Artificial Food Color Additives and Child Behavior

A 15 Landrigan PJ, Goldman LR. 2011. Children's vulnerability to toxic chemicals: a challenge and opportunity to strengthen health and environmental policy. Hunt PA, et al. 2011. Similarity of bisphenol A pharmaco-kinetics in rhesus monkeys and mice: relevance for human exposure. Environ Health Perspect 119:422–430. vom Saal FS, Hughes C. 2005. An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment. We agree with Schwartz and Landrigan that there is a need for change in the regulatory system for chemicals used in products in the United States. Bisphenol A (BPA) is one of thousands of chemicals of concern, but it provides a striking example of what happens when there is no requirement for premarket testing. Full estrogenic activity was demonstrated for BPA when it was tested for use as a pharmaceutical drug in 1936, which should have precluded its use in the wide range of products that results in continuous exposure (Stahlhut et al. 2009). The findings we reported in our article (Taylor et al. 2011) show that clearance of BPA in mice, monkeys, and humans does not differ, and years of research has demonstrated that mice and rats are valid models for predicting the long-term adverse consequences of developmental exposure to estrogenic chemicals. A vast and rapidly growing number of studies with experi mental animals (Richter et al. 2007) and humans (Braun and Hauser 2011) report adverse effects later in life as a result of exposure to BPA during development. study, the Centers for Disease Control and Prevention estimated that 93% of people in the United States are exposed to BPA, with higher exposures in children than adults. The potential exposure of fetuses and infants to BPA is especially concerning because BPA is not metabolized effectively during these highly sensitive stages of human development. Our data (Taylor et al. 2011) indicate that to reach the median serum levels of unconjugated (bioactive) BPA reported in multiple biomonitoring studies (Vandenberg et al. 2010), exposure must be far higher than predicted by the Food and Drug Administration (FDA) based on its risk assessment of BPA (FDA 2008); these govern ment estimates (FDA 2008) are based on kinetics after acute oral exposure and the assumption that food and beverage packaging is the only source of BPA exposure. However, data from the 2003–2004 NHANES (Stahlhut et al. 2009) confirmed that BPA exposure is likely to be …