans. Our multidisciplinary research program produces Methods, Measurements, and Models to identify relationships between and characterize processes that link source emissions, environmental concentrations, human exposures, and target-tissue dose. The impact of these tools is improved regulatory programs and policies for EPA.
Description:
Cognitive development (COGDEV) is marked by a number of critical periods during early childhood in which brain development is influenced by myriad chemical and non-chemical stressors from the built, natural, and social environments. Inherent factors and behaviors can also directly impact COGDEV or influence exposure to environmental stressors. As such, the cumulative effect of stressors a child is exposed to may be more important than the impact of a single stressor. The objective of this study was to summarize the effects of key stressors from the total environment on a child’s general cognitive score (GENCOG) through systematic review and meta-analysis. Over 100 potential stressors of GENCOG were evaluated from 258 epidemiological studies identified through a multi-database search of recent publications (2003-2013). Meta-analyses were conducted for those evaluated in two or more studies. The strongest negative stressors of GENCOG (i.e., -0.4<r<-0.3) were low birth weight, preterm birth, prenatal (PRE) stress and sleep health. Weaker negative stressors (i.e., -0.3<r<-0.1) included parity, PRE depression, PRE environmental tobacco smoke (ETS), postnatal (POST) lead, POST fluoride, and domestic violence. The strongest positive stressors of GENCOG (i.e., 0.2<r<0.3) were maternal IQ and cognitive stimulation at home. Weaker positive stressors (i.e., 0.1<r<0.2) included breastfeeding, child care, housing quality and population density. No association with GENCOG (i.e., r<0.1) was found for gender, sibling number, PRE smoking or cocaine. Evidence was inconclusive (i.e., P>0.05) for POST ETS and manganese, PRE and POST arsenic, PRE alcohol (low amounts), essential fatty acids and thyroid health due to heterogeneity across a small number of studies. In sum, we identified several stressors from the total environment that are associated with GENCOG differences. However, there is insufficientevidence to quantify cumulative effects of exposure to multiple stressors on COGDEV.
